Determinants of cardiac involvement in children and adolescents with essential hypertension

Left ventricular hypertrophy is often found in association with systemic hypertension and may be an independent risk factor for cardiovascular disease morbidity and mortality. Few studies have investigated the determinants of left ventricular mass (LVM) in young patients with essential hypertension. Therefore, we studied 104 children and adolescents with blood pressure persistently greater than the 90th percentile for age and sex and with no known cause of blood pressure elevation. LVM was determined by echocardiography and was indexed by height to account for body size. The mean LVM index was 90.2 +/- 26.0 g/m. Using the gender-specific 95th percentile from normal children, 40 subjects (38.5%) had left ventricular hypertrophy. Using multiple regression analysis, the significant independent direct correlates of LVM index were male sex, body mass index, dietary sodium intake, age at diagnosis, and systolic blood pressure at maximum exercise. The significant independent inverse correlate of LVM index was resting heart rate (p less than 0.05). These variables accounted for a substantial portion of the LVM index variance in this population (multiple R2 = 0.56, p less than 0.001). The results indicate that left ventricular hypertrophy is prevalent in children and adolescents with essential hypertension. The direct association of LVM index with body mass index and dietary sodium intake suggests weight reduction and dietary salt restriction might be useful to prevent or treat the development of left ventricular hypertrophy in pediatric patients with essential hypertension.     

Risk for cardiac involvement in essential hypertension

The evidence is inescapable that even mild essential hypertension is associated with left ventricular hypertrophy, regardless of the age of the patient. Increased left ventricular afterload must play a major role in the pathogenesis of the hypertrophy; however, further proof of this awaits our improved understanding of the quantitation of afterload in the clinical setting. Other factors, including the adrenergic nervous system and blood viscosity, may play an additional role, possibly mediated through alterations in afterload or by direct myocardial action. Left ventricular hypertrophy exerts a positive benefit by normalizing wall stress in patients with hypertension. Especially in patients without coexistent coronary abnormalities, systolic function is normal and abnormalities of diastolic function are of uncertain clinical importance. Because echocardiography now provides a convenient and sensitive noninvasive means of following patients with left ventricular hypertrophy, long-term studies are now needed to document the incremental risk (or benefit) of left ventricular hypertrophy over blood pressure itself in the eventual morbidity of essential hypertension. The recognition of left ventricular hypertrophy in a patient with borderline elevation of blood pressure poses a new clinical dilemma. Should treatment be instituted based on this additional finding? In view of the data correlating stress, exercise, and mean daily blood pressure with left ventricular hypertrophy and the reduction of left ventricular mass following lowering of blood pressure, it has been our practice to treat patients with left ventricular hypertrophy more readily than those without left ventricular hypertrophy. The rationale in this approach is not that left ventricular hypertrophy per se is harmful, but rather that it indicates a greater degree of afterload than may be evident from office blood pressure measurements.     

Ambulatory blood pressure monitoring in pediatric end-stage renal disease: chronic dialysis and transplantation.

Hypertension is highly prevalent in pediatric patients with end-stage renal disease (ESRD). Ambulatory blood pressure monitoring (ABPM) has been used to characterize the altered circadian blood pressure patterns in ESRD in order to improve our understanding of the blood pressure dysregulation that occurs in these children. In children receiving chronic hemodialysis, 24-h blood pressure load elevation and a high prevalence of non-dipping are reported for both systolic blood pressure (SBP) and diastolic blood pressure ((DBP). When comparing casual and ABPM measurements for diagnosing hypertension, ABPM reclassified approximately one third of patients from normotensive to hypertensive and from hypertensive to normotensive. ABPM has also been used to confirm experimentally that interdialytic weight gain is positively associated with increases in interdialytic blood pressure. In children who have undergone renal transplantation, 24-h blood pressure load elevation and non-dipping are also highly prevalent. A non-dipping pattern in transplant patients may be indicative of underlying renal parenchymal, renovascular disease or effect of medications. The prevalence of left ventricular hypertrophy (LVH) in pediatric patients after transplantation is approximately 20%, and left ventricular mass index (LVMI) is correlated with 24-h, daytime, and night-time ambulatory blood pressure. Since ESRD is a lifetime disease, addressing the high prevalence of hypertension and altered circadian blood pressure patterns in childhood may help prevent cardiovascular morbidity and mortality in early adulthood. Further studies are therefore needed to establish the utility of ABPM for the management of hypertension and prevention of end-organ injury in children with ESRD.     

