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.

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.

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.

Prevalence of aortic regurgitation by color flow Doppler in relation to aortic root size.

To determine whether there is a correlation between aortic root size and the prevalence of aortic regurgitation, we performed color flow Doppler echocardiographic studies on 1015 consecutive patients during a 3-month period. Patients were grouped according to their M-mode aortic root diameter as measured in the left parasternal position. The measured groups ranged from 2.0 to 4.5 cm, grouped at 0.1 cm intervals. As the aortic root size enlarged, the prevalence of aortic regurgitation increased linearly (p less than 0.001; correlation coefficient, r = 0.75). At an aortic root size in the "small normal" range of 2.0 to 2.4 cm, the prevalence of aortic regurgitation was 0% to 15%. In the "intermediate" and "top normal" ranges of 2.9 to 3.7 cm, the prevalence of aortic regurgitation increased linearly from 15% to 47%. With aortic root dilation, the prevalence of aortic root regurgitation was generally more than 50%. The severity of aortic regurgitation was semiquantified. Aortic root size was not a good indicator for the severity of aortic regurgitation. Patients with moderate and severe aortic regurgitation had variable aortic root sizes. Throughout the range of aortic root sizes, mild aortic regurgitation predominated. We conclude that aortic regurgitation is a common finding in patients with aortic roots that are dilated or are in the "top normal" size range, that the prevalence of aortic regurgitation increases linearly with aortic root size, and that aortic root size does not correlate with the severity of aortic regurgitation.

Left ventricular mural thrombi complicating acute myocardial infarction. Long-term follow-up with serial echocardiography.

To determine the clinical significance of left ventricular thrombi, we used two-dimensional echocardiography to study 261 patients with acute transmural myocardial infarction. Mural thrombi were found in 46 patients. This complication occurred in 34% (44 of 130) of anterior wall infarctions but in only 1.5% (2 of 131) of inferior wall infarctions. An apical wall motion abnormality was present in all patients with thrombus. Severe depression of left ventricular function was not a prerequisite for thrombus formation: the mean left ventricular ejection fraction was 37 +/- 1.5%. Forty-three patients with left ventricular thrombi were followed for a mean duration of 15 months with serial echocardiography. None of the 25 patients who received anticoagulation treatment had an embolic event. Embolization occurred in 7 of 18 patients who had not received anticoagulation treatment. All embolic events occurred within 4 months of infarction. Although anticoagulation treatment appeared to provide protection against embolic events, the prevalence of left ventricular thrombi on follow-up echocardiographic study was essentially the same whether or not this treatment was used.

Immediate diagnosis of acute myocardial infarction by two-dimensional echocardiography.

To define the role of portable two-dimensional echocardiography (2-D echo) in the immediate diagnosis of acute chest pain syndrome, 80 consecutive patients were studied. Adequate 2-D echo studies were obtained in 65 (81%). Thirty-three patients had clinical evidence of transmural or nontransmural acute myocardial infarction (AMI), 18 of whom had nondiagnostic initial ECGs. Thirty-two did not have a clinical AMI. Thirty-one of the 33 (94%) patients with clinical AMI had regional wall motion abnormalities on the initial 2-D echo; the other two had uncomplicated nontransmural AMIs, diagnosed only by ECG in one and by ECG and moderate elevation of CK-MB isoenzyme in the other. Twenty-seven of the 32 patients without clinical AMI had normal regional wall motion on the initial 2-D echo and none had a complication (severe arrhythmia, recurrent pain, heart failure or death) during the hospital course. Conversely, 10 of the 36 patients with initial 2-D echo regional wall motion abnormalities had a complication (p less than 0.05). Thus, in patients with acute chest pain syndrome, an initial 2-D echo that shows no regional wall motion abnormality suggests that such patients will not develop an AMI or clinical complication during the hospital course. An initial 2-D echo with regional wall motion abnormality identifies a high-risk group of patients who are likely to have AMI and important cardiac complications and may, therefore, benefit from admission to an intensive care unit.

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.

Delayed peak of the posterior wall. A new echocardiographic index of posterior wall aneurysm.

Delayed posterior wall (PW) peak in the detection of PW asynergy was studied by M-mode echocardiography in 53 patients with angiographically proven PW aneurysm, hypokinesis and normal PW. The timing of the PW peak was evaluated by the intervals between (1) the aortic valve closure (Ac) and the PW peak, and (2) the R wave of the electrocardiogram and the PW peak (R-peak). The PW excursion predicted only 39 percent with aneurysm and none with hypokinesis. In contrast, 13 of 18 patients with aneurysm and 4 of 13 patients with hypokinesis demonstrated significantly delayed PW peaks occurring between 0.05 and 0.1 sec following Ac (normal 0 to 0.05 sec). A new index, a ratio of R-peak to ejection time (R-peak/ET) of 1.35 or greater was found to be highly indicative of PW aneurysm in 16 of 18 patients.