bunrab: (Default)
Sodium, Potassium Intake Tied to Heart Disease
Study finds 24% greater risk per unit increase in salt-to-mineral ratio
MONDAY, Jan. 12 (HealthDay News) -- Too much sodium and too little potassium in one's diet may increase one's risk of cardiovascular disease, a new study suggests.

The findings, based on a long-term analysis by the U.S. National Heart, Lung, and Blood Institute of almost 3,000 people with pre-hypertension, also suggests that increasing potassium consumption along with the common wisdom of lowering one's salt intake may reverse the risk.

Researchers found that for people with high normal blood pressure levels (120 to 139/80 to 89 mmHg), every unit increase in the person's sodium-to-potassium ratio raised his or her chance of cardiovascular disease by 24 percent.

The findings were published in the Jan. 12 issue of the Archives of Internal Medicine.
bunrab: (heart)
Viagra May Shield Heart From Blood Pressure Damage
Sildenafil appears to delay dangerous heart muscle expansion in mice
MONDAY, Jan. 5 (HealthDay News) -- Tests in mouse hearts show that sildenafil, the key ingredient in Viagra, may shield hearts from damage caused by high blood pressure, a new study suggests.

Investigators said that sildenafil appears to influence RGS2, a single protein essential in the reactions that initially protect the heart's blood-pumping function from spiraling into heart failure. The findings, published online Monday in The Journal of Clinical Investigation, suggest that sildenafil may prove useful in the treatment or prevention of heart damage due to chronic high blood pressure.

"Sildenafil clearly prolongs the protective effects of RGS2 in mouse hearts," senior investigator Dr. David Kass, a cardiologist and professor of medicine at the Johns Hopkins University School of Medicine and its Heart and Vascular Institute in Baltimore, said in a Hopkins news release.

After a week of inducing high blood pressure in the mice, the team found that the hearts engineered to lack RGS2, or regulator of G-protein signaling 2, expanded in weight by 90 percent, and almost half of the experiment animals died of heart failure. In the mice with RGS2, the dangerous muscle expansion, known as hypertrophy, was delayed, growing by only 30 percent, the researchers found, and none of those mice died.

Later testing showed that treating hypertensive mice that had RGS2 with sildenafil showed enhanced buffering, less hypertrophy, and stronger heart muscle contraction and relaxation. In addition, these mice showed as much as 10 times lower stress-related enzyme activity compared to their untreated counterparts. The study also found that sildenafil had no effect in mice lacking RGS2.

The study involved more than a half-dozen experiments, all performed within the last three years, designed to zero in on RGS2's role in stalling hypertrophy.

"The evidence is piling up that unbridled Gq signaling is driving a central biological chain reaction in heart failure, and that by extending the protective effects of RGS2 or by developing a test for its presence, researchers can develop new therapies or improve existing ones, including ACE inhibitors and possibly sildenafil, for people with heart failure who will benefit most," Kass said.

Doctors currently use so-called ACE inhibitor and ARB inhibitor drugs to block Gq signaling. These drugs are the most common treatment for heart failure, which afflicts more than 5 million Americans each year, killing more than a quarter million of them, according to the study.
bunrab: (Default)
From Health Day News:
A new genetic cause of enlarged heart has been identified by an international team of scientists, who said their finding could lead to new treatments.

In research with rodents and humans, the scientists found that the gene osteoglycin (Ogn) regulates the growth of the heart's left ventricle, it's main pumping chamber. When Ogn behaves abnormally, the heart can become enlarged, BBC News reported.

The study appears in the journal Nature Genetics.

It was already known that irregular heart growth can be caused by obesity, high blood pressure and strenuous exercise, but the influence of genes is largely unknown, BBC News reported.

"But, now that we are unraveling how genes control heart growth, we can gain a better understanding of common forms of heart disease. This could lead to new and more effective ways of treating people," said researcher Dr. Stuart Cook.
bunrab: (Default)
As I've mentioned before, I get a weekly summary of articles from Medscape Pharmacy. This article is from this week's; I've reprinted the abstract here, but not the whole article.
From Pharmacotherapy

Controversy and Conflict in the Treatment of Acute Decompensated Heart Failure: Limited Role for Nesiritide

John A. Noviasky, Pharm.D.
Abstract

The use of nesiritide for acute decompensated heart failure (ADHF) has been clouded with controversy since its approval in 2001. Extensive marketing and many review articles have established this drug as a safe and superior product to current standards. However, its safety has been called into question by the results of a meta-analysis, and its superiority of important outcomes (length of stay, mortality, decreased readmission rate) has never been proved by a randomized trial against agents with similar vasodilator properties (e.g., nitroglycerin). A review of the available literature on nesiritide in the areas of mortality, renal effects, retrospective studies, use in off-label indications, length of stay, and mortality is presented and illustrates why its use should be limited or even eliminated. After review of this article, the reader should be able to answer the question—if nesiritide had never been approved for use in patients with ADHF, would we have missed it?—with a negative reply.



The gist of the whole article is, neseritide appears to increase mortality, rather than decrease it. This includes results from a study done *by the manufacturer* of the drug.

What I wonder is, if all the preliminary studies showed that it was safe and effective, how does it happen now that all the after-approval studies show either no statistically significant effect whatsoever compared to other drugs used for the same purpose (that is, it's no better than older treatments), or else a slight negative effect? Thaat's a rhetorical question, by the way, as we already know that there are a lot of problems with the pharmaceutical approval process in the USA, and that our government agencies are far too heavily influenced by Big Pharma money. The article itself answers the question, pointing out the manufacturer's aggressive marketing campaign, which included a "guide" for hospitals on how billing Medicare for this drug could be more profitable for the hospital than other drugs. 

The EU has not approved this drug, and probably won't, according to the article.
bunrab: (Default)

One of the sites I'm registered at is MedScape from WebMD, and specifically I signed up for their pharmacists' newsletter. If one carefully reads the fine print, one does not have to be a medical professional to register for these sites. So, here's a link to the article, for those who would care to register at MedScape and get the news on a current basis. They don't seem to sell their list nor spam their subscribers with stuff, just the newsletter on a regular basis.

For those who can't register, here's the highlights of the article, which was originally published in the journal Pharmacotherapy, V. 27 No. 4:

bunrab: (Default)
Okay, I think I have most of the entries bagged and tagged - that is, I've cleaned up the crap code, added keywords/tags, and got 'em pretty much in date order. One thing I've noticed as I went through them - I sure do have a lot of ice cream recipes! Anyway, here's a bunch of stuff I've been wanting to post for the last couple months:
bunrab: (Default)

Thursday, December 14, 2006

Easy recipe time!
Roasted Winter Vegetables
1 bag "Golden Nugget" or other fingerling (tiny) potatoes
1 bag pearl onions
1 sweet potato
1 butternut squash
1 bag parsnips (giant white carrots)
optional: 1 small box brussels sprouts, if you're not a supertaster who hates them
olive oil
fresh rosemary
fresh thyme

Scrub the potatoes, but you don't have to peel them. Peel the outer layer off the onions. Peel the sweet potato and cut it into 1" cubes. Peel the butternut squash and cut it into 1" cubes. Scrub and peel the parsnips, cutting off the tops, and cut them into 2" long segments at the thin end, 1" long segments at the thick end. Remove any wilted leaves from the brussels sprouts.

Place all the veggies in a large baking dish or casserole dish. Bloop a few tablespoons of olive oil over them, and toss till everything has a very slight touch of olive oil on it. Now strip the leaves from 4-5 branches of rosemary, and from 4-5 branches of thyme, and sprinkle them over the veggies. Toss the veggies again, so that the herbs are distributed throughout. Roast, uncovered, in a 350° to 375° F oven for about one hour, or until a fork stuck in a potato or cube of sweet potato goes in easily. Serve hot. This makes a lot - 8 people or so's worth - so if there are leftovers, they taste just fine rewarmed the next day.

The even easier version of this recipe:
Instead of all those kinds of veggies, just get one bag of the Golden Nugget potatoes and one bag of some other kind of tiny potatoes - "new potatoes" or "fingerlings" or anything else where each potato is only golf-ball size. Do the same bit with the olive oil and the herbs. But you don't have to do all that peeling and cutting. Same baking instructions.
This week's article:
Magnets may interfere with pacemakers and ICDs
Dec 08 (HealthCentersOnline) - Certain types of magnets that are becoming increasingly popular in clothing and jewelry may interfere with the function of pacemakers and other implanted cardiac devices, according to new research.
Implanted in the chest, pacemakers and implantable cardiac defibrillators (ICD) are two types of battery-powered devices that monitor and, if necessary, correct an abnormal heart rhythm by sending electrical charges to the heart.

Researchers in Europe recently evaluated several types of magnets to see if they were capable of interfering with pacemakers and ICDs that had been implanted in patients.

The study found that while traditional magnets commonly found in the home and office are not dangerous, other types of magnets can be. Specifically, the research found that powerful magnets made from neodymium-iron-boron (NdFeB) are capable of interfering with cardiac devices implanted in the chest.

NdFeB magnets are becoming increasingly popular in office products, toys, jewelry and some clothing. Because of this, the researchers urge the manufacturers of the magnets to place warning labels on their products.

The study included 70 patients, 41 with pacemakers and 29 with ICDs. Each of the patients was tested with two spherical magnets that were 8 and 10 millimeters in diameter, as well as a necklace made of 45 spherical magnets. In every instance, the magnets interfered with the implanted heart devices of the patients. After the magnets were removed, the devices all resumed their normal function.

"Physicians should caution patients about the risks associated with these magnets. We also recommend that the packaging include information on the potential risks that may be associated with these types of magnets," explained Thomas Wolber, a cardiologist at the University Hospital of Zurich in Switzerland and lead author of the study, in a recent press release.

The results of the study were published in the December 2006 issue of the journal Heart Rhythm.
This week's article:
Possible cause found for deadly rapid heartbeats
Nov 30 (HealthCentersOnline) - A recent study may help researchers to better understand the mechanism involved in a certain type of heart failure.
Heart failure is a chronic condition in which at least one chamber of the heart is not pumping well enough to meet the body's needs. This leads to congestion in the lungs or pulmonary blood vessels and may cause fluid backup or swelling in the lungs, legs and ankles.

Ventricular tachyarrhythmia is a type of tachycardia, or abnormally rapid heart rate, that originates in the lower chambers (ventricles) of the heart. Ventricular tachyarrhythmia can lead to ventricular fibrillation and/or heart failure.

Researchers from Germany may have found an explanation for why ventricular tachyarrhythmia occurs in some instances. Using mice and heart muscle cells from rabbits, the researchers were able to find a possible molecular reason for the abnormal heartbeats.

The study showed that a substance known as an "effector" for a protein called calmodulin may be improperly regulating the influx of sodium ions into the muscle of the heart. Previous research has shown that genetic problems with the regulation of the sodium ion influx puts a person at increased risk for ventricular tachyarrhythmia.

The researchers suspect that the disruption observed during the study may be a contributing factor to the onset of dangerous ventricular tachyarrhythmias that are associated with heart failure.

The results of the report were published online on November 22 in advance of its print publication in the December issue of the Journal of Clinical Investigation.
bunrab: (Default)

Thursday, November 23, 2006

This week's article:
Blood pressure may help predict heart failure risk
 
posted by Kelly : 11:38 PM  

Friday, November 17, 2006

My local newspaper (the Baltimore Sun) had an article a few days ago entitled "Working on MRIs that are safe for pacemakers." Subhead: "Patients with heart implants may be able to undergo diagnostic scanning procedure."

