New CHF Drugs
Coreg & beta-blockers
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October, 1993 - A patient with severe heart failure often requires hospitalization. In the hospital, IV therapy may begin with nitroprusside sodium (Nipride, Nitropress) or nitroglycerin, combined with IV diuretics (Lasix, Bumex). It is sometimes necessary to add dobutamine (Dobutrex) or dopamine (Dopastat, Intropin). After 48 hours of IV therapy, most patients can be put on oral meds and discharged.
In patients who don't respond well, IV Inocor (amrinone lactate) or Primacor (milrinone lactate) may be used; then epinephrine or rarely norepinephrine (Levophed). If that doesn't control symptoms, use of a balloon inside the heart to help it pump (intra-aortic balloon counterpulsation) or surgically putting in an LVAD may be tried. Heart transplant is used in patients who qualify and cannot be helped any other way.
Title: Advanced congestive heart failure. Inpatient treatment and selection for cardiac transplantation.
Author: Stevenson L W Ahmanson at UCLA Cardiomyopathy Center, UCLA School of Medicine
Source: Postgrad Med, 1993 Oct, 94:5, 97-100, 103-7
Unique Identifier: 94021953
July, 1995 - CHFers usually have shortness of breath and get very tired during exercise. Whether these symptoms are related only to heart function is uncertain. We studied the relationship between symptoms during activity and actual heart function, in CHF patients.
Fifty-two CHF patients were monitored during treadmill testing. During exercise, shortness of breath and fatigue were measured on a scale of 6 to 20 (Borg scale). How much daily activity each patient thought he could do was measured with the Minnesota Living With Heart Failure Questionnaire and the Yale Dyspnea-Fatigue Index (patient surveys).
Maximum treadmill exercise showed Vo2max of 13.4; and increased shortness of breath score to 15.7, fatigue score to 14.8, and PCWP to 28 mmHg.
Perceived shortness of breath had no relation to PCWP. Perceived fatigue corresponded only weakly to fatigue poisons in the blood (lactate). Twenty-one percent of the patients showed normal cardiac output with PCWP less than 20 mmHg during exercise; 42% showed normal cardiac output but PCWP higher than 20 mmHg; and 37% showed reduced cardiac output and wedge pressure greater than 20 mmHg during exercise.
Despite these different responses, all 3 groups showed similar levels of fatigue and shortness of breath at identical workloads and had similar total scores on both questionnaires. There was no relation between the Living With Heart Failure Questionnaire and peak Vo2, and only a weak relationship between the Dyspnea-Fatigue Index and peak Vo2.
The inability to exercise perceived by CHF patients has little or no relation to objective measurements of circulatory, breathing, or metabolic dysfunction during exercise.
Title: Dissociation between exertional symptoms and circulatory function in patients with heart failure
Authors: Wilson JR, Rayos G, Yeoh TK, Gothard P, Bak K
From: Circulation 1995 Jul 1;92(1):47-53
PMID: 7788915, UI: 95308752
February 27, 1996 - High dose oxygen is not good for healthy people but CHF patients are routinely given supplemental oxygen. Whether oxygen changes heart function in CHFers is unknown. We studied 10 patients with class 3 to 4 heart failure who inhaled room air and 100% oxygen for 20 minutes.
We measured cardiac output, stroke volume, PCWP, vascular resistance, arterial pressure, and heart rate. Different oxygen concentrations were studied: room air, 24% oxygen, 40% oxygen and 100% oxygen.
The 100% oxygen reduced cardiac output from 3.7 to 3.1 liters/minute, and lowered stroke volume from 46 to 38 ml/beat per minute, and increased PCWP from 25 to 29 mmHg (none of these are good things). Other oxygen concentrations also lowered cardiac output and stroke volume.
In heart failure, oxygen may have a harmful effect on cardiac output, stroke volume, and PCWP.
