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Objective. Assess impact of Medicare Part D benefit phases on adherence with evidence-based medications after hospitalization for an acute myocardial infarction. Data Source. Random 5 percent sample of Medicare beneficiaries. Study Design. Difference-in-difference analysis of drug adherence by AMI patients stratified by low-income subsidy (LIS) status and benefit phase. Data Collection/Extraction Methods. Subjects were identified with an AMI diagnosis in Medicare Part A files between April 2006 and December 2007 and followed until December 2008 or death (N = 8,900). Adherence was measured as percent of days covered (PDC) per month with four drug classes used in AMI treatment: angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARBs), beta-blockers, statins, and clopidogrel. Monthly exposure to Part D benefit phases was calculated from flags on each Part D claim. Principal Findings. For non-LIS enrollees, transitioning from the initial coverage phase into the Part D coverage gap was associated with statistically significant reductions in mean PDC for all four drug classes: statins (-7.8 percent), clopidogrel (-7.0 percent), beta-blockers (-5.9 percent), and ACE inhibitor/ARBs (-5.1 percent). There were no significant changes in adherence associated with transitioning from the gap to the catastrophic coverage phase. Conclusions. As the Part D doughnut hole is gradually filled in by 2020, Medicare Part D enrollees with critical diseases such as AMI who rely heavily on brand name drugs are likely to exhibit modest increases in adherence. Those reliant on generic drugs are less likely to be affected. Key Words. Medicare Part D, benefit design, AMI, evidence-based drugs, The advent of the Medicare Part D drug benefit presents an opportunity to explore the impact of cost sharing on patients' use of and adherence with evidence-based medications following an [...]

PURPOSE: To evaluate the pharmacokinetics of furosemide and torsemide before and after diuresis in patients presenting with marked fluid overload. SUBJECTS AND METHODS: We studied 44 patients with New York Heart Association class III or IV heart failure, ejection fraction [less than or equal to] 40%, and an estimated excess fluid body weight [greater than or equal to] 6.8 kg. Oral furosemide or torsemide was administered before and after diuresis. Pharmacokinetic parameters were assessed before and after diuresis. RESULTS: Following diuresis, maximum plasma concentration increased from 11.0 [+ or -] 5.0 [Mu]g/mL to 13.9 [+ or -] 6.8 with torsemide (P [less than] 0.05) and from 3.1 [+ or -] 1.5 to 3.9 [+ or -] 1.9 with furosemide (P = 0.16). Maximum concentration increased by more than 30% in only one third of the patients. Total absorption (by area under the curve method) increased 6% among patients on torsemide (P = 0.38) and 7% among patients on furosemide (P = 0.63) and increased [greater than] 30% in only 1 torsemide and 2 furosemide patients. The time to maximum concentration decreased from 1.40 [+ or -] .82 h to 0.81 [+ or -] 0.36 with torsemide (P [less than] 0.01). There were no differences between furosemide and torsemide in the effects of edema on absorption. CONCLUSION: Marked diuresis altered the pharmacokinetics of both furosemide and torsemide in only a small percentage of patients. The use of adequate doses of oral diuretics in edematous patients may be successful, thereby permitting home treatment with oral diuretics and avoiding the cost of hospitalizations or home intravenous administration services. Am J Med. 1998;104:533-538. [C] 1998 by Excerpta Medica, Inc.

The impact of nonsteroidal anti-inflammatory drugs (NSAIDs) on renal function has not been evaluated in patients with congestive heart failure. Therefore, the renal effects of indomethacin were examined in patients with chronic heart failure, and the relation between the changes in glomerular filtration rate and renal plasma flow after indomethacin administration was assessed. Twenty-five patients with congestive heart failure and an ejection fraction

Previous studies have indicated that patients with an acute myocardial infarction have marked activation of all neurohumoral systems on admission to the hospital. This activation begins to subside within the first 72 hours so that by 7-10 days, all plasma neurohormones have returned to normal. The only documented exceptions were found to occur in patients with left ventricular dysfunction and overt heart failure, where both plasma renin activity and atrial natriuretic peptide were increased, and in patients with left ventricular dysfunction but no overt heart failure, where only atrial natriuretic peptide was increased. Although these studies suggest that neurohumoral activation rarely occurs at that time of hospital discharge, they were small and may have missed an important subgroup of patients with persistent neurohumoral activation. In the Survival and Ventricular Enlargement (SAVE) study, 522 patients had plasma neurohumoral levels measured at a mean of 12 days postinfarction. All SAVE patients had left ventricular dysfunction (left ventricular ejection fraction [is less than or equal to] 40%), but no overt heart failure. In this group of patients, all neurohumoral levels (plasma renin activity, norepinephrine, arginine vasopressin, and atrial natriuretic peptide) were found to be increased compared with age-matched control subjects. These results indicate that, in fact, a subgroup of patients without overt heart failure has persistent neurohumoral activation at the time of hospital discharge postinfarction, and that this activation involves several neurohumoral systems. Since patients with persistent neurohumoral activation postinfarction are likely those most of risk of developing complications and the ones most likely to benefit from pharmacologic interventions blunting the effects of neurohumoral activation, measurement of predischarge neurohumoral levels may be useful. (Am J Cardiol 1991;68:80D-86D)

