Cardiologists question some CHF drug therapies
Cardiologists question some CHF drug therapies
Calcium channel blockers are under new scrutiny
As the American College of Cardiology (ACC) holds its 46th annual meeting this month, the news for patients is generally promising. Hospitals are treating more patients with congestive heart failure (CHF) now than 10 years ago, but they’re doing it faster and with better results, according to data from the National Hospital Discharge Survey.
In 1983, the survey showed about 463,000 hospital discharges for CHF. The average length of stay was nearly 10 days and the mortality nearly 10%. By 1993, the last year available for study, CHF discharges had nearly doubled, but hospital stays had dropped to 7.5 days and mortality to 6.1%.
Better drug therapy has contributed to the outcome improvement for heart disease, and many presenters at the ACC meeting are focusing on specific drugs and patient outcomes that is, which therapies are keeping patients with chronic heart disease out of the hospital and which aren’t. Among their findings:
Warfarin
A Massachusetts General Hospital study raises an important question: Why bother with the anticoagulant warfarin? Researchers found that CHF patients discharged on warfarin were worse off six months later than those not taking the drug. Rehospitalization rates both for heart problems and other disorders were higher in the warfarin group, sometimes significantly. Rehospitalizations for CHF averaged 32.5% in the warfarin group, vs. 23.1% in the non-warfarin group.
Metoprolol
One drug that ought to be considered on discharge at least from a cost-control perspective is the beta-blocker metoprolol. Swedish researchers found huge differences in future health care costs between a metoprolol-treated group of patients with idiopathic dilated cardiomyopathy and a similar group taking a placebo. The study suggests that inexpensive metoprolol can slash the cost of cardiac care by 200%.
Haldol
Think twice before using IV haloperidol in critically ill patients. Researchers at Henry Ford Hospital and Wayne State University in Detroit found a substantial risk of torsades de pointes a potentially fatal arrhythmia in critically ill patients given the antipsychotic. While the overall incidence of torsades de pointes averaged 3.6% in critically ill patients, the risk nearly tripled in patients given 35 mg or more of IV haloperidol. A bout with torsades can add as much as a week to the average hospital stay of a critically ill patient.
ACE inhibitors
The ACE inhibitors are once again getting lots of attention from cardiologists, thanks to recent studies that show the drugs reduce mortality and morbidity among CHF patients. ow there’s a new problem: getting doctors to properly prescribe these antihypertensives. Two reports one from the St. Louis College of Pharmacy, the other from Massachusetts General Hospital suggest utilization of ACE inhibitors has increased over the past five years. But in Louisiana, the local chapter of the ACC found that some Medicare patients hospitalized with heart failure may still not be getting ACE inhibitors on discharge.
And researchers at Loma Linda (CA) University think they have the ACE inhibitor cough puzzle solved that is, what causes it? The key is in the effect of ACE inhibitors on the breakdown of two substances: Substance P and Neurokinin A. Substance P stimulates secretion in the bronchioles, while Neurokinin A causes bronchoconstriction. In a comparison of three drugs enalapril, fosinopril, and losartan the researchers found that any time Neurokinin A levels were elevated, patients coughed while on the drugs.
Nearly all patients studied showed increased levels of Substance P while taking ACE inhibitors, but only those with accompanying increased levels of Neurokinin A coughed. Enalapril was the worst offender in the cough department; losartan, the least likely to cause the side effect.
Betaxolol
A University of California Medical School study suggests that preoperative use of the beta-blocker betaxolol can dramatically cut the number of cardiac events in patients undergoing surgery for coronary atherosclerotic disease. Twenty-four patients stabilized on a daily dose of 10 to 20 mg of betaxolol for two weeks prior to peripheral vascular surgery suffered no perioperative cardiac events. However three of 10 patients not taking the betaxolol did.
Amiodarone
The antiarrhythmic amiodarone can’t budge the circadian pattern of sudden cardiac death (SCD). Georgetown University Hospital researchers in Washington, DC, found chronic administration of the antiarrhythmic failed to change the most likely time of SCD. Sudden cardiac death is most likely between six in the morning and noon.
Calcium channel blockers
Mixed press for the calcium antagonists. Australian researchers found an increased risk of repeat myocardial infarction in patients taking diltiazem or nifedipine vs. those on beta-blockers. On the other hand, amlodipine the successor product to nifedipine may help curb the progression of congestive heart failure, according to researchers at the University of Pennsylvania in Philadelphia. Amlodipine appears to reduce levels of interleukin-6, a cytokine that in excess may contribute to a decline of cardiac function in CHF patients.
Hydrochlorothiazide (HCTZ)
The old, inexpensive diuretic does more than lower blood pressure. According to Georgetown University Hospital researchers, HCTZ was the only drug in a six-product comparison that decreased blood pressure and caused a sustained decrease in the size of the left atrium. The other drugs studied included prazosin, atenolol, diltiazem, clonidine, and captopril. The efficacy of HCTZ at lowering blood pressure was confirmed in a Cornell University study in Ithaca, NY, but researchers there found the drug inferior to ramipril in decreasing left ventricular mass. Increased cardiac mass can indicate a poor outcome for hypertensive patients.
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