Heart failure in hypertensive patients with left ventricular hypertrophy

Left ventricular hypertrophy (LVH) is supposed to be a useful marker of cardiovascular complications during the course of hypertension. Authors compared the presence of heart failure, left ventricular diastolic dysfunction and chronic atrial fibrillation in hypertensive patients with and without left ventricular hypertrophy defined by echocardiography. Hospital records of 192 hypertensives treated in our medical department during years 1996-1999 were analysed. Left ventricular hypertrophy was defined by echocardiography (Penn convention) as left ventricular mass index > 134 g/m2 in men and > 110 g/m2 in women. Presence of LVH was found in 128 patients (mean age 65.9 years), absence of LVH in 64 patients (mean age 64.8 years). Both groups of hypertensives were matched by demographic parameters, by the presence of hyperlipidemia, by smoking habits. Hypertensive patients with left ventricular hypertrophy were more often treated by ACE inhibitors. There were statistically significant more patients with heart failure, left ventricular diastolic dysfunction and chronic atrial fibrillation in LVH-positive patients than in LVH-negative once. There was also statistically significant lower ejection fraction (50.3 +/- 11.4% vs 56.5 +/- 7.4%) in LVH-positive patients than in LVH-negative once. Left ventricular hypertrophy in patients with hypertension brings usually a complicated course of the disease with a high contribution to the development of chronic heart failure.     

The etiology and associated risk factors in a sample of 300 patients with atrial fibrillation]

PURPOSE: To analyze the etiology and the prevalence of risk factors in patients with atrial fibrillation. PATIENTS AND METHODS: Applying an unpaired case controlled study, we examined 300 consecutive patients (143 men) with atrial fibrillation and a mean age of 66 +/- 8 years. This group is compared with a control group of 700 patients (mean age 64 +/- 12 years). RESULTS: In the group with atrial fibrillation the etiology in 32% was arterial hypertension, in 20% coronary heart disease, in 13% valvular heart disease, in 11% heart failure, in 4% hyperthyroidism and in 20% idiopathic. 50% presented hypertension, 29% tobaccoism, 26% left ventricular hypertrophy, 20% consumption of alcohol, 19% hypercholesterolemia and 16% diabetes. Compared with the control group, patients with atrial fibrillation had coronary heart disease (p < 0.05), VHD (p < 0.01), myocardiopathy (p < 0.05), HT (p < 0.001), left ventricular hypertrophy (p < 0.001), diabetes (p < 0.01) and alcohol consumption (p < 0.01) more frequently. In the multivariant analysis heart failure (odds ratio 2.1 [1.2-3.3]), the valvular heart disease (odds ratio 2.2 [1.4-3.5]), the coronary heart disease (odds ratio 1.8 [1.2-2.6]), the arterial hypertension (odds ratio 1.7 [1.2-2.3]), the left ventricular hypertrophy (odds ratio 2.6 [1.7-3.8]), the diabetes (odds ratio 1.9 [1.2-2.9]) and alcoholic habits (odds ratio 2 [1.3-3.9]) were independent risk factors for atrial fibrillation in our population. CONCLUSIONS: Atrial fibrillation in our study, is more frequent in patients with arterial hypertension, coronary heart disease or valvular heart disease. There are other risk factors such as arterial hypertension, diabetes and consumption of alcohol too, the modification of which could diminish the risk of the appearance of atrial fibrillation.     

An autopsied case of marked cardiac hypertrophy due to multifactorial heart disease in an 85 year-old man who had been socially active]

An autopsied 85-year-old man had suffered from a mild form of diabetes mellitus since the age of 67 and had experienced the first episode of heart failure with arapid ventricular rate of atrial fibrillation at the age of 72. He had remained socially active until he died suddenly of ventricular fibrillation, although he had complications of aortic regurgitation at the age of 76 and later mitral regurgitation at the age of 80. Chest roentgenograms showed gradual increase in the cardiothoratic ratio which reached 68.1% at the final stage. Autopsy revealedmarked left ventricular hypertrophy with a heart weight of 580 g, degeneration ofaortic valves, thickening of mitralvalve cusps and moderate coronary atherosclerosis without ischemic myocardial lesions. There were no specific lesions suggestive of primary cardiomyopathies on microscopic observations and the lesions of both aortic and mitral valves were not significant enough to explain the clinical findings of aortic and mitral regurgitation. Because the pathological examination failed to identify a single disease which was responsible for the marked cardiachypertrophy, we eventually reached the conclusion that the cardiac hypertrophy developed based on a multifactorial heart disease.     