The article was cautiously optimistic; a study of the first pacemaker designed to withstand MRIs is scheduled to start at the end of this year. However, the article doesn't say whether this study applies to ICDs, or just plain pacemakers, and it doesn't make it completely clear whether the difference between ICDs and plain pacemakers matters for these purposes.

MRIs are used, among other things, to detect cancers.

Wednesday, November 15, 2006

Three magazines that might be useful (put 'em on your wish list for Chanukah/Christmas/Solstice/Festivus):

First off, strange as it may sound, I find the magazine Diabetic Living to be very useful for someone with heart failure. Many, many of the health concerns are the same for the two chronic illnesses, including the need to watch one's weight, to get regular medical care, to be very careful in evaluating proposed treatments (especially new ones). Plus, the magazine makes a very strong effort to make all its recipes low-sodium, or at least lower-sodium, as well as low-fat and low-sugar. I've gotten several excellent recipes out of there that suited me (low-sodium diet), my dad (diagnosed as diabetic a couple years ago at age 80, and also had a heart attack a year ago) and my spouse (borderline high cholesterol). The one catch to this magazine for CHF patients is that you may want to buy it off the magazine racks in the drug store or supermarket rather than subscribe, because if you subscribe, you'll get all kinds of bulk mail advertising assorted diabetic supplies you don't need. I buy it at CVS; most national drug store chains carry it and I've seen it in Safeway supermarkets. Diabetic Living

Prevention, put out by Rodale: this one's aimed at health in general. It used to be a bit flaky - Rodale publishes a lot of stuff having to do with alternative medicine and living lifestyles that tend toward the green/off-the-grid/deeply-into-yoga stuff. And they used to be completely uncritical about alternative medicine and all sorts of supplements. However, the past few years, they have tempered it a bit toward the real world, and they do more critical evaluations of the usefulness of alternative treatments, and offer lots of helpful advice for people undergoing any kind of medical care, as well as offering a lot of ways to live a healthier lifestyle. Many of their recipes use reduced-sodium ingredients, and are pretty healthy. Prevention

Science News, a weekly newsmagazine that offers 12 pages or so of very short articles about the latest in medicine and science. Although they emphasize science in their title, they give summaries of a lot of medical news, and any time there's a national meeting of one of the big medical associations, such as the American College of Cardiology, they have an entire page with summaries of half a dozen or so of the most important papers presented at the meeting. Intended for the regular educated person, not highly technical but the editors assume you are familiar with at least the general vocabulary of science. Science News

This week's news article:
Pump, with drugs, can reverse heart failure 
posted by Kelly : 11:04 PM  
bunrab: (Default)

Thursday, October 26, 2006

An article from a few weeks ago:
Stomach acid drug may slow heart failure

Sep 26 (Reuters Health) - Treatment with famotidine, which is sold under the names Pepcid and Fluxid as a stomach acid blocker, appears to improve the symptoms occur with chronic heart failure, new research shows.
Famotidine blocks histamine receptors that exist on gastric cells, and this decreases stomach acid production. However, these receptors also exist in heart muscle cells, so Dr. Masafumi Kitakaze and colleagues thought famotidine could benefit people with heart failure.

To investigate, Kitakaze, at the National Cardiovascular Center in Suita, Japan, and colleagues compared cardiac symptoms and function in heart failure patients who were treated with famotidine or with a different type of acid blocker for reflux disease or gastritis.

As they report in the Journal of the American College of Cardiology, the researchers found that famotidine therapy had a beneficial effect on the function of the main pumping chamber of the heart. Moreover, treatment with famotidine seemed to dramatically reduce hospital readmission rates for worsening heart failure.

In a statement, Dr. Gary S. Francis, a cardiologist at the Cleveland Clinic and co-author of a related editorial, sounded a caution: "I certainly would not recommend that patients go out and start taking Pepcid three times a day or anything like that."
SOURCE: Journal of the American College of Cardiology, October 3, 2006.

Monday, October 23, 2006

Hey, did I tell you that my new ICD fired up only 5 days after I got it put in? At the data dump* a couple days later, it showed my fibrillation at about 300 beats per minute, and the doc swears I wouldn't have been sitting there talking to him without this ICD. Odd, though, since the previous ICD had not fired in 2.5 years... We have to wonder a bit if the surgery perhaps acted in some sort of catalytic way to make things a bit worse, even while providing a fix for them.

*Data dump being more formally known as interrogation, carried out by means of telemetry.

It feels odd - not the big thwack in the chest I was expecting from the tests on the previous ICD, but instead just an odd electrical fizzy feeling, as though a small automobile fuse had shorted, and a few sparklies in front of my eyes. Very mild feeling, didn't knock me over, let alone out, but it was a real incident, the telemetry says so!


It may have fired again this past morning, I'm not sure; my next data dump isn't for another 2 months, and unless it fires repeatedly in a short period, one doesn't call the doctor for just one incident.


Well, I've just been busy. Busier than I should be, perhaps - we had houseguests for a weekend, and between the clean-up before-hand, the staying up late talking, and the running around doing stuff, I was wiped out - pretty much slept straight through afterwards, waking up only briefly for lunch and dinner the next day. My sleep schedule is still a bit rocky after that.

On the bright side, my 6 weeks is up since the surgery, so I can now raise my right arm above shoulder level, and carry my saxophone, and get back on the motorcycle. I hadn't been able to put on t-shirts for the 6 weeks - it is possible, though difficult, to get a t-shirt ON without raising one's arm above the head, but it is completely impossible to get a t-shirt OFF without doing so.

The scar is still sort of odd - a very pronounced ridge, although at least it doesn't have the strange tuck under it any more - but the week or so that it took that tuck to loosen up and flatten out some was quite some pain. A great deal of nerve pain, under the shoulder and radiating out along the right arm, feeling like I was being stabbed with daggers. Not fun. But that's gone now. I wish doctors were better about warning one about that sort of thing!!

bunrab: (Default)

Tuesday, July 25, 2006

This week's article:

Thursday, July 20, 2006

Well, the stress echo shows that my ventricles are discordant - one side blobs OUT when it should be squeezing in; when I exercise, my EF DROPS from 20% down to the 10-15% range. (In the middle of the walk, my blood pressure started dropping because of this. Apparently, this is significantly abnormal enough to wind the test down early.) The bi-ventricular pacemaker would definitely be at least a partial fix for this, if they could get that bi-v lead in, and it looks like it would be worth a third try at it. So, my cardiologist called another EP (electrophysiologist, the pacemaker surgeon) and I go in to see him in a few weeks, and we discuss what we'd need to do to make sure that a third try at putting in a third lead would not be a complete waste of time and money; what can he do differently to avoid the stuff the other EPs ran into? Since the new pacemaker would need to go in a different spot, because the old location is all scar tissue now, where, precisely, would we put it? (And if I was freaking out airline security before, having a pacemaker when I'm not a little old lady, imagine if I have a pacemaker in some spot other than the upper left thorax!) And a few other questions. But anyway, there's no question but that my heart needs the help.

I asked Dr. G, "Why don't people just believe me when I TELL them I get really tired when I walk?" (This is sort of a running thing, because every cardiologist I've ever seen says things like "Oh, you've got to walk more, it will help!" And I keep saying, no, it doesn't build up my stamina, it makes me feel worse! And they never believe me.) And he says it's because I don't panic enough. When I was on the treadmill, I was muttering that it was boring and that I'd like something to read, and maybe I'd just critique the technique of the painting I was staring at, and when the speed and incline increased, I told him that I really wouldn't want to do this for very long, and that it's not a pace I would choose if he weren't making me. Well, that was true. However, according to him, from what the echo was showing, what I *should* have been saying was "This is too much, stop the test, let me off this thing" while panting for breath. Because I wasn't panting for breath, and I could still finish a whole sentence, they didn't believe it till they could see the heart itself.

So OK, I'm supposed to get more upset and panic more often and get hysterical if I want people to take me seriously? C'mon.

Can I help it if playing the saxophone all these years has done wonders for my breath control?

Anyway. I also asked him about the beta blocker research I mentioned in my previous post, and he has read about that, and thought of me, too, and will be keeping an eye out for testing as soon as it's available. He's not so concerned with how much the Coreg costs me and my insurance company, as he is with not having the side effects if I don't have to. He expects the test to be available pretty soon, as these things go.
Baked potatoes with "steak" sauce:
2 large baking potatoes
1 tbsp unsalted butter
1 4-ounce can NSA sliced mushrooms (see the link to Healthy Heart Market at right)
1 tsp minced garlic
1/4 cup pine nuts
4 ounces Mr. Spice Garlic Steak Sauce (HHM has this, too)

IN saucepan, melt butter and stir in the pine nuts; stir them around for a minute or so. Add the mushrooms and garlic, and stir them occasionally till the pine nuts brown slightly. Add the steak sauce, stir, turn down heat, and simmer, while you nuke the potatoes for 8-10 minutes.

Slice potatoes open, serve sauce over them. This is a lot of sauce for 2 people (the way I like it) or a modest amount of sauce for 4 potatoes. The Mr. Spice sauce is both low-sodium and fat-free. To make a balanced meal out of this, serve it with salad that has diced fresh mozzarella in it - the kind that comes packed in liquid, in round balls - fresh mozzarella is only about 15-25 mg of sodium per ounce. This'll add some protein to the meal, 'cause the pine nuts alone aren't a whole lot of protein.

Sunday, July 16, 2006

I read a short blurb somewhere recently, that said that researchers have discovered a genetic basis for whether or not heart failure patients respond successfully to beta blockers, and that they are developing a fairly quick genetic test for it. This should mean that it will be possible to test new patients and see whether or not to waste anyone's time, energy, and money on expensive drugs such as Coreg, which also need complicated titration over a period of weeks. Since even my co-pay is expensive for stuff that's still brand-name only such as Coreg, and since the insurance company's share is even more, I'm sure they'd be happy to pay for the test the minute it's available. Since my EF has never noticeably improved, despite all the meds, it could be that I'm one of the people for whom beta-blockers don't work. It would be nice to be able to discontinue one of the meds, if that's the case. I mean, it would be nice if the drugs DID work, but if they don't, I can save some money and eliminate a few side effects.

I'll keep an eye peeled for more details about this one, and keep you posted.

