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Echocardiographically determined left ventricular structural and functional correlates of complex or frequent ventricular arrhythmias on one-hour ambulatory electrocardiographic monitoring.

The associations between 6 echocardiographic measurements and ventricular arrhythmias on 1-hour ambulatory electrocardiograms were evaluated in 3,348 subjects of the Framingham Heart Study who were free of symptomatic coronary artery disease, congestive heart failure and valvular heart disease and were not receiving diuretic drugs or other blood pressure or cardiac medications. Age-adjusted estimates of association between echocardiographic measurements of left ventricular (LV) structure and function and complex or frequent (Lown grade 2 or greater) ventricular arrhythmia were computed using logistic regression. In this bivariate model only LV internal diameter (systolic and diastolic) and fractional shortening were associated with arrhythmia in both sexes (p less than 0.01). When all variables were entered into a multivariate model, only age and systolic LV internal diameter remained independently associated with arrhythmia (p less than 0.001). Thus, LV chamber size and function are important predictors of risk for ventricular arrhythmia. Systolic LV internal diameter, which reflects both functional and structural information, is the only measurement independently predictive of arrhythmia risk in persons free of apparent heart disease.

Adult

Differences in left ventricular structural and functional changes between pheochromocytoma and essential hypertension. Role of elevated circulating catecholamines.

Experimental findings suggest that catecholamines increase protein synthesis and play a role in cardiac hypertrophy. We hypothesize that elevated circulating plasma catecholamines in pheochromocytoma influence cardiac structural and functional remodeling. We compared 15 patients with surgically proven pheochromocytoma and 15 with untreated essential hypertension; we matched the patients for age, sex, body surface area, and blood pressure (BP) levels. Left ventricular hypertrophy (LVH) was identified by M-mode echocardiography in six patients with pheochromocytoma and in four with essential hypertension. Among both groups there were no differences in cardiac structure, no correlation between left ventricular mass and BP, no significant differences in mitral E-F slope, no correlation between either plasma norepinephrine or plasma epinephrine levels, and no differences in the left ventricular structural indices measured. In the pheochromocytoma group, left ventricular end systolic stress and end systolic diameter were significantly lower and left ventricular percent fractional shortening was higher. Plasma norepinephrine levels were higher in the pheochromocytoma group, but did not differ among patients of that group with and without LVH. We conclude that in both pheochromocytoma and essential hypertension, only a subset of patients develop evidence of LVH, and that in pheochromocytoma, the elevation of circulating plasma catecholamines is not necessarily associated with LVH. These results indicate that factors other than catecholamines and BP determine the development of LVH in pheochromocytoma.

Adolescent

Effect of training on left ventricular structure and function. An echocardiographic study.

To study the cardiac effects of running, 15 healthy non-athletic male volunteers underwent a moderate training schedule for six weeks; thereafter five continued to run at a similar intensity for a further six weeks and 10 stopped. Left ventricular wall thickness and dimension, relaxation, and diastolic function were studied by digitised echocardiography at entry and at two, four, and six weeks, and again at 12 weeks. Significant increases in running ability and maximum oxygen consumption were observed. Maximum oxygen consumption was unchanged in those who continued to run but a reduction was noted in those who stopped. No significant changes in left ventricular dimensions were observed, but the thickness of the posterior wall and the septum increased during six weeks' running. Left ventricular mass (cube volume formula) increased significantly during the first six weeks. Comparison of those who continued to train and those who stopped showed that the former had no change in mass, whereas in the latter mass returned towards pre-exercise values. Systolic function (fractional shortening) was unchanged throughout the study. In addition, no abnormalities of relaxation or diastolic function were detected. Exercise induced left ventricular hypertrophy may develop rapidly during training and the increased myocardial mass resulting from six or 12 weeks' running is not associated with impaired relaxation and diastolic function as found in pathological forms of hypertrophy.

Body Weight

Effects of aging on left ventricular structure and function.

