Importance of heart weight, weights of cardiac ventricles and left ventricle plus septum/right ventricle ratio in assessing cardiac hypertrophy.

The present communication deals with the observations made during the study of 140 hearts (138 from medico-legal postmortems and 2 from post-natal deaths). The formalin fixed heart was dissected to separate non-muscular portion (NMP), right ventricle (RV), and left ventricle with septum (LV + S). The weights of the different components of the adult heart were affected by sex and body built not by age or body length. In most of the hearts the total weight varied from 180 to 320 Gm, the weight of RV, from 40 to 80 Gm, and LV + S, from 100 to 180 Gm. NMP was neither affected by age nor by ventricular weight. The coefficient of correlation between the heart weight and NMP was 0.93. Heart weight in Gm could be represented as equaled to 38.89 + 4.09 NMP. LV + S/RV ratio ranged from 1.64-3.84 : 1 in males and 1.73--3.1 : 1 in females, averaged being 2.52 : 1 and 2.44 : 1 respectively. No correlation between the weights of RV and LV + S was found. An attempt has been made to lay down the criterion for normal heart and for ventricular hypertrophy. The importance of total heart weight, weights of ventricles and the ratio is assessment of cardiac hypertrophy is discussed.     

Genetics of left ventricular hypertrophy and its regression.

Genetics of left ventricularophy and its regression The importance of left ventricular hypertrophy (LVH) in hypertension is well established. The development of LVH results from the interaction of genetic, hemodynamic, neurohumoral and environmental factors. In this review we describe the principal genetic alterations of cardiac hypertrophy and the genetic polymorphisms that are most consistently related to its development and particularly to the therapeutic induction of regression. The identification of a particular genetic profile could, in the future, help to predict the regression of left ventricular hypertrophy in response to different antihypertensive drugs.     

The impact of hypertension and hypertension-related left ventricle hypertrophy on right ventricle function

AIM: The aim of our study is to determine the effect of hypertension and hypertension-related left ventricle hypertrophy on right ventricle (RV) morphology and function by using RV standard Doppler echocardiographic indices, myocardial Doppler imaging, and strain/strain rate imaging indices. METHODS: We studied 35 patients with arterial hypertension and 30 age- and sex-adjusted control subjects who had no other pathological conditions. Standard transthoracic Doppler echocardiographical measurements, pulsed-wave tissue Doppler from tricuspid anulus (Peak systolic-st, peak early diastolic-et, peak late diastolic velocity-at), reconstructed spectral pulsed-wave tissue Doppler velocities (peak systolic-S, peak early-E, peak late diastolic velocity-A), and strain/strain rate imaging of RV free wall mid region (peak systolic strain-in, peak systolic strain rate-SR) were obtained. RESULTS: Age, body surface area, blood pressure, and heart rate were comparable between two groups. Hypertensive subjects had significantly increased LV end-diastolic septal and posterior wall thickness, left atrial diameter, LV mass, LV mass index, and relative wall thickness during diastole. At the level of right ventricular lateral tricuspid annulus without systolic changes, the majority of diastolic measurements were altered in hypertensives (early diastolic velocity et; 13 +/- 2 vs. 18 +/- 4 m/sec, P < 0.0001, late diastolic velocity at; 20 +/- 4 vs. 14 +/- 3 m/sec, P < 0.0001, early to late diastolic velocity ratio; 0.69 +/- 0.14 vs. 1.32 +/- 0.38, P < 0.0001). The velocity data from two-dimensional color myocardial imaging at the level of RV free wall mid region again showed altered diastolic measurements in hypertensives (E; 8.01 +/- 2.6 vs. 10.4 +/- 3.14 m/sec, P < 0.001, A; 11.5 +/- 2.6 vs. 9.12 +/- 3.7 m/sec, P < 0.0001, E/A ratio; 0.75 +/- 0.41 vs. 1.87 +/- 0.48, P < 0.00). The peak systolic strain of RV free wall mid region was significantly lower in hypertensive individuals than controls (25.666 +/- 5.64 vs. 30.03 +/- 6.78%, P < 0.05). No significant differences were found in other parameters of RV function between hypertensive and control subjects. CONCLUSIONS: The present study demonstrates that besides the manifest morphologic LV adaptations, significant RV functional alterations can be determined by TDI and strain/strain rate imaging in patients arterial hypertension. Both tissue velocities by TDI and strain imaging may be new tools to define and quantitate subtle change in systolic and diastolic function of right ventricular function in arterial hypertension that cannot be determined in standard echocardiographic parameters.     