左房容积指数与慢性心力衰竭病人的预后

左房客积反映左室充盈压、心房结构重塑及神经激素的活动。国外研究表明,左房容积扩大是预测慢性心力衰竭不良预后的一个强有力的标志。现回顾近年来相关临床研究的结果,分析左房容积指数与慢性舒张性心力衰竭、收缩性心力衰竭、冠心病及心房颤动患者的不良预后的相关性。     

Heart failure and cardiac hypertrophy

Opinion statement Left ventricular failure is the final common pathway for a wide spectrum of myocardial insults, including systemic hypertension and myocardial infarction. Although left ventricular hypertrophy is an adaptive response to pressure and volume overload, this process becomes maladaptive if left untreated and pathologic cardiac hypertrophy then becomes an important and independent risk factor for the development of heart failure. Despite its importance, the transition from hypertrophy to heart failure in humans is poorly understood. The focus of treatment should be prevention of heart failure and other cardiovascular events, such as stroke and atrial fibrillation. When heart failure is present, treatment with medical and device therapy is then focused on improving functional capacity, increasing survival, and preventing progression to end-stage heart failure.     

Role of transthoracic echocardiography in atrial fibrillation

Atrial fibrillation is a major clinical problem that is predicted to be encountered more frequently as the population ages. The clinical management of atrial fibrillation has become increasingly complex as new therapies and strategies have become available for ventricular rate control, conversion to sinus rhythm, maintenance of sinus rhythm, and prevention of thromboembolism. Clinical and transthoracic echocardiographic features are important in determining etiology and directing therapy for atrial fibrillation. Left atrial size, left ventricular wall thickness, and left ventricular function have independent predictive value for determining the risk of developing atrial fibrillation. Left atrial size may have predictive value in determining the success of cardioversion and maintaining sinus rhythm in selected clinical settings but has less value in the most frequently encountered group, patients with nonvalvular atrial fibrillation, in whom the duration of atrial fibrillation is the most important feature. When selecting pharmacological agents to control ventricular rate, convert to sinus rhythm, and maintain normal sinus rhythm, transthoracic echocardiography (TTE) allows noninvasive evaluation of left ventricular function and hence guides management. The combination of clinical and transthoracic echocardiographic features also allows risk stratification for thromboembolism and hemorrhagic complications in atrial fibrillation. High-risk clinical features for thromboembolism supported by epidemiological observations, results of randomized clinical trials, and meta-analyses include rheumatic valvular heart disease, prior thromboembolism, congestive heart failure, hypertension, older (> 75 years old) women, and diabetes. Small series of cases also suggest those with hyperthyroidism and hypertrophic cardiomyopathy are at high risk. TTE plays a unique role in confirming or discovering high-risk features such as rheumatic valvular disease, hypertrophic cardiomyopathy, and decreased left ventricular function. Validation of the risk stratification scheme used in the Stroke Prevention in Atrial Fibrillation-III trial is welcomed by clinicians who are faced daily with balancing the benefit and risks of anticoagulation to prevent thromboembolism in patients with atrial fibrillation.     