Thursday, July 06, 2006

The July issue of Prevention magazine has ratings of various salsas they tested. Salsa certainly adds zing to food, and has the added advantages of being low-fat and generally low-cal. However, finding low-sodium salsa can be a pain. So, from among the 9 salsas that they gave the highest ratings to, here are the ones that are

Green Mountain Gringo Mild Salsa - 90 mg sodium per 2 Tbsp; available at natural foods stores and some grocery stores
Stonewall Kitchen Mango Lime Salsa - 35 mg sodium per 2 Tbsp; order at http://www.stonewallkitchen.com
Newman's Own Black Bean and Corn Salsa - 140 mg sodium per 2 Tbsp, which is right on the top edge of "low sodium" but this one has the advantage of being available in most supermarkets.
Robert Rothschild Farm Fiery Raspberry Salsa - 109 mg. sodium per 2 Tbsp; order at http://www.robertrothschildfarm.com

Sunday, July 02, 2006

New recipe:

Meatless Loaf

1 can NSA (no salt added) chickpeas/garbanzos
1/2 cup to 3/4 cup NSA bread crumbs
1/4 cup grated or shredded cheese - whatever you have on hand. Mozzarella, parmesan, romano, lo-so-cheddar... whatever.
about 1/3 to 1/2 cup finely chopped carrots - I started with shredded carrots and then chopped them further in the food processor
one 4-ounce can NSA mushrooms
2 eggs or equivalent egg substitute (e.g., EggBeaters)
4 to 6 tablespoons of barbecue sauce, to taste
1 heaping teaspoon all-purpose saltless seasoning (whatever brand you like - the kind with onion powder, garlic powder, parsley, and a bunch of spices)

Drain and rinse the chickpeas, then "rice" them. If you don't have a ricer (a sort of potato masher) then you should smush them with a fork. You don't want to use a food processor, unless it's a very weak one, because processing will turn it to mush, which won't have the same texture that ground meat does.
Drain the mushrooms, and chop them fine - a food processor pulsed for just a second or two will work for this.
Mix all ingredients thoroughly together, including the barbecue sauce.*
Pack the mixture into an 8 x 4 or 5" loaf pan. Smoothe the top.
Topping:
Sprinkle another Tbsp of bread crumbs and another Tbsp of grated cheese across the top. Then spoon 2 more Tbsp of barbecue sauce on top, and spread it around so it covers most of the loaf.

Bake at 375-400 degrees for about 35-40 minutes, or until the top looks done. Let sit in pan for 5 minutes before slicing. Makes 6 slices.

This is pretty complete protein-wise, and has the carrots and mushrooms in it, just about any sort of green vegetable or salad is a good side dish to make it a balanced meal.


*That's what really makes this taste like a meatloaf! If you are a strict vegetarian, make sure you get a barbecue sauce that has no animal products; some have worcestershire sauce in them, and worcestershire sauce has anchovies. So read the ingredients!! If all you're looking for is low-sodium, and you're not worried about the animal products, then you can try, among others, Stubb's - although it's not "low" sodium, it's about half the sodium of most other barbecue sauces. And tasty, too.

bunrab: (Default)

Tuesday, June 13, 2006

This week's article:
Being overweight or obese can enlarge a teen's heart
Jun 08 (HealthCentersOnline) - The heart health of adolescents may suffer from excess body weight, causing abnormal heart enlargement and impaired pumping function by age 20.
Being overweight and obese has long been associated with an increased risk of heart disease. Obesity is the second leading cause of preventable death, contributing to serious health problems such as cancer, heart disease, diabetes, stroke and cancer. Over the past 30 years, childhood obesity has tripled in the United States. According to the U.S. Centers for Disease Control and Prevention (CDC), 16 percent of children ages 6 to 19 are considered overweight and childhood obesity has tripled in the United States.

The study examined data gathered from the Strong Heart Study (SHS), a 4,549-person study of cardiovascular risk factors and cardiovascular disease. The study specifically looked at information obtained during the examination of 460 participants, ranging in age from 14 to 20 years old. This group included 245 girls and 215 boys.

The researchers, made up of a team of physicians from the United States and Europe, used several diagnostic tools, including an ultrasound, to measure the size, shape and pumping function of the teens' hearts.

The study found that severe abnormalities in body build (such as being overweight or obese) paralleled cardiac changes, even in people as young as 18. The excess body mass appears to make the heart work harder, leading to an abnormally large heart.

"The main findings are that, when obesity is present, something happens in our hearts to increase its size and wall thickness, which cannot be understood by measurement of blood pressure," explained study author Giovanni de Simone, M.D., F.A.C.C. from the New York Presbyterian Hospital-Weill Medical College of Cornell University in New York, New York and the Federico II University Hospital School of Medicine in Naples, Italy, in a recent press release.

"This excess of cardiac mass, which we call 'inappropriate' in connection to cardiac workload, is also associated with a general impairment of the function of the heart to push blood into the arterial tree and also to distend its cavity to receive the blood returning from the periphery."

The results of this latest study appear in the June 6 issue of the Journal of the American College of Cardiology.

bunrab: (Default)

Tuesday, May 30, 2006

Ladies Home Journal had a short blurb, which I can't find amongst my clippings right now, about how and why blood thinners help reduce the chances of SCD from atrial fibrillation. I don't remember the details of how it does that, but I do remember the statistics they cited in the column: if you are at risk of atrial fibrillation, and you don't take any blood thinners, you have a 1 in 20 chance of having an incident that could kill you, each year. [Note, my own EP says it's one in 17, not one in 20; I suppose they were rounding off.] If you take low-dose aspirin as a blood thinner, that lowers your risk to 1 in 40 - only half the chance. And if you take coumadin, it lowers your risk to a 1 in 70 chance each year.

So, even if you don't need blood thinners because of clotting risks, apparently you should take them because of fibrillation risks. While taking a strong blood thinner such as coumadin can carry its own risks - I ride a motorcycle, so I'd never take a prescription strength blood thinner, since it could make even a mild accident fatal - taking "baby aspirin" has far fewer risks and apparently accomplishes a lot. And, according to my cardiologist, if you take a proton pump inhibitor, such as Prilosec (available over the counter), it reduced the chances that aspirin will give you stomach ulcers. On the other hand - and isn't there always an other hand? - proton pump inhibitors such as Prilosec and Protonix (one of the newest prescription ones) are in one of the classes of drugs that can lead to increased risk of arrhythmia (see post about 9 posts down from this one). So it sounds like we've come full circle, hasn't it!! Apparently, if possible, to reduce your fibrillation risk in an optimum manner, you should take the low-dose aspirin without the proton-pump inhibitor, if possible.

It gets more complicated all the time.


This week's article:
Common painkillers may raise risk of heart failure

May 23 (Reuters Health) - Patients who use non-steroidal anti-inflammatory drugs (NSAIDs), which include over-the-counter analgesics such as ibuprofen or naproxen, have a small increased risk of experiencing a first hospitalization for heart failure, researchers from Spain report. They also found that for patients with pre-existing heart failure, NSAIDs may worsen the condition, triggering the need for hospital admission. ...

With current NSAID use, the overall risk of a first hospitalization for heart failure was increased by 30 percent after accounting for major heart failure risk factors, report Huerta and colleagues from Centro Espanol de Investigacion Farmacoepidemiologica in Madrid.

The increased risk of heart failure hospitalization associated with individual NSAIDs ranged from 10 percent with diclofenac to more than threefold with indomethacin. The dose and duration of use of the drugs had no apparent effects.

Heart failure hospitalization was also associated with known risk factors including high blood pressure, diabetes, kidney failure, other heart disease and anemia. Obesity, smoking, alcohol use, and recent hospitalizations and specialists' visits -- two indicators of other illness -- were also associated with an increased risk of hospitalization.

However, a prior diagnosis of heart failure was the main risk factor triggering a first hospitalization for heart failure, increasing the risk by more than sevenfold.

The investigators point out that their results are compatible with the findings of other published studies indicating that NSAIDs exacerbate heart failure symptoms, leading to hospitalization among susceptible patients, such as those with a history of cardiovascular disease and, in particular, previous heart failure.

The new study adds the finding that NSAIDs trigger the risk of hospitalization for heart failure in patients without a history of heart failure, the researchers conclude.

SOURCE: Heart, May 2006.

Monday, May 29, 2006

Science News has a short blurb mentioning that they've found out exactly what it is that makes it a bad idea to eat grapefruit or drink grapefruit juice when taking certain medications. Lipitor, for example, and the other statins, which most of us with almost any heart problem seem to be taking. So anyway, it turns out to be certain compounds called furanocoumarins, which are in grapefruit juice but not in other citrus juices, that are the metabolism-interfering compounds. Since the furanocoumarins can be filtered out of grapefruit juice, this may mean that in the not too distant future, those of us on medication can start drinking grapefruit juice for breakfast again! Whee! Don't know as there's any way to do that with fresh grapefruit, though; I guess we'll have to keep on eating those high-in-potassium canteloupe halves instead of grapefruit halves. Oh well.

Friday, May 26, 2006

More ICD news

Boston Sci finds battery problem in some devices

May 16 (Reuters) - Boston Scientific Corp. on Monday said it had notified doctors that some of its implantable cardiac devices, which it acquired as part of its purchase of Guidant Corp. last month, could be at risk for early battery depletion.
Boston Scientific, whose shares fell 1 percent, said the problem occurred in a single lot of 996 implantable cardioverter defibrillators and cardiac resynchronization therapy defibrillator devices that had been implanted in patients globally. No deaths or injuries were reported.

Implantable cardiac devices, or ICDs, are used to jolt a dangerously racing heartbeat back to a normal rhythm. Several models of the life-saving devices have been the subject of recalls or safety alerts by Guidant and other manufacturers in recent years.

Boston Scientific said 30 of its Guidant devices had been returned by May 8, and it had received an additional 46 reports of devices that remained implanted but showed signs of premature battery depletion.

The devices, which contain a faulty component from the single manufacturing batch, are in the Vitality DS, Vitality AVT and Vitality 2 ICD lines and the Contak Renewal 3, Contak Renewal 4 and Contak Renewal 4AVF lines of CRT-Ds.

In information posted on its Web site, Boston Scientific advised doctors to schedule follow-up appointments as soon as possible with patients who had received the devices and contact the company for instructions to determine remaining battery life of the devices.

The battery problem came to light after an overall review of Guidant's product lines, Boston Scientific said.

Boston Scientific swooped in to buy Guidant for about $27 billion after Guidant initiated a series of device recalls and was stung by criticism over its failure to promptly notify physicians and the public about life-threatening defects.

"We understand and acknowledge we have to do a better job of communicating, and this is a step in that direction," Boston Scientific spokesman Paul Donovan said.

Boston Scientific also advised doctors of two device malfunctions linked with implantation of Guidant defibrillators in an unusual position.

Planting one of these devices below the chest muscle, rather than below the skin, can result in mechanical stress to an area of the titanium case that can cause the product to malfunction, the company said. The uncommon technique could affect devices in the Renewal 3, Renewal 4 and Vitality HE product lines.

The two patients whose devices malfunctioned underwent successful replacement procedures, Boston Scientific said.

Morgan Stanley analyst Glenn Reicin said the product notifications stem from an approach adopted by Guidant last year to update physicians regularly about performance issues.

"Investors should view these communications as normal course of business," Reicin said in a note to clients.

Boston Scientific is currently working to resolve a warning letter from the U.S. Food and Drug Administration over quality control issues. The Guidant division also faces its own FDA warning letter over its ICDs.

Tuesday, May 09, 2006

Here's a relatively low-sodium macaroni and cheese recipe. Please note that this recipe is NOT low-fat; I don't know of any way to make mac-n-cheese that is low-fat, low-sodium, and tasty all at once; at most, you can get two of those together. This one is low-sodium and tasty. There are footnotes telling you where some of the ingredients are available.

