Left ventricular hypertrophy in patient on dialysis

Left ventricular hypertrophy (LVH) is a significant factor for higher mortality caused by cardiovascular diseases, which are the main cause of death (45%) in hemodialysis patients. In this study we analyzed the link between hypertension nad anemia, which are the main risk factors for the occurrence of LVH. The study included 40 patients (20 M and 20 F, age 20-80 years) who were treated with chronic dialysis. Using the method of transthoracic echocardiography, in M-mode, 38 patients underwent measurement of the thickness of intraventricular septum and posterior wall of the left ventricle at the end of diastole. LVH was expressed through the left ventricle mass index (LVMI) > 131 g/m2 for male and > 100 g/m2 for female. The efficiency of dialysis was calculated with the standard formula (Kt/V1,2). The patients on erythropoietin therapy received medium maintenance dose of 4000 units per week. Blood pressure and hemoglobin data were included in the calculations. A statistically higher rate of hypertension was found in males (M 17/20, F 10/20, p = 0.04), and of myocardial hypertrophy in females (M 7/20, F 17/20, p = 0.004). Overall patient data analysis showed LMVI to be statistically significantly higher (p = 0.0004) in hypertensive patients, and so were the values of systolic and diastolic pressure (p = 0.0006) in spite of applied medication. Hemoglobin was significantly higher (p = 0.04) in LVH patients. A significant positive correlation was found between LVMI and arterial pressure (p = 0.006), and negative between LVMI and hemoglobin concentration (p = 0.03). There was no statistically significant correlation between LVMI and age, interdialytic fluid intake and Kt/V. These results indicate that among patients on chronic dialysis treatment, LVH is more frequent in those with hypertension. The higher hemoglobin concentration found in patients with LVH was probably due to the relatively small number of patients. It is necessary to reduce the effect of risk factors for LVH by using better therapeutic options, thus to decrease the mortality in dialysis patients.     

Left ventricular hypertrophy regression during antihypertensive treatment

For more than 20 years hypertrophy regression has been in the focus of hypertension research. Many studies in animals have shown impressive reduction of left ventricular hypertrophy after medical treatment of hypertension. The most important result seems to be that hypertrophy can be almost completely reversed in young animals, whereas in older animals regression of left ventricular hypertrophy appears to be less complete. Hypertrophy regression in man seems much more difficult to prove. The direct correlation between left ventricular muscle mass and ECG changes has been disappointing in many studies. Echocardiography is able to show a comparatively good impression of left ventricular muscle mass and therefore can also demonstrate regression of left ventricular hypertrophy within its methodological limits. There is no doubt that today magnetic resonance imaging has by far the best imaging quality of all the clinical methods and is able to demonstrate both hypertrophy and its regression with incomparable accuracy. In the present clinical study hypertrophy regression has been demonstrated after 6 months of treatment with Carvedilol.     

Left ventricular hypertrophy improves cardiac performance in spontaneously hypertensive rats

Cardiac function was studied in spontaneously breathing, adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY). By rapid intravenous blood infusion, the relation between left ventricular end-diastolic pressure (LVEDP) and stroke volume (SV) was determined while the cardiac nervous control was pharmacologically blocked. Since SV is greatly influenced by the level of afterload (mean arterial pressure, MAP), SV was also determined at increased MAP (constriction of abdominal aorta) and at decreased MAP (vasodilation by hydralazine). At low LVEDP levels, a righward shift of the Frank-Starling relationship was observed in SHR. This rightward shift seems mainly to depend on the increased MAP present in SHR since it was less prominent if MAP was lowered to normotensive levels in SHR. Maximal SV during volume infusion was similar in SHR and WKY, despite a much higher MAP in SHR. When peak SV was instead compared at similar MAP levels for both (either at ‘normotensive’ or ‘hypertensive’ levels) it was always significantly greater in SHR, and was increased largely in proportion to their increased left ventricular weight. This indicates that the left ventricular hypertrophy present in SHR is, at least at this stage, a physiological adaptation of the heart to increase its performance, in order to maintain a normal SV and hence cardiac output, despite an increased arterial pressure.     

Left ventricular cellular hypertrophy in pressure- and volume-overload valvular heart disease

To determine the dependence of myocyte hypertrophy in chronic valvular heart disease on the site and type of lesion, the myocardium was studied from 11 patients with either pressure-overload hypertrophy (PO; four patients with aortic stenosis and two with mixed aortic stenosis/insufficiency) or pure volume-overload hypertrophy (VO; two patients with mitral regurgitation and three with aortic insufficiency). These patients, all without coronary artery disease, died zero to 34 days after valve replacement surgery. Diameters of 25 longitudinally oriented myocytes in the circular midwall myocardium were measured with a calibrated light microscope eyepiece reticle on each of five transmural, transverse, histologic sections from the apical, anterolateral, posterolateral, anteroseptal, and posteroseptal left ventricle. Statistical analysis by modified two-way analysis of variance (ANOVA) demonstrated that mean myocyte size (based on 125 measurements) varied widely among cases but was not statistically different among sites. The myocyte diameter for PO lesions (25.9 +/- 1.1 micron, mean +/- SEM) was significantly greater (P less than 0.05) than that for pure VO lesions (20.4 +/- 0.7 micron), despite equal relative heart weights (measured/predicted from body weight: 2.5 +/- 0.2 [mean +/- SD] versus 2.5 +/- 0.5). This study suggests that 1) cellular hypertrophy in valvular heart disease occurs uniformly throughout the left ventricular myocardium; and 2) mean myocyte diameters are greater in PO than in VO hypertrophy for equivalent cardiac enlargement.     