Title: Hemodynamic effects of supplemental oxygen administration in congestive heart failure
Authors: Haque WA, Boehmer J, Clemson BS, Leuenberger UA, Silber DH, Sinoway LI
Source: J Am Coll Cardiol 1996 Feb;27(2):353-7
PMID: 8557905, UI: 96152300
1998 - 4.8 million Americans have congestive heart failure. Each year, there are at least 400,000 new cases. The number of deaths per year directly from heart failure increased from 10,000 in 1968 to 42,000 in 1993, with another 219,000 related to the condition. Heart failure is the first-listed diagnosis in 875,000 hospitalizations a year. It is the most common diagnosis in hospital patients age 65 and older. In that age group, 20% of all hospitalizations have a primary or secondary diagnosis of heart failure.
Visits to doctors' offices for heart failure increased from 1.7 million in 1980 to 2.9 million in 1993. More than 65,000 persons with CHF receive home care each year. In 1993, an estimated $17.8 billion was spent for the care of heart failure patients.
The following estimates are from the Framingham study: One in 10 people over age 65 will get heart failure. CHF is twice as common in people with high blood pressure and 5 times greater in people who have had a heart attack, compared to people who have not.
According to the National Health and Nutrition Examination Surveys, equal numbers of men and women have heart failure. Almost 1.4 million people with CHF are less than 60 years old. The disease is present in 2% of persons aged 40 to 59, more than 5% of persons age 60 to 69, and in 10% of persons age 70 and older. Heart failure occurs at least 25% more often among black Americans than among white Americans.
Survival after CHF diagnosis is worse in men than women but even in women, only about 20% survive longer than 8 to 12 years. The outlook is not much better than for most forms of cancer. The fatality rate for heart failure is high, with 1 in 5 persons dying within one year. Sudden death is common in these patients, occurring at a rate about 9 times higher than in the general population.
From: National Heart, Lung and Blood Institute -- Data Fact Sheet
Title: CHF in the United States: A New Epidemic
1998 - Simple tests measuring white blood cell levels (lymphocytes) may predict long-term survival in heart failure patients. This could help cardiologists decide which patients are most in need of heart transplant.
Heart disease raises levels of a stress hormone called cortisol. This stress response can also increase levels of the brain chemical norepinephrine. High levels of norepinephrine wear out the heart quickly, shortening life.
Cortisol levels change over time and are hard to accurately measure. However, researchers say "increased cortisol levels decrease lymphocytes." So, they suspected that low lymphocyte levels in the blood might point to added risk. They studied the one-year and 4-year survival rates of 211 CHFers diagnosed between 1988 and 1995. These patients were considered for heart transplant, so they all had blood lymphocyte tests.
78% of patients with lymphocyte levels below 21% of total white cell count, survived for one year after the test compared to 90% of patients with levels from 21% to 47%. Only 34% of low-lymphocyte patients were alive 4 years later, compared to 73% of those in the higher range. The test is no good for patients who have other conditions that can affect white cell count, such as infection, surgery, heart attack, steroid use, or history of cancer.
The Mayo Clinic team notes that the equipment needed for the test is already in most labs. Expense shouldn't be an issue because white blood cell counts are already a standard part of diagnostic blood tests.
From: Circulation (1998;97:19-22)
January 1, 1998 - New info from the heart failure trial ATLAS shows big differences in drug use from country to country, despite published international guidelines for treating CHF. ATLAS compared low-dose versus high-dose Zestril (lisinopril) (an ACE inhibitor) on survival in 3164 patients in 19 countries. All patients had ejection fraction less than 31% and had class 2, 3 or 4 CHF.
Major differences included:
November, 1998 - Jon's Note: As recently as January of 2000, the CDC has issued warnings about increasing deaths in the United States from germs that cannot be killed even with hospital-strength antibiotics.
It was nothing more than a routine complication. A 4-month old boy in a Tokyo hospital developed a stubborn staph infection after surgery. When tests showed that the microbes were resistant to methicillin (standard treatment), doctors tried vancomycin, considered the "unstoppable antibiotic" of last resort.