Correlation between arterial pressure at rest and during effort and left ventricular mass in hypertensive patients who were never treated

A poor correlation has been found between blood pressure at rest and left ventricular mass in the course of several echocardiographic studies on hypertensive patients. The aim of this work was to determine if this finding could be the result of previous antihypertensive therapy, which had been suspended a few weeks previously in most of the studies. In addition, we tested whether blood pressure values during physical exercise correlate with the echocardiographic indices of left ventricular mass better than the values at rest. In our group of 43 patients with mild to moderate essential hypertension who had never been pharmacologically treated, the correlation between both systolic and diastolic blood pressure and left ventricular mass was poor (r = 0.41 and 0.30 respectively). This result suggests that one or more factors other than hypertension may determine the development of left ventricular hypertrophy. However, in 10 patients with left ventricular hypertrophy a more significant correlation was found between cardiac mass and diastolic pressure (r = 0.52), rather than systolic pressure (r = 0.33). This finding supports data indicating that cardiovascular risk is related more to diastolic pressure increments than to systolic pressure. As for blood pressure values during physical exercise, in our study they did not show a better predictivity of ventricular mass than the values at rest.     

Risk Reduction Following Regression of Cardiac Hypertrophy

Cardiac hypertrophy in essential hypertension is documented to be an independent risk factor for congestive heart failure, coronary heart disease and cardiac sudden death. Reduction of left ventricular hypertrophy therefore emerged as a new challenge of antihypertensive treatment. Sympatholytic agents, calcium entry blockers, and angiotensin converting enzyme inhibitors have been found to reduce left ventricular hypertrophy, whereas vasodilators (and most likely also diuretics) are unable to reduce left ventricular mass despite good control of arterial hypertension. Several studies indicated that reduction of left ventricular hypertrophy is not detrimental to cardiac pump function: systolic and diastolic function were found to be maintained at rest and during exposure to increased pressure load. In hypertensive patients with left ventricular hypertrophy ventricular arrythmias have been reported to be increased and to be the pathophysiological link for the increased risk of cardiac sudden death. Reduction of cardiac hypertrophy was found to be accompanied by a reduction of prevalence and severity of ventricular arrhythmias if treated with betablockers, calcium entry blockers or converting enzyme inhibitors. Whether reduction of cardiac hypertrophy indeed decreases the cardiovascular risk attributed to left ventricular hypertrophy is unknown at present, although clinical studies support such a viewpoint.     

Development and regression of left ventricular hypertrophy

Left ventricular hypertrophy is an important adaptive response to chronic pressure or volume overload of the left ventricle. The different types and the pathophysiologic mechanisms of the development of left ventricular hypertrophy in various disease states are reviewed. Detection of left ventricular hypertrophy may be accomplished by electrocardiography and cardiac angiography. Echocardiography, however, is the most accurate noninvasive method to detect the presence and estimate the severity of increased left ventricular mass. The clinical significance of left ventricular hypertrophy and its prognostic implications in several cardiac diseases associated with hypertrophy are discussed. The critical transition stage from adaptive, compensatory and reversible left ventricular hypertrophy to "pathologic" hypertrophy with impaired left ventricular contractility and irreversible myocardial damage is yet unknown. Recent data are presented that provide evidence of regression of left ventricular hypertrophy after medical treatment of patients with hypertension and after aortic valve replacement in patients with aortic valve disease. The clinical importance of regression of hypertrophy and its effects on long-term prognosis remain to be determined.     

Obesity and the heart

Obesity has been identified as an independent risk factor for coronary heart disease and congestive heart failure. Although congestive heart failure can be secondary to coronary heart disease, in morbid obesity these conditions can be independent. Cardiac structure and function can be altered even in the absence of systemic hypertension and underlying organic heart disease. In obese patients total blood volume increases and creates a high cardiac output state that may cause ventricular dilatation and ultimately eccentric hypertrophy of the left (and possibly the right) ventricle. Eccentric left ventricular hypertrophy produces diastolic dysfunction. Systolic dysfunction may ensue due to excessive wall stress if wall thickening fails to keep pace with dilatation. This disorder is referred to as obesity cardiomyopathy. The frequent coexistence of systemic hypertension in obese individuals facilitates development of left ventricular dilatation and hypertrophy. Congestive heart failure may occur and may be attributable to left ventricular diastolic dysfunction or to combined diastolic and systolic dysfunction. The risk of coronary heart disease seems to be more strictly correlated to central obesity than to increased body mass index. Insulin resistance seems to be the key factor that links obesity and ischaemic heart disease. In such a condition the so called Syndrome X appears. It is characterized by: obesity, systemic hypertension, diabetes mellitus, hypertriglyceridaemia and reduced HDL cholesterol levels. Considering that left ventricular hypertrophy is often present, many risk factors coexist in obese patients. Weight loss is very useful in obese patients. It may reduce mortality and morbidity for coronary heart disease and delay or avoid the appearance of congestive heart failure. It is proved that after weight loss, blood pressure, glucose, cholesterol, triglycerides and left ventricular mass decrease.     

