Cardiac Left Ventricular Mass Research Articles

Echocardiographic evaluation of cardiac functions and left ventricular mass in children with malnutrition.

This study was undertaken to assess the left ventricular mass (LV Mass) and systolic and diastolic functions of the left ventricle in children with protein energy malnutrition (PEM). Thirty children, aged between 2 months and 2 years with PEM (four kwashiorkor, seven marasmic- kwashiorkor, 19 marasmus), and 17 healthy, age-matched children, using Doppler echocardiography were studied. The mean LV Mass in the patients was lower than that in the controls (14.5 +/- 5.2 vs 19.8 +/- 4.7 g, P < 0.05). However, the LV Mass/body surface area was not different in the patients with PEM and in the control group (52 +/- 9.2 vs 53.9 +/- 8.2g/m(2), P > 0.05), indicating that LV Mass was reduced in proportion to decrease in body size in malnutrition. Left ventricular septal and posterior wall thickness in PEM were also lower than that in the controls, and the most significant reduction in the LV Mass, septal and posterior wall thickness were found in the kwashiorkor group. Cardiac output was reduced in proportion to decrease in body size in the patient group (1.6 +/- 0.5 vs 2.1 +/- 0.8 L/min, P < 0.05), therefore cardiac index was not significantly different between the patients and the control subjects (5.9 +/- 1.4 vs 5.7 +/- 1.6 L/min/m(2), P > 0.05). Systolic function indices including ejection fraction, fractional shortening, and diastolic function indices were not significantly different in the groups. We demonstrated that LV Mass and cardiac output were reduced in proportion to decrease in body size in patients with PEM, and LV systolic and diastolic functions were preserved in atrophic hearts.

Quantitative trait loci for blood pressure exist near the IGF-1, the Liddle syndrome, the angiotensin II-receptor gene and the renin loci in man.

Blood pressure (BP) is heritable and finding quantitative trait loci that influence BP is an important step in identifying genes responsible for BP regulation. Sixty-six pairs of dizygotic (DZ) twin subjects and their parents were used in a sib-pair analysis to look for linkage of selected candidate genes to the quantitative trait BP. Microsatellite markers were tested in the vicinity of the gene loci for insulin-like growth factor-1 (IGF-1), Liddle syndrome, autosomal-dominant hypertension with brachydactyly, angiotensinogen, angiotensin II type 1 receptor, angiotensin-converting enzyme, renin, and lipoprotein lipase. BP was measured in a standardized manner. Heart size was determined echocardiographically. Significant linkage was found at the IGF-1, Liddle syndrome, and AT1 receptor gene for systolic BP. Linkage for diastolic BP was found at the autosomal-dominant hypertension with brachydactyly locus. Both systolic and diastolic BP were linked to the renin gene locus. The linkage was most consistent for the IGF-1 gene locus and systolic BP. Linkage was also found between the IGF-1 gene locus and posterior cardiac wall thickness, septal thickness, and left ventricular mass index. It is suggested that these quantitative trait loci may be important for the subsequent detection of allelic variants for elevated BP. Furthermore, these results linking the IGF-1 gene locus to both BP and cardiac dimensions underscore the importance of the IGF-1 gene as a candidate gene for cardiovascular disease.

Effect of short-term hormone replacement therapy on left ventricular mass and contractile function

Objective: To determine the effect of hormone replacement therapy (HRT) on cardiac structure and function and whether these changes are related to changes in blood volume. Design: Open-label pilot study. Setting: Academic medical center. Patient(s): Eighteen healthy postmenopausal women. Intervention(s): We administered medroxyprogesterone acetate orally, 5 mg/d for 2 months followed by 2 months of oral sequential 17β-estradiol, 1 mg/d plus medroxyprogesterone acetate, 10 mg/d for the last 12 days of each month. Main Outcome Measure(s): Cardiac output, stroke volume, heart rate, end diastolic volume, end systolic volume, ejection fraction, and left ventricular mass were measured by echocardiography; blood and plasma volumes were measured using 125I-albumin dilution. Result(s): Cardiac output, stroke volume, left ventricular mass, end diastolic volume, and ejection fraction increased by 12.8%, 11.7%, 9.4%, 7.2%, and 10.9%, respectively, by 16 weeks. End systolic volume decreased, whereas heart rate was unaffected. There was a significant increase in blood volume (5.2%) and plasma volume (4.8%) from baseline during treatment, which could explain the increased cardiac output but not the increased ejection fraction. Conclusion(s): Hormone replacement therapy causes modest but significant increases in cardiac output, ejection fraction, and left ventricular mass. These pilot data suggest a direct myocardial effect of HRT that is preload independent.