Macaroni Quattro Formaggio
Cook 12 ounces of elbow macaroni or other small-to-medium pasta (tiny shells, rotini, radiatore, etc.) according to directions on package.
Grate an 8 ounce bar of low-sodium cheddar cheese(1). Dice up 4 ounces of FRESH mozzarella cheese(2). (If you have an ounce or so of leftover swiss(3) (gruyere, emmenthaler) cheese, you can grate that and add it too.) Mix these cheeses with the macaroni, and place in a casserole dish. Over the top of the macaroni, sprinkle about 2 ounces of grated Parmesan and Romano cheese(4), then on top of that, about 2 ounces (1/4 cup) of low-sodium seasoned dry bread crumbs(5), spreading the Parmesan/Romano and the crumbs as evenly as possibly across the whole top of the casserole. Then slice up 2 tablespoons of unsalted butter, and dot the top of the casserole with little chunks of butter. Over the whole thing, pour a can of evaporated milk - depending on where you live, that's somewhere around 8 to 12 liquid ounces; the exact amount isn't critical as long as it's at least 1 cup and not more than about a cup and a half. Place the dish, uncovered, in a 350°F oven, for 25 minutes, then switch the oven to BROIL and 400°F for 3 minutes, to brown the crumbs on top. Let the dish cool for about 5 minutes before serving.Serves 4 to 6 people as a main course, depending on the people.

To fancy it up some, drain a can of no-salt-added diced stewed tomatoes, and add them in when you are first mixing the macaroni with the cheddar and mozzarella.

The leftovers are extremely tasty cold, too; it can be served as slices, along with a salad.

(1) Heluva Good makes low-sodium cheddar; if you can't get your local supermarket to order some, you can order directly from the company. You'd better like cheese though, since it's a minimum of 4 bars.
(2) Most larger supermarkets will carry a national brand of fresh mozzarella, such as Bel Giorno, which has about 70 mg of sodium per ounce. Fresh mozzarella comes in round balls floating in liquid, by the way. If you can find some from a local dairy, though, those fresh mozzarellas often have as little as 15 mg of sodium per ounce. High-end markets such as Whole Foods, Central Market, etc. will usually have local-dairy mozzarella in their cheese assortments.
(3) Swiss cheeses vary greatly in their sodium, so you have to check the labels, but there are quite a few brands that run only 50-75 mg of sodium per ounce, including the house brand from Giant, and the commonly available Alpine Lace brand.
(4) Parmesan and Romano, or any grated cheese intended for spaghetti, can vary widely in sodium, too. This will be the highest in sodium of the cheeses in this recipe. But you can find one that has 75-100 mg of sodium per serving compared to others that have 150-180 mg of sodium per serving, and that's what to look for.
(5) Healthy Heart Market, see the link at right, carries low-so bread crumbs. They also have the canned no-salt added tomatoes, if you decide to add those.

<hr>
This week's article:
How exercise helps heart failure patients
May 04 (HealthCentersOnline) - A small study may help explain why aerobic training helps to reverse the abnormal heart patterns that appear in patients after experiencing heart failure.
Heart failure is chronic condition in which at least one chamber of the heart is not pumping well enough to meet the body's needs. This leads to congestion in the lungs or pulmonary blood vessels and may cause fluid to back up in the lungs, legs and ankles.

Previous research has demonstrated that aerobic exercise can help a person with heart failure feel and function better. Now, new research suggests that this response works by suppressing certain neurohormones that cause many of the severe symptoms of heart failure.

Following certain cardiac events (e.g., heart attack), the body works to protect itself in the short term by increasing its production of certain types of B-type natriuretic peptides (BNP). These neurohormones constrict blood vessels and help heart cells to retain sodium, which allows the heart to continue to pump blood effectively.

However, over a period of time an imbalance of the BNP neurohormones can become detrimental, leading to irregular heart rhythms, tissue buildup and the accumulation of fluid in the heart.

Researchers from Italy have found that aerobic exercise helps to improve the effects of heart failure by lowering some types of BNP. The researchers studied 47 heart failure patients who had entered a nine-month aerobic training program. The 44 patients who completed the program reported an improvement in their quality of life significantly greater than a similar control group (that did not include heart failure patients). Testing also revealed the heart failure patients had lowered levels of three types of BNP.

"Reversing neurohormonal activation by physical training adds to the current clinical practice a novel non-pharmacological aid. Out of 85 patients who completed the protocol, only the 44 randomized to the training program improved functional capacity, systolic function, and quality of life, in contrast to the controls. These beneficial effects were associated with a decrease in plasma level of BNP, NT-proBNP, and norepinephrine, only in the training group," explained Claudio Passino, M.D. from the CNR Institute of Clinical Physiology in Italy, in a recent press release.

The results of the study appear in the May issue of the Journal of the American College of Cardiology.

bunrab: (Default)

Wednesday, April 26, 2006

another article
 

Tuesday, April 18, 2006

This week's interesting article:

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Tuesday, February 21, 2006

The "Speed Bump"* comic in yesterday's paper was funny. There's a guy lying in a hospital bed, and a doctor talking to him: "We successfully replaced your pacemaker with an iPod, Mr. Wyatt... Now you can march to the beat of any damn drummer you want."


*it's a single-panel cartoon that runs in daily newspaper, by Dave Coverly.

Monday, February 20, 2006

As predicted, Johns Hopkins has indeed phoned me twice since my last visit, to get my address and insurance info and mother's maiden name and first 10 digits of pi, in preparation for my surgery next month. Why can't they get their computers to talk to one another, instead of phoning me at 8:15 in the morning?

Friday, February 17, 2006

From an article a couple months ago in the Baltimore Sun, some medical websites. You've probably already found most of these, but if not, try them:
http://www.medlineplus.gov (NIH and National Library of Medicine)
http://www.healthfinder.gov (Dept. of Health & Human Services)
http://www.ahrq.gov (Agency for Healthcare Research and Quality - reportedly not very user-friendly)
http://www.pubmed.gov (National Library of Medicine)
http://www.consumerreportsmedicalguide.org (Consumer Reports; mostly free but some info requires a subscription)
http://www.healthratings.org (Consumer Reports' ratings of other medical websites)
http://www.mayoclinic.com
http://hms.harvard.edu (Aetna and Harvard Medical School)
http://www.pdrhealth.com (medicines)
http://www.safemedication.com (medicines, run by Amer. Soc. of Health System Pharmacists)
http://www.crbestbuydrugs.org (Consumer Reports again)

This week's news articles:
First, as the overweight, couch-potato, baby-boom generation starts edging into the "normal" age range where heart failure becomes more common, what a surprise! Heart failure rates increase! What is of note, regardless of age, here, is that survival rates are improving - finally! We were getting tired of those mortality statistics not budging, despite newer meds and newer surgeries. Finally, it appears, the cumulative effects of those things are having an effect on mortality.
Heart failure increasing in older adults
Feb 08 (Reuters Health) - The rate of heart failure in the US among older adults increased from the 1970s to the 1990s, but survival rates have improved, new research shows. Both of these trends were more apparent in men than in women.
"Hospitalizations for heart failure have more than doubled between the two periods," Dr. William H. Baker, from the University of Rochester in New York, said in a statement. "Heart failure is the most common discharge diagnosis for men and women over age 65."

The findings, which appear in the American Heart Association's journal Circulation, are based on study of new cases of heart failure in the early 1970s and 1990s using data for more than 300,000 older adults enrolled in an HMO in Oregon or Washington.

From 1970 to 1974, a total of 387 patients were diagnosed with heart failure. The number of new cases from 1990 to 1994 was 1555. After accounting for age, a 14 percent increase in the rate of heart failure was observed between the two periods. As noted, this rise was greater in men than in women.

Deaths due to heart failure fell during the 20-year period by 33 percent for men and by 24 percent for women, the report indicates.

As to why survival did not improve as much in women, the researchers believe that it may be because older women have more additional diseases than men or because they are more physically frail.

"The increase in incidence and survival for heart failure suggests an accelerating rise in this disabling and costly disease that is of public health and clinical importance," Baker emphasized. "In the future, heart failure deserves the highest research priority into its precipitating factors and its management."

SOURCE: Circulation, online February 6, 2006.

Next, a reminder to us all that we should have our kidney function checked regularly.
Poor kidney function ups death risk in heart failure

Feb 07 (Reuters Health) - Impaired kidney function raises the risk of death and hospital admission in patients with chronic heart failure, even among those patients with fairly well preserved heart-pumping action, study findings suggest.
So-called "renal insufficiency" has been shown to increase the risk of death in chronic heart failure patients, but most studies have involved patients with markedly reduced left ventricular ejection fraction (LVEF) -- a measure of the heart's blood-pumping strength.

Less is known about the impact of kidney function on heart failure in the presence of preserved heart-pumping power.

To investigate, Dr. Hans L. Hillege, from the University of Groningen in the Netherlands and associates studied 2,680 heart patients -- 1087 of whom had an LVEF greater than 40 percent indicating preserved heart-pumping action.

At baseline, 36 percent of patients had poorly functioning kidneys. During a median follow-up of 34.4 months, 950 patients died of cardiovascular causes or were admitted to the hospital for heart failure, and there were 625 deaths from all causes.

The authors report that both poorly functioning kidneys and lower LVEF were significant independent predictors of worse outcomes.

"The strong independent effect of renal function in our analysis after adjustment for numerous cardiac risk factors shows that renal function is a valuable predictive variable in evaluating outcomes," the authors maintain, "even if it probably represents partly underlying atherosclerotic or hypertensive vascular disease."

SOURCE: Circulation, February 6, 2006.

Tuesday, February 14, 2006

Reading KateMonster's post reminds me to also be thankful to the doctor who diagnosed me. I had been taking drugs to treat asthma, which are directly harmful to hearts with cardiomyopathy, and the same thing could have happened to me. However, when my GP, frustrated with my nonresponsive "asthma," referred me to a pulmonologist, it took him about 5 minutes to correct the diagnosis - even though he was a lung specialist, not a heart specialist, he looked at my heart in the x-rays, not just the lungs, and listened to my heart as well as my lungs. He was so sure of the diagnosis that he wrote out a couple of the necessary prescriptions - Lasix and digoxin - right away, even as he wrote up a referral to a cardiologist. So thank you to him, and to his ready box of Kleenex and kind nurse. That was 3 years ago, and I'm still alive now. Yay!

Friday, February 03, 2006

On the first of Feb., I got to see an electrophysiologist at Johns Hopkins - one of the reasons we moved up here to Baltimore!!
My regular cardiologist over in Howard County had referred me, and this EP had an opening relatively soon in his schedule. I swear, the longest part of the whole deal was waiting in lines once I got to Johns Hopkins Outpatient Clinic. First you walk in the lobby and wait in a check-in line, to then be told that since you are new you have to go wait in another line to get a "history card" after which you are finally permitted to approach the elevators and go up to the correct floor, where you wait in line for a floor concierge to direct you to the correct wing, where you finally wait in line at the check-in desk for the group of doctors you are actually there to see. At each and every one of these stops, you wind up repeating your name, and your mother's maiden name, and the first 6 digits of pi, and... well, not quite that, but an awful lot of repetitive info - especially given that I had already given all this info during not one, but TWO phone calls the previous week.

Then I got to sit in a waiting area - there are several of them in the cardiology pod, each with at least one more person waiting than there are chairs. I did get a chair, however, and got some knitting done. I am finished with the first wrist-warmer made out of self-striping sock yarn for my friend Fade!! Yeeha!