Heart failure with normal ejection fraction

Opinion statement Heart failure with normal ejection fraction, also known as diastolic heart failure, is a major problem for patients and health-care providers and is a substantial expense to society. The main pathophysiologic processes involved are increased left ventricular stiffness and abnormal relaxation, with resulting impaired left ventricular filling. These processes typically displace the pressure-volume relationship in an upward direction, resulting in increased left ventricular end-diastolic, left atrial, and pulmonary capillary wedge pressures, leading to symptoms of pulmonary congestion. The most common clinical disorders leading to diastolic heart failure are 1) hypertension with concentric left ventricular hypertrophy, 2) coronary artery disease with decreased left ventricular compliance, 3) hypertrophic cardiomyopathy, and 4) aortic stenosis with concentric left ventricular hypertrophy. Echocardiography and cardiac catheterization with magnetic resonance imaging hold promise as future diagnostic tools. The approach to the treatment of diastolic heart failure is focused on four treatment goals: 1) persistent control of elevated blood pressure, with regression of left ventricular hypertrophy, 2) careful reduction of central blood volume (diuretics), 3) maintenance of atrial contraction and control of heart rate (beta-blockers, digoxin, atrioventricular pacing); and 4) improvement of left ventricular relaxation. There is currently no drug treatment specific for abnormal relaxation, although efforts are being made to develop such compounds. A promising future therapy includes agents that lyse advanced glycation end-products as an approach to relieving increased ventricular stiffness. In addition to pharmacotherapy, maintaining ideal body weight and a regular exercise program are also helpful in the treatment of diastolic heart failure. Although the overall prognosis of patients with diastolic dysfunction is more favorable than that of patients with systolic dysfunction, the frequency of treatment failure and recurrent symptoms underscores the need for further improvement in treatment of this condition.     

908例室性心律失常动态心电图分析

目的：探讨室性心律失常与心脏病的病因及临床相关因素的相关性。方法：对动态心电图检测出的908例室性心律失常病例进行病因及临床相关因素分类，并进行分析。结果：在有、无器质性心脏疾病的患者中均可发生室性心律失常。其发生率由多至少依次为冠心病、高血压、瓣膜病、心肌病、先心病、病因不明、病窦＋房室传导阻滞（SSS＋AVB）、糖尿病。而相关因素中，室性心律失常的发生率依次为左室肥大、心功能损害及心房颤动。结论：动态心电图监测能提高室性心律失常的检出率，有利于心脏病及心律失常的诊治，改善其预后。     

Clinicopathological study on left ventricular hypertrophy in elderly hypertensive patients

The correlations between blood pressure, left ventricular hypertrophy and left atrial enlargement were examined in 2,010 autopsied cases. The cases were classified into 3 groups: 972 (48.2%) normotension cases, 313 cases (15.5%) of systolic hypertension and 725 cases (36.1%) of diastolic hypertension. The incidence of left ventricular hypertrophy (LVH) was significantly higher in systolic and diastolic hypertensive cases than in normotensives (p less than 0.05), but no significant difference in LVH incidence was found between the 2 hypertensive groups. The incidence of an enlarged left atrium was also significantly higher in both hypertensive groups than in the normotensive group (p less than 0.05). The incidence of congestive heart failure and a large CTR were also higher in both hypertensive groups. However, there were no intergroup differences in atrial fibrillation incidence, despite significant differences in atrial size. Finally, the incidence of moderate to severe coronary artery stenosis was significantly higher in both hypertensive groups, but no difference was found between the 2 types of hypertension. We concluded that both systolic and diastolic hypertension contributed to the genesis of left ventricular hypertrophy, left atrial dilatation, coronary sclerosis and congestive heart failure.     

Stellenwert der antiarrhythmischen Therapie mit Dronedaron nach den Ergebnissen der PALLAS-Studie

The results of the PALLAS study triggered a significant change regarding indication and safety related to the use of dronedarone. In permanent atrial fibrillation, symptomatic heart failure, or impaired left ventricular function, the use of dronedarone is now contraindicated. In addition, the relevance of dronedarone for rhythm control in paroxysmal atrial fibrillation is reduced and alternative approaches, such as catheter ablation and treatment with class IC drugs or amiodarone are strengthened. However, all these treatment procedures also exhibit a specific potential for complications and adverse events. With respect to the very limited drug treatment possibilities in patient cohorts with hypertension and left ventricular hypertrophy or coronary artery disease it is beneficial to have dronedarone available in the treatment armamentarium for atrial fibrillation in these patients. It is of major importance to gain a better understanding of the adverse effect of dronedarone that became apparent from the PALLAS data as compared to the ATHENA cohort, to better allow identification of clinical risk factors to define patients at risk better.     