Inhibitory Effect of Tranilast on Hypertrophic Collagen Production in the Spontaneously Hypertensive Rat Heart

Tranilast, N-(3,4-dimethoxycinnamoyl) anthranilic acid, a widely used antiallergy drug in Japan, has been shown to inhibit transforming growth factor-β1 release from fibroblasts and reduce collagen synthesis in keloid cells. In the present study, we have investigated the effect of this drug on cardiac hypertrophy in spontaneously hypertensive rats (SHR), with a focus on the cardiac collagen matrix, which is associated with myocardial stiffness. Twenty-four-week-old SHRs and Wistar Kyoto rats (WKYs) were administered tranilast (300 mg/kg) orally once a day for 4 weeks. This treatment significantly suppressed increases in left ventricular collagen concentration (P<0.05) and the left ventricular weight / body weights ratios (P<0.05) in SHRs, and tranilast was ineffective on collagen concentration and ventricular weight / body weights ratios in WKYs. Tranilast did not affect systolic or diastolic blood pressure, end-diastolic left ventricular pressure and heart rate in both SHRs and WKYs, and the agent did not change positive dp/dt or cardiac output in SHRs. The pressure-volume relationship curve was shifted to the left by the drug; the slope (k) of the logarithm of the pressure-volume relationship curve was significantly increased (P<0.05) in SHRs. It is concluded that the suppression of increases in cardiac collagen and left ventricular mass by tranilast results in a corresponding prevention of cardiac stiffness as studied in the SHR.

Increased left ventricular muscle mass after long-term altitude training in athletes.

The effects of long-term altitude training on altitude and sea-level physiological characteristics in elite endurance athletes were investigated. Seven Swedish elite cross-country skiers (five men, two women; mean age 27 years) spent 1 month training at 1900 m above sea level in Italy. Rollerski treadmill tests were performed before and 5 and 11 days after the altitude sojourn; three tests were also performed at altitude. Before and 1, 11 and 35 days after the altitude camp, echocardiographic and blood volume measurements were performed. The heart rates at both maximal (P < 0.05) and submaximal (P < 0.01) work loads were decreased by 5-9 beats min-1 at altitude. The haemoglobin concentration and haematocrit increased quickly at altitude with a corresponding decrease on return to sea level. The blood volume (7%) and total haemoglobin (3%) tended to be higher day 11 post-altitude (NS). There were no significant changes in diastolic internal diameter or wall thickness of the left ventricle, but the calculated cardiac left ventricular muscle mass was increased post-altitude (9-10%, P < 0.01). The maximal oxygen uptake increased in six of the seven skiers after the altitude training (day 11, mean 3%, NS). In conclusion, training at moderate altitude may cause a reduction in heart rates during exercise. Moreover, after long-term training at altitude, there may be an increase in the cardiac left ventricular muscle mass.

Body Composition and Source of Weight Loss After Bariatric Surgery

Little is known about the composition and source of weight loss after bariatric surgery for morbid obesity. This study was undertaken to determine changes in weight, body mass index (BMI), lean body weight (LBW), fat weight (FW) and left ventricular cardiac mass (LVM) following vertical banded gastroplasty (VBG). After VBG for morbid obesity, 26 women and four men (mean age = 39.1 years) were weighed and had body composition analysis undertaken at intervals. Thirteen patients underwent echocardiography preoperatively and 1 year postoperatively to determine change in LVM and LVM index. Over 12 months there was significant weight loss for all weight parameters examined (p < 0.05). Fat weight loss was most significant; total weight loss and reduction of BMI were significant but less so than fat loss (Wilcoxon's signed ranks test). LBW loss had the smallest contribution to weight loss (p < 0.0001). There was a significant loss of LVM and posterior cardiac wall thickness (p < 0.05). VBG can lead to loss of lean body weight and left ventricular mass, and more dramatically, fat weight, body weight, and BMI. Cardiac mass and lean body mass are preferentially conserved relative to body fat with weight loss after VBG.

