Increased distance between mitral valve coaptation point and mitral annular plane: significance and correlations in patients with heart failure.

OBJECTIVE: To measure the distance between the mitral leaflet coaptation point and the mitral annulus (CPMA) and assess the relation of this index to structural and functional characteristics of the failing left ventricle. DESIGN: Echocardiographic indices and CPMA were measured at baseline and again during dobutamine infusion and leg lifting. Left ventricular diastolic and systolic dimensions, left ventricular ejection fraction (LVEF) by Simpson's rule, mitral annulus dimension, and E point septal separation were correlated with CPMA. SETTING: Tertiary referral centre. PATIENTS: The total study population of 129 patients included 94 with LVEF < 35% and 35 with LVEF 35%-45%; 76 had coronary artery disease and 53 had dilated cardiomyopathy. INTERVENTIONS: A dobutamine infusion was given in 18 patients and preload increase by leg lifting in 28. MAIN OUTCOME MEASURES: Correlations between CPMA and contractility indices at baseline and during interventions. RESULTS: CPMA was correlated with left ventricular diastolic dimension (r = 0.52), left ventricular systolic dimension (r = 0.53), LVEF (r = -0.44), fractional shortening (r = -0.42), E point septal separation (r = 0.48), and mitral annulus dimension (r = 0.44) (all p < 0.001). Dobutamine decreased CPMA from (mean (SD)) 12.04 (3.64) mm to 8.92 (2.56) mm and increased LVEF from 27 (6.2)% at baseline to 33.4 (6.9)% at 10 microg/kg/min (both p < 0.001). These changes were strongly related (r = 0.68, p < 0.007). After leg lifting, CPMA decreased from 13 (4) mm at baseline to 10 (3) mm (p < 0.001), and LVEF increased from 32 (11)% at baseline to 39 (11)% (p < 0.001). Fractional shortening and left ventricular diastolic dimension also increased (p < 0.001) and mitral annulus dimension and E point septal separation decreased (p < 0.002), but left ventricular systolic dimension did not change. CONCLUSIONS: The mechanism displacing the mitral coaptation point towards the left ventricular apex is multifactorial. The correlations between CPMA difference (before versus after interventions) and ejection fraction difference (before versus after interventions) shows that this index depends mainly on left ventricular function.

Pressor hormone profile during stress in hypertension: does vasopressin interfere with left ventricular hypertrophy?

Neurohormonal factors may account for the fact that patients with similar severity and duration of hypertension develop different degrees of left ventricular hypertrophy (LVH). The purpose of this work was to compare the pressor hormone profiles of hypertensive subjects off medication during exercise testing. Nineteen patients, stratified according to echocardiographically diagnosed absence (Group I n = 6) or presence (Group II n = 13) of LVH, underwent testing on the treadmill according to the Bruce protocol. Both groups were comparable in age, severity and duration of hypertension and reached similar double product at peak exercise. Measurements of plasma renin activity (PRA), plasma catecholamines and vasopressin (AVP) at baseline, peak exercise and post exercise revealed significant differences between groups: Group I had suppressed PRA levels throughout and had significantly higher baseline AVP levels, which increased further at peak effort. Group II had significantly higher baseline PRA levels, which tended to increase further at peak effort, and had suppressed AVP levels throughout. There was a significant negative correlation between percent increments in AVP and increments in double product. Norepinephrine increased significantly with effort in both groups, but the levels attained were higher in Group I. In view of the known negative inotropic action of AVP and the trophic effect of angiotensin, we speculate that lower baseline AVP and higher PRA, together with inability of AVP to increase with effort, may be causally related to development of LVH.

Detection of atherosclerotic lesions in the aorta by transesophageal echocardiography.

Transesophageal echocardiographic studies were prospectively performed in 152 consecutive patients older than age 40 years referred to the echocardiography laboratory to assess the prevalence of atherosclerosis in the thoracic aorta and relate this to a history of systemic embolization. Forty-four patients (29%) had at least 1 atherosclerotic lesion in the thoracic aorta. This was associated with a higher prevalence of coronary artery disease (78% of all patients with coronary artery disease), carotid artery disease (88% of all patients with carotid artery disease) and peripheral vascular disease (all symptomatic patients). Forty-two of all patients (28%) had systemic emboli, 20 (48%) of whom had at least 1 atheromatous lesion in the thoracic aorta. Conversely, only 24 of 110 patients (22%) without previous systemic emboli had atheromatous lesions (p < 0.001). It is concluded that atherosclerotic lesions in the thoracic aorta can readily be identified with transesophageal echocardiography. The detection of atherosclerotic plaques of the aorta represents a marker of diffuse atherosclerotic disease, often associated with carotid, coronary and peripheral vascular disease and with the occurrence of systemic emboli. Transesophageal echocardiography may be used serially to investigate whether dietary or pharmacologic maneuvers, or both, can shrink established atherosclerotic plaques in the thoracic aorta.

Regression of left ventricular hypertrophy with isradipine in previously untreated hypertensive patients.

The regression of left ventricular hypertrophy (LVH) is considered a desirable goal of antihypertensive treatment. Isradipine was used as first-line antihypertensive treatment in 15 patients who had mild-to-moderate hypertension and LVH, and who were studied before and after 6 months of treatment. Left ventricular mass and function were assessed by Doppler echocardiography. Systolic and diastolic blood pressure were reduced from 161 +/- 14 mm Hg and 103 +/- 3 mm Hg to 136 +/- 8 mm Hg and 87 +/- 6 mm Hg, respectively (P < .001). The interventricular septal thickness was reduced by 11.9% (P < .001), posterior wall thickness by 11.1% (P < .001), left ventricular end-diastolic diameter by 2%, and left ventricular mass index by 17% (P < .02). In conclusion, 6 months of antihypertensive treatment of mild-to-moderate hypertension with isradipine achieves a significant regression (17%) of LVH.

Myocardial infarction caused by blunt chest injury: possible mechanisms involved--case reports.

Two cases are reported in which blunt chest trauma caused myocardial infarction. Coronary angiography revealed apical aneurysms in both patients with normal coronary arteries in the first and total occlusion of left anterior descending artery in the other. The main possible mechanisms of myocardial infarction after blunt chest trauma are discussed.