Left ventricular hypertrophy is associated with inflammation in sodium loaded subtotal nephrectomized rats

The pathological influences of inflammation on left ventricular hypertrophy (LVH) were studied in subtotal nephrectomized (SNx) rats after 0.3% NaCl loading for 5 weeks. We found that mild hypertension, increased plasma levels of creatinine, inorganic phosphate, asymmetric dimethylarginine (ADMA), and parathyroid hormone (PTH) were observed in the present SNx rats without LVH. In the present study, the NaCl-loaded SNx (SNx + NaCl) rats were characterized by significant LVH and hypertension with aggravated values of all the parameters. We further confirmed that glomerular sclerosis, tubulointerstitial fibrosis, and inflammatory cell infiltration into the tubulointerstitial area, observed in the SNx rats, were more severely caused in the SNx + NaCl rats. In addition, plasma interleukin-6 (IL-6) levels in the SNx + NaCl rats were significantly increased compared to those in the SNx rats. These findings indicated that NaCl-loaded SNx rats developed LVH and hypertension, which were accompanied with increased plasma levels of PTH, creatinine, inorganic phosphorus, ADMA, and IL-6. Thus, these results suggest that inflammation as well as endothelial dysfunction would be correlated with LVH as non-traditional risk factors at the early stage in the present renal failure model.     

Left ventricular image processing

Left ventricular image processing methods of x-ray cineangiocardiograms and ultrasound echocardiograms are discussed. 3-D reconstruction methods of the left ventricle from ultrasound echocardiograms and magnetic resonance images are also discussed. Boundary detection of the left ventricle and the quantitative analysis of the left ventricular function and wall motion are discussed. To reconstruct 3-D shapes, we need several cross sectional shapes or silhouettes of the left ventricle. Several cross sectional echo images of apical long axis view are taken by changing the angles of rotation of the probe of echo transducer around its axis. Gated multi-phase MRI method is used to obtain each 2 cross sectional images in transverse, coronal and sagittal directions. Some results of 3-D shapes of the left ventricle and myocardium reconstructed are shown and 3-D functional images which give us regional functions of the left ventricular wall on three dimensional shape are shown.     

Left ventricular mechanoenergetics in small animals

Studies on left ventricular mechanical work and energetics in rat and mouse hearts are reviewed. First, left ventricular linear end-systolic pressure-volume relation (ESPVR) and curved end-diastolic pressure-volume relation (EDPVR) in canine hearts and left ventricular curved ESPVR and curved EDPVR in rat hearts are reviewed. Second, as an index for total mechanical energy per beat in rat hearts as in canine hearts, a systolic pressure-volume area (PVA) is proposed. By the use of our original system for measuring continuous oxygen consumption for rat left ventricular mechanical work, the linear left ventricular myocardial oxygen consumption per beat (VO2)-PVA relation is obtained as in canine hearts. The slope of VO2-PVA relation (oxygen cost of PVA) indicates a ratio of chemomechanical energy transduction. VO2 intercept (PVA-independent VO2) indicates the summation of oxygen consumption for Ca2+ handling in excitation-contraction coupling and for basal metabolism. An equivalent maximal elastance (eEmax) is proposed as a new left ventricular contractility index based on PVA at the midrange left ventricular volume. The slope of the linear relation between PVA-independent VO2 and eEmax (oxygen cost of eEmax) indicates changes in oxygen consumption for Ca2+ handling in excitation-contraction coupling per unit changes in left ventricular contractility. The key framework of VO2-PVA-eEmax can give us a better understanding for the biology and mechanisms of physiological and various failing rat heart models in terms of mechanical work and energetics.     

Left ventricular noncompaction in Sotos syndrome

Sotos syndrome is an autosomal dominant condition characterized by pre- and postnatal overgrowth (tall stature and macrocephaly), a typical facial appearance, advanced bone age, and developmental delay. The syndrome is caused by mutations or deletions of the nuclear receptor binding SET domain protein 1 (NSD1) gene, which encodes a histone methyltransferase implicated in the regulation of chromatin. Left ventricular noncompaction (LVNC), also called left ventricular (LV) hypertrabeculation, is a rare disorder classified as a primary genetic cardiomyopathy by the American Heart Association. This condition is characterized by an altered myocardial wall due to arrest of embryonic compaction of the loose interwoven meshwork that makes up the fetal myocardial primordium. The cardiac manifestations of this cardiomyopathy are variable, ranging from an absence of symptoms to a progressive deterioration in cardiac function, with heart failure, arrhythmias, and systemic thromboemboli. We describe two unrelated patients who had LVNC, as based on echocardiographic findings, and Sotos syndrome, as based on physical features and molecular analysis. To our knowledge, the literature contains no previous reports of concomitant LVNC and Sotos syndrome. In the light of these two cases, we suggest that patients with Sotos syndrome be evaluated for LVNC cardiomyopathy when being screened for heart defects.     

高血压病患者室性心律失常与左心室舒张功能损害

目的: 探讨高血压患者的室性心律失常与左心室舒张功能损害的关系。方法: 149例高血压病患者24 h动态心电图检测,多普勒超声检测左心室舒张功能。室性心律失常(按Lown分级)与左心室舒张功能指标(A/E比值)作相关分析。结果: 高血压患者A/E比值与室性心律失常Lown分级正相关。结论: 高血压患者的左心室舒张功能损害程度越严重, 室性心律失常相应较重。