To better characterize the cardiac structural and functional changes that are associated with aging, Doppler-echocardiography was performed on 23 young (mean age, 25 years) and 30 old (mean age, 70 years) healthy normotensive subjects. Left ventricular cavity dimensions and wall thickness were determined and left ventricular mass index was calculated from M-mode echocardiograms. Stroke volume was calculated from Doppler-measured aortic flow. Diastolic filling was evaluated by pulsed Doppler echocardiography of mitral inflow. Posterior wall thickness (1.0 vs 0.8 cm, p less than 0.05) and relative wall thickness (0.42 vs 0.35, p less than .05) were significantly greater in the elderly subjects compared with the younger subjects. Left ventricular mass index increased on average 0.25 gm/m2/yr but was not significantly increased in the elderly compared with the younger subjects (89 vs 77 gm/m2). Shortening fraction and stroke volume did not differ between the two groups. Diastolic filling was dramatically altered with aging, and the elderly subjects demonstrated a doubling of percent atrial contribution (37% vs 19%, p less than 0.0001) and halving of peak early-to-peak atrial velocity ratio (0.85 vs 1.77, p less than .01).

Adult

Left ventricular structure and function by echocardiography in congenital muscular dystrophy.

Cardiac involvement in congenital muscular dystrophy (CMD) has not previously been reported in the literature excepting Japanese ones. The purpose of this study was to investigate the probability of cardiac muscle involvement in 25 patients with CMD. Left ventricular dimensions, wall thicknesses and function were investigated by M-mode and Doppler echocardiography in patients and healthy control subjects. The M-mode echocardiographic data were similar in the two groups. However, the left ventricular mass index in the study group was significantly lower than that of the control group. Left ventricular diastolic function also differed significantly when compared with that of the control group. Mild diastolic dysfunction of the left ventricle might precede manifestations of probable cardiac muscle involvement or subclinical cardiac involvement.

Child

Effects of captopril on left ventricular structure and function in SHR with established hypertension.

While antihypertensive therapy is considered to be an important clinical intervention in hypertensive patients, its effects on cardiac structure and function have not been intensely evaluated. In this study we tested the hypotheses that lowering blood pressure (BP) with the angiotensin I-converting enzyme inhibitor captopril, would: 1) normalize left ventricular mass and increase the cardiocyte mitochondria/myofibrils volume (Vmito/Vmyo) ratio; and 2) not compromise peak ventricular performance. We treated 16-week-old SHR and WKY with captopril (40-80 mg/kg) and hydrochlorothiazide (500 mg/l) via their drinking water. After six weeks of treatment peak cardiac performance was measured during rapid volume overload. Tissue samples from the left ventricular wall were analyzed by electron microscopy and stereology. Captopril lowered BP in SHR and WKY but had no affect on the left ventricular/body weight ratio. The only intracellular change in treated SHR was an increase in sarcoplasmic volume density. Treated WKY exhibited decreased midmyocardial mitochondrial volume density. At peak cardiac output, acceleration of flow and cardiac index were not affected by treatment. Stroke work at peak cardiac output was decreased in the treated groups due to a decrease in mean arterial pressure. In addition, captopril treatment resulted in a shift of the cardiac output (CO)-left ventricular end diastolic pressure (LVEDP) curves, such that LVEDP at peak cardiac output was approximately 50% less in the treated groups compared to their respective control groups. Although captopril was efficacious in lowering BP, it is suggested that lowering BP with this agent does not, at least within six weeks, lead to a reversal of hypertrophy or to a significant alteration in the volume densities of myofibrils and mitochondria. However, an important effect of this antihypertensive drug which may be of clinical significance, is that it leads to a leftward shift of the CO-LVEDP curve in both hypertensive and normotensive rats.

Animals

Myocardial structure and left ventricular function in hypertrophic and dilative cardiomyopathy and aortic valve disease.

Left ventricular biopsies from 126 patients with advanced (EF less than 50%, n = 45) and mild (EF 50-60%, n = 21) and latent cardiomyopathy (EF greater than 60%, n = 60) and 18 additional patients with aortic valve disease and 22 cases with hypertrophic cardiomyopathy were analyzed to define possible correlations between myocardial structure and function. Deterioration of ventricular function was combined with increasing muscle cell diameters (r = 0.47) and increasing nuclear size of the myocytes (r = 0.74) in latent and dilative cardiomyopathies and in patients with aortic valve disease (cell diameter, r = 0.6; nuclear size, r = 0.9). Patients with HCM showed a wide range of cell diameter and nuclear size. 24% of the latter patients had no bioptic evidence of myocardial hypertrophy. The mitochondrial volume of the myocytes was 23% in the normal and hypertrophied myocardium independent of the kind of disease and ventricular function. The volume fraction of the myofibrils continuously decreased with worsening of the left ventricular function in patients with latent and dilative cardiomyopathy (from 45 +/- 6.9 to 37.6 +/- 6.3%) and aortic valve disease (from 46.2 +/- 3.4 to 27.9 +/- 9.3%). Patients with hypertrophic cardiomyopathy presented with normal or slightly decreased values of myofibrils consistent with normal ventricular function (42.5 +/- 5.0). The data demonstrate that the degree of myocardial hypertrophy and certain ultrastructural findings are inversely correlated with left ventricular function.