Correlates of left atrial size in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study

Left ventricular hypertrophy has been suggested to mediate the relation between hypertension and left atrial enlargement, with associated risks of atrial fibrillation and stroke. However, less is known about correlates of left atrial size in hypertensive patients with left ventricular hypertrophy. We assessed left atrial size by echocardiography in 941 hypertensive patients, age 55 to 80 (mean, 66) years, with electrocardiographic left ventricular hypertrophy at baseline in the Losartan Intervention For Endpoint reduction in hypertension study. Enlarged left atrial diameter (women, >3.8 cm; men, >4.2 cm) was present in 56% of women and 38% of men (P<0.01). Compared with the 512 patients with normal left atrial size, the 429 patients with enlarged left atrium more often had mitral regurgitation, atrial fibrillation, and echocardiographic left ventricular hypertrophy. They also had higher age, systolic blood pressure, pulse pressure, weight, body mass index, left ventricular internal chamber dimension, stroke volume, and mass and lower relative wall thickness and ejection fraction (all, P<0.05). In logistic regression analysis, left atrial enlargement was related to left ventricular hypertrophy and eccentric geometry; greater body mass index, systolic blood pressure, and age; female gender; mitral regurgitation; and atrial fibrillation (all, P<0.05). Thus, left atrial size in hypertensive patients with electrocardiographic left ventricular hypertrophy is influenced by gender, age, obesity, systolic blood pressure, and left ventricular geometry independently of left ventricular mass and presence of mitral regurgitation or atrial fibrillation.     

Noncompaction and neuromuscular disease with positive troponin-T in a nonagenerian

In a 94-year-old male with a history of atrial fibrillation, aortic stenosis, heart failure, apical thrombus, arterial hypertension, aneurysm of the abdominal aorta, and a urinary bladder carcinoma, cardiologic investigations revealed pulmonary rales, enlarged heart, absolute arrhythmia, and positive troponin-, myocardial thickening, enlarged cardiac cavities, hypocontractility, aortic stenosis, slight aortic insufficiency, severe mitral insufficiency, and surprisingly left ventricular hypertrabeculation. Upon neurological investigations, a polyneuropathy was suspected but a myopathy not completely excluded. The presented case shows that LVHT occurs also in nonagenarians and is associated with neuromuscular disease and positive troponin-T, in the absence of ischemic heart disease or severe renal failure. The cause of troponin-T-positivity remains multi-factorial.     

Pathophysiology of heart failure following myocardial infarction

The structural and functional abnormalities that lead to cardiac death are coronary artery disease and left ventricular abnormalities related to remodelling (left ventricular hypertrophy, left ventricular systolic dysfunction, and left ventricular fibrosis). Aldosterone adversely affects all of these processes. It produces both a vasculopathy and left ventricular dysfunction and fibrosis. Endothelial dysfunction in the coronary arteries can lead to acute coronary events. Left ventricular dysfunction will cause the progression of heart failure, and left ventricular fibrosis and dysfunction provide an arrhythmic substrate. The combination of acute coronary events and arrhythmias can lead to sudden cardiac deaths, while acceleration of the heart failure disease process can lead to deaths from progressive heart failure. The increased understanding of the mechanistic role of aldosterone in cardiovascular disease provides a rationale for the positive results that have been seen in clinical trials of aldosterone blockade.     

