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At least 19 recordsLinked to original sources
PubMed1991

A comparative study of left ventricular structure and function in elite athletes.

Adaptations to left ventricular (LV) structure and function appear to be dependent on the type, intensity and duration of exercise training. We therefore studied two clearly defined groups of elite athletes, by M-mode and Doppler echocardiography, with a group of inactive individuals as controls. All groups were age matched. Group 1 comprised ten elite endurance athletes with maximal oxygen consumption (VO2 max) of 74.7 +/- 1.43 (mean +/- SEM). Group 2 consisted of ten elite weightlifters with VO2 max 45.3 +/- 2.00. Group 3 comprised of ten inactive individuals with VO2 max 44.5 +/- 2.13. Left ventricular end diastolic dimension was significantly higher in group 1 (5.72 +/- 0.07) than in groups 2 or 3 (5.29 +/- 0.09 and 5.19 +/- 0.09 respectively, p less than 0.001). Left ventricular mass index was significantly higher in groups 1 and 2 (156.4 +/- 5.97 and 138.6 +/- 7.27 respectively) than in group 3 (104.1 +/- 3.16 p less than 0.001). Percentage fractional shortening was used as an index of systolic function and no significant difference was found between groups. Doppler E:A ratio was taken as an index of diastolic function and was found to be significantly elevated in group 1 at rest (3.37 +/- 0.24) compared with 2.38 +/- 0.16 and 1.99 +/- 0.10 in groups 2 and 3 respectively (p less than 0.003). On exercise, the E:A ratio in group 1 was significantly higher than in group 3 (1.95 +/- 0.14 and 1.23 +/- 0.05 respectively p less than 0.001), and tended to be higher than group 2 (1.68 +/- 0.15 p = ns). These data show that both modes of intense training produce left ventricular hypertrophy. Diastolic function is not impaired in the athletes and may be augmented in the endurance athletes.

Adolescent↗
PubMed1991

The inheritance of left ventricular structure and function assessed by imaging and Doppler echocardiography.

The heritability of left ventricular structure and function was studied in 53 pairs of monozygotic and dizygotic twins, aged 18 to 31 years, by means of M-mode and Doppler echocardiography. A significant fraction of the phenotypic variances of left ventricular wall thickness was explained by genetic variance. For the left ventricular internal dimension, however, no genetic effect was found after correction for body weight. After appropriate adjustment a genetic component of 32% was found for aortic peak flow velocity, 55% for stroke distance, and 47% for minute distance. The early and late diastolic peak flow velocities at the mitral valve showed a genetic component estimated at 43% and 26%, respectively. The inheritance of the late/early diastolic peak flow velocity ratio was estimated at 53%. In conclusion, these data suggest a significant genetic component for left ventricular structural features but not for cavity dimension. A significant influence of heredity was detected for left ventricular inflow and outflow characteristics.

Adult↗
PubMed1986

Left ventricular structure and function by echocardiography in ultraendurance athletes.

To determine left ventricular (LV) structural and functional changes induced by ultraendurance exercise training, M-mode LV echograms and Doppler recordings of LV inflow velocity in 26 triathletes and 17 normal subjects were studied. All triathletes trained 20 to 40 hours/week in swimming, cycling and running for more than 2 years. Structurally, triathletes had normal LV systolic and diastolic cavity dimensions, but increased wall thickness (1.05 +/- 0.26 vs 0.80 +/- 0.27 cm in normal subjects, p less than 0.001), increased relative wall thickness, or h/R ratio (0.41 +/- 0.10 cm vs 0.33 +/- 0.11 cm in normal subjects, p less than 0.001), and increased LV mass (226 +/- 60 vs 143 +/- 54 g in normal subjects, p less than 0.001). LV mass correlated closely with mean exercise blood pressure during an 8-hour exercise test in 14 triathletes (r = 0.88). Systolic function at rest was similar in both groups, with no differences in fractional shortening or end-systolic stress. Diastolic LV function measured by digitized M-mode echo was similar in normal subjects and triathletes, with no differences in peak rates of cavity enlargement and wall thinning by echocardiogram. In contrast, the Doppler-derived ratio of early-to-late LV inflow velocities was slightly increased in triathletes (p less than 0.05). It is concluded that ultraendurance training produces a physiologic pattern of moderate pressure overload LV hypertrophy, in proportion to the hemodynamic load imposed during prolonged exercise. Unlike the abnormal hypertrophy of systemic hypertension, early diastolic function remains normal in the triathlete heart.

Adult↗
PubMed1992

Effects of 4 weeks endurance training on cardiac left ventricular structure and function.