And in other good news, Dr. Sinha is sure that he can indeed put the third lead in, so that I will have bi-V pacing finally, and he is quite convinced that he can persuade my insurance to pay for it. The fact that my EF is still only 21%, when after 3 years and all the medication and so forth they would expect it to improve to 30%, is prima facie evidence that something needs to be done.

So something will be done, on Thursday, March 2. I have to be there at 6:30 a.m. - I told him I would not even need a sedative, let alone anesthesia, at that hour. Anyway, I am sure they will phone at least once more to ask all the same questions over again about my name and medications and mother's maiden name and pi and the lost treasures of the Incas.

bunrab: (Default)

Tuesday, January 24, 2006

This week's article:
'Statin' drug may be helpful in heart failure

Jan 20 (Reuters Health) - Treatment with Lipitor (atorvastatin), one of the popular cholesterol-lowering "statin" drugs, can help the heart pump better in patients with heart failure, according to a new report.
By contrast, findings from a much smaller study showed that aside from lowering cholesterol levels, Lipitor did not benefit patients with heart failure. Both reports are published in the Journal of the American College of Cardiology.

"Although the reasons for these discrepant findings are not known, the most logical explanation is that the (group in the second study) had relatively mild heart failure" and thus there was less chance for Lipitor to show a benefit, Dr. Douglas L. Mann and Dr. Kumudha Ramasubbu, from Baylor College of Medicine in Houston, note in a related editorial.

Still, the second study is important because it shows that cholesterol lowering can be achieved in these patients without any obvious side effects using high-dose statin therapy, the editorialists point out.

In the first study, Dr. Srikanth Sola, from Emory University in Atlanta, and colleagues assessed the outcomes of 108 heart failure patients who were randomly assigned to receive Lipitor (20 milligrams per day) or inactive "placebo" for 12 months.

A significant improvement in the heart's pumping ability was noted in the Lipitor group during the study period, whereas a drop was observed in the placebo group. In addition, use of the drug appeared to reduce inflammation.

In the second study, Dr. Barry E. Bleske, from the University of Michigan at Ann Arbor, and colleagues assessed the outcomes of 15 patients with heart failure who were treated with Lipitor (80 milligrams per day) or placebo for 12-weeks and then crossed over to the other treatment for another 12 weeks.

With the exception of a significant drop in LDL ("bad") cholesterol levels, Lipitor therapy produced no beneficial, or harmful, effects in this patient group.

At present, statins can be recommended to heart failure patients with known heart disease and elevated levels of LDL cholesterol, Mann and Ramasubbu note. The broader question of whether these drugs should be given to all patients with heart failure remains unanswered, but several ongoing trials are addressing this topic, they add.

SOURCE: Journal of the American College of Cardiology, January 17, 2006.

I just realized I hadn't ever mentioned the results of the MUGA scan. I saw my cardiologist last week to discuss them. The MUGA gives an exact number, instead of the range that an echo gives. My EF is, therefore, 21%.
And while I'm relatively asymptomatic compared to most people with EFs that low, he finds it frustrating that despite all the meds and my reasonable weight and all that, we haven't managed to improve that to at least 30%. So he's referred me to an electrophysiologist with Johns Hopkins, to be evaluated for going back in and implanting that third lead on the pacemaker. As I mentioned when I started this blog, the EP who did it couldn't get the third lead in; the vein at the back of my heart was too "tortuous." Anyway, that was nearly 3 years ago; since then, surgeons have become more experienced at laparascopic implantation, and also there's a possibility that the doctors at Johns Hopkins might just be better than the ones back in Austin... anyway, he's gonna look at me and see if it might be possible now to do that.

If he judges that it's not, then we have to decide whether it's worth it to do a limited thoracotomy, cracking open a couple ribs to get at the heart - much less invasive and quicker recovery than cracking the sternum for open-heart, but a lot more trouble than laparascopic surgery, and it would actually require a couple of nights in the hospital and a couple of weeks of recovery time. And not playing a large saxophone that hangs from around my neck for a couple of months. So I'd have to think about that. Maybe wait until the summer, after the 4th of July concerts are over!


A short article from New Scientist, 14 January 2006:
Implantable defibrillators have saved countless lives by applying electric shicks to jump-start failing hearts. But these devices have one serious flaw: they often go off when they are not needed, giving unsuspecting and perfectly healthy recipients the fright of their lives. [BunRab's 2 cents worth: if they were perfectly healthy, they wouldn't have implanted defibrillators, would they now.] "People often don't realise just what unpleasant and flawed devices standard defibrillators are," says Andrew Grace... For this reason, he has been working with Cameron Health of an Clemente, CA, to develop a defibrillator that may spell an end to unnecessary shocks by more thoroughly assessing electrical activity in the heart.
Standard defibrillators are connected to the heart via wires, and judge how well the organ iz functioning by monitoring the small area of tissue that is usually the origin of rhythm disturbances. However, electrical anaomalies in this area are not always morrored elsewhere in the heart, and are therefore not always significant. But defibrillators still kick in and give the heart an unnecessary shock.
The new device scans the whole heart in the same way as an ECG, and will only provide a shock if it picks up a major, organ-wide irregularity. Like an ECG it uses sensor electrodes and magnets to pick up the electric fields generated by electrical activity in the heart muscle.
As well as avoiding false alarms, the device is less invaive than standard defibrillators as it is not attached to the heart itself but fits on the chest just under skin. This makes fitting it simpler and safer.

There's a couple paragraphs more, but that's the gist of it. What I get from this is that it's ONLY a defibrillator, not a pacemaker; it wouldn't be used for anyone who needs a pacemaker as well as an ICD, and doesn't therefore apply to anyone who is getting bi-ventricular pacing out of their device.
Plus, I'd have to say I haven't heard of any noticeable number of people getting unnecessary shocks; I've met many people with the ICD/pacemaker devices, and most have *never* had their ICD shock them. Let alone unnecessarily. So I'm not convinces that this was as big a problem as the developer of the new device is making out. However, others' experience may vary. Certainly, for people who need only an ICD, smaller and easier would be better. I wonder, though, whether it eats up more battery power monitoring more of the heart? Would that mean more frequent, if less invasive, surgery?

This week's news article:

Resistance training OK for heart failure patients
Dec 27 (Reuters Health) - Contrary to qualms about deleterious effects on the heart, people with chronic heart failure can safely undertake a resistance training program, Australian researchers report. In fact, such training appears to have a beneficial effect on how strongly the heart is able to pump blood.
Resistance training has been shown to improve the functional ability of people with chronic heart failure to perform activities of daily living, and to improve their overall quality of life. However, there have been concerns that it may accelerate the remodeling process that affects the main pumping chamber of the heart -- the left ventricle -- when chronic heart failure sets in.

To investigate, Dr. Itamar Levinger, from Victoria University of Technology in Melbourne, and colleagues used ultrasound to assess the structure and function of the left ventricles of eight men with heart failure who participated in an 8-week resistance training program and seven similar men who did not.

The investigators' findings appear in the International Journal of Cardiology. The resistance training did not appear to have a significant effect on left ventricle measurements, the report indicates.

Yet, the patients who undertook the resistance training showed significant increases in the amount of blood the heart was able to pump with each beat, compared with the non-training group.

"Since resistance training improves functional ability and quality of life of patients with chronic heart failure without causing a reduction in left ventricular contractile function or structure it is recommended to add this training regime to the regular exercise rehabilitation programs of these patients," Levinger's team concludes.

SOURCE: International Journal of Cardiology, November 2, 2005.
Publish Date: December 27, 2005

bunrab: (Default)

Tuesday, December 20, 2005

News:
Micronutrients helpful for heart failure patientsec 07 (Reuters Health) - Micronutrient supplementation improves heart function and quality-of-life in elderly patients with chronic heart failure, according to a report from investigators in Germany and the UK.
"The vitamin story has been confused with studies examining the response to single vitamin supplements in relatively low-risk patients," Dr. Klaus K. A. Witte from Castle Hill Hospital, Cottingham, told Reuters Health.

On the other hand, "CHF patients are at higher risk and might have multiple deficiencies. Replacing just one micronutrient might expose deficiency elsewhere (the vitamin E and C interaction, for example), so a combination is important," Witte explained.

He and his and colleagues investigated the effects of long-term multiple micronutrient supplementation in 32 patients older than age 70 years with stable heart failure.

After an average of 295 days, the patients who had been assigned to get micronutrient supplements experienced significant improvements in cardiac pumping ability, the team reports in the European Heart Journal.

Also, patients taking micronutrients had an increase in their quality-of-life score, whereas the participants who had been given placebo supplements had a decrease in their quality-of-life score.

The differences in overall quality-of-life score were mainly due to improvements in scores for breathlessness on exertion, quality of sleep, and daytime concentration among the patients taking micronutrients.

"At present there are few supplements that include the constituents we used," Witte said. "I would generally recommend a combined multivitamin supplement along with zinc, copper, and selenium. I also feel strongly that a high dose Coenzyme-Q10 is important. Most currently available supplements do not have enough Co-Q10."

SOURCE: European Heart Journal, November 2005.

Sunday, December 18, 2005

Top Ten List: Ten Reasons Why CHF is Not the Worst Thing That Could Happen

10. No chemotherapy, radiation, dialysis, or daily injections.
9. You get to use handicapped parking spaces at the mall.
8. Perfect excuse for getting out of parties you'd rather not go to in the first place.
7. Lots of chances to lecture people endlessly when they say "you don't LOOK disabled"
6. ICD support groups serve free dinner at quarterly meetings.
5. Get to take part in medical studies and maybe even get paid for them.
4. Take naps in mid-afternoon even if you're under 65.
3. Improve your on-line research skills hunting for low-sodium products.
2. Takes your mind off worrying about getting Alzheimer's when you get old.
And the number one reason why CHF INTWTTCH:
1. Cardiologists' waiting rooms have such great magazines!

It's the beginning of the holiday season! That means, for many people, FOOD.
And all those parties. Snacks and alcohol - what do we do about them?

First off, if you want to be sure there's something at a party that you can eat, bring something yourself; a bowl of my fruit salad with ginger dressing will work nicely. I can't seem to find the old post from a couple of years ago where I put this, so I'll re-print it below.

Eggnog is pretty much off limits. High in fat, higher in sodium than you'd think for a sweet beverage, and often has alcohol in it. A little alcohol will not hurt you, but eggnog can pack a surprising amount in it, with all the sugar disguising the alcohol content. So just say no to eggnog. You'll see "lite" varieties in the supermarket; these are lower in fat and cholesterol, but not any lower in sodium, and they tend to taste like vaguely rum-flavored thin milkshakes - worse, if they have artificial sweeteners in them. So they're not worth bothering with.

If you want to have a festive beverage that's very holidayish, consider mulled apple cider - there are thousands of recipes out there on the web. One way to make the making of mulled cider easier: instead of using cheesecloth balls to hold the spices (who even owns cheesecloth any more? How many of us would know where to find any if we wanted some? [The answer to that is: fabric stores.]}, use wire mesh tea balls. A large tea ball will hold the spices and brown sugar and allow the brown sugar to dissolve out into the cider just as cheesecloth would. And it's then washable and re-usable for your pot of tea.