老年住院患者心脏结构和功能指标及其影响因素与氨基末端脑利钠肽前体的相关性研究

目的分析老年患者心脏结构和功能指标异常与氨基末端脑利钠肽前体(NT-proBNP)水平的相关性;了解年龄、血红蛋白、肾功能和肺部感染等对NT-proBNP水平的影响。方法选取148例老年住院患者,根据ACC/AHA心功能分期方法分为3组:对照组(心脏结构及功能正常者,ACC/AHA标准A阶段);异常组(ACC/AHA标准B阶段患者)及心力衰竭组(ACC/AHA标准C+D阶段的患者)。采用ELISA法测定血浆NT-proBNP水平。二维及脉冲多普勒超声心动图测量心脏各结构及功能。结果 NT-proBNP的水平在对照组、异常组及心力衰竭组3组之间比较,依次为对照组<异常组<心力衰竭组(P<0.05);与对照组相比,心力衰竭组患者NT-proBNP水平明显升高(P=0.005);与异常组相比,心力衰竭组患者NT-proBNP水平升高,差异无统计学意义(P=0.057);对照组与异常组间的差异无统计学意义(均为P>0.05)。不同心脏异常数量间NT-proBNP水平的比较,NT-proBNP水平随心脏异常指标数量的增多而升高(均为P<0.05),两两比较后发现3个以上心脏异常组NT-proBNP水平较无心脏异常组高(均为P<0.01)。超声心动图指标中,左心房扩大(r=0.251,P=0.002)、瓣膜疾病(r=0.242,P=0.003)及心房颤动(r=0.260,P=0.001)与NT-proBNP水平呈正相关,射血分数(r=-0.191,P=0.020)与其呈负相关。冠心病(r=0.188,P=0.022)、肺部感染(r=0.200,P=0.015)与NT-proBNP水平呈正相关;血红蛋白(r=-0.186,P=0.024)与NT-proBNP水平呈负相关。结论 NT-proBNP水平在对照组、异常组及心力衰竭组中逐渐升高,异常组与心力衰竭组NT-proBNP水平有重叠;NT-proBNP水平随着心脏结构与功能指标异常的增多而升高;心房颤动、左心房扩大、瓣膜疾病、LVEF、冠心病、肺部感染及血红蛋白均与NT-proBNP水平有相关性。     

Etiology and pathogenesis of thromboembolism.

Thrombus formation in the left atrium and left ventricle is primarily due to stasis of blood which causes activation of the coagulation system. Migration of thrombotic material into the circulation depends on the dynamic forces of the circulation. Atrial fibrillation is the commonest underlying cardiac disorder predisposing to thromboembolism. Rheumatic mitral stenosis, left atrial enlargement, prior myocardial infarction, hypertension, and echocardiographic left ventricular hypertrophy are risk factors for thromboembolic stroke in elderly patients with chronic atrial fibrillation. Non-valvular atrial fibrillation accounts for 45% of cardiac sources of thromboembolic stroke and includes patients with ischemic heart disease, hypertension, thyrotoxic heart disease, hypertrophic cardiomyopathy, chronic sinoatrial disorder, and idiopathic atrial fibrillation. 15% of cardiac sources of thromboembolic stroke are associated with acute myocardial infarction, 10% with left ventricular aneurysm and mural thrombi remote from an acute myocardial infarction, 10% with rheumatic valvular heart disease, and 10% with prosthetic cardiac valves. Mitral valve prolapse, mitral annular calcium, nonischemic cardiomyopathies, infective endocarditis, nonbacterial thrombotic endocarditis, left atrial myxoma, paradoxical embolism associated with congenital heart disease, calcific aortic stenosis, and complex atherosclerotic plaque within the proximal aorta also contribute to thromboembolism.     

Heart failure with preserved systolic function

Optional statement At least 30% of patients with congestive heart failure have preserved systolic function in the absence of significant valvular heart disease. These patients have diastolic dysfunction. Patients are frequently older and hypertensive. The rate of hospitalization in these patients is similar to that in patients with systolic dysfunction. Mortality is intermediate between that of patients with systolic dysfunction heart failure and normal subjects. Diagnosis requires a clear demonstration of the presence of the heart failure syndrome, normal systolic function, and the absence of valvular disease that could increase left atrial pressures. The diagnosis is supported by evidence of diastolic dysfunction that, from a practical point of view, will be provided most frequently by tissue Doppler imaging. Few randomized data are available on efficacy of therapeutic approaches. Acute treatment centers on reducing central blood volume with diuretics and nitrates and controlling heart rate, particularly in the setting of atrial fibrillation. Further treatment centers on reversing underlying pathophysiologic changes, particularly left ventricular hypertrophy. Control of hypertension and antagonism of the renin-angiotensin-aldosterone system appear to be promising therapeutic approaches.     