INCREASED LEFT VENTRICULAR MUSCLE MASS AFTER LONG-TERM ALTITUDE TRAINING IN ATHLETES 810

The effect of long-term altitude training on altitude and sea-level physiological characteristics in elite endurance athletes were investigated. Methods. Seven Swedish elite cross-country skiers (5 men, 2 women; mean age 27 years) spent one month of training at 1900 m above sea level in Italy. Rollerski treadmill tests were performed before and 5 and 11 days after the altitude sojourn; 3 tests were also performed at altitude. Before and 1, 11 and 35 days after the altitude camp, echocardiographic and blood volume measurements were performed. Results. The heart rates at both maximal (p<0.05) and submaximal (p<0.01) work loads were decreased by 5-9 beats·min-1 at altitude. The haemoglobin concentration and haematocrit increased quickly at altitude with a corresponding decrease on return to sea level. The blood volume (7%) and total haemoglobin (3%) tended to be higher day 11 post-altitude (NS). There were no significant changes in diastolic internal diameter or wall thickness of the left ventricle, but the calculated cardiac left ventricular muscle mass was increased post-altitude(9-10%, p<0.01). The maximal oxygen uptake increased in 6 of the 7 skiers after the altitude training (day 11, mean 3%, NS). Conclusion. Long-term training at moderate altitude may increase the cardiac left ventricular muscle mass. A relation to lowered exercise heart rates in spite of a decreased plasma volume at altitude cannot be excluded.

Athletic heart: a metabolic, anatomical, and functional study.

Previous studies have suggested a reduced glucose uptake by the athlete's heart at rest. To examine whether there is a compensatory increase in the myocardial fatty acid utilization, we studied nine male endurance-trained athletes (age 26 +/- 2 yr, VO2max 60 +/- 1 ml.kg-1.min-1, mean +/- SEM) and eight sedentary subjects (age 26 +/- 1 yr, VO2max 38 +/- 2 ml.kg-1.min-1) by single photon emission tomography using 123I-heptadecanoic acid (HDA) and mathematical modeling. Magnetic resonance imaging (MRI) and echocardiography were performed for the measurements of cardiac dimensions and left ventricular (LV) mass. No significant differences were found in the myocardial HDA beta-oxidation index (5.2 +/- 2.0 vs 7.4 +/- 1.6 mumol.min-1.100 g-1, P = NS) between endurance-trained and sedentary subjects. Fractional amounts of HDA beta-oxidation, backdiffusion, and esterification were also similar. In MRI study, LV mass was greater in the trained subjects (213 +/- 9 vs 179 +/- 10 g, P < 0.01) and in particular, LV long-axis diameter measured from the mitral valve level to the apex was increased (102 +/- 2 vs 88 +/- 2 mm, P < 0.001, trained vs sedentary subjects). VO2max correlated with LV long-axis diameter (r = 0.77, P < 0.001). In contrast to our hypothesis, myocardial HDA utilization was not enhanced in endurance-trained athletes at rest. Increases in LV mass and especially in LV long-axis diameter were observed in the athletes, indicating LV longitudinal remodeling.

Assessment of cardiac volumes and left ventricular mass by cine computed tomography before and after mitral balloon commissurotomy