The prevalence and correlates of echocardiographic left ventricular hypertrophy among employed patients with uncomplicated hypertension

To determine the prevalence and correlates of echocardiographic left ventricular hypertrophy among subjects in a general population, we studied 621 employed subjects. Patients with uncomplicated essential hypertension in a worksite-based treatment program included 145 with borderline hypertension and 316 with sustained hypertension by World Health Organization criteria. Normotensive subjects were randomly selected from members of the same unions. M-mode echocardiographic left ventricular dimensions were used to calculate left ventricular mass and other indexes of left ventricular anatomy. The specificity of 13 echocardiographic criteria of left ventricular hypertrophy was determined in normotensive individuals, and the prevalence of left ventricular hypertrophy by each criterion was assessed in patients with borderline or sustained essential hypertension. The results suggest that the most suitable reference standard for detection of left ventricular hypertrophy in a heterogeneous urban population utilizes sex-specific cutoff values for left ventricular mass index of 110 g/m2 or greater for women and 134 g/m2 or greater for men. With 97% specificity, the prevalence of left ventricular hypertrophy by these criteria is approximately 12% among patients with borderline hypertension and 20% among patients with relatively mild, uncomplicated sustained essential hypertension. Wall thickness measurements performed slightly less well. At similar levels of blood pressure, black patients were more likely than white patients to exhibit concentric left ventricular hypertrophy, especially among borderline hypertensive patients. Left ventricular hypertrophy occurred in patients with sustained hypertension who also exhibited increased cardiac output, strongly associated with low plasma renin activity.     

Left Ventricular Hypertrophy in Hypertensive Children and Adolescents: Predictors and Prevalence

Left ventricular hypertrophy is an independent predictor of cardiovascular morbidity and mortality in adults. In children, the primary correlate of left ventricular mass (LVM) is lean body mass, but fat mass, gender and systolic blood pressure are also contributors. LVM can be estimated from echocardiographic measurements, and by indexing this allometrically to height to the 2.7 power, the left ventricular mass index (LVMI) can be calculated. LVMI optimizes detection of left ventricular hypertrophy with established normal curves for children from birth to 18 years. In children with sustained hypertension, 8–41 % have LVMI above the 95th percentile and in 10–15.5 % of these, LVMI is elevated above levels associated with increased mortality in adults. The presence of obesity is associated with higher LVMI than is found in children with hypertension alone. In children with chronic kidney disease, left ventricular hypertrophy develops relatively early and becomes more prevalent as kidney function decreases. In summary, left ventricular hypertrophy is a sensitive marker of target organ damage in children with BP elevation, obesity and chronic kidney disease providing important management information.     

Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension.

The spectrum of left ventricular geometric adaptation to hypertension was investigated in 165 patients with untreated essential hypertension and 125 age- and gender-matched normal adults studied by two-dimensional and M-mode echocardiography. Among hypertensive patients, left ventricular mass index and relative wall thickness were normal in 52%, whereas 13% had increased relative wall thickness with normal ventricular mass ("concentric remodeling"), 27% had increased mass with normal relative wall thickness (eccentric hypertrophy) and only 8% had "typical" hypertensive concentric hypertrophy (increase in both variables). Systemic hemodynamics paralleled ventricular geometry, with the highest peripheral resistance in the groups with concentric remodeling and hypertrophy, whereas cardiac index was super-normal in those with eccentric hypertrophy and low normal in patients with concentric remodeling. The left ventricular short-axis/long-axis ratio was positively related to stroke volume (r = 0.45, p less than 0.001), with cavity shape most elliptic in patients with concentric remodeling and most spheric in those with eccentric hypertrophy. Normality of left ventricular mass in concentric remodeling appeared to reflect offsetting by volume "underload" of the effects of pressure overload, whereas eccentric hypertrophy was associated with concomitant pressure and volume overload. Thus, arterial hypertension is associated with a spectrum of cardiac geometric adaptation matched to systemic hemodynamics and ventricular load. Concentric left ventricular remodeling and eccentric hypertrophy are more common than the typical pattern of concentric hypertrophy in untreated hypertensive patients.     