Function and reserve of the hypertrophic left ventricle in aortic valve disease]

Left ventricular function was analyzed by angiography in 31 patients with aortic valve disease and in 12 patients without heart disease (control group). Ejection fraction, percentage shortening of minor equator, mean velocity of fiber shortening and men left atrial pressure were considered as parameters of left ventricular function. Contractile reserve was tested by a single postextrasystolic beat. Patients with pure aortic stenosis and an increase of left ventricular muscle mass to 220% of the normal value showed no impairment of left ventricular function. Patients with pure aortic regurgitation and a left ventricular muscle mass of 260% of normal showed no significantly impaired function. Both groups increased ejection fraction and percentage shortening of the minor equator after premature beat comparable to the control group. Patients with combined lesions of the aortic valve had a left ventricular muscle mass of 360% of normal. This group showed decreased ejection fraction, percentage shortening of minor equator and mean velocity of fiber shortening as compared to the control group while mean left atrial pressure was significantly elevated. After premature beat all parameters remained depressed as compared to control group. We conclude that the degree of hypertrophy determinates cardiac function in aortic valve disease. Moderate hypertrophy shows normal function at rest, while severe hypertrophy shows impaired function.     

高血压病心律失常发生机制的临床分析

目的分析高血压病心律失常的发生机制。方法对100例高血压病患者和20例健康者的超声心动图、24小时动态心电图和临床资料进行比较。结果(1)高血压病患者的左心房(左房)增大,并随年龄增大,高血压病史延长,左房扩大越明显,发生严重房性心律失常几率也越高。高龄组发生持续性房颤为30.77%,显著高于其他年龄组。(2)室性心律失常发生率为36%(36例),房性心律失常发生率为85%(85例)。(3)多元回归分析显示:高血压病患者房性心律失常的发生与左房的大小、二尖瓣返流、左室大小以及左室质量指数相关,尤其与左房大小的相关性更明显,室性心律失常与左房、二尖瓣返流、主动脉瓣返流、左室质量指数相关性不显著,而与左室腔大小相关。结论(1)年龄、高血压病史、左房大小是影响高血压房性心律失常的重要因素,二尖瓣返流、左室增大、左室质量指数增高也与发生房性心律失常相关。(2)高血压患者室性心律失常发生率低于房性心律失常,高血压离心性心脏扩大比向心性肥厚更容易发生室性心律失常。     

动态血压参数与原发性高血压患者靶器官损害的关系

目的探讨24h动态血压参数与原发性高血压患者靶器官损害的关系。方法对140例原发性高血压患者进行24h动态血压监测,根据血压昼夜节律变化消失与否将其分为两组,对两组患者靶器官损害的情况进行对比分析,并对心、脑、肾各靶器官损害的危险因素进行Logistic回顾分析。结果两组脑卒中、左室肥厚、心力衰竭和肾功能损害的发生率差异有统计学意义(P<0.05),24h动态血压参数与各种靶器官损害的相关性不同。结论24h动态血压各参数对高血压患者靶器官损害的影响不同,血压负荷、昼夜血压曲线消失和血压波动幅度与靶器官损害显著相关。     

Hypertensive heart disease with left ventricular diastolic dysfunction demonstrating restrictive hemodynamics: a case report]

A 47-year-old man with hypertensive heart disease and left heart failure due to left ventricular diastolic dysfunction was admitted to our hospital because of emergent hypertension. Chest radiography on admission showed slight cardiomegaly and mild pulmonary congestion with right pleural effusion Echocardiography showed concentric hypertrophy and normal contraction of the left ventricular wall Pulsed Doppler left ventricular inflow velocity wave and pulmonary venous flow velocity wave disclosed restrictive filling patterns. After Ca antagonist, nitrate, and diuretics were administered, blood pressure was normalized, and left ventricular inflow velocity wave showed the relaxation abnormality pattern and pulmonary venous flow velocity wave showed the normal pattern. Radioiodinated iodine-123 metaiodobenzyl guanidine (123I-MIBG) imaging in the state of normalized blood pressure showed decreased heart to mediastinum ratio and increased washout rate. Left heart catheterization and angiography revealed normal end-diastolic pressure and coronary arteries, but coronary flow reserve evaluated with Doppler flow wire and intracoronary adenosine triphosphate administration was impaired: Plasma level of atrial and brain natriuretic peptides, which were markedly elevated on admission, decreased with the improvement of heart failure. Doppler flow velocity patterns, plasma levels of atrial natriuretic peptide and brain natriuretic peptide, cardiac sympathetic nerve activity, and coronary flow reserve might be useful for evaluating the severity of left ventricular diastolic dysfunction in patients with hypertensive heart disease.