The baby did not respond even after a full month, so the doctors tried an experimental treatment: they combined vancomycin with arbekacin (an antibiotic available only in Japan), even though this therapy has a 20% risk of causing kidney failure. At first it seemed to work. "The fever went down. White blood cell count came down. The patient was doing well," says Keiichi Hiramatsu, one of Japan's leading experts in bacterial genetics. "After about 12 days things looked stable and drugs were stopped," he says. Within 2 weeks, the infection was back.
The tiny patient, who had a congenital heart defect that would require several surgeries, spiked a fever. Pus began to drain from the incision. Doctors found abscesses under his skin. The infection had come back with a vengeance. When researchers tested a specimen from the baby boy, they were stunned by what they found: a strain of Staphylococcus aureus that was resistant to both methicillin and vancomycin. "Usually with vancomycin, a small concentration called level 2 is enough to kill off staph," Dr. Hiramatsu says. "This new strain required level 8. Nothing like it has ever been seen before."
For years experts have feared a super germ. A strain of staph became resistant to penicillin in 1944. By 1996, 35% of all staph were resistant to methicillin. That leaves only vancomycin, and scientists know it will eventually lose its power. "The question was not whether a vancomycin-resistant staph would happen," says Fred Tenover from Centers for Disease Control. "It was only a matter of when."
News of the Tokyo strain was announced by the CDC in 1997. Within days, strains of the new bug (called VISA) showed up in the USA. Doctors reported the first case in a Michigan patient on dialysis. He had to be treated with a ferocious combination of antibiotics. The second case, reported a month later in New Jersey, was also cured with a combination of antibiotics. The third patient died in March of 1998 from complications that included a runaway staph infection.
For now, the new germ is just resistant - not invincible. However, doses of vancomycin 16 to 32 times the usual strength are needed to kill it. Soon that won't be enough to stop it, says Stuart Levy, a professor of medicine at Tufts University School of Medicine. "Resistance emerges in stages. Within a year or two, we'll see a strain of Staphylococcus totally resistant to everything we can throw at it. That's very frightening."
Some 90,000 patients die every year of hospital-acquired infections in the USA. That could double if staph infections become untreatable. Surgical procedures that are now common could become very, very dangerous again - like they were before antibiotics were used at all. Perhaps worst of all, we could find ourselves helpless against certain bacteria and a simple kitchen cut or scraped knee that got infected could prove fatal.
Staph isn't the only worry. Many disease-causing bacteria are finding ways to brush aside the drugs used against them. Several strains of common bacteria are already untreatable, including vancomycin-resistant enterococcus, Myco-bacterium tuberculosis, and Pseudomonas aeruginosa.
Mutating with every new generation, pathogens develop ways to escape drugs that target them. Germs have an advantage because they reproduce very fast. A population of bacteria can double in size every 20 minutes, offering lots of chances for mutations to happen. Once a strain of bacteria develops the genes for drug resistance, it can share them with other strains, even in different species of bacteria. As resistant genes enter the gene pool, bacteria gain multi-drug resistance by putting together sequences of movable genes called plasmids one after another, like beads on a chain.
That vacomycin resistance happened at all is scary, says Paul Axelsen, from the University of Pennsylvania. "The chance of one mutation is probably one in a million," he says, "and vancomycin resistance depends on the mutation of 8 enzymes. So we're looking at 8 new proteins, each made up of hundreds of amino acids. That means the odds of evolving resistance to vancomycin may be something like a million to the millionth power. It's almost inconceivable." But it has happened.
The minute any new antibiotic comes into wide use, germs start mutating to survive it. Because weaker germs are killed off, our medical treatment gives resistant bugs more room to reproduce. "That's the problem," says Dr. Levy. "The more widely these drugs are used, the more quickly they lose their power." Using a drug on and off in a patient is the ideal way to create resistance. Once a resistant germ appears, it can spread easily wherever seriously ill people or patients with weak immune systems contact each other - in hospitals and intensive care units, for example. This is where resistant microbes first occur.