We used cine computed tomography (CT) to determine whether decreased mitral valve gradients and pulmonary artery pressures resulted in decreased right ventricular and atrial volumes after percutaneous mitral balloon commissurotomy (MBC). In patients treated for severe mitral stenosis, previous studies have shown that after the mitral valve gradient decreases, the left atrial volume is reduced and left ventricular stroke volume is increased. The effects of commissurotomy on right heart chamber sizes have been difficult to assess with angiography and echocardiography. Moreover, in follow-up studies performed after surgery, changes in cardiac chamber volumes occurring after the mitral valve gradient and pulmonary pressure are reduced are confounded by the effects of thoracotomy. Our group has previously demonstrated that cine CT can accurately measure both left and right cardiac chamber volumes. We studied 11 female patients before, immediately after, and at 1 year after MBC, and 9 female control subjects of comparable age. To assess cardiac chamber volumes, we used cine CT. To assess the effects of MBC, we used cardiac catheterization and Doppler echocardiography. Compared to the control subjects, patients with mitral stenosis before MBC had larger total cardiac volumes (sum of all four chambers plus left ventricular myocardium) at ventricular end-diastole (381 ± 50 ml for controls vs 529 ± 102 ml for patients, p < 0.0005), larger left atrial (LA) end-diastolic volume and end-systolic volume (LA EDV: 72 ± 14 ml vs 186 ± 59 ml, p < 0.0005; LA ESV 31 ± 8 ml vs 143 ± 52 ml, p < 0.0005), and larger right atrial (RA) ESV (28 ± 6 vs 58 ± 23 ml; p < 0.005). RA EDV tended to be large (74 ± 18 ml vs 100 ± 31 ml; p < 0.10). Right ventricular (RV) EDV were similar (111 ± 23 ml vs 119 ± 23 ml; difference not significant). During cardiac catheterization immediately after MBC, the mitral valve gradient decreased (11 ± 3 mm Hg to 4 ± 1 mm Hg, p < 0.0001), mean pulmonary artery pressure decreased (29 ± 9 mm Hg to 20 ± 4 mm Hg; p < 0.025), and mitral valve area increased (1.1 ± 0.3 cm 2 to 2.8 ± 1.2 cm 2; p < 0.0005). These hemodynamic changes were confirmed by Doppler echocardiography. When cine CT studies obtained 5 ± 6 days after MBC were compared to studies obtained before MBC, LA ESV was found to decrease significantly to 119 ± 44 ml ( p < 0.0005). RV EDV tended to increase (144 ± 24 ml) and was significantly larger than in controls ( p < 0.025). At 1 year after MBC, the mitral valve area was unchanged from soon after MBC as measured by Doppler echocardiography (2.1 ± 0.5 cm 2 vs 1.9 ± 0.5 cm 2). Although the total cardiac volume was unchanged (552 ± 132 ml), significant changes in the individual cardiac chamber volumes occurred. Compared to before MBC, LA volumes decreased further (LA EDV was 158 ± 52 ml, p < 0.001; LA ESV was 102 ± 39 ml, p < 0.0005) and RV EDV increased further to 148 ± 46 ml ( p = 0.057). The LV EDV tended to increase compared with before MBC and compared with control subjects (119 ± 34 ml; p < 0.10). The LV and RV end-systolic volumes and the RA end-systolic and end-diastolic volumes remained remarkably similar throughout. The LV mass increased (63 ± 11 vs 71 ± 12 gm/m 2; p < 0.005). Thus in patients with mitral stenosis, the left and right atria are enlarged. After MBC, redistribution of cardiac chamber volumes occurs without a change in total cardiac volume.

Effects of Long-term Treatment with Prazosin on Left Ventricular Diastolic Function in Mild to Moderate Hypertension

It is not well established if blood pressure control is associated with an improvement in diastolic function, whose impairment represents an early marker of cardiac involvement in systemic hypertension. The purpose of this study was to evaluate whether a prolonged treatment with an alpha 1-blocking agent can lead to a reversal of the abnormalities of left ventricular filling. Eleven never-treated patients with mild to moderate essential hypertension were examined before and after at least six months of treatment with prazosin. Cardiac function and left ventricular mass were measured by means of radionuclide ventriculography and echocardiography. Average blood pressure values significantly decreased during the treatment period: from 163.54 +/- 17.80 mm Hg to 146.81 +/- 13.14 mm Hg for systolic blood pressure and from 106.09 +/- 6.96 mm Hg to 92.90 +/- 8.93 mm Hg for diastolic blood pressure. All the indices of left ventricular mass showed a trend toward reduction, but the differences with respect to the baseline values did not reach statistical significance. Average value of ejection fraction was normal before treatment and did not change significantly after treatment. All indices of diastolic function were significantly lower than normal controls' values at the beginning of the study and tended to worsen at the end of the study. Our findings suggest that diastolic function is not consistently affected by the therapy with alpha 1-adrenoreceptor antagonists despite good blood pressure control.

Hemodynamic differences between black patients and white patients with essential hypertension. State of the art lecture.

Physiological studies reported from our laboratory over the past several years have been reviewed and support epidemiological reports indicating that hypertensive cardiac and vascular disease runs a more severe course in the black patient. Although comparison of systemic hemodynamics failed to demonstrate that, for any level of arterial pressure, the magnitude of total peripheral resistance (which is the hemodynamic hallmark of hypertensive disease) differed between black patients and white patients, there are more subtle differences that were ascertained. Thus, although intravascular (plasma) volume contracts as arterial pressure and total peripheral resistance increase in both racial groups, this relation may differ quantitatively. At least in some black patients (43%), intravascular volume may be more expanded; in these patients, this relation is less closely correlated with the renopressor system (i.e., plasma renin activity). Moreover, these studies indicated that, at any level of arterial pressure, cardiac (left ventricular mass and posterior wall thickness) and renal hemodynamic involvement is more severe in the black patient. These findings point to important differences that operate in black patients and white patients with essential hypertension. With further study, these findings may be translated into more specific antihypertensive therapeutic implications for patients of both racial groups with essential hypertension.