Adrenergic nervous system and left ventricular mass in primary hypertension

A link between the activity of the adrenergic nervous system and left ventricular hypertrophy has frequently been found in hypertensives. In 16 patients with untreated primary hypertension of mild to moderate degree, we have evaluated the possible correlations between echocardiographic left ventricular mass (LVMe) and sympathetic nervous system activity, using pressor response to exogenous noradrenaline infusion, measurement of 24-h catecholamine urinary excretion and pressure response to ergometric exercise. Pressor response to noradrenaline infusion was significantly related to echocardiographic measures of left ventricular hypertrophy (correlation coefficients were: -0.60 for LVMe; -0.51 for septal thickness (ST); -0.51 for posterior wall thickness). Left ventricular mass was also related to systolic blood pressure measured during ergometric exercise (correlation coefficients were: 0.52 with LVM index, 0.51 with LVMe and 0.61 with ST). Arterial wall hypertrophy has been identified as being responsible for the vascular hyperreactivity in hypertension. A likely explanation of our findings is that the degree of left ventricular hypertrophy is associated with the degree of structural alterations of the resistance vessels and that the vascular impairment is responsible for the increased pressure response to noradrenaline.     

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.     

Heart rate variability in left ventricular hypertrophy.

BACKGROUND--Electrocardiographic left ventricular hypertrophy and strain are associated with increased cardiac morbidity and mortality. Impaired cardiac autonomic function, assessed non-invasively by spontaneous heart rate variability on Holter monitoring, is associated with an increased risk of sudden death after myocardial infarction. AIM--To study the effect of left ventricular hypertrophy on heart rate variability. PATIENTS--36 controls and 154 patients with left ventricular hypertrophy (94 with hypertension and 60 with aortic valve disease). SETTING--Tertiary referral centre. METHODS--Heart rate variability was measured on 24 h Holter recordings by non-spectral methods. Left ventricular mass index and fractional shortening were measured by echocardiography. RESULTS--Patients with left ventricular hypertrophy had a higher left ventricular mass index (P < 0.001) and reduced heart rate variability (P < 0.001) compared with those of the controls. A continuous inverse relation was apparent between heart rate variability and left ventricular mass index (r = -0.478, P < 0.001). Heart rate variability was not affected by age, the presence of coronary artery disease in patients with left ventricular hypertrophy, or beta blocker treatment for hypertension. Multivariate analysis showed that left ventricular mass index is the most important determinant of heart rate variability. CONCLUSION--Heart rate variability is significantly reduced in patients with left ventricular hypertrophy secondary to hypertension or aortic valve disease. A continuous inverse relation exists between heart rate variability and left ventricular mass index. Impaired cardiac autonomic function in left ventricular hypertrophy may contribute to the mechanism of sudden death.     

Blood pressure pattern importance in the development of left ventricular hypertrophy in hypertension.

Heterogeneous results regarding correlations between blood pressure, (measured by various methods and in different conditions), and left ventricular mass in arterial hypertension have been reported. Fifty-three essential hypertensives, I-II WHO stage, have been studied in order to verify the relationship between office and average 24-hour blood pressure, and its day- and night-time pattern with left ventricular hypertrophy. All patients had newly diagnosed essential hypertension, and no subject had received any antihypertensive therapy before entry. The subjects underwent 24-hour blood pressure monitoring, evaluating the average of 24 hours, day- and night-time blood pressures, and M-mode echocardiography. Neither subjects with nor without left ventricular hypertrophy showed correlations between office blood pressure and left ventricular mass. On the contrary, average 24-hour systolic and diastolic blood pressure resulted related to left ventricular mass (r = 0.36 and 0.40, p less than 0.01 respectively). Furthermore, in the subgroup with left ventricular hypertrophy, left ventricular mass was correlated directly with nocturnal systolic blood pressure (r = 0.46) and inversely with the rate of nocturnal decrease in systolic pressure (r = -0.60, p less than 0.01). These results appear to confirm the usefulness of 24-hour blood pressure monitoring in evaluating cardiac afterload in essential hypertension, and the important role that the 24-hour systolic pressure has in the development of left ventricular hypertrophy in these subjects.     