Aortic Valve

The limited utility of the plain chest film in the assessment of left ventricular structure and function.

The determination of radiographic cardiac size as an estimation of the state of cardiac function is one of the more common correlations made. Despite the widespread use of these measurements, the correlation between cardiac function and radiographic appearance, and the validity of clinical judgments based on this correlation, has not been fully determined. Similarly, the increment in left ventricular chamber size necessary to produce a change in the plain film appearance of the left ventricle has not been defined. The results of a two observer, blind, retrospective analysis of plain film radiographs of the chest, and related quantitative left ventricular angiograms, and left ventricular pressure studies performed on 256 patients is presented. The sensitivity, speficity, predictive value and accuracy of six previously described plain film measurements of left ventricular size together with determinations of the extent of left ventricular volume change necessary to produce a perceptible change in the plain film radiographic appearance of the left ventricle are reported. The performance of each of these measurements proved to be disappointing. A sensitivity of 75% was not possible using any of the methods unless the left ventricular chamber volume was more than 66% above the upper limit of normal.

Cardiac Volume

[Changes in left ventricular function and structure in hypertensive patients treated with methyldopa and urapidil].

In a randomized cross-over and double-blind trial twenty mild-to-moderate hypertensives (11 males, 9 females, mean age 48.4 +/- 7.6 years) were receiving methyldopa (250 mg b.i.d.) or urapidil (30 mg b.i.d.) for 7 weeks and then treated with alternative drug for additional 7 weeks, separated by one week of wash-out period. Both antihypertensives induced significant reduction (P less than 0.01) in systolic and diastolic arterial pressure, while no significant changes (P greater than 0.20) in the body weight and the heart rate were observed. The echocardiographic features of left ventricular hypertrophy (LVH) did not decrease significantly (P greater than 0.05) on either drug, except for the left ventricular posterior wall thickness (LVPWd), which decreased on methyldopa from 10.4 +/- 1.3 to 9.8 +/- 1.4 mm (P less than 0.05). The drugs under study did not change significantly the echocardiographic indices of left ventricular function. Echocardiography resulted to be more sensitive in detecting LVH than electrocardiography. It is concluded that methyldopa might successfully reduce LVH, while direct and indirect vasodilators (such as urapidil) are less effective.

Adult

Comparison of the effects of isradipine and lisinopril on left ventricular structure and function in essential hypertension.

The effects on cardiac structure and function of antihypertensive regimens with different effects on the renin-angiotensin system were compared. In a 1-year study, 32 patients with essential hypertension were randomized to treatment with either the converting enzyme inhibitor lisinopril or the calcium antagonist isradipine; hydrochlorothiazide could be added. Blood pressure (BP) decreased significantly (p less than 0.001) and similarly in the 2 treatment groups. Left ventricular (LV) mass was already significantly reduced after 16 weeks of treatment (p less than 0.001) and remained decreased thereafter, with no difference in the response to the 2 treatment regimens. The change in LV mass was related to the decrease in systolic BP for the total study group (p less than 0.001) and for each treatment group separately. During the 3-week run-out period on placebo, BP and LV mass increased again (p less than 0.01). Afterload decreased during active treatment (p less than 0.001), and fractional shortening of the LV internal diameter was significantly increased (p less than 0.01) to a similar extent in both groups. The ratio of peak mitral flow velocities during atrial contraction and early filling was reduced after 1 year of active treatment in the total study group (p less than 0.01); this change was similar in both groups. The data suggest that the regression of LV mass during antihypertensive therapy is mainly related to the decrease in systolic BP.

Adult

Left ventricular structure and function in normotensive adolescents with a genetic predisposition to hypertension.