1. The effect of 4 weeks of moderate exercise training on cardiac left ventricular structure and function was examined by repeated echocardiographic/Doppler examination in 10 previously sedentary volunteers participating in a single blind, sedentary phase controlled, cross-over study. 2. Left ventricular internal diastolic diameter increased after 4 weeks of training from 4.98 to 5.11 cm with a further increase to 5.24 cm after 2 weeks of detraining (s.e.d. 0.05 cm, P < 0.01). These increases were still significant after adjustment for heart rate which fell from a pretraining average of 67.0-59.9 beats/min after 4 weeks of training. 3. There were no significant changes in systolic diameter or function and left ventricular wall thicknesses were unchanged during training, but were thinned after 2 weeks subsequent detraining. 4. The ratio of early to late transmitral filling velocity (E/A ratio) was significantly increased by training. Although E/A ratio was shown to be heart rate sensitive, training effects were still evident after adjustment for heart rate. 5. These changes in left ventricular volumes and function may contribute to the cardiovascular reflex changes previously shown to be produced by identical training programmes.

Adult↗
PubMed1992

Gender differences in left ventricular structure and function in young adults with normal or marginally elevated blood pressure.

Gender differences in left ventricular structure and function were evaluated in 68 male and 69 female young adults (mean age 30 +/- 7 years) with normal or marginally elevated blood pressure. Left ventricular mass index was greater in men than in women, even after controlling for blood pressure. There were no significant gender differences in left ventricular systolic function. Doppler indices of diastolic filling were also similar in men and women. Thus, men have a significantly greater left ventricular mass index than women, but this difference in ventricular size is not associated with differences in systolic or diastolic function.

Adult↗
PubMed1992

Effect of chronic supraventricular tachycardia on left ventricular function and structure in newborn pigs.

OBJECTIVES: The purpose of this study was to examine the effects of supraventricular pacing tachycardia on left ventricular function and myocardial structure in newborn, immature pigs and to determine whether immature pigs respond to supraventricular tachycardia differently from adults. BACKGROUND: Previous studies have shown that supraventricular tachycardia causes dilated cardiomyopathy in adult animals; however, in humans, supraventricular tachycardia-induced congestive heart failure occurs most frequently in children and newborns. Because some clinical diseases may cause myocardial failure in adults but rarely do so in children, it was hypothesized that the effects of supraventricular tachycardia in newborns may be different from those in adults. METHODS: In two groups of newborn swine (3 weeks of age), left ventricular volume, mass and function were assessed with simultaneous echocardiography and cardiac catheterization and myocardial structure was examined with light and electron microscopy. Six piglets underwent 3 weeks of left atrial pacing tachycardia (240 beats/min) and six littermates served as a control group. Both groups were followed up for 3 weeks. RESULTS: At the end of the protocol, left ventricular dimensions increased in the piglets with supraventricular tachycardia compared with values in the control group, but there were no differences in left ventricular mass. Systolic function, assessed by fractional shortening, peak ejection rate and maximal rate of pressure development, was decreased in the group with supraventricular tachycardia. The fractional shortening-end-systolic stress relation in the piglets with supraventricular tachycardia decreased below normal values. Left ventricular diastolic function assessed by the relaxation time constant was prolonged, the peak filling rate was decreased and left ventricular stiffness was increased in the supraventricular tachycardia group. The morphologic data demonstrated that supraventricular tachycardia did not change total myocyte volume but did decrease total myofibrillar volume. CONCLUSIONS: Supraventricular tachycardia caused dilated cardiomyopathy in immature pigs. These changes in left ventricular function were associated with a decrease in cellular contractile proteins. Thus, the effects of supraventricular tachycardia on left ventricular function and structure in immature animals were comparable to previous findings in mature animals.

Age Factors↗
PubMed1989

Echocardiographic observation on changes of left ventricular structure and function in healthy elderly.

The method of M-mode and 2-dimensional echocardiography was employed in 81 healthy persons to compare the difference in left ventricular structure and function between the elderly group (n = 41, aged 60-76 years) and the control group (n = 40, 22-58 aged years). The results revealed: 1) Aging of cardiovascular system was structurally as well as functionally reflected by echocardiogram, with echocardiographic findings appearing earlier than clinical manifestations. 2) Myocardial contractility and pump function of the elderly were often maintained in good status at rest. 3) Latent depression of left ventricular diastolic function was frequently seen in the elderly. LAD, AE, MVV and EPSS were found to be sensitive compared with the control group, (P less than 0.05, less than 0.001, less than 0.001, less than 0.001, respectively) and useful indices, which can be readily determined. Therefore, in order to evaluate the status of cardiac structure and function of the elderly accurately, it is important to refer to the normal values of relevant age group and draw conclusions from multi-parameters.

Aged↗
PubMed1988

Left ventricular structure and function, assessed by imaging and Doppler echocardiography, in athletes engaged in throwing events.