放射性核素电子计算机断层摄影测量左室心肌质量与儿童青少年血压关系的研究

高血压合并左心室肥厚早已被人熟知。近年来研究发现左室心肌质量的增加伴随着血压明显增高达９０百分位或以上在儿童时期即已出现。一般认为左室心肌质量的增加是高血压或血压偏高的结果。仅在最近几年才有少数作者发现左室心肌质量的增加出现在儿童发生血压增高之前。血压正常儿童或青少年之父母有高血压者，其左室心肌质量均高于无高血压家族史者。本研究者在观察血压增高与高血压家族史及左室心肌质量之间的关系时，结果发现在高血压高危儿童并有家族史者左室心肌质量高于高血压高危儿童无高血压家族史者，提示除血压增高可能为左室心肌质量增加之原因外，而且左室心肌质量之增加尚可能为高血压之原因，即有可能在先天因素中存在左室心肌质量易于增加的因子或者说不能除外心室肌异常基因的存在。     

Relation of hemodynamic load to left ventricular hypertrophy and performance in hypertension

Left ventricular hypertrophy and dysfunction in patients with hypertension are often poorly related to the level of blood pressure. To evaluate the reasons for this, 100 untreated patients (44 +/- 14 years) with essential hypertension were studied using cuff blood pressure and quantitative echocardiography to measure left ventricular mass index and end-diastolic relative wall thickness as 2 indexes of left ventricular hypertrophy. Left ventricular hypertrophy, as measured by either left ventricular mass index or end-diastolic relative wall thickness, correlated weakly with all indexes of blood pressure including systolic, diastolic, and mean blood pressure (r = 0.16 to 0.32). In contrast, end-diastolic relative wall thickness, an index which assesses the severity of concentric hypertrophy, showed a closer direct relation with total peripheral resistance (r = 0.52 p less than 0.001) and a significant inverse relation with cardiac index (r = -0.47, p less than 0.001). Left ventricular performance as assessed by fractional systolic shortening of left ventricular internal dimensions was not significantly related to left ventricular mass index, blood pressure, or peak systolic wall stress, but declined significantly with increasing mean systolic wall stress (r = -0.42, p less than 0.001) and even more with increasing end-systolic wall stress (r = -0.71, p less than 0.001). It is concluded that in patients with hypertension (1) left ventricular hypertrophy is correlated only modestly with measurements of resting blood pressure; and (2) the classic pattern of concentric left ventricular hypertrophy, as measured by relative wall thickness, is more closely related to the "typical" hypertensive abnormality of elevated peripheral resistance, suggesting that these anatomic and hemodynamic changes may be pathophysiologically interdependent. Furthermore, left ventricular performance declines when the pressure overload in hypertension is not offset by compensating hypertrophy, allowing wall stresses to increase.     

Left ventricular hypertrophy and geometry in a population sample of elderly males

BACKGROUND: Recent studies have shown that left ventricular geometric adaptationto hypertension is complex. The spectrum of geometric adaptationsin a general population and its relationship to systolic anddiastolic function has, however, not been investigated. OBJECTIVES AND METHODS: This echocardiographic and Doppler study investigated the relationshipsbetween left ventricular geometric shape (normal, concentricremodelling, concentric hypertrophy and eccentric hypertrophy)and left ventricular systolic and diastolic function in a populationsample of 584 males aged 70 in Uppsala, Sweden. The influencesof hypertension, coronary heart disease and diabetes mellituswere also evaluated. RESULTS: Sixteen percent of the healthy population (n=167) demonstratedthe presence of left ventricular hypertrophy (mainly eccentric).Subjects with hypertension (n=115) showed an increased leftventricular mass (eccentric left ventricular hypertrophy 31%,concentric left ventricular hypertrophy 15%), when comparedwith healthy subjects (P<0.001). Subjects with coronary heartdisease (n=32) without hypertension also showed an increasedleft ventricular mass (most often eccentric) (P<0.05). UsingDoppler determinations of cardiac index, no differences werefound in cardiac index between the geometric groups. Raisedtotal peripheral resistance, increased blood pressure and enlargedleft atrium were found in both concentric and eccentric leftventricular hypertrophy (P<0.01–0.05). Disturbed diastolicfunction was seen with a prolongation of the isovolumic relaxationtime in eccentric (P<0.01) and increased atrial-dependentleft ventricular filling in concentric left ventricular hypertrophy(P<0.05). CONCLUSIONS: Alterations in left ventricular geometry were common in thispopulation-based study of elderly males, both in healthy subjectsand in subjects with hypertension or coronary heart disease.Raised total peripheral resistance and left ventricular diastolicdysfunction were common findings in both concentric and eccentricleft ventricular hypertrophy.     