Other beverages include sparkling cider - Martinelli's makes a non-alcoholic sparkling apple cider, as well as apple-cranberry and a couple other varieties. A chilled bottle or two of this with a festive bow is as welcome a hostess gift as wine, and drinkable by all. I served sparkling cider with Thanksgiving dinner, and everyone enjoyed it; we never even got around to opening the wine.

And then there's tea. Chai tea is a rich, spicy tea. It can be served sweetened or un; with milk or without. And there's decaf versions, if you are supposed to limit your caffeine intake. I also served chai at Thanksgiving - I made a huge pot of decaf chai, we sweetened it with Splenda, and drank it with dessert and afterward. One of my sisters-in-law is pregnant, so she really appreciated the non-alcoholic options. You can find decaf chais in various supermarket brands, such as Celestial Seasonings, or some good whole-leaf chais from on-line vendors, such as Plymouth Tea.

Finally, alcohol itself: a teeny tiny bit will not hurt most of us. I take 9 pills a day, including 5 that say on the label not to drink any alcohol. I have discovered, though, that I can handle 1/4 of a serving of alcohol without any ill effects. So I can allow myself a couple of gulps of beer or hard cider, or the bottom of a wine glass of white wine or champagne, or a bottle-cap-ful of Bailey's or other liquer poured over ice cream or into hot cocoa. I don't do it that often, but I can do it. Check with your doctor, and see if he or she goes into screaming fits at the idea, or instead says "yeah, you can have a sip of that as long as you don't drink a whole glass." Once you have that permission, though, don't overdo it!!

Festive Fruit Salad
suitable for bringing to parties or serving to company
1 banana
1 box of strawberries (more is OK- if you want to get a quart box instead of a pint box, that's fine)
1 large (quart) container of cubes of melon - most supermarkets have these, cubed honeydew and cantaloupe, sometimes watermelon too
1 can mandarin orange slices in juice
1 can pineapple chunks in juice
2 kiwi fruits (melon and kiwi are even higher in potassium than bananas!!)
several pieces of candied ginger

Use a bowl with a liquid-tight lid, such as Tupperware, to make this salad in.

1. Open the 2 cans and drain the juices into a separate bowl. Put the fruit in the bowl you're making the salad in.
2. Dice up the candied ginger into teeny pieces. Put it in the juices to steep. You can add a little bit of sugar to this if you want, but not too much!
3. Chop the banana into bite-sized chunks. Halve the strawberries. Cut the melon cubes, which are usually pretty large, into bite-size chunks. Put them in the salad bowl, and toss a couple of teaspoons of the fruit juice with them to keep everything fresh - the vitamin C (ascorbic acid) in the juice will do that.
4. Peel one kiwi, slice it in half, and then slice into thin slices to toss with the rest of the fruit. (You'll use the other kiwi at the end.)
5. Pour the rest of the fruit juice/ginger mix over the tossed fruit, and stir thoroughly. Cover, stick in the refrigerator, and let sit for at least 2 hours, and preferably more. At least once, more often if you think about it, tip the bowl around to stir up the ginger-juice so the fruit at the top gets to marinate in it.
6. Just before serving or setting off to the party, peel the other kiwi fruit and cut into thin circles. Toss the salad one last time, then place these kiwi circles decoratively on top - arrange them in a pattern, or cut snowflake shapes out of them first, or something decorative. Cover the bowl again until the minute you're ready to serve it or to put it on the buffet table at the party you're attending.

bunrab: (Default)

Tuesday, July 26, 2005

Fresh articles via the Heart Center Online:
Insulin resistance associated with heart failure
Estrogen therapy may help prevent enlarged heart

Insulin resistance associated with heart failure
Jul 22 (HeartCenterOnline) - Insulin resistance appears to increase the risk of developing heart failure, according to a new study published in a leading medical journal.

Congestive heart failure (CHF) is a condition in which the heart does not pump enough blood to adequately supply the body. It is considered a degenerative condition with no cure, and it is a major cause of death. People with CHF are 4 to 8 times more likely to die than people without the condition, according to background information in the study.

The most common causes of CHF are high blood pressure and atherosclerosis. Other risk factors include diabetes and obesity.

Insulin resistance is a condition in which the body does not respond to available insulin as well as it should and is considered a forerunner of diabetes Until this study, insulin resistance, had not been considered a risk factor for developing CHF.

During the study, a team of physicians in Sweden tracked 1,187 men over the age of 70 between 1990 and 2002. During that time, 104 men developed CHF. After controlling for all the possible risk factors, including previous heart attack, high blood pressure, diabetes, smoking and high cholesterol, the research team found that insulin resistance is a valuable predictor for CHF.

The researchers speculated that the connection between obesity and CHF may be mediated by insulin resistance and called for further study. The study was published in the July 20 edition of the Journal of the American Medical Association.
Copyright 2000-2005 (HealthCentersOnline)
Publish Date: July 22, 2005

Estrogen therapy may help prevent enlarged heart
Jul 22 (HeartCenterOnline) - It may be premature to declare that estrogen replacement therapy has no place in preventing all forms of heart disease, according to researchers at the University of California, Irving (UCI).

In recent years, hormone replacement therapy with estrogen (HRT) has come under scrutiny because of findings released by the large, multi-year Women's Health Initiative. That study found that HRT did not prevent heart disease among post-menopausal women, as was once thought. Since those results were released, millions of women stopped taking HRT as a means to prevent heart disease.

However, the research team at UCI found that HRT prevented hypertrophic cardiomyopathy, or enlarged heart, among post-menopausal women who had experienced a heart attack.

According to a release describing the study, hypertrophic cardiomyopathy occurs in as many as 80 percent of people who experience heart attacks. It may lead to heart failure.

Among pre-menopausal women, heart disease rates are significantly lower than among men the same age. However, after menopause, the rate of heart disease among women climbs rapidly, eventually becoming more common among women than men. Heart disease is the leading killer of American women.

In prepared remarks, the authors of the study say that HRT deserves further study, despite the "intense reaction" to the findings of the Women's Health Initiative. The study appeared in the July 15 edition of the Journal of Biological Chemistry.
Copyright 2000-2005 (HealthCentersOnline)
Publish Date: July 22, 2005

Friday, July 22, 2005

It has been a while. We moved from Texas to Maryland. Where up until this week, it has been 10-15 degrees cooler than Texas. This week, the temperatures are about identical. But that's OK - it's the middle of July, it's supposed to be summer. At least here in the Baltimore area, summer will last for another few weeks, and it'll be getting cooler again by the end of August. In Austin, it will stay in the 90's till October.

Nothing much to write about. Gotta find a new cardiologist now that I'm here. That should be fun. Gotta figure out what my health plan will pay for, now that I'm out-of-state with reference to the Employees Retirement System of Texas. Yeeha.

Anyone taking beta-blockers is going to have problems with heat. If you are taking furosemide/Lasix or related diuretics, you will also have problems with the sun. Suggestion: invest in several cooling bandanas. (Like this one, http://www.brandsonsale.com/zecoba.html , although that's just an example. I have not personally ordered from these people, so I don't know if it's any good. It's just to show you the kind of thing I mean.) For playing in the band in outdoor 4th of July concerts, I wear 2-3 of these - one tied around my forehead, one around my neck, one sorta draped down the center of my back. They really help. I could stand being out in the heat for almost 3 hours with these. Don't overexert yourself, though - you shouldn't try to "tough it out."

bunrab: (Default)

Thursday, June 09, 2005

From Science News, Vol. 167, No. 22, May 28, 2005, p. 341.

Positive Jolt: Electroshock therapy may have side benefit
Nathan Seppa

People with depression have high concentrations of norepinephrine, a nervous system hormone that signals blood vessels to constrict and ratchets up blood pressure, researchers report. Treating these individuals with electroshock therapy lowers their norepinephrine concentrations—and their heart rate and blood pressure too, scientists find.

A fast pulse, vessel constriction, and high blood pressure are valuable tools in a person's fight-or-flight response. But if high norepinephrine concentrations chronically keep a person in that state, it puts a strain on the heart, says Mitchel A. Kling, a psychiatrist at the National Institute of Mental Health in Bethesda, Md. Excess norepinephrine, he says, could partly explain the long-standing connection between depression and heart failure, which is a weakening of the heart. Depression doubles the risk of death in people with heart failure, as do high norepinephrine concentrations.

"Depression is not good for your heart, basically," says Kling.

He and his colleagues conducted standard clinical tests on 22 people with the most severe form of depression and 23 people free of depression. The groups were similar in age. Volunteers with depression had a higher average pulse rate and higher blood pressure than did people in the comparison group. Blood and spinal-fluid samples revealed higher concentrations of three stress hormones—norepinephrine, cortisol, and epinephrine—in study participants with depression than in the others. The stress-hormone differences showed up even during sleep.

Next in the study, eight of the depressed patients volunteered to receive a series of electroshock treatments, which are also called electroconvulsive therapy. Among psychiatrists, electroshock treatment remains controversial. Many depressed people show gains from it, but some complain of memory loss and other side effects. Its benefit sometimes lasts only a few days and, at other times, endures for months or years, Kling says.

The eight patients in Kling's study averaged nine electroshock treatments apiece over roughly 3 weeks. Four weeks after the last treatment, the patients again provided blood and spinal-fluid samples. These showed a clear drop in the concentration of norepinephrine, but not cortisol or epinephrine, the researchers report in an upcoming Proceedings of the National Academy of Sciences.

"To my knowledge, no one has ever looked at the effect of electroconvulsive therapy on the levels of norepinephrine," says cardiologist Inder S. Anand of the Veterans Affairs Medical Center and University of Minnesota in Minneapolis. Combined with other work, this research is "pretty convincing" that stress chemicals such as norepinephrine are being overproduced in the depressed brain, he says.

Even more interesting, he says, is that electroshock can change conditions in the brain to the point of reversing norepinephrine's oversupply.

Made by nerve cells, norepinephrine carries signals between the cells. Electroshock therapy might "reset" overzealous nerve cells in the brain and reduce their norepinephrine production, Kling hypothesizes. But the therapy's long-term benefits in this regard are unknown, he says.

Suppressing norepinephrine might nevertheless offer benefits for patients with heart failure, Kling says. Some of the many antidepression drugs on the market may reduce norepinephrine concentrations too, he says, "but there is surprisingly little data on that."
--------------------------------------------------------------------------------

If you have a comment on this article that you would like considered for publication in Science News, send it to editors@sciencenews.org. Please include your name and location.

References:

Gold, P.W. . . . and M.A. Kling. In press. Cardiac implications of increased arterial entry and reversible 24-h central and peripheral norepinephrine levels in melancholia. Proceedings of the National Academy of Sciences. Abstract available at http://www.pnas.org/cgi/doi/10.1073/pnas.0503069102.

Further Readings:

Aggarwal, A., et al. 2002. Norepinephrine turnover is increased in suprabulbar subcortical brain regions and is related to whole-body sympathetic activity in human heart failure. Circulation 105(March 5):1031-1033. Available at http://circ.ahajournals.org/cgi/content/full/105/9/1031.

Anand, I.S., et al. 2003. Changes in brain natriuretic peptide and norepinephrine over time and mortality and morbidity in the Valsartan Heart Failure Trial (Val-HeFT). Circulation 107(March 11):1278-1283. Available At http://circ.ahajournals.org/cgi/content/full/107/9/1278.