Ten male athletes engaged in throwing events and ten control subjects, matched for age, height, and weight, were investigated with echocardiography and Doppler velocimetry to assess cardiac structure and systolic and diastolic left ventricular function at rest. Left ventricular (LV) internal diameter, wall thickness, LV mass, and systolic LV function were not different between athletes and nonathletes. The possibility that strength training could alter LV diastolic function was further investigated. Both early diastolic function, estimated from the velocity of LV relaxation and the LV inflow pattern, and late diastolic function, assessed by Doppler velocimetry, were similar in throwers and controls. The unchanged ratio of the peak velocities of LV filing during atrial contraction and early filling suggests that LV distensibility is unaltered in these athletes. In conclusion, the amount and type of training performed by these throwers was not associated with changes in LV structure and function.

Adolescent↗
PubMed1992

[Myocardial structure and left ventricular function in aortic valvular diseases].

In this study 13 patients with aortic stenosis (AS) and 19 patients with aortic regurgitation (AR) were analyzed to investigate the correlation between myocardial structure and left ventricular (LV) function. LV end-diastolic dimension (Dd), LV end-systolic dimension (Ds), LV Mass Index (LVMI), FS, mVcf and the normalized rate of change of LV dimensions during systole and diastole (-V/Dd, +V/Dd) were assessed using M-mode echocardiography before and after aortic valve replacement. The myocardial structures were investigated from the biopsied specimen in the operation using both light and electron microscopes. Then muscle fiber diameter (Diameter), the degree of interstitial fibrosis (%Fibrosis) and the myocyte volume fraction (%MF, %MT, %SA) were quantitatively evaluated by using a computerized system. And semi-quantitative analysis was made with electron microscopic score (EM-score). The results were as follows. 1. AS group: Left ventricular myocardial degeneration was mild. Significant positive correlationships were found between preoperative LVMI and Diameter (p < 0.01), and between the former and the volume fraction of the myofibrils (%MF) (p < 0.05). And significant positive correlationship was seen between Diameter and %MF (p < 0.05). However, no significant correlationship was seen between preoperative LVMI and %Fibrosis. Both LV systolic and diastolic function (-V/Dd, +V/Dd) showed significantly negative correlationship to LVMI preoperatively (p < 0.01, p < 0.05) and postoperatively (p < 0.05, p < 0.05). And in the patients with preoperative LVMI larger than 300 g/m2 and Diameter larger than 30 microns, +V/Dd was irreversible postoperatively. 2. AR group: EM-score in AR was significantly higher than that in AS (p < 0.05). Preoperative LVMI showed significantly positive correlationship to %Fibrosis (p < 0.01). And postoperative LVMI showed significantly positive correlationship to fibrous content (p < 0.01). Both LV systolic and diastolic function -V/Dd, +V/Dd) showed significantly negative correlationship to LVMI preoperatively (p < 0.05, p < 0.01) and postoperatively (p < 0.01, p < 0.01). And in the patients with preoperative LVMI larger than 300 g/m2 and %Fibrosis larger than 16%, both -V/Dd and +V/Dd were irreversible postoperatively. The above mentioned results indicated that preoperative LVMI and the morphologic parameters were useful to predict the reversibility of the postoperative LV function in both AS and AR.

Adult↗
PubMed1988

Left ventricular structural and functional changes in young men at increased risk of developing essential hypertension. Assessment by echocardiography.

In order to evaluate if left ventricular structural changes are present in young subjects with increased risk of developing essential hypertension, we have investigated young normotensive and borderline hypertensives with and without hypertensive parents. Our results showed, that left ventricular hypertrophy (LVH) was found in these risk subjects and that LVH was associated to borderline hypertension.

Adult↗
PubMed1992

Late onset renal hypertension in old rats alters left ventricular structure and function.

This study was designed to test the hypothesis that the left ventricle of the senescent rat has a limited compensatory response to late onset hypertension. Data were obtained from middle-aged (15 mo) and senescent (24 mo) Sprague-Dawley rats either 1 or 3 mo after the initiation of one-kidney figure-8 renal wrap (Grollman) hypertension. Peak left ventricular (LV) function assessed during acute volume expansion was not markedly affected 1 mo after induction of hypertension with the exception of a decrement in the acceleration of aortic flow (dF/dt) in the senescent hypertensive group. Three months after the surgery was performed, peak LV function (stroke index, stroke volume/g LV, and dF/dt) was depressed in the senescent hypertensive rats, compared with the controls. In contrast, these indexes in the 15-mo-old rats were similar in the experimental and control groups after either 1 or 3 mo of hypertension. Developed pressure, however, was not compromised by hypertension at either age. Cardiocyte hypertrophy due to pressure overload occurred in both age groups but to a greater extent in the senescent group. This cellular response did not cause an absolute increase in LV mass and was associated with endomyocardial foci of cellular degeneration and fibrosis suggestive of cell loss. Mitochondria-to-myofibril volume ratios were not significantly altered in the experimental groups at either age, thus the cellular hypertrophy in these rats was characterized by uniform organelle growth. These data support two important conclusions regarding late onset hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1987

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↗
PubMed1992

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↗
PubMed1991

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↗
PubMedDate not supplied

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↗
PubMed1987

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↗
PubMedDate not supplied

[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↗
PubMed1992

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↗