Haemodynamic alterations of the left ventricle during right atrial pacing.

The left ventricular haemodynamic alterations during right atrial pacing were studied in 12 cases. Cardiac index varied little: during maximal rate however, its mean value was slightly lower than the resting one. Stroke index decreased inversely to the heart rate. The course of these indices did not separate the normal from abnormal cases. Ventricular function curves (VFCs) were constructed by relating the changes of left ventricular (LV) end-diastolic pressure (EDP) to those of stroke index (SI). In 4 normal cases the curves were steep, showing a fall of EDP with relatively large decrease of SI; in 3 cases of congestive myocardiopathy they were flat, showing fall of EDP in two and increase in one, with relatively small decrease of SI; in 5 patients with effort angina LVEDP initially decreased. This initial fall of VFCs was steep in two with normal and flattened in three with impaired resting LV function. Increase of EDP, evidently due to development of ischaemia, followed in all; it exceeded resting EDP in two out of three cases developing angina and in one out of two not developing angina. Our findings support the view that the increase of LVEDP is due to decrease of both myocardial contractility and compliance.     

Mechanical alterations of the left ventricle during right atrial pacing.

The effect of increasing heart rate by right atrial pacing on the peak value of the first derivative of left ventricular (LV) pressure(dp/dt) and the maximal velocity of the contractile element (KVmax) was studied in 12 cases. Peak dp/dt was poor as regards its sensitivity in reflecting the changes of contractility, due to its strong dependence on LV end-diastolic (EDP) and systolic pressure. KVmax increased constantly in the 4 normals and in 2 cases of ischaemic heart disease which did not develop angina; the increase exceeded 90 ml sec-1 in the former and one of the latter cases in which resting LV function was normal. In contrast, it decreased during the development of ischaemia in two of the three cases which developed angina; in the third case, in which also resting LV function was seriously impaired, the course of KVmax was almost flat. A similar flat course was observed in the three cases of congestive myocardiopathy. the above alterations of KV max were independent of the EDP and proportional to the basic contractility and its anticipated changes during pacing.     

Synthesis and degradation of myocardial protein during the development and regression of thyroxine-induced cardiac hypertrophy in rats.

Cardiac hypertrophy was induced in rats by daily injections of L-thyroxine (1.0 mg/kg). Regression from hypertrophy was studied 4 days after discontinuing thyroxine. Isolated, Langendorff-perfused hearts were perfused with Krebs-Henseleit buffer, glucose, insulin, and amino acids. To measure protein synthesis, left ventricular tissue was assayed for incorporation of tritiated phenylalanine into protein. Indices of rates of protein degradation were obtained by measuring the release of cold phenylalanine after blocking protein synthesis with cycloheximide. After 3 days of thyroxine (when cardiac growth was maximally increased), the rate of protein synthesis increased by 22% (P less than 0.001). After 1 week, synthesis was 8% greater than control (P less than 0.05), and by 2 weeks (when hypertrophy was stable and the rate of cardiac growth was similar to controls), synthesis had returned to control levels. In hearts regressing from hypertrophy, synthesis was reduced to 68% of control (P less than 0.001). The rate of protein degradation was decreased by 12% (P less than 0.05) after 3 days of thyroxine, but was not different from control at 1 or 2 weeks. During regression, degradation was 12% below control (P less than 0.05). Changes in the release of several amino acids that are synthesized or metabolized in heart (e.g., alanine, glycine, serine) were different from changes in phenylalanine release. In conclusion thyroxine-induced cardiac hypertrophy and regression are accompanied by changes in protein synthesis and degradation, and amino acid metabolism. The predominant change in hypertrophy is increased protein synthesis with a minor contribution from reduced degradation. Regression of hypertrophy is accompanied by decreased synthesis, not increased degradation.     

Biloculate false aneurysm of the right ventricle after cardiac surgery.

A case of a 12-year-old boy who had double false aneurysms of the right ventricle after incomplete closed pulmonary valvotomy six years earlier is presented. The aneurysms were successfully treated surgically, and the aetiology is discussed.     