Determinants of Blood Pressure in the First Decades of Life

The blood pressure (BP) in children has been studied since the beginning of this century, and in the past decade the potential association between childhood BP levels and adult hypertension has gained increasing interest. From several longitudinal studies, many of them comprising large numbers of children and youngsters, it appears that the BP of children is significantly associated with BP on follow-up measurements and that childhood BP is related to adult levels. Whether the objective is to predict future BP, or the aim is to shed light on the early pathogenesis of primary hypertension, it is of major importance to find out why BP rises in some and stays the same in others. To achieve this, characteristics need to be detected that are related to changes in BP in the first decades of life. Although not many reports on these dynamic relations are presently available, age, height, body weight, initial BP level, and a family history of hypertension have been put forward as determinants of children's BP change over time. Moreover, there are data to support the effect of dietary factors, most notably certain electrolytes, on BP regulation early in life. Also, certain hemodynamic and neural characteristics, such as changes in cardiac output and left ventricular mass, renal blood flow, and sympathetic nervous system activity, may be related to a subsequent rise in BP and future hypertension. Findings from nonexperimental and experimental studies on determinants of BP in children and youngsters will be reviewed.

Quantitative assessment of growth and function of the cardiac chambers in the normal human fetus: a prospective longitudinal echocardiographic study.

We assessed the changes in cardiac chamber size, architecture and function in the normal fetus in a prospective, longitudinal, two-dimensional, and two-dimensionally directed M mode echocardiographic study. Serial echocardiograms were recorded in 16 normal fetuses at 4 week intervals from 20 weeks gestation to parturition. Fetal gestational age was assessed by biparietal diameter. Left ventricular, right ventricular, and left atrial chamber sizes and aortic diameter all increased linearly with age. The ratios of right and left ventricular diameter, left atrial to aortic diameters, and relative left ventricular wall thickness that we used as an index of short-axis left ventricular architecture remained constant. Fractional right ventricular and left ventricular wall thicknesses were similar both on echocardiograms and in postmortem hearts over the same range of gestational ages. In addition, postmortem right ventricular and left ventricular free wall weights were indistinguishable and contributed the same proportion to total heart weight throughout gestation. Left ventricular echocardiographic mass increased linearly from a mean of 0.86 +/- 0.09 to 7.47 +/- 2.43 g at term and corresponded closely with postmortem left ventricular weight. We conclude that (1) fetal cardiac chamber dimensions, wall thicknesses, and left ventricular mass increased with gestational age, (2) cardiac architecture in terms of the ratios of right ventricular/left ventricular diameters, left atrial/aortic diameters, and relative wall thickness remained constant, (3) right and left ventricular fractional shortening did not change with age, (4) left ventricular mass assessed echocardiographically corresponded closely with postmortem left ventricular weights in fetal hearts of similar gestational ages, and (5) the similarities between right and left ventricular sizes, wall thicknesses, and free wall weights in this study do not support the theory of right ventricular dominance in the human fetus.

BP as a determinant of cardiac left ventricular muscle mass

BP as a determinant of cardiac left ventricular muscle mass

BP as a Determinant of Cardiac Left Ventricular Muscle Mass

The relationship between casual BPs and measures of cardiac hypertrophy, derived from the ECG, has been described as fairly weak. In this study, ECG and echocardiographic measurements of left ventricular muscle mass were related to various measures of BP obtained during circadian ambulatory BP monitoring in 12 patients with hypertension. Casual BP did not correlate substantially with ECG voltages or with echocardiographic measurements of muscle mass. The correlations between whole-day, daytime, or nighttime BP averages and ECG voltages were not significant. However, echocardiographic left ventricular muscle mass correlated significantly with the averages of whole-day, daytime, and nighttime, and two-hour morning systolic pressures. The correlations between diastolic BP and left ventricular muscle mass were not significant. Therefore, serial BP measurements are required to evaluate the relationship between BP and left ventricular muscle mass as measured by the M-mode echocardiogram. The ECG is of little value in this relationship.