肥胖与原发性高血压患者心肌肥厚的相关性分析

目的　探讨肥胖对原发性高血压患者心肌肥厚的影响。方法　回顾性分析2012年1月至2015年12月于我院就诊的280例原发性高血压患者,按照国际糖尿病联盟设定的亚洲人肥胖的诊断标准,其中肥胖组130例,对照组150例。通过二维引导的M模式进行测量记录左心室结构,计算左心室质量指数及左室肥厚在两组患者中的发生率,应用多元线性逐步回归分析患者的年龄、性别、收缩压、舒张压、平均血压、脉压差,体质指数、血糖、糖化血红蛋白、TC、TG、LDL-C、HDL-C、肌酐、尿酸与心肌肥厚的相关性。结果　肥胖组患者的左心室质量指数显著高于对照组,且左室肥厚的发生率明显高于对照组,差异具有统计学意义(Ｐ<0.05)。患者的体重指数、血压、血糖、糖化血红蛋白、TC、TG、LDL-C及HDL-C与心肌肥厚相关。结论 除血压因素外,肥胖与高血压患者的左室肥厚发生密切相关,差异具有统计学意义(Ｐ<0.05)。     

Importance of left ventricular mass as a predictor of cardiovascular morbidity in hypertension

Arterial hypertension is a powerful risk factor for cardiovascular disease, but the ability to use blood pressure measurements to predict complications in individual patients or small groups is limited. One possible approach to identifying hypertensive patients at high risk is based on the observation that the presence of electrocardiographic left ventricular hypertrophy (ECG-LVH) identifies individuals at severalfold higher risk than other individuals with similar blood pressure but no ECG-LVH. The suggestion that the increased risk associated with ECG-LVH is related to increased left ventricular (LV) mass has been supported by autopsy studies in which heart weight was found to be increased in patients dying of cardiovascular diseases. Unfortunately, the usefulness of LVH to predict prognosis in hypertension has been limited practically by the fact that ECG-LVH is present in only 3% to 8% of average hypertensive patients, and by the possibility that certain electrocardiographic patterns, particularly involving repolarization, might reflect undiagnosed coronary artery disease rather than myocardial hypertrophy. The development over the past dozen years of anatomically validated echocardiographic methods of measuring LV muscle mass has provided a probe that is more sensitive than electrocardiography for detection of hypertensive LVH. This method has now been utilized in studies which suggest that LV mass may be more important than blood pressure as a predictor and possible determinant of cardiovascular morbid events. It is the purpose of this review to evaluate critically these findings and other clinical and experimental evidence related to the prognostic significance and possible mechanisms of risk associated with increased LV mass.     

Increased right ventricular wall thickness in left ventricular pressure overload: echocardiographic determination of hypertrophic response of the "nonstressed" ventricle

Left ventricular hypertrophy in left ventricular pressure overload occurs in response to excessive work load imposed on the left ventricle by increased impedance to ejection. Right ventricular hypertrophy may occur in patients with these findings, but has been considered to be secondary to pulmonary hypertension. To determine the frequency of right ventricular hypertrophy and its relation to increased left ventricular wall thickness in patients with left ventricular pressure overload, right ventricular wall thickness was measured using M-mode echocardiography with two-dimensional echocardiographic guidance in 65 patients with left ventricular pressure overload; 49 patients had essential hypertension and 16 had aortic valve stenosis. These measurements were compared with data from 13 patients with "thin-walled" dilated cardiomyopathy and 20 normal subjects. Average right ventricular wall thickness in hypertensive patients (7 +/- 2 mm) and patients with aortic stenosis (6 +/- 2 mm) was significantly greater than that in normal subjects (4 +/- 1 mm) and patients with dilated cardiomyopathy (4 +/- 1 mm) who had normal left ventricular wall thickness, even though left ventricular mass was increased in all patient groups. Increased right ventricular wall thickness was present in 40 (80%) of 49 patients with hypertension and 10 (63%) of 16 patients with aortic stenosis. The magnitude of increase in right ventricular wall thickness was linearly correlated (r = 0.76, p less than 0.005) with left ventricular wall thickness, but was not associated with pulmonary hypertension. It is concluded that increased right ventricular wall thickness is common in patients with left ventricular pressure overload, is directly related to increases in left ventricular wall thickness, and is independent of right ventricular hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)