Even using anti-bacterial soaps can cause genetic changes that produce resistance. More troubling is the use of antibiotics in animals. Of the 50 million pounds of antibiotics produced in the United States each year, more than 40% is used in livestock and other animals. Of that, less than 20% is prescribed to fight infections. The rest is used to stimulate growth - a practice many blame for spurring development of resistant bacteria.
"There's been a tendency to think of human resistance and animal resistance as very different but they're not," says Dr. Levy. "When genes for resistance happen, whether from human or animal use of a drug, they're part of the shared gene pool." The widespread use of the drug avoparcin in cattle helped spawn vancomycin immunity. In one case, a drug resistant form of salmonella found in hamburger meat was traced to a farm that used antibiotics to increase growth in cattle.
A number of drugs have been designated not for use in humans to keep resistance from crossing over. But as old standbys fail, researchers have turned to animal drugs to create new drugs, some of which are already less potent because of their use in animals to increase growth. The use of virginiamycin in animals led to bacteria resistant to Synercid, an antibiotic approved by the FDA not long ago for humans. That's very troubling because Synercid is one of the few drugs that may be able to replace vancomycin.
Some European nations have restricted the use of antibiotics as growth agents for livestock. FDA officials say they are looking into the issue. (Jon's Note: As of 2002, the FDA is still sitting on its thumbs on this issue) Meanwhile, even drug makers have agreed there could be real danger. One major drug company recently warned against overuse of fluoroquinolones in animals because the drugs would become less effective in humans.
Can doctors do anything to stop this trend? Yes. As many as one of every 6 office visits results in an antibiotic prescription, many of them unnecessary. Of the 145,000,000 prescriptions for antibiotics written in doctors' offices each year, up to half are not medically justified, said the National Academy of Sciences' Institute of Medicine in 1997. Of the 190,000,000 antibiotic prescriptions written for hospitalized patients, 25 to 45% are not needed.
Consider the common cold. In 1992, about 12,000,000 antibiotic prescriptions were written for colds, upper respiratory infections, and bronchitis. That's about 20% of all antibiotics prescribed to adults. A researcher at the University of Colorado Health Sciences Center found that antibiotics were prescribed for 50 to 70% of these conditions - an astonishing figure, considering that viruses account for about 90% of all such cases and viruses do not respond to antibiotics.
Patients want something to show for the time and expense of an office visit. According to a 1997 study, doctors are 10 times more likely to prescribe an antibiotic when they think a patient expects it. In another study, 21 doctors were asked why they prescribed antibiotics for sore throats when the drugs don't help. One doctor said, "You can't just say, 'It's viral, you don't need antibiotics' because they feel they're being blown off. They feel their illness is not being taken seriously."
Parents of sick kids are no different. In some cases, day care centers insist that a child who's been sick be on antibiotics before he comes back to school. Managed care programs want to reduce costs so there is strong pressure to treat a patient the first time around to reduce the odds of a return visit. It's just easier to write a prescription. Even when an antibiotic is called for, doctors are quick to prescribe a broad-spectrum drug instead of a narrowly targeted one, despite the fact that this shotgun approach causes resistance.
Limiting antibiotic prescriptions could go a long way toward slowing resistant organisms, but even wise use of existing antibiotics will only slow it. We'll continue to need new drugs. Unfortunately, lulled into complacency by the strength of drugs like vancomycin and reluctant to face huge research and testing costs for new drugs, many drug companies scaled back antibiotic development in the 1980s. No new antibiotics were approved in 1993 or 1994 by the FDA.
In some cases, research that might have led to success was abandoned. In the early 1980s the Schering-Plough Research Institute began to develop an alternative to vancomycin. With no profit to be made as long as vancomycin was effective, the company canceled development. Scientists at Eli Lilly now know that a version of that drug works against resistant organisms but the research has been stopped.