Carney, R.M., et al. 1999. Major depression, heart rate, and plasma norepinephrine in patients with coronary heart disease. Biological Psychiatry 45(Feb. 15):458-463. Abstract available at http://dx.doi.org/10.1016/S0006-3223(98)00049-3.


Sources:

Inder S. Anand
University of Minnesota, Minneapolis
Veterans Affairs Medical Center
1 Veterans Drive
Minneapolis, MN 55417

Mitchel A. Kling
National Institute of Mental Health
National Institutes of Health
Building 10, Room 2D-46
10 Center Drive
Bethesda, MD 20892-1284

Someone sent me this article, which is interesting because I've been taking medication for an underactive thyroid for more than 20 years before my heart failure was diagnosed:

Researchers discover thyroid, heart failure connection
Plain Talk ^ | May 27,2005

Researchers at The University of South Dakota School of Medicine believe they are on the verge of changing the way physicians view the treatment of heart disease.

Along with several colleagues, A. Martin Gerdes, director of the School of Medicine's Cardiovascular Research Institute in Sioux Falls, has recently published groundbreaking research in a nationally recognized medical journal for establishing a connection between low functioning thyroid glands and the development of heart disease. Although treatment on human patients may be some time away, the team is excited at the prospect of standing on the cutting edge in a new trend in the field of heart medicine research.

The study, titled "Thyroid Hormones Induce Unique and Potentially Beneficial Changes in Cardiac Myocyte Shape in Hypertensive Rats Near Heart Failure," appears in the May issue of the American Journal of Physiology-Heart and Circulatory Physiology, published by the American Physiological Society. During the course of his study, Gerdes and his colleagues established that not only can a poorly functioning thyroid contribute to congestive heart failure; it also indicates a reduced likelihood of recovery, and an increased chance of death.

This study builds upon earlier work at the institute which showed researchers that whatever leads to heart failure is always preceded by changes in the shape heart cells. As pressure within the heart increases, stress causes the heart cells to stretch and flatten, and thereby weaken. The new study demonstrates that a moderate dose of thyroid hormones (TH) over 30 days "normalizes" the shape of the cardiac cells (myocytes) and reduces stress on the heart's wall nearly 40 percent.

The research team was pleased not only because the hormone therapy appeared to have a positive effect upon the distorted heart cells, but also because this research involves a new treatment approach.

"This is the first study to look at the implications of thyroid hormone therapy on hypertensive heart failure," Gerdes said.

Based on these encouraging findings, the authors of the paper feel that this new avenue of treatment warrants further study. However, Gerdes warned since "this is the first study to disclose these positive effects with TH, we don't yet have enough information to do this intelligently in humans. Care should be taken in administering TH to humans for heart disease since there is so little information available from animal studies," Gerdes said.

However, Gerdes was optimistic that the successes he and his research team have enjoyed will someday be applied to the treatment of heart disease in humans.

"We're really just looking at the tip of the iceberg here, but we believe this could be the beginning of the next big thing in the treatment of heart disease," Gerdes said.


http://www.plaintalk.net/stories/05...0526050167.html

bunrab: (Default)

Thursday, April 28, 2005

Can you make a cake without sodium? Yes. First off, you DON'T need to add salt to make the cake rise. Many people think that yeast breads and quick breads/cakes won't rise if there's no salt. This is not true. The yeast in bread feeds off of sugar, not salt; salt just speeds it up a little. You can leave salt out of homemade bread willy-nilly. To me, it still tastes fine, but if you are going to be serving bread to people who aren't used to low-sodium cooking, you can do the following: Add a pinch (a spot about the size of the head of a nail) of regular salt to the bread, which is so much less than the recipes call for that the mgs of sodium will still be well under five mg per slice, and 2 pinches of potassium salt (such as NuSalt). You don't want to add more potassium salt for two reasons: (1) it tastes off to people who aren't used to it, and (2) normal people don't need that much potassium and it could even be problematic for them. So don't just substitute a teaspoon of NuSalt for a teaspoon of regular salt. You can also throw in a pinch of powdered ginger, along with your pinches of salt; the bread will not taste like ginger specifically, but it will taste a little less bland.

Back to cakes. Cakes don't use yeast; they use baking powder or baking soda to rise. Baking soda is sodium bicarbonate; baking powder is a mixture of baking soda, cream of tartar, and corn starch - still mostly baking soda, though. However, this is true mainly only in North America. In Europe, it is a lot more common to use baking powder made with calcium rather than with sodium. Calcium has many of the same properties as sodium - the three elements potassium, sodium, and calcium, are near each other on the table of chemical elements and all do similar things. This is why you'll see substitutes for salt involving potassium, and substitutes for baking powder involving potassium OR sodium. As I mentioned above, the substitutes involving potassium have to be used carefully, so that normal people don't get too much potassium; calcium doesn't cause that kind of concern. Most Americans don't get ENOUGH calcium in our diets, and may even benefit from the substitution of calcium-based baking powder instead of sodium-based.

The calcium baking powder most easily available in the USA is Rumford; it uses calcium phosphate instead of sodium bicarbonate. In my opinion, it's also an excellent baking powder; you are not going to lose anything in your baking by switching over to it. It does as good or better a job in cakes as regular baking powder. If your local supermarket doesn't carry Rumford, you can order it here. (Incidentally, according to their web site, Rumford also makes a cornbread mix that uses the calcium baking powder and is completely wheat-free as well.)

Another brand of sodium-free baking powder is Featherweight; it's available from Healthy Heart Market, whose link is to the right of this post. It is made of a mixture of monocalcium phosphate, potato starch, potassium bicarbonate. The potato starch gives it a very slightly different texture from corn starch, and in my opinion it does not rise as well as Rumford; you need to use a little bit more of it. If a recipe calls for a teaspoon of baking powder, try using between one-and-a-quarter teaspoons and one-and-a-half.


And now for something completely different:
A few recent articles about heart failure; I've provided links, but in case you aren't a MedScape member, I've copied the abstracts as well, so you can get the gist of the articles.

The Role of Candesartan in the Treatment of Chronic Heart Failure
http://www.medscape.com/viewarticle/502413?src=mp

Hugh F. Mcintyre
From British Journal of Cardiology
Abstract
The renin-angiotensin system (RAS) plays a fundamental role in cardiovascular pathophysiology. In particular, angiotensin II (AII) has been identified as a culprit in endothelial and vascular damage, elevated blood pressure, and cardiac failure. Pharmacological inhibition of this system is available through two mechanisms; the reduction of AII formation by inhibition of angiotensin-converting enzyme (ACE), and by direct blockade of the type 1 angiotensin II receptor by angiotensin II receptor blockers (ARBs).

Angiotensin-converting enzyme (ACE) inhibitors have a proven role in the management of elevated blood pressure and diabetes and may confer specific vascular benefit. In patients with chronic heart failure (CHF) secondary to left ventricular systolic dysfunction (LVSD), there is extensive evidence that, when compared to placebo, ACE inhibitors reduce morbidity and mortality. Randomised placebo controlled trials have also shown ACE inhibitors reduce all-cause mortality and major cardiovascular events after myocardial infarction.

Given the unequivocal benefit of ACE inhibitors, initial studies with ARBs in patients with LV dysfunction (in CHF and following myocardial infarction) have focused on two areas: the role of ARBs when compared with ACE inhibitors, and when combined with ACE inhibitors.

Only recently, with the results of the CHARM study, have the role of ARBs when compared to placebo in a population with CHF been clarified. This study also addressed the benefit of ARBs in patients with heart failure and preserved LV systolic function.


BNP Levels May Help Guide Carvedilol Therapy for Heart Failure
http://www.medscape.com/viewarticle/503627?src=mp
BY Megan Rauscher
NEW YORK (Reuters Health) Apr 20 - Carvedilol therapy is associated with a sustained decline in brain natriuretic peptide (BNP) levels in patients with congestive heart failure (CHF), research shows. This suggests, according to the investigators, that "serial BNP levels can provide some guidance" regarding the odds of carvedilol-driven improvement left ventricular function.

"Beta-blocker therapy improves symptoms, left ventricular ejection fraction, and survival in patients with CHF, but chronic effects on neurohormones have not been extensively investigated," Dr. Robert P. Frantz, from the Mayo Clinic in Rochester, Minnesota and colleagues explain in the March issue of the American Heart Journal.

They examined the relationship between clinical and echocardiographic parameters and serial neurohormones in 55 patients with CHF, most of whom had nonischemic dilated cardiomyopathy, treated with carvedilol over the course of 1 year. Forty-six patients completed 12 months of follow-up.

"We found that carvedilol therapy is usually associated with a decline in plasma BNP peptide levels," Dr. Frantz told Reuters Health. "The extent of change in BNP levels correlates with extent of change in left ventricular ejection fraction."

Specifically, at 12 months, left ventricular ejection fraction improved from 26% at baseline to 39%, and NYHA class improved from 2.3 to 1.8. BNP levels fell from 453 to 208 pg/mL at 6 months. Compared with baseline, levels remained significantly lower (233 pg/mL) at 12 months (p = 0.01).

"The relationship between changes in BNP levels and ejection fraction suggests that serial measurements of BNP may be a useful guide in monitoring patients with CHF who are being treated with carvedilol, but the relationship is not sufficiently strong to obviate the role for measurement of ejection fraction," Dr. Frantz said.

"If elevated BNP levels do not decline in a patient who is being treated chronically with carvedilol, it suggests that this patient may not have had improvement in ejection fraction and should be evaluated carefully," he added.

Am Heart J 2005;149:541-547.


FDA Approvals: Hyzaar, Panzem, Decapinol
http://www.medscape.com/viewarticle/503708?src=mp

Yael Waknine

April 21, 2005 — The U.S. Food and Drug Administration (FDA) has approved a new indication for losartan potassium plus hydrochlorothiazide tablets, allowing their use to reduce the risk of stroke in patients with hypertension and left ventricular hypertrophy; an orphan drug indication for 2-methoxyestradiol capsules, allowing their use for the treatment of ovarian cancer; and an oral rinse with a barrier mechanism of action for the reduction of gingivitis in patients aged 12 years and older.

Losartan Plus Hydrochlorothiazide (Hyzaar) for Stroke Risk Reduction in Hypertensive Patients With LVH

On April 5, the FDA approved a new indication for losartan potassium plus hydrochlorothiazide (HCTZ) tablets (Hyzaar, made by Merck & Co.), allowing its use to reduce the risk of stroke in patients with hypertension (HTN) and left ventricular hypertrophy (LVH). There is evidence, however, that this benefit does not apply to black patients.

The indication was approved in March 2003 for losartan tablets (Cozaar, made by Merck & Co.), the angiotensin II receptor blocker component of the combination product.

Approval of the indication was based on the results of the landmark Losartan Intervention for Endpoint Reduction (LIFE) study in 9,193 patients, showing that a losartan-based regimen reduced the risk of fatal and nonfatal stroke by 25% in patients with HTN and LVH compared with atenolol-based therapy for a median follow-up period of 4.8 years (total number of strokes, 232 vs 309; P = .001).

Both regimens achieved similar reductions in blood pressure and no significant differences were observed between groups with respect to risk of myocardial infarction or cardiovascular death.

The extension of this indication to the losartan-HCTZ combination tablet was based on the frequency of HCTZ coadministration with the study drug to achieve target blood pressure in both groups of the LIFE trial (losartan, 73.9%; atenolol, 72.4%). In addition, the company demonstrated that the losartan and HCTZ tablets used in the trial were bioequivalent with the combination drug.

