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Myocardial ischemia is a compromised blood supply to the heart muscle that affects patients with coronary artery disease (CAD). Ischemic CAD patients sometimes experience episodes of arrhythmia abnormal heart beats. Life-threatening arrhythmias known as ventricular premature complexes (VPCs) are treated with antiarrhythmic drugs. It is not known whether this therapy actually reduces the risk of sudden death. Long-term antiarrhythmic therapy to prevent VPC was evaluated in 28 patients receiving the antiarrhythmic drug moricizine for one to 56 months. A transient reduction in drug efficacy was evident in 36 percent of the patients at follow-up. An increase in moricizine was needed in four (14 percent) of the patients. The drug ceased to be effective in another four patients (14 percent). Some patients experienced spontaneous resolution of arrhythmias, late arrhythmic events and delayed side effects. Although moricizine is a safe and effective drug for treating arrhythmias, its long-term ability to control arrhythmias is problematic. It is suggested that drug efficacy assessments be made every year. (Consumer Summary produced by Reliance Medical Information, Inc.)

We hypothesized that patients suffering acute myocardial infarction who have reperfusion arrhythmias (RPA) during intracoronary streptokinase infusion (ICSK) would have different clinical and angiographic characteristics and a larger infarction size than those who achieved reperfusion without RPA. Of 35 patients who received intracoronary streptokinase, 27 had successful reperfusion documented by angiography. Successful reperfusion was accompanied by RPA in eight patients and no RPA in 19 patients. RPA included episodes of ventricular tachycardia in one, idioventricular rhythm in four, junctional bradycardia in one, or AV block in two patients which occurred at the time of reperfusion. Myocardial infarction size was calculated using creatine kinase-MB (CK-MB) isoenzyme time activity curves using standard methods. The mean CK-MB g equivalents (eq) for those with RPA was 71 ± 25 (± 1 SD) and for those with no RPA was 45±24 (p <.04). In patients with RPA, ejection fraction rose 5 ± 14 percentage points before discharge, but fell 10± 13 points in those with RPA (p <.03). There was no difference between groups in total dose of streptokinase, final degree of stenosis of the affected vessel, reocclusion rate, or time from onset of symptoms to reperfusion. We conclude that patients suffering acute myocardial infarction who have RPA during ICSK in most cases have a larger infarction site or a more “stunned myocardium,” as indicated by greater CK-MB release and fall in ejection fraction which is not due to increased time of ischemia.

The relative decrease in cardiac output with ventricular pacing versus “physiologic” modes was measured noninvasively using Doppler echocardiography in 26 patients. Standard echocardiographic measurements of left ventricular size (diastolic diameter), left ventricular function (shortening fraction) and left atrial size were examined to determine which of these variables might best identify patients more likely to benefit from maintenance of atrioventricular (AV) synchrony. Decreases in relative cardiac output, expressed as reduction in the Doppler-derived flow velocity integral, with loss of AV synchrony ranged from 0 to 43% (mean decrease 21%). There was no correlation between left ventricular size or function and effect of pacing mode on relative cardiac output. There was, however, correlation between left atrial size and sensitivity to pacing mode.

The purpose of this study was to determine if baseline Doppler-echocardiographic variables of systolic or diastolic function could predict the hemodynamic benefit of atrioventricular (AV) synchronous pacing. Twenty-four patients with a dual chamber pacemaker were studied. Baseline M-mode and two-dimensional echocardiograms were obtained and Doppler-echocardiographic measurements of mitral inflow and left ventricular outflow were made in VVI mode (single rate demand) and in VDD (atrial synchronous, ventricular inhibited) and DVI (AV sequentially paced) modes at AV intervals ranging from 50 to 300 ms. Forward stroke volume and cardiac output were determined in each mode at each AV interval from the left ventricular outflow tract flow velocities, and the percent increase in cardiac output over VVI mode was determined.

The ability to program different atrioventricular (AV) delay intervals for paced and sensed atrial events is incorporated in the design of some newer dual chamber pacemakers. However, little is known regarding the hemodynamic benefit of differential AV delay intervals or the magnitude of difference between optimal AV delay intervals for paced and sensed P waves in individual patients. In this study, Doppler-derived cardiac output was used to examine the optimal timing of paced and sensed atrial events in 24 patients with a permanent dual chamber pacemaker. The hemodynamic effect of utilizing separate optimal delay intervals for sensed and paced events compared with utilizing the same fixed AV delay interval for both was determined.

To determine the effect of ventricular function on the exercise hemodynamics of variable rate pacing, 16 selected patients underwent paired, double-blind, randomized exercise tests in single rate demand (VVI) or variable rate (VVIR) pacing modes. Ejection fraction and cardiac index were determined by two-dimensional and Doppler echocardiography at baseline and during peak exercise.