Antibiotic research is now cranking up again. About 25 new ones are in the research pipeline but none are expected to take the place of vancomycin. A promising new class of drugs is at least 7 years away, and there are roadblocks to commercial development. Drug makers have a huge interest in promoting the widespread use of new antibiotics, but that kind of overuse is exactly what creates resistance and shortens the life span of antibiotics! The trick is to convince drug makers that it's worth their while to develop such drugs.
For now, doctors have fewer and fewer weapons in the war against microbes. Four months after the doctors found that staph infection in the hospitalized baby, the patient was finally released. When the patient returned to the hospital 6 months later for a planned second surgery, the medical team checked into a cough reported by the baby's mother. A chest x-ray showed nothing, so doctors decided to proceed. Opening up the child's chest, they were appalled to discover an infection of vancomycin-resistant staph.
"The frightening part was that the strain had stayed there for 6 months," says Dr. Hiramatsu. "Even in the absence of vancomycin, it kept its resistance. That tells us this is a very stable strain, here to stay." This super germ is rare so far, but Dr. Hiramatsu has identified what he calls the mother cell - called Mu3 - that converts to vancomycin resistance when the drug is used. It's alarmingly common. No one knows how common Mu3 may be in USA hospitals.
Doctors at Juntendo had to keep that baby's chest cavity open for 2 months in order to swab it with antiseptics 3 times a day. The time-consuming and painful procedure seemed to work but when the patient returned for a third operation months later, doctors once again found vancomycin-resistant staph.
Title: The Antibiotic Crisis
Author: Peter Jaret
Source: Hippocrates 12(11):26-33, 1998
1999 - "You are born with all the heart cells you'll ever have," says Duke molecular biologist Doris Taylor, "Once you damage some heart muscle, it's gone forever. The heart can't regenerate." Yet if you strain your biceps pumping iron, they respond by building new muscle. Taylor decided to try to get that kind of muscle - skeletal muscle - to rebuild dead heart muscle. "The skeletal muscles have specialized cells called myoblasts that reproduce to fix damaged muscles."
She wants to use myoblasts taken from a "plug" of a patient's leg muscle to boost the pumping strength of a failing heart. When enough heart muscle is damaged, it can no longer pump efficiently. The result is CHF.
The advantage of using muscle cells from each patient is that it is their own tissue, which won't be rejected by their immune system. She is testing her idea using rabbits, which have hearts similar to human hearts. Unlike some animals, rabbits have heart attacks just like people. Her early studies show that it is possible to isolate muscle cells from arm or leg muscles, grow them in a lab dish for a few days, and then inject them into the heart, where they live in existing heart muscle. This is called "cellular cardiomyoplasty."
In that study, 2 ways of getting the muscle plugs into the heart were tried. They injected the cells directly into the heart muscle using a needle and syringe. Using this method, the myoblasts took up residence in an area around the injection site but if they injected too much fluid, the heart rhythm became unstable and the rabbits died.
In a second method, they used a catheter to spread the cells into the heart. In this experiment the cells became much more broadly distributed across the damaged section of heart and integrated into the heart muscle. "Usually, if 30 to 40% of the left ventricle is damaged, it leads to heart failure," Taylor said. "We can replace up to 75% of the damaged tissue."
New research is testing how well the cells actually boost pumping strength. Early findings suggest the cells are working and that they improve the heart's function. Since myoblasts are skeletal muscle, which by its nature contracts when stretched, the cells should contract when they are stretched - when the heart's chambers fill with blood.
Taylor also plans to combine her work with Dr. Thomas-Joseph Stegmann's work at in Germany. Those researchers were able to make damaged heart muscle grow new blood vessels using a human growth factor called FGF1. They produced FGF1 with genetic engineering techniques. "If we could combine new blood vessel growth with new muscle formation, we could regenerate heart muscle," said Taylor.
She plans to extend their work into larger animals such as pigs, to see how long they can maintain active pumping in the new cells. If that works, they will try for approval to start human trials.
Source: Science Daily
December 7, 1999 - Less may be better when it comes to taking aspirin after a surgical procedure called carotid endarterectomy. Patients taking lower doses of aspirin were much less likely to have a stroke, heart attack, or die than patients taking higher doses.