Biloculate false aneurysm of the right ventricle after cardiac surgery.

A case of a 12-year-old boy who had double false aneurysms of the right ventricle after incomplete closed pulmonary valvotomy six years earlier is presented. The aneurysms were successfully treated surgically, and the aetiology is discussed.     

开搏通逆转高血压性心肌肥大过程中心肌超微结构的变化

目的 :探讨开搏通逆转高血压性心肌肥大对心脏超微结构的作用。方法 :用多道生物信号系统记录血压和心率 ,用电子显微镜观察心肌超微结构。结果 :第 4、8、12周 ,高血压组的 SBP,DBP,MAP比对照组高 ,第 16周差别不明显 ,假手术组和对照组的差别无统计学意义 ;在第 4、8、12周 ,T管和肌浆网扩张 ,第 16周大部 T管和肌浆网恢复正常 ;在第 4周 ,粗、细肌丝溶解 ,第 16周 ,大部分粗、细肌丝清晰 ,排列正常。结论 :开搏通能降低腹主动脉缩窄大鼠的血压和逆转心肌肥大 ;在第 4周 ,高血压组肌纤维和肌管出现病理变化 ,在第 16周大多数粗、细肌丝和 T管、肌浆网恢复正常     

Coronary blood flow during the development and regression of left ventricular hypertrophy in renovascular hypertensive rats

Left ventricular (LV) coronary flow (CF) was determined by left atrial injection of microspheres in conscious rats during the development and after the reversal of LV hypertrophy in 2-kidney, 1-clip Goldblatt hypertension. Two groups of untreated renal hypertensive rats (RHR) were studied, the first (RHR₁, n = 17) at 10 weeks and the second (RHR₂, n = 9) at 24 weeks after clipping. Beginning 9 weeks after clipping, 2 other groups were treated either with captopril (40 to 60 mg/kg/day) in drinking water (RHR-C, n = 8) or left nephrectomy (RHR-N, n = 9) and followed for 15 weeks. Sham-operated animals followed for similar periods of time served as controls (Sham-1, n = 12, as a control for RHR₁, and Sham-2, n = 11, as a control for RHR₂). In all groups, LV mass increased or decreased in close correlation with changes in arterial blood pressure, and minimal total LV coronary resistance remained unchanged. The development of hypertrophy was associated with a tendency toward reduction in CF reserve (defined as maximal CF/unit mass); this flow reserve was restored with reversal of hypertrophy. The importance of the relation between pressure and LV mass as a determinant of CF reserve was investigated in a second study in which this relation was changed by altering the periods of captopril therapy; in these cases, CF reserve correlated significantly with the ratio of arterial pressure to LV mass (r = 0.76, n = 12, p < 0.01). The results suggest that maintenance of CF reserve in LV hypertrophy depends on an appropriate balance between arterial pressure and LV mass, and might be disturbed by antihypertensive therapy that leaves LV hypertrophy unchanged.     

Coronary blood flow after the regression of pressure-overload left ventricular hypertrophy.

Abnormal coronary blood flow (CBF) in long-standing left ventricular (LV) pressure-overload hypertrophy has been associated with ischemia and LV dysfunction. Thus, goals of therapy in pressure overload are not only the relief of the overload itself but also regression in hypertrophy and subsequent improvement in CBF. However, little is known about CBF in humans or in large mammals after the relief of pressure overload, when the hypertrophy has regressed. This study was performed to test the hypothesis that, even 6 months after the relief of pressure overload in the dog, CBF would still be abnormal. Three groups of dogs were studied: 1) normal control dogs (NL group), 2) dogs with LV pressure-overload hypertrophy (LVH group), and 3) dogs that had developed LV pressure-overload hypertrophy but in whom the pressure overload was relieved 6 months before the final study (LVH Reg group). CBF was studied in conscious dogs by use of the radiolabeled microsphere technique at rest, during rapid atrial pacing, and during maximum coronary vasodilation produced by adenosine infusion. The ratio of LV weight (g) to body weight (kg) (LVBW) was 4.2 +/- 0.3 in the NL group, 7.1 +/- 0.6 in the LVH group, and 7.7 +/- 0.5 in the LVH Reg group before pressure-overload relief (p = NS, LVH versus LVH Reg). Six months after removal of the pressure overload, the LVBW in the LVH Reg group had fallen to 5.5 +/- 0.3 (p < 0.05), but this LVBW was still greater than that in the NL group (p < 0.05). During rapid atrial pacing, endocardial and epicardial CBF rose significantly in NL dogs. However, during rapid atrial pacing, endocardial CBF fell from 1.18 +/- 0.22 to 0.7 +/- 0.20 ml/min per gram in the LVH group (p < 0.05) and did not rise in the LVH Reg group. During adenosine infusion, endocardial blood flow increased in NL dogs from 1.63 +/- 0.13 to 4.0 +/- 0.3 ml/min per gram and increased to a similar level in the LVH Reg group. Although CBF increased during adenosine infusion in the LVH group, the increase was less than that in the NL or LVH Reg group (p < 0.05). Minimum coronary vascular resistance was similar in NL dogs (14 +/- 2 units) and LVH Reg dogs (18 +/- 3 units, p = NS) but was significantly elevated (32 +/- 10 units) in LVH dogs (p < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)     