Congestive heart failure (CHF) is a condition in which the left side of the heart is unable to pump sufficient blood to supply oxygen and nutrients to the body. This is partially attributable to insufficiency of the left ventricle (the chamber of the heart from which blood is pumped to all portions of the body except the lungs) resulting from excessively high vascular resistance. An accepted treatment strategy for decreasing vascular resistance is to administer drugs that cause the blood vessels to relax. Angiotensin-converting enzyme inhibition therapy in the treatment of (ACE) inhibitors are one type of drug used for this purpose. It has been reported that kidney function, which is often compromised in patients with CHF, is also affected by treatment with ACE inhibitors. However, the nature of the change is controversial. In some patients, a dramatic improvement in kidney function is observed; in others, just as precipitous a decline is seen. ACE treatment alters a number of physiological factors influencing the kidney, including blood flow, glomerular perfusion pressure, and others; some of these alterations tend to improve kidney function, other are detrimental. In most patients, the detrimental effects of ACE inhibition are compensated for by other mechanisms, allowing the positive effects (such as improved blood flow) to manifest themselves. In some cases, concurrent therapy for CHF such as blood volume reduction induced by diuretics, or administration of prostaglandin inhibitors, can limit the effectiveness of the compensatory mechanisms; in these cases deterioration of kidney function is seen. (Consumer Summary produced by Reliance Medical Information, Inc.)

* Objective: To examine resting metabolic rate in patients with congestive heart failure as a cause of cardiac cachexia and associated weight loss. * Design: Cross-sectional study. * Setting: Baltimore Veterans Affairs Medical Center. * Patients: 20 men with heart failure (mean age [+ or -] SD, 69 [+ or -] 7 years) and reduced ejection fraction (mean, 0.24 0.10) and 40 healthy men (mean age, 69 [+ or -] 7 years). * Results: Patients with heart failure had smaller fat-free mass than did controls (53 [+ or -] 8 kg compared with 56 [+ or -] 6 kg; P < 0.09), but no difference in fat mass existed (21 [+ or -] 8 kg compared with 19 [+ or -] 8 kg). Measured resting metabolic rate was 18% higher in patients with heart failure than in controls (1 828 [+ or -] 275 kcal/d compared with 1543 [+ or -] 219 kcal/d; P < 0.01); no difference in caloric intake existed (2144 [+ or -] 479 kcal/d compared with 2174 [+ or -] 826 kcal/d). The difference in resting metabolic rate between the two groups was even more striking when indexed per kilogram of fat-free mass. * Conclusions: Higher resting metabolic rate in patients with heart failure at least partially accounts for otherwise unexplained weight loss. Present caloric guidelines, which were established in healthy elderly persons, substantially underestimate the resting caloric needs of elderly persons with heart failure., Weight loss among elderly men with congestive heart failure appears to be at least partially due to an increase in resting metabolic rate. Twenty men aged 62 to 76 years in congestive heart failure were compared with 40 healthy men in the same age range. Despite reporting similar intake of calories, patients in heart failure had smaller fat-free mass but equal amounts of body fat. This was considered a sign of muscle wasting. Resting metabolic rate was 18% higher in patients with congestive heart failure. This higher metabolic rate accounts at least partially for unexplained weight loss. It also suggests that calorie guidelines, which were established in healthy elderly persons, may underestimate the needs of those with congestive heart failure.

Background: Coenzyme [Q.sub.10] is commonly used to treat congestive heart failure on the basis of data from several unblinded, subjective studies. Few randomized, blinded, controlled studies have evaluated objective measures of cardiac performance. Objective: To determine the effect of coenzyme [Q.sub.10] on peak oxygen consumption, exercise duration, and ejection fraction. Design: Randomized, double-blind, controlled trial. Setting: University and Veterans Affairs hospitals. Patients: 55 patients who had congestive heart failure with New York Heart Association class III and IV symptoms, ejection fraction less than 40%, and peak oxygen consumption less than 17.0 mL/kg per minute (or [is less than] 50% of predicted) during standard therapy were randomly assigned. Forty-six patients completed the study. Intervention: Coenzyme [Q.sub.10], 200 mg/d, or placebo. Measurements: Left ventricular ejection fraction (measured by radionuclide ventriculography) and peak oxygen consumption and exercise duration (measured by a graded exercise evaluation using the Naughton protocol) with continuous metabolic monitoring. Results: Although the mean ([+ or -] SD) serum concentration of coenzyme [Q.sub.10] increased from 0.95 [+ or -] 0.62 [micro]g/mL to 2.2 [+ or -] 1.2 [micro]g/mL in patients who received active treatment, ejection fraction, peak oxygen consumption, and exercise duration remained unchanged in both the coenzyme [Q.sub.10] and placebo groups. Conclusion: Coenzyme [Q.sub.10] does not affect ejection fraction, peak oxygen consumption, or exercise duration in patients with congestive heart failure receiving standard medical therapy., Coenzyme Q (sub 10) does not appear to improve symptoms in people with congestive heart failure. Researchers randomly assigned 46 patients with congestive heart failure to take coenzyme Q (sub 10) or a placebo and measured the heart's response to the treatment. Although patients taking coenzyme Q (sub 10) had higher blood levels of coenzyme Q (sub 10), the compound had no positive effect on the heart compared to the placebo. It also had no effect on exercise duration or oxygen consumption during exercise