In a double-blind trial, Taylor randomized 2800 patients scheduled for the procedure to take daily doses of 81mg, 325mg, 650mg, or 1300mg of aspirin in coated tablets, beginning before surgery and continuing for 3 months afterward.
Thirty days after surgery, the rate of serious vascular events was 5% in both low-dose groups and 7% in both high-dose groups. At 3 months, the rate was 6% for low-dose patients and 8% for high-dose patients. Eighty-five percent of events occurred within 30 days of surgery. Risk of stroke was slightly lower in the low-dose groups but rates of other complications were not affected by aspirin dose.
Researchers also analyzed the data to exclude patients who had been taking 650mg or more of aspirin per day before the trial. In the remaining 1116 patients, the 30-day rate of stroke, heart attack, and death was 4% for low-dose patients versus 8% for high-dose patients. At 3 months, it was 4% versus 10%. No differences were seen between the 81mg and 325mg groups, or between the 650mg and 1,300mg groups.
The researchers discourage reading too much into these results, but as one doctor put it, "Don't take a whole aspirin - just lick it."
Title: Low-dose and high-dose acetylsalicylic acid for patients undergoing carotid endarterectomy: a randomised controlled trial
Authors: Taylor DW, Barnett HJM, Haynes RB, et al for the ASA and Carotid Endarterectomy (ACE) Trial Collaborators
Source: The Lancet, 1999;353:2179-2184
October 1, 1999 - Vasomedical Inc said today that 2 studies on EECP for heart failure were presented at the Third Annual Scientific Meeting of the Heart Failure Society of America.
One study reviewed data from an ongoing safety trial. In this study, patients got 35 one-hour EECP sessions over 7 weeks, in addition to standard drug therapy. This 12-patient study showed EECP to be safe, with no adverse effects. Careful follow-up of these patients did not show any worsening of their heart condition. Benefits by the end of treatment showed a 25% increase in exercise time and a 31% improvement in quality of life scores.
The second study reviewed data on 106 patients with severe left ventricular dysfunction and 278 patients without. Improvement was seen in quality of life and in angina class in both groups after EECP. It was found to be safe and effective for patients with chronic angina regardless of their ventricular dysfunction. EECP treatment is approved for coverage by Medicare.
1999 - When we think of heart failure, we usually think of a person who has an enlarged heart and low EF. We now know that a lot of CHFers have normal systolic heart function: the part of the heart beat cycle when the heart squeezes/contracts - pumping blood out into the body.
In the 1950s, digoxin, mercurial diuretics, and morphine were the only drugs for heart failure. Digoxon was first used in England in 1785 after the active ingredient - foxglove - was recognized in an herbal compound made by an old woman. The woman had successfully treated dropsy (edema) with it.
In the 1800s there were several ways to treat heart failure. Southey tubes were used in France in 1877 to remove edema - up to 40 lbs of fluid in 2 days. These tiny tubes (each one inch long) were pushed through the skin of the foot and lower leg. Southey tubes were connected to tubing which drained into a bucket. Starling's Law of the Heart was discovered in 1912.
In 1948, Hellems and Dexter showed that PCWP gave useful information about the filling pressure of the heart. That led to the Swan-Ganz catheter (right-heart cath, through the neck). Then we were able to measure pulmonary pressures and cardiac output. In the mid-1960s, Dr. Gorlin invented the concept of ejection fraction. Caths came after the lucky discovery by Sones that contrast dye injected into the right coronary artery didn't kill a patient.
Loop diuretics like Lasix became important, as did vasodilators like isosorbide dinitrate, hydralazine, and ACE inhibitors. Franciosa and Cohn found the importance of afterload reduction when they gave nitro to heart attack and heart failure patients. Unfortunately, inotropic drugs usually increase mortality. Surprisingly, beta-blockers give benefit. When metoprolol therapy in CHF patients was first reported in 1975 in Sweden, other researchers thought they were nuts to even try it.