Molecular characterisation of neonatal cardiac hypertrophy and its regression

Neonatal cardiac hypertrophy associated with diabetic pregnancy is transient and regresses naturally, but is associated with increased morbidity and mortality. This study was undertaken to analyse the changes in expression of 5 cardiac genes, including atrial natriuretic peptide, alpha- and beta-myosin heavy chain, and cardiac and skeletal alpha-actin genes, using a rat neonatal model, in which cardiac hypertrophy was induced via maternal diabetes. In the hypertrophied left ventricle of neonates from diabetic mothers, the levels of mRNA from all the above genes except skeletal alpha-actin were increased by between 1.8- and 12-fold compared with the controls at birth (p < 0.05). In the first 28 days, the level of mRNA for alpha-myosin heavy chain increased slightly, while that for atrial natriuretic peptide and beta-myosin heavy chain decreased continuously similar to the controls, but at a significantly faster rate. No significant difference between the two groups of neonates was observed in all 5 genes after 1 month, indicating complete regression. Expression of 5 cardiac genes in the neonatal cardiac hypertrophy was characterised in both hypertrophic and regressive phases. Hypertrophic regression provides a unique model for the testing of new drugs or genetic modifying factors in cardiac hypertrophy.     

Perioperative hemodynamic and geometric changes of the left ventricle during cardiomyoplasty in goats with dilated left ventricle

OBJECTIVE: Clinical data have suggested the occurrence of temporary short-term deterioration of the heart following cardiomyoplasty. The purpose of this study was to monitor the short-term hemodynamic effects of cardiomyoplasty in a goat model of a dilated left ventricle, using conductance catheters (ie, pressure-volume loops) and cardiac output measurements. METHODS: Eight female goats underwent acute cardiomyoplasty 8 to 12 weeks after left ventricular (LV) dilatation was induced by a carotid jugular arteriovenous shunt. The cardiomyoplasty procedure was monitored using a Swan-Ganz catheter for cardiac output measurements and a 12-electrode (dual-field) conductance catheter to LV pressure-volume loops. RESULTS: After wrapping the heart with the latissimus dorsi muscle, there was a significant reduction in both cardiac output and LV end-diastolic volume (LVEDV) at 10 min. Partial recovery was observed 45 min later. CONCLUSION: A decrease in both cardiac output and LVEDV was observed following myocardial wrapping. This may explain some of the perioperative and postoperative morbidity and mortality observed following cardiomyoplasty.     

药物逆转左心室肥厚研究进展

高血压引起的左心室肥厚(LVH)已被公认为是心血管并发症的独立危险因素[1],引起高血压LVH的主要原因是血流动力学和神经内分泌激活两方面。高血压LVH时心脏的组织结构发生的改变,包括心肌细胞肥大和心肌间质纤维化。下面就药物逆转左心室肥厚研究进展简单综述如下。1血管紧张素转换酶抑制剂现已证实多种血管紧张素转换酶抑制剂如苯那普利、依那普利、赖诺普利,均能有效逆转高血压LVH。一项多研究分析表明,血管紧张素转换酶抑制剂是逆转高血压LVH的最有效药物[2]。以往认为血管紧张素转换酶抑制剂主要通过抑制AngⅡ形成来防止LVH,但…