The FDA notes that in the LIFE trial black patients with HTN and LVH receiving losartan had a higher risk of stroke compared with those receiving atenolol. This finding has not been confirmed thus far because of the difficulty of interpreting subset differences in large clinical trials. However, trial data do not support use of losartan for the reduction of cardiovascular risk in hypertensive black patients with LVH.

Losartan potassium plus HCTZ fixed-dose combination tablets were previously approved for the treatment of HTN. Their use for initial therapy is only warranted in patients with severe HTN in whom the necessity of achieving prompt control of blood pressure outweighs the associated risks

bunrab: (Default)

Thursday, March 31, 2005

Below are a whole bunch of excerpts, with references to the original articles. I'll summarize what they say, though: CHF patients who have left bundle branch blockage (LBBB) have a worse prognosis than other CHF patients. Biventricular (3-lead) pacing may improve the odds slightly for some such patients.

Why do I care about this? Guess who has LBBB - and in fact, said LBBB was noticed almost 10 years ago, when I was getting my gall bladder removed, and had an EKG. At the time, the doctors thought nothing much of it except that I should remember to mention it before any future EKGs or surgery; in and of itself, LBBB is not supposed to be dangerous. (Sort of like those prolapsed mitral valves aren't supposed to be too bad if that's all that's wrong...) And then, the partial fix for this is the 3-lead pacemaker... that would be the one they couldn't do on me, I have the pacemaker but they couldn't implant the third lead, something weird about the veins back there. Bleah.

Oh well. I've still got other factors in my favor, including having lost lots of weight.

Most of these articles are pretty technical; if you follow the links, be prepared for some very medical-research-y wordiness.

http://www.eurheartj.org/cgi/content/full/25/1/97
Mortality in congestive heart failure complicated by atrial fibrillation
... It is interesting that the proportion of patients with ischaemic heart disease (IHD) was found to be higher (53.3%) in group A (no LBBB or AF) than in the groups of patients with LBBB, AF or both (33.3–35.4%). This suggests that LBBB and AF are more commonly found in association with non-ischaemic cardiomyopathy, and secondly, patients with non-ischaemic cardiomyopathy have a worse prognosis than their counterparts with IHD. The aetiology of CHF may therefore be a confounding factor in this analysis, and it would be interesting to see the effect of AF and LBBB analysed separately for the ischaemic and non-ischaemic subgroups of patients. ...

http://www.eurheartj.org/cgi/content/abstract/23/21/1692
Cumulative effect of complete left bundle-branch block and chronic atrial fibrillation on 1-year mortality and hospitalization in patients with congestive heart failure. A report from the Italian network on congestive heart failure (in-CHF database)
Abstract
Background Many clinical variables have been proposed as prognostic factors in patients with congestive heart failure. Among these, complete left bundle-branch block and atrial fibrillation are known to impair significantly left ventricular performance in patients with congestive heart failure. However, their combined effect on mortality has been poorly investigated. The aim of this study was to determine whether left bundle-branch block associated with atrial fibrillation had an independent, cumulative effect on mortality for congestive heart failure.
Methods and Results We analysed the Italian Network on congestive heart failure (IN-CHF) Registry that was established by the Italian Association of Hospital Cardiologists in 1995. One-year follow-up data were available for 5517 patients. Complete left bundle-branch block and atrial fibrillation were associated in 185 (3·3%) patients. In this population the cause of congestive heart failure was dilated cardiomyopathy (38·4%), ischaemic heart disease (35·1%), hypertensive heart disease (17·3%), and other aetiologies (9·2%). This combination of electrical defects was associated with an increased 1-year mortality from any cause (hazard ratio, HR: 1·88; 95% CI 1·37–2·57) and sudden death (HR: 1·89; 95% CI 1·17–3·03) and 1-year hospitalization rate (HR: 1·83; 95% CI 1·26–2·67).
Conclusions In patients with congestive heart failure, the contemporary presence of left bundle-branch block and atrial fibrillation was associated with a significant increase in mortality. This synergistic effect remained significant after adjusting for clinical variables usually associated with advanced heart failure. We can conclude that this combination of electrical disturbances identifies a congestive heart failure specific population with a high risk of mortality. Copyright 2002 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved
http://adam.about.com/reports/000013_4.htm
...Conditions Associated with Left-Side Heart Failure and Their Effect on Severity
Left-side heart failure tends to be more severe than right-side heart failure, particularly when it is associated with the following conditions:
  • Coronary artery disease.
  • HIV infection.
  • Amyloidosis.
  • Chemotherapy with doxorubicin.
    The outlook is better in patients with left-side heart failure associated with the following:
  • Idiopathic cardiomyopathy (the cause is unknown).
  • Heart failure due to childbirth.

...Other Conditions Associated with Increased Severity in Heart Failure
Weight Issues. If heart failure patients are overweight to begin with, their condition tends to be more severe. Once heart failure develops, however, an important indicator of a worsening condition is the occurrence of cardiac cachexia, which is unintentional rapid weight loss (a loss of at least 7.5% of normal weight within six months).
Impaired Kidney Function. In one study of patients with advanced heart failure, impaired kidney function was the most important indicator for a poor outlook, even more so than heart function itself. (In the study, impaired kidney function was not associated with heart failure.)
Congestion (Fluid Buildup). According to one study, patients with severe symptoms who have congestion (fluid buildup) have poorer survival rates than those without fluid build up. In fact, two-year survival rates are 87% in those who were congestion-free compared to 41% to 67% in patients with various signs of congestion (e.g., swelling, difficulty breathing when lying down, weight gain from fluid buildup).
Atrial Fibrillation. This abnormal rhythm is a rapid quivering beat in the upper chambers of the heart. It is a major cause of stroke and very dangerous in people with heart failure.
Left Bundle Branch Block. Left bundle-branch block is an abnormality in electrical conduction in the heart. It develops in about 30% of heart failure patients and is a major risk factor for serious adverse heart events.
Sleep Apnea. With this disorder a person stops breathing during the night, perhaps hundreds of times, usually for periods of 10 seconds or longer. It is a very strong risk factor for heart failure, and patients with apnea have a higher mortality rate than those without it.
Depression. The presence of depression indicates a poorer outlook. Studies indicate that depression may have adverse biologic effects on the immune and nervous systems, blood clotting, blood pressure, blood vessels, and heart rhythms.
Seasonal and Daily Patterns. More emergency room visits and higher mortality rates have been observed during winter months and on Mondays in patients with heart failure. One factor in this higher risk may be sudden and strenuous exertion, particularly snow-shoveling, which is associated with a risk for heart attack in people with heart problems.


This one's an explanation of what LBBB is and why bi-ventricular pacing may help:

 

http://www.brighamandwomens.org/cvcenter/Patient/crt.asp
... Some patients with cardiomyopathy and CHF have an abnormality of the electrical system. The most common abnormality is a delay in electrical conduction through the left bundle branch. This is known as left bundle branch block (LBBB). Because the electrical signal to the left ventricle is delayed by left bundle branch block, the right ventricle begins to contract a fraction of a second before the left ventricle instead of simultaneously. The result is an asynchronous, or uncoordinated contraction of the ventricles. This uncoordinated ventricular contraction further reduces the pumping efficiency of an already weakened heart muscle in CHF patients. It is estimated that up to 40% of patients with cardiomyopathy and CHF have an uncoordinated ventricular contraction caused by electrical delay, most often LBBB. This electrical delay is visible on an electrocardiogram (ECG) as widening of the QRS complex and helps to identify patients who might benefits from CRT. (figure 3)... What is cardiac resynchronization therapy?
The idea behind CRT is simple: restoration of the normal coordinated pumping action of the ventricles by overcoming the delay in electrical conduction caused by bundle branch block (also called resynchronization).This is accomplished by means of a unique type of cardiac pacemaker. Common pacemakers are typically used to prevent symptoms associated with excessively slow heartbeats. The pacemaker continuously monitors the patient's heartbeat and delivers a tiny, imperceptible electrical charge to stimulate the heartbeat when necessary. Most pacemakers typically have 2 electrodes (or leads) one in the right atrium and one in the right ventricle, which permits the pacemaker to maintain the normal coordinated pumping relationship between top and bottom of the heart. These leads are connected to a battery pack (pulse generator) placed under the skin in the upper chest. In addition to the 2 leads (right atrium and right ventricle) used by a common pacemaker, CRT pacemakers have a 3rd lead that is positioned in a vein on the outer surface of the left ventricle. (figure 4) ...What to expect from CRT?
The response to CRT may vary greatly between patients. Scientific study involving more than 2,000 patients worldwide have consistently demonstrated modest improvements in exercise tolerance, CHF class and quality of life in most patients. Though these improvements may be noticed almost immediately in many patients, they may not be fully realized for weeks or months in others. Unfortunately, there are a small number of CHF patients who do not benefit from CRT therapy. Further research is needed to identify those patients who are mot likely to benefit.


And off on a tangent,
http://circ.ahajournals.org/cgi/content/full/103/3/375Clinical Investigation and Reports Sex Differences in the Prognosis of Congestive Heart Failure Results From the Cardiac Insufficiency Bisoprolol Study (CIBIS II)
Abstract
Background—Whether female sex is associated with a better prognosis in patients with congestive heart failure (CHF) remains uncertain. The Cardiac Insufficiency Bisoprolol Study (CIBIS) II showed that bisoprolol reduced all-cause mortality and morbidity rates in CHF patients treated with diuretics and ACE inhibitors. We examined whether survival was different in men (n=2132) and women (n=515) enrolled in CIBIS II. Methods and Results—Women differed from men with regard to age, NYHA functional classification, primary cause of CHF, and risk factors such as left bundle-branch block. After adjustment for baseline differences, the probability of all-cause mortality was significantly reduced by 36% in women compared with that in men (hazard ratio 0.64, 95% CI 0.47 to 0.86, P=0.003). Women also had a 39% reduction in cardiovascular deaths (hazard ratio 0.64, 95% CI 0.45 to 0.91, P=0.01) and a 70% reduction in deaths from pump failure (hazard ratio 0.30, 95% CI 0.13 to 0.70, P=0.005) compared with men. Kaplan-Meier survival analysis revealed a significant reduction in all-cause mortality among women treated with bisoprolol compared with men (6% versus 12% P=0.01) but not among women treated with placebo (13% versus 18%, P=0.10). However, this sex/ß-blocker effect was not significant in multivariate analysis. Conclusions—These results indicate that regardless of ß-blocker treatment and baseline clinical profile, female sex is a significant independent predictor of survival in patients with CHF.

Wednesday, March 23, 2005

An article I tore out of Science (www.sciencemag.org) from 9 April 2004, that got lost in a stack and just now came to light, talks about "Renovating the Heart." The abstract says:
Inspired by reports that cell infusions can heal animal hearts, cardiologists are rapidly moving to test the idea in humans."

The therapy being tested involves taking cells from a patient's own body, and injecting them into the ailing heart. No really show-stopping results yet but there have been some successes and some warning signs that cell therapy can be dangerous. Some patients in one study developed arrhythmias - [but then, heart failure patients have a high risk of arrhythmia anyway, so is this due to the cell therapy, or something that would have happened anyway?].

Stay tuned.

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