It is impossible to overstate the benefit of surgical procedures over the past 50 years. Valve surgery and bypass surgery improve life span and relieve symptoms. heart transplant saves lives. Other mechanical devices, such as ventricular assist devices, pacemakers, and ICDs, have played a large role.
Until recently, diastolic heart failure (dysfunctin during the part of the heart beat cycle when the heart relaxes) was poorly understood. Systolic dysfunction is when the heart can't pump out enough blood. Diastolic dysfunction, on the other hand, is when the heart cannot properly fill the left ventricle with blood when it relaxes. The left ventricle is not enlarged, diastolic pressures are high, and ejection fraction may be normal. However, patients still have heart failure.
Diastolic dysfunction progresses in 3 phases:
Many factors are at work in DHF. Negative diastolic pressures can create temporary suction in a non-filling heart. There is an "untwisting" action of the heart as it relaxes that can change during heart failure, or in rejection after transplant.
The A-V interval greatly influences the heart's filling times and can be changed for the better with beta-blockers, and biventricular pacemakers. Atrial size, pressure, and stiffness influence the left ventricle's action. Stiffness plays a major role. Heart cell relaxation is strongly influenced by cellular calcium levels and other hormones. Hopefully, a positive lusitropic drug (heart relaxation enhancer) will be found.
Usual treatment for DHF is diuretic use and nitrates to reduce preload, vasodilators such as ACE inhibitors to reduce afterload and slow or stop remodeling; beta-blockers to lower heart rate, and possibly calcium channel blockers to lower afterload and heart rate. There are only 2 trials dealing with CHFers having normal systolic heart function. They were both in 1990.
Thickening of ventricle walls can occur with high blood pressure and aging. Reduced heart relaxation is worsened by improper functioning of the sarcoplasmic reticulum calcium pump called SERCA (sarcoplasmic reticulum calcium ATPase). This pump should return the cellular calcium level to normal, allowing heart cells to relax. Reduced functioning of this pump causes slower heart pumping and relaxation. During stress, fast heart rate shortens the filling period, leading to incomplete relaxation.
Taken from: Heart Failure With Normal Systolic Function CME
January 18, 2000 - Oxygen and CPAP are equally effective for treating Cheyne-Stokes respiration in CHFers.
In this study, Dr. Samuel Krachman detected Cheyne-Stokes respiration in 14 of 25 patients with stable heart failure and an average EF of 17%. The 9 patients with Cheyne-Stokes respiration who completed the study were randomized to a night of oxygen therapy followed by a night of nasal CPAP, or the reverse.
The researchers found that both therapies were equally effective in reducing severe apnea, increasing oxygen saturation, and keeping oxygen saturation above 90% more of the time patients were asleep. Apnea cycle length and heart rate did not change with either therapy.
Sleep-disordered breathing of the Cheyne-Stokes type often happens in patients with severe but stable CHF, Dr. Krachman writes. "Oxygen therapy and nasal CPAP therapy are equally effective in decreasing the apnea index and improving night time oxygen levels in these patients."
Source: Chest 1999;116:1550-1557, Reuters Health
March 20, 2000 - Aspirin's ability to prevent stroke may depend on whether the patient has CAD, says Dr. Robert Hart. His team reviewed 5 trials of aspirin for stroke prevention, covering a total of 52,000 patients. They also reviewed 4 observational aspirin studies.
In the randomized trials, aspirin use had no effect on stroke risk in patients without CAD. Aspirin use did significantly reduce stroke risk in patients with CAD. Aspirin use also reduced risk of heart attack in all patients. In all 4 observational studies, aspirin use in healthy people actually raised risk of stroke.
In the randomized trials, long-term regular aspirin use increased the risk of brain hemorrhage, whether or not aspirin was used before or after a heart-related event. Dr. Hart said, "A small reduction in heart attack risk must be balanced against small increase in risk of major bleeding in the brain."
Source: Arch Neurol 2000;57:326-332
March 28, 2000 - Use of NSAIDs by elderly patients doubles their risk of being hospitalized for heart failure. For those with a history of heart disease, NSAIDs increase the risk by more than 10 times.
