ACE Inhibitors and Aspirin
Therapeutics and Drugs Briefs
ACE Inhibitors and Aspirin
Source: Guazzi MD, et al. Clin Pharmocol Ther 1998;63:79-86.
Cyclooxygenase inhibitors, such as aspirin (ASA), may counteract the vasodilatory effects of angiotensin converting enzyme (ACE) inhibitors by blocking prostaglandin effects. ACE inhibitors increase prostaglandin levels by increases in bradykinin levels. Thus, Guazzi and colleagues studied 26 patients with mild to moderate hypertension on enalapril monotherapy (40 mg/day) and 26 patients with severe hypertension on enalapril, long-acting nifedipine (30 mg/day), and atenolol (50 mg/day). ASA was tested at doses of 100 mg/day and 300 mg/day. Each drug combination was administered for five days, and an attenuation of ACE inhibitor effect was defined as a 20% reversal of the blood pressure lowering effect by ASA. The 100 mg dose produced no effects. The 300 mg dose antagonized the beneficial blood pressure lowering effects of drug therapy in both groups in about 50% of the patients, which were then termed responders to ASA. No clinical difference between the responders and the nonresponders could be identified. Guazzi et al conclude that about half of the patients on ACE inhibitor therapy for hypertension are susceptible to 300 mg of ASA/day attenuating hypertension control, regardless of the severity of their hypertension.
The major limitations of this study were the fixed sequence of drug administration and the short treatment periods (5 days) without drug washout periods in-between. On the other hand, the investigators and the patients were blinded to the treatment, and the short treatment periods enhanced compliance. Several questions remain about this issue. Whether this attenuating effect will persist long term is unknown. Whether it will apply to heart failure patients treated with ACE inhibitors is unknown. Also, the mechanism of this effect was not elucidated in this study. If the results are reproducible, it would suggest that any attenuating effects of ASA can be avoided by sticking to baby ASA (81 mg). -mhc
Hypertension and Regression of LVH
Source: Ofili EO, et al. JAMA 1998;279:778-780.
Among the original participants in the Systolic Hypertension in the Elderly Program (SHEP), 94 volunteer subjects enrolled in an echocardiographic substudy group. Study subjects were evenly divided between placebo and active treatment (diuretic as initial therapy, adding beta blocker if target blood pressure was not achieved). Most patients required only diuretic for BP control (80%). Baseline echocardiographic data were similar in both active drug and placebo groups.
Over a three-year follow-up period, LV mass increased in placebo recipients (6%) and decreased in the actively treated group (13%). Change in systolic blood pressure and, to a lesser extent, change in diastolic blood pressure correlated with change in LV mass.
Short-term trials of diuretic therapy have generally shown much less favorable results for LV mass reduction than this trial. Similarly, the correlation between BP reduction and LV mass reduction in earlier studies has been weak. Combining these results with the favorable LV regression seen in the Treatment of Mild Hypertension Study (TOMHS), where diuretic fared most optimally in LV changes, suggests that diuretics be viewed more positively in their capacity to regress LVH. -lk
Ineffectiveness of Pneumococcal Vaccine
Source: Ortqvist A, et al. Lancet 1998;351:399-403.
Since middle-aged and elderly individuals may suffer substantial morbidity and mortality at the hands of pneumococcal pneumonia, the efficacy of vaccination in this group is of considerable importance. In order to reduce the size of a study group necessary to demonstrate the relative efficacy of the vaccine, a high-risk group may be selected, in which the prevalence of the investigated end point is predictably higher. This study selected immunocompetent adults, ages 50-85, who had been admitted to the hospital with community-acquired pneumonia (n = 691), and randomized them to Pneumovax or placebo. Duration of follow-up was five years.
A new episode of pneumonia occurred in 16% of the placebo recipients and 19% of Pneumovax recipients (not a statistically significant difference). Similarly, there was no reduction in pneumococcal pneumonia or overall mortality. There was a trend toward a reduction in the rate of bacteremia in Pneumovax recipients (P = > 0.05). Pneumococcal vaccine was safe, without serious adverse events. The authors conclude that Pneumovax did not prevent pneumonia overall, or pneumococcal pneumonia specifically. -lk
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