Two populations of patients with mitral valve prolapse were analyzed to identify factors predisposing to the development of cerebral emboli. Of 760 patients followed for up to five years by our cardiologists with echocardiographically demonstrated mitral valve prolapse (MVP), only one, aged 82 years, has had a stroke. In contrast, of 43 patients admitted to our neurology service with a cerebral embolus and no evidence of carotid or other cardiac lesion and in whom echocardiography was performed, MVP was present in 9. No contributing etiologic mechanisms were uncovered to account for the disparity between the cardiology and neurology populations. However, with the apparent increased incidence of MVP in young patients with cerebral ischemia, both groups require longitudinal follow-up to understand better the factors that predispose a small percentage of patients with mitral valve prolapse to the development of cerebral ischemia.

An asymptomatic 14-year-old male was found at cardiac catheterization to have a coronary artery fistula involving a vessel originating from the left main coronary artery and terminating in the right heart. Chest X-ray and electrocardiogram were within normal limits and shunt flow was too small to be detected by oximetry although a large vessel was seen angiographically. One year later, the previously loud continuous murmur had disappeared and repeat catheterization demonstrated near closure of the fistula. This is the first report documenting the spontaneous closure of a coronary artery fistula.

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Lisinopril, a long-acting, angiotensin-converting enzyme inhibitor, was compared with placebo in a randomized, parallel, double-blind, 12-week study of 193 patients with heart failure. All patients were New York Heart Association Functional Class II, III, or IV and had remained symptomatic despite optimal dosing with digoxin and diuretics. After 12 weeks of therapy, the improvement in treadmill exercise duration was greater in the lisinopril group (113 seconds) compared with the placebo group (86 seconds). This improvement in exercise duration was particularly evident in patients with left ventricular ejection fractions less than 35% (lisinopril = 130 seconds; placebo = 94 seconds). In patients receiving lisinopril, the increase in exercise duration was accompanied by an improvement in quality of life as measured by the Yale Scale Dyspnea/Fatigue Index and in signs and symptoms of heart failure. In addition, the lisinopril group had a larger mean increase (3.7%) in left ventricular ejection fraction when compared with the placebo group (1.3%). Thus, lisinopril, administered once daily for 12 weeks, was well tolerated and efficacious in the treatment of heart failure when used concomitantly with diuretics and digoxin.

No abstract