Dr. David Henry and Dr. John Page interviewed 365 patients with an average age of 77 years, who were admitted to hospitals with a primary diagnosis of heart failure. Controls were 658 age and sex-matched patients without heart failure admitted to the same hospitals.
NSAID use during the week before hospital admission was linked with 2 to 1 risk for CHF, compared to patients who had not used NSAIDs. Patients with a history of heart disease who used NSAIDs had even higher odds for their first heart failure admission compared to those without such a history.
The higher the dose of NSAIDs taken the previous week, the higher the risk for heart failure hospitalization. "We should discourage use of NSAIDs in people with damaged but compensated heart function," the doctors suggest. "These drugs should be used with caution in such patients, in the lowest possible dose."
Source: Arch Intern Med 2000;160:777-784
June 1, 2000 - Anemia is common in CHF patients and treating their anemia improves heart function and reduces hospitalizations. Dr. Donald Silverberg reviewed the records of 142 heart failure patients and found that 56% were anemic (hemoglobin less than 12g/dL). The worse the CHF, the more likely a patient was anemic: from 9% anemic in class one patients to 79% in class 4.
Twenty-six were still anemic and had severe CHF even after 6 months of maximum heart failure treatment. Treating these anemic CHFers with erythropoietin and IV iron raised their hemoglobin and their EF, even though their heart failure meds were not changed. This treatment also reduced hospitalizations by 92%, improved heart class, reduced Lasix doses, and slowed progression of kidney failure.
Source: J Am Coll Cardiol 2000;35:1737-1744
March 6, 2001 - A gene linked to heart disease is also linked to skeletal muscle disorders. Dr. Jeffrey Towbin identified alpha-dystrobrevin - a protein - in left ventricular disease.
"It is intriguing that all cardiomyopathy genes lead to skeletal muscle disease as well," says Towbin. He says doctors need to recognize the connection between structural heart disease and other muscle disorders. For example, based on this link between muscle and heart disease, patients with muscular dystrophy should be screened early for heart disease.
He added that each gene discovery adds to the understanding that heart disease is linked with complex interaction of proteins. "In heart disease, it's not one gene and one protein that causes the problem. It's many proteins and genes. In most cases, the gene mutations are individual," Towbin said. "Your mutation is not likely to be the same as anyone else's, except those in your family."
Source: Baylor College Of Medicine
May 24, 2001 - Danish researchers recently found little or no "placebo effect" in dozens of studies. In most medical trials, one group of patients takes a new treatment while another group gets a look-alike dummy pill. Neither the patients nor the doctors know who is getting what. Studies sometimes include a third group called a control, who get nothing or just continue standard treatment for their condition.
Researchers combined the findings of 114 studies on all kinds of medical conditions to see how placebo stacked up against no treatment at all. The placebo group usually did about the same as the group getting no treatment at all. Exceptions were in studies using subjective measures, such as when patients tried to describe how much pain they had. Placebo patients in those studies averaged only 15% reduction in pain.
Many textbooks suggest that 1/3 of patients given placebos in trials get better, probably because they believe they are getting an effective treatment. The new research casts doubt on this idea.
Dr. Stephen Schneider has worked on many trials where patients on placebo improved. He said some of those patients would have gotten better with no treatment at all. Also, he said that being in a medical study guarantees regular access to doctors' care, and encourages patients to eat better, exercise more, and otherwise pay more attention to their health.
Source: Associated Press
All information on this site is opinion only. All concepts, explanations, trials, and studies have been re-written in plain English and may contain errors. I am not a doctor. Use the reference information at the end of each article to search MedLine for more complete and accurate information. All original copyrights apply. No information on this page should be used by any person to affect their medical, legal, educational, social, or psychological treatment in any way. I am not a doctor. This web site and all its pages, graphics, and content copyright © 1997, 1998, 1999, 2000, 2001, 2002, 2003, 2004 Jon C.