Search

Left ventricular (LV) ejection fraction may not adequately detect a reduction in LV systolic performance resulting from chronic mitral regurgitation (MR), due to ventricular unloading into the low-impedance left atrium. To determine whether LV ejection fraction sufficiently gauges myocardial function in MR, nine patients were studied using micromanometer-measured LV pressures and biplane cineventriculography before and 1 year after mitral valve surgery. Six control patients were also studied. LV ejection fraction was normal in MR patients, despite an increase in LV end-systolic volume index. LV end-systolic pressure-volume and stress-volume ratios in MR patients were lower than in controls (P <0.05 and P <0.01), suggesting that LV systolic performance fell. One year after mitral valve surgery, LV ejection fraction decreased (P <0.05) even though LV end-systolic volume index (P <0.05), pressure-volume (P <0.05), and stress-volume ratios (P <0.01) all improved. Thus, LV ejection fraction inadequately reflected LV systolic function in MR patients before and after mitral valve surgery. Cathet. Cardiovasc. Intervent. 49:290-296, 2000. © 2000 Wiley-Liss, Inc.

The autonomic nervous system appears to modulate ventricular arrhythmias associated with acute myocardial ischemia. This study investigated the electrophysiologic effects and antifibrillatory actions of subacute left stellectomy in a conscious, post-infarction canine model of sudden cardiac death. Twenty-two dogs with a previous anterior wall myocardial infarction and inducible ventricular arrhythmias were randomized to undergo either left stellectomy (n = 12) or remain as sham-denervated controls (n = 10). Five to 7 days post left stellectomy, there were no significant changes in heart rate, electrocardiographic intervals or ventricular refractoriness compared to sham-denervated controls. Acute posterolateral ischemia was produced in left stellectomy and sham-denervated dogs by anodal current-induced thrombosis via a previously positioned electrode in the left circumflex coronary artery. Ventricular fibrillation developed within 1 hour of the onset of ischemia (early ventricular fibrillation) in 3/12 (25%) left stellectomy dogs versus 8/10 (80%) sham-denervated controls (P P = 0.072). Small differences in regional myocardial norepinephrine content, which is a marker for neuronal integrity, occurred in the mid-posterolateral and mid-anteroseptal regions of the left ventricle after left stellectomy. Overall norepinephrine concentration after left stellectomy was 409.70 +/- 9.90 ng/g vs 428.07 +/- 10.84 ng/g in sham controls (P = NS). In summary, subacute left stellectomy significantly reduces the incidence of ventricular fibrillation occurring within 1 hour of the onset of acute posterolateral ischemia at a distance to a previous myocardial infarction in conscious dogs, and tends to reduce the ischemic post-infarction mortality at 24 hours after the onset of ischemia. This protective effect of left stellectomy is not due to any alteration in cardiac electrophysiologic parameters measured prior to the development of acute posterolateral ischemia, nor is it related to re

The electrophysiologic actions of pirmenol, an investigational class I antiarrhythmic agent, were evaluated in eight anesthetized dogs, 5 to 10 days after anterior myocardial infarction. Before administration of the drug, programmed ventricular stimulation failed to initiate nonsustained or sustained ventricular tachyarrhythmias (VT) in any of the postinfarction dogs. After the cumulative administration of 2.5, 5.0, and 10.0 mg/kg pirmenol, programmed stimulation initiated sustained VT in six of the eight postinfarction dogs tested, with one additional dog responding with reproducible nonsustained VT (15 to 20 monomorphic complexes) after pirmenol adminstration. Only one of eight postinfarction dogs tested remained noninducible throughout the primenol dosing schedule. Administration of pirmenol tended to increase ventricular excitation thresholds, relative (p p p <0.01 after 2.5, 5, and 10, mg/kg) refractory periods between ischemically injured and normal noninjured ventricular myocardium. These findings suggest a potential for the provocation or aggravation of ventricular arrhythmias by pirmenol in the setting of recent myocardial infarction.

The antiarrhythmic and antifibrillatory actions of the dextrorotatory isomer of sotalol, administered in a multiple-dose regimen, were evaluated in conscious dogs 3 to 5 days after anterior myocardial infarction. The intravenous administration of d-sotalol, four 8 mg/kg doses over a 24-hour treatment period, suppressed the induction of ventricular tachycardia by programmed electrical stimulation in six of nine dogs tested, slowed the rate of the induced tachyarrhythmia in two of the remaining three dogs, and provided significant protection (5 of 8 d-sotalol vs 0 of 8 vehicle control) against the development of ventricular fibrillation in response to ischemia at a site distant to a previous myocardial infarction. Increases in ventricular myocardial refractoriness and in QTc and paced QT intervals suggest that class III electrophysiologic actions contribute to the antiarrhythmic properties of dextrorotatory sotalol in this animal model. The degree of beta-adrenergic receptor blockade produced by d-sotalol in this dose regimen was negligible. These findings suggest the potential utility of d-sotalol in the prevention of ventricular tachycardia and ventricular fibrillation in the setting of myocardial infarction, particularly when beta-adrenergic receptor blockade is undesirable or contraindicated.

The relationship between inducible ventricular tachycardia in the convalescent phase of myocardial infarction and subsequent spontaneous ventricular fibrillation is uncertain. Thirty conscious instrumented dogs underwent programmed ventricular stimulation 5 days after anterior infarction; 15 had inducible ventricular tachycardia and 15 were noninducible. Following programmed ventricular stimulation, the application of a 150 uA current to the intima of the proximal circumflex artery initiated intimal damage, thrombosis, and acute ischemia of the posterolateral wall. After 20 minutes of ischemia, 73% inducible and 15% noninducible anlmals developed ventricular fibrillation (p p p <0.001) animals. Inducible ventricular tachycardia following infarction was highly predictive of spontaneous ventricular fibrillation during a later ischemic episode in this model. The mass of previously injured myocardium was a critical determinant of both.