Diagnosis and management of pericardial effusions

Pericardial effusions are a relatively common phenomenon, largely in part due to its many possible etiologies. Although a considerable amount of cases are idiopathic, careful history and physical examination will reveal the etiology in a vast majority of patients. The most effective tools, echocardiography and right heart catheterization, should be aimed not only at the diagnosis of the pericardial effusion, but also to the assessment of the severity of the pericardial effusion, since this will determine that individual patient's management. A small, asymptomatic pleural effusion of known etiology can be treated conservatively, mostly by treating the underlying cause and with careful observation for signs or symptoms of deterioration. Large effusions can be treated with closed pericardiocentesis after routine evaluation for possible etiologies. For patients presenting actual or impending tamponade, the definitive treatment is either closed or open pericardiocentesis, depending on fluid accumulation characteristics, and it should not be delayed for the administration of medical treatment (inotropes, intravenous fluids). Routine evaluation of pericardial fluid is warranted in those cases in which a clear etiology was not established prior to pericardiocentesis.

Effects of enalaprilat on hemodynamics and ventricular activation duration in hypertensive patients with left ventricular hypertrophy: clinical evidence of improved excitation-contraction coupling with angiotensin converting enzyme inhibition in human hypertension.

Hypertension is a major risk factor for the development of heart failure. Despite significant progress in our knowledge of the physiopathology of heart failure, the cause for decompensation in patients with left ventricular hypertrophy (LVH) is still obscure. The angiotensin converting enzyme inhibitor enalaprilat has been found to improve electromechanical coupling of heart cells in animal models. To assess the effects of enalaprilat on ventricular electromechanical coupling in humans, we studied the His bundle electrograms and hemodynamics in 22 hypertensive patients with LVH. Patients received either 2.5 mg enalaprilat or saline placebo intravenously in a double-blind protocol. There were no significant changes in heart rate, and atrioventricular and His-Purkinje conduction times. Ventricular activity duration was reduced from 110 +/- 11 msec to 88 +/- 13 msec after enalaprilat administration (P < .01). Enalaprilat decreased peak-systolic and end-diastolic left ventricular pressures, and arterial and pulmonary pressures, as well as pulmonary and systemic vascular resistances. End-systolic wall stress decreased 18% (P < .01), ejection fraction increased 11% (P < .01), and end-diastolic pressure-volume ratio decreased 50% (P < .001) after enalaprilat administration. There were no significant changes in these parameters after saline infusion. It is concluded that enalaprilat reduces ventricular activation duration and improves ventricular performance in hypertensive patients with LVH. Data suggest that enalaprilat significantly improves excitation-contraction coupling in these patients.

The use of biosensors in pacemaker technology: experience with a ventricular rate responsive pacemaker.

Ten elderly patients each had a ventricular rate responsive pulse generator (Activitrax) placed in them to help correct severe conduction abnormalities; none had suspected ischemic heart disease. The pulse generator was programmed to a maximal pacing rate of 125 ppm, a medium activity threshold, and a rate response of 6. Six weeks after implantation of the pulse generator, the patients were evaluated before exercising and again when the pacing rate reached 125 ppm. The evaluation protocol included an M-mode echocardiogram from which the following measurements were taken: the left ventricular end-diastolic volume (EDV), the end-systolic volume (ESV), the ejection fraction (EF), and the peak systolic pressure/end-systolic volume (PSP/ESV). The numerical values were recorded, calculated, and compared statically with the following results: the EDV increased from 91 +/- 10 to 125 +/- 20 cc (p less than .05); the ESV decreased from 64 +/- 10 to 24 +/- 6 cc (p less than .005); the EF increased from 41 +/- 5 to 61 +/- 10% (p less than .05); and the PSP/ESV ratio increased from 1.70 +/- 1 to 4.10 +/- 2 mm Hg/cc (p = 10). Also, during the maximal pacing rate, the septum of all patients showed paradoxical septal motion. All patients in our study have been asymptomatic and have shown an increase in their exercise capacity. We conclude that during exercise the left ventricular function ins influenced more by heart rate than by AV synchrony, as indicated by an elevated EDV in most patients.