Ferrel J. Pauletto

Effect of Left Ventricular Hypertrophy and Its Regression on Ventricular Electrophysiology and Vulnerability to Inducible Arrhythmia in the Feline Heart

BACKGROUND Left ventricular hypertrophy (LVH) is associated with an increased risk of death, susceptibility to ventricular arrhythmia, and multiple electrophysiological abnormalities. The purpose of the present study was to determine whether the susceptibility to arrhythmia and electrical abnormalities persists after regression of hypertrophy in an animal model of LVH. METHODS AND RESULTS We placed constricting bands on the ascending aorta of cats (n = 9) or performed sham operations (n = 9). Serial cardiac echocardiography was performed to measure left ventricular wall thickness. After LVH had developed in the banded animals, the constricting bands were removed and serial echocardiograms were used to monitor for regression of hypertrophy. Electrophysiological studies were performed in cats that showed regression of LVH (Regress, n = 5), those that showed no change in LV wall thickness (No Regress, n = 4), and in the sham-operated animals (Sham). Cats with persistent LVH had a higher incidence of inducible polymorphic ventricular tachycardia (4 of 4) compared with Regress (1 of 5) or Sham (1 of 9) cats (P < .05) and had lower ventricular fibrillation thresholds (9 +/- 2 mA) than Regress (17 +/- 4 mA) or Sham (16 +/- 3 mA) cats (P < .05). Persistent LVH in the No Regress group was associated with prolongation of epicardial monophasic action potential duration (MAPD) in the left but not the right ventricle. Dispersion of refractoriness was greater in the No Regress group (P < .05 versus Regress or Sham). Regress cats were identical to Sham cats in having a low incidence of inducible polymorphic ventricular arrhythmia, high fibrillation threshold, and MAPD measurements (P = NS versus Sham). CONCLUSIONS LVH produces multiple electrophysiological abnormalities and increased vulnerability to inducible polymorphic ventricular arrhythmia in this model of LVH. Cats that show regression of hyperthrophy have normal ventricular electrophysiology and have the same low vulnerability to inducible ventricular arrhythmia as Sham animals.

A new approach to visualize the left main coronary artery using apical cross-sectional echocardiography

Patients undergoing coronary arteriography were studied to evaluate the feasibility of use of cross-sectional echocardiography to detect the left main coronary artery. Visualization of the left main coronary artery from the cardiac apex was attempted using a cranial transducer angulation. With this approach, the left main coronary artery was adequately visualized in 27 of 35 consecutive patients (77 percent) who were prospectively evaluated; in 12 of the 27 the bifurcation was clearly seen. In 26 of the 27 patients cross-sectional echocardiography correctly assessed the patency of the left main coronary artery as judged with coronary angiography. One patient had a false positive echocardiographic study; there were no false negative studies. A comparison of the short axis versus apical cross-sectional techniques in another group of 30 patients revealed the superiority of the apical approach in visualization of the left main coronary artery and its bifurcation; combined use of both techniques allowed for a 93 percent (rate of) success. Thus, apical cross-sectional echocardiography permits visualization of the left main coronary artery and its bifurcation and, therefore, has the potential for detecting left main coronary obstructive lesions.

Use of multiple views in the echocardiographic assessment of pulmonary artery systolic pressure

The purpose of this study was to determine which echocardiographic views most reliably demonstrate the maximum velocity of a tricuspid regurgitant jet in the evaluation of pulmonary artery systolic pressure. Consecutive patients seen in three echocardiographic laboratories during a 3-month period were enrolled. A complete Doppler examination was performed on each patient, including a continuous-wave Doppler evaluation of tricuspid regurgitation in each of seven views. All seven views were used to determine the maximum velocity of tricuspid regurgitation. Of the 1163 studies, 866 (75%) had some tricuspid regurgitation by color-flow Doppler and 614 (53%) had a measurable velocity of tricuspid regurgitation in at least one view. No single echocardiographic view consistently yielded the maximum velocity of tricuspid regurgitation. The apical four-chamber view alone was inadequate. All seven views must be used to be certain that the maximum velocity of tricuspid regurgitation has been obtained.

Effect of an intravenous angiotensin-converting enzyme inhibitor on the electrophysiologic features of normal and hypertrophied feline ventricles

Left ventricular hypertrophy is associated with an increased risk of ventricular arrhythmia and multiple electrophysiologic abnormalities that normalize with regression of hypertrophy. For patients who have hypertension, treatment with angiotensin-converting enzyme (ACE) inhibitors produces regression of hypertrophy and a reduction in ventricular arrhythmia. It is unclear whether the reduction in ventricular arrhythmia associated with ACE inhibitor therapy is due to regression of hypertrophy alone, a direct antiarrhythmic effect of ACE inhibition, or both. We performed electrophysiologic studies in normal cats and cats with fixed left ventricular hypertrophy before and after acute intravenous administration of trandolopril. Trandolopril produced a small, consistent prolongation of monophasic action potential duration in normal and hypertrophied ventricles although this prolongation did not reach statistical significance. Trandolopril had no significant effect on effective refractory period, inducibility of arrhythmia, or ventricular fibrillation threshold in normal or hypertrophied ventricles. These data suggest that the reduction in arrhythmia associated with ACE inhibitors is not caused by a direct electrophysiologic effect but is more likely caused by regression of hypertrophy.