It has been suggested that the heart plays an active role in the pathogenesis of arterial hypertension. If this is true, there must be early cardiac involvement in young normotensive subjects who develop hypertension later in life and differences in cardiac morphology or function may exist between young normotensive subjects with different risks of developing hypertension. M-mode echocardiography was performed in 51 normotensive male adolescents with at least one hypertensive parent (SHT). These subjects were compared with 55 normotensive sons of normotensive parents (SNT) and with 25 adolescents with borderline hypertension (BH). Control groups were matched for sex and age. The following morphologic parameters were significantly greater in the SHT group than in the SNT group: interventricular septum (0.54 +/- 0.08 vs 0.49 +/- 0.09 cm/m2; p less than 0.01) and posterior wall (0.54 +/- 0.11 vs 0.50 +/- 0.08 cm/m2; p less than 0.05) thickness, left ventricular mass (125.0 +/- 29.1 vs 109.2 +/- 25.4 gm/m2; p less than 0.005), and cross-sectional area (9.9 +/- 1.8 vs 8.9 +/- 1.6 cm2/m2; p less than 0.005). No significant differences between SHT and BH subjects were observed. Excursion of left ventricular posterior wall was significantly higher in the BH group. No differences were observed between SHT and SNT subjects. These data show that the same kinds of changes in cardiac morphology are present in normotensive subjects with a family history of hypertension and in subjects with borderline hypertension, suggesting that cardiac involvement may precede elevation of blood pressure.

Adolescent

Assessment of left ventricular structure and function by cross sectional echocardiography.

Cross sectional echocardiography can be used to give semiquantitative estimates of ventricular volumes and ejection fraction which are very valuable in detecting the severe abnormalities seen clinically. The technique has also been widely used to study regional abnormalities of wall motion. However, with a frame rate of 30 s-1 and lateral resolution of 3-4 mm critical analysis of disturbances of timing is not possible, so the method should be used in conjunction with M-mode and Doppler techniques. In spite of physical limitations, based on the underlying mechanisms of image generation, its advantages of real time application and noninvasive nature, its ability to demonstrate myocardial thickness as well as echo intensity, and its relative cheapness have made cross sectional echocardiography a major tool in documenting abnormalities of left ventricular function occurring in disease.

Cardiac Volume

Chronic exercise and left ventricular structure and function in healthy human subjects.

Twelve healthy well-trained participants in a supervised exercise program (mean age, 41.3 yr) were compared with 12 sedentary control subjects (mean age, 38.9 yr) with physical characteristics similar to the exercised group (EG) before training. Resting echocardiograms revealed significantly lower heart rates (HR) in the EG compared with control group (CG) but no evidence for cardiac structural differences between groups. Radionuclide angiograms performed at rest and during two levels of supine cycling (HR targets: 120 and 140 beats X min-1) resulted in increases in background-corrected end-diastolic counts [EDC(bc)] and confirmed use of the Frank-Starling mechanism in the majority of subjects. Mean values (+/- SD) for ejection fraction (EF) and normalized peak systolic ejection rate (PSER) (P greater than 0.05 between groups) were the following. (Formula: see text) The results suggested that fitness training does not induce significant cardiac enlargement as apparent from measurements at rest or important changes in contractile state during exercise. Increases in exercise stroke volume with such training may be the result of an increased end-diastolic volume.

Adult

Premature ventricular complex morphology. A marker for left ventricular structure and function.

The shape of a premature ventricular complex (PVC) might reflect the presence or absence of myocardial disease. To test this, 100 patients with a PVC on a 12-lead electrocardiogram at cardiac catheterization or nuclear angiography were classified according to PVC morphology. Group 1 (n = 50) had PVC QRS complexes with either smooth and uninterrupted contour or with narrow (less than 40 msec) notching. Group 2 (n = 50) demonstrated PVC with broad (greater than or equal to 40 msec) notching or shelves. Clinical, electrocardiographic and angiographic variables were assessed to define group differences. All patients had one or more etiological forms of heart disease none of which distinguished either group. Groups 1 and 2 differed with respect to a history of congestive heart failure (12% vs. 66%, p = 0.0004), dilated cardiomyopathy (2% vs. 38%, p = 0.0005), and the presence of mitral regurgitation (13% vs. 58%, p = 0.001), respectively. In group 1, 45 of 50 (90%) patients with a PVC had no notching. Patients in group 2 had greater PVC QRS duration as compared with patients in group 1 (181 +/- 6 vs. 134 +/- 3 msec, p = 0.0001). End-diastolic volume index (EDVI) (78 +/- 3 vs. 139 +/- 11 ml/m2, p = 0.0000) and ejection fraction (EF) (0.59 +/- 0.02 vs. 0.34 +/- 0.03, p = 0.0000) significantly discriminated between group 1 and 2, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult