Arrhythmias in mitral valve prolapse. Effect of selection bias.

To assess the contribution of bias in subject selection to the prevalence of arrhythmias in cases of mitral valve prolapse (MVP), we compared ambulatory arrhythmias in 63 patients with MVP and 28 symptom-matched control subjects. All subjects were in sinus rhythm. Mean 24-hour heart rate of the prolapse population was lower than that of the control group (76 v 82 beats per minute). Mean atrial premature complex (APC) density per 1,000 beats (0.9 v 0.7 for patients with MVP and control subjects, respectively) and mean ventricular premature complex (VPC) density per 1,000 total beats (1.2 v 1.5) did not differ between groups. Small differences between groups in APC and VPC complexity did not reach statistical significance. Our findings suggest that, compared with similarly symptomatic controls, patients with MVP do not have as high an excess prevalence of arrhythmias as previously believed.

Effect of age, sex, and body surface area on echocardiographic left ventricular wall mass in normal subjects.

M-mode echocardiography was used to estimate left ventricular wall mass in 136 older normal subjects (Group I: 78 men and 58 women, ages 20 to 97 years) and 105 younger normal subjects (Group II: 52 male and 53 female subjects, ages 1 day to 23 years). Echocardiographic left ventricular mass (in grams) was estimated from the following formula: left ventricular mass = 1.05 ([ left ventricular internal diastolic dimension + ventricular septal thickness (diastole) + posterior wall thickness (diastole)] - [left ventricular internal diastolic dimension]). In both groups, female subjects had a slightly smaller left ventricular mass than male subjects (mean difference 7.2% in Group I, p less than 0.05, and 3.6% in Group II, p = 0.05) for any given age and body surface area. Left ventricular mass varied linearly with body surface area and increased as a function of age. In group I subjects, echocardiographic left ventricular mass (in grams) could be estimated by the general formula: left ventricular mass = 124 (body surface area) + A +/- C, where A is the age-dependent intercept; +/- C encompasses a 95% prediction interval for normal values, which is assumed to be nearly constant (+/- 58 g); and body surface area is expressed in square meters. In the Group II (younger) subjects, with age not considered, left ventricular mass (in grams) could be estimated from the following formula: left ventricular mass = 115 (body surface area) -11 +/- C, where +/- C = +/- 32% and this 95% prediction interval varies as a percentage of the mean.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular hypertrophy and function in high, normal, and low-renin forms of essential hypertension.

To assess the relative importance of the level of blood pressure (BP) and renin profile status as determinants of hypertensive left ventricular hypertrophy (LVH) and dysfunction, we studied, by quantitative echocardiography, 118 hypertensive patients off medication. The 19 high-renin patients were younger (31 +/- 13 years; p less than 0.01) but had hypertension of severity (152 +/- 13/95 +/- 11 mg Hg) similar to the 79 normal-renin patients (42 +/- 14 years; 152 +/- 17/98 +/- 12 mg Hg) and 20 low-renin patients (49 +/- 13 yrs; 157 +/- 17/95 +/- 11 mm Hg). Left ventricular (LV) mass index (normal = 70 +/- 25 g/m2) was similar in the high- (113 +/- 21 g/m2, p less than 0.001), normal = (114 +/- 31 g/m2, p less than 0.001), and low-renin patients (115 +/- 18 g/m2, p less than 0.01). End-diastolic relative wall thickness (nl = 0.32 +/- 0.05) was equally elevated in high- (0.41 +/- 0.09), normal (0.42 +/- 0.08) and low-renin groups (0.41 +/- 0.08) (all p less than 0.001). In the entire population, there was a closer correlation of relative wall thickness with total peripheral resistance (r = 0.54, p less than 0.001) than with mean blood pressure (r = 0.31, p less than 0.05). LV dysfunction (LV fractional systolic shortening less than 26%) occurred only in two high-renin patients, whereas LV fractional shortening was significantly increased in the low-renin subgroup (p less than 0.01). We conclude that the degree of LVH is similar in low-, normal-, and high-renin hypertensives and is proportional to the degree of hypertension, even though the high-renin patients were significantly younger; but that the low-renin patients with similar level of blood pressure, even though significantly older and with a longer duration of hypertension than the other patient groups, manifest increased LV function compared to normals.

Considerations in the use of echocardiography in epidemiology. The Framingham Study.

To quantify potential biases in the use of echocardiography in epidemiologic studies, we assessed the relationship of sex, age, vital capacity, body fatness, and overt cardiovascular disease to prevalence of acceptable echocardiograms in 6148 Framingham men and women aged 17 to 90 years. Echocardiograms adequate to assess left ventricular chamber dimensions and wall thickness, aortic root, and left atrial dimensions as well as mitral and aortic valves were obtained in 4947 (80%) of the 6148 subjects. The prevalence of acceptable echocardiograms ranged from less than 50% for those more than 80 years of age to more than 96% for subjects under 30 years of age. A significant learning curve was apparent, particularly in the older subjects (more than 60 years of age) for whom prevalence of acceptable echocardiograms rose from a minimum of 28% during the first 5 months of studies to a maximum of 74 to 81% during studies 2 years later. The likelihood of unacceptable echocardiograms was slightly greater in men. Obesity (in subjects younger than 60 years of age), lower vital capacity, and overt cardiovascular disease were associated with unacceptable echocardiograms, independent of age. Consideration of these biases should aid in the interpretation and planning of epidemiologic and other studies using echocardiography.

Kindled seizure-induced reduction of muscarinic cholinergic receptors in rat hippocampal formation: evidence for localization to dentate granule cells.

The binding of [3H] quinuclidinyl benzilate ( [3H] QNB) to muscarinic cholinergic receptors in dentate gyrus of rat hippocampal formation was analyzed by membrane binding assay and in vitro autoradiography. The destruction of dentate granule cells, either by neonatal irradiation or colchicine injection, resulted in nearly complete elimination of [3H] QNB binding sites in the molecular and granule cell layers. By contrast, neither perforant path transection nor destruction of the septal-hippocampal cholinergic afferents caused a decline of [3H] QNB binding sites. Amygdala kindled seizures resulted in a 30% reduction of [3H] QNB binding sites which was distributed uniformly across the entire molecular and granule cell layers. Thus, most, if not all, of the muscarinic cholinergic receptors present in dentate gyrus appear to reside on the somata and dendritic trees of the dentate granule cells. We propose that this kindled seizure-induced decline of muscarinic receptors represents an endogenous compensatory mechanism designed to stabilize granule cell excitability.

Sudden unexpected death during ambulatory electrocardiographic monitoring. The Framingham Study.

This report documents the clinical and electrocardiographic events of sudden unexpected death in a 52-year-old man without known heart disease during ambulatory electrocardiographic monitoring. This death occurred two and a half hours after detailed noninvasive testing, including treadmill exercise, that was unrevealing. The sequence of S-T change suggesting epicardial injury, multiform ventricular premature depolarizations, and frequent and early cycle ventricular premature depolarizations followed by ventricular tachycardia-flutter-fibrillation precipitated by an early cycle ventricular premature depolarization were documented. The delay in cardiopulmonary resuscitation in this witnessed cardiac arrest punctuates the need for widespread dissemination of the skills of cardiopulmonary resuscitation.

Echocardiographic assessment of cardiac anatomy and function in acromegalic patients.

Echocardiography was used to evaluate cardiac anatomy and function in 25 patients with accromegaly. Eighty per cent of the patients (20 of 25) had abnormal echocardiograms including 13 patients without other signs or symptoms of cardiac involvement. The most common abnormality was increased left ventricular mass with concentric left ventricular wall thickening, which was found in 64 per cent (16 of 25) of the patients. Increased left ventricular transverse dimension at end diastole was found in 36 per cent (nine of 25) of the patients. Other echocardiographic abnormalities found included left atrial or aortic root enlargement (three patients), disproportionate septal thickening (one patient) and depressed left ventricular ejection fraction (three patients). Since five of the patients with increased left ventricular mass had no history of hypertension or hyperthyroidism, the increased mass cannot be ascribed solely to these conditions commonly associated with acromegaly. Furthermore, the degree of cardiac hypertrophy showed no significant correlation with pre- or post-treatment growth hormone levels, or with known duration of acromegaly prior to treatment. Thus, although the pathophysiology and significance of cardiac abnormalities in acromegalic patients is not yeat fully understood, echocardiography does provide a sensitive tool for detecting such abnormalities before they are otherwise apparent.

Risk factors for pulmonary embolism. The Framingham Study.

To assess potential long-term risk factors for major pulmonary embolism, 46 subjects from the Framingham Heart Study with autopsy-confirmed and clinically significant pulmonary embolism were identified in whom age, systolic blood pressure, cholesterol level, cigarette use, glucose level, Metropolitan relative weight, and varicose veins were ascertained at entry into the Study. These variables were compared among these 46 subjects, all 3,470 subjects in whom these variables were measured at the inception of the Study, and the 998 of these subjects who died within 26 years of follow-up. In multivariate analysis of subjects with autopsy-confirmed major pulmonary embolism and all subjects who died, only Metropolitan relative weight was significantly and independently associated with pulmonary embolism and only among women (p less than 0.001). These findings indicate that, in this cohort, increased adiposity in women is an important long-term factor for significant pulmonary embolism at autopsy. This raises the possibility that weight reduction in obese women may decrease the chances of pulmonary embolism.

Fibrosing mediastinitis causing pulmonary arterial hypertension without pulmonary venous hypertension. Clinical and necropsy observations.

Clinical and morphologic observations are described in two patients with severe pulmonary arterial hypertension without pulmonary venous hypertension from fibrosing mediastinitis. In one patient, both main pulmonary arteries and one major pulmonary vein were severely narrowed by dense fibrous tissue; in the second patient, only the right main pulmonary artery was severely narrowed. Both patients had normal intrapulmonary arteries and normal pulmonary parenchyma. Of nine previously described necropsy patients with pulmonary hypertension due to fibrosing mediastinitis, seven had severe narrowing of multiple large pulmonary veins and in six of them the pulmonary hypertension was entirely due to pulmonary venous obstruction. In one other patient, the pulmonary hypertension was due to obstruction of one main pulmonary artery and several large pulmonary veins. Each of these seven previously described patients had severe changes in the small intrapulmonary arteries. Of the other two previously described patients with pulmonary hypertension from fibrosing mediastinitis, one had severe narrowing of only the main right pulmonary artery, and the other, of both main pulmonary arteries. Thus, although pulmonary arterial hypertension in patients with fibrosing mediastinitis is usually due to obstruction of multiple large pulmonary veins and to severe secondary changes in small intrapulmonary arteries, fibrosing mediastinitis can cause severe pulmonary hypertension by obstructing the right or both main pulmonary arteries.

Evidence of altered T-lymphocyte number and proliferative responses in genetically epilepsy-prone rats.

Genetically epilepsy-prone (GEPR-9) rats exhibit decreased antibody plaque-forming cell responses following immunization. We examined the hypothesis that this immunosuppression was due to deficits in the number or proliferative responses of T-lymphocytes. Splenocyte responses to concanavalin A and pokeweed mitogen were significantly greater in GEPR-9 rats than controls. Flow cytometric analysis indicated that GEPR-9 rats possess an increase in T-cells associated with the T-helper phenotype. The increased proportion of T-helper cells in GEPR-9 rats may underlie their enhanced proliferative responses to T-cell mitogens. These results clearly indicate that the failure of the GEPR-9 rat to respond to a T-dependent antigen in vivo is not due to a lack of T-helper activity.

Decrease in hippocampal [3H]vinylidene kainic acid binding in genetically epilepsy-prone rats.

Specific [3H]vinylidene kainic acid binding to the kainate-sensitive subtype of glutamate receptor was studied in brain of 31-day-old non-epileptic Sprague-Dawley control and two colonies of genetically epilepsy-prone rats using in vitro autoradiographic techniques. At 37.5 nM [3H]vinylidene kainic acid, specific [3H]vinylidene kainic acid binding was reduced significantly by 18 and 22% in dorsal and ventral hippocampal formation stratum lucidum of 31-day-old genetically epilepsy-prone-9 rats compared with non-epileptic controls. Hippocampal [3H]vinylidene kainic acid binding was reduced in genetically epilepsy-prone-3 rats by 15 and 18%, but these reductions were not statistically significant. Saturation of [3H]vinylidene kainic acid binding studies indicated that the total number of ventral hippocampal [3H]vinylidene kainic acid binding sites was decreased by 21% in genetically epilepsy-prone-3 rats and 28% in genetically epilepsy-prone-9 rats. The reduction in ventral hippocampal [3H]vinylidene kainic acid binding in genetically epilepsy-prone rats resembles the reduction in ventral hippocampal [3H]vinylidene kainic acid binding sites observed in perinatal hypothyroid rats. As genetically epilepsy-prone rats are hypothyroid during the neonatal period, the reduction in hippocampal [3H]vinylidene kainic acid binding in the genetically epilepsy-prone rats may be a consequence of a hypothyroid-induced defect in the development or maturation of the hippocampal mossy fiber projection in genetically epilepsy-prone rats. An alternative hypothesis is that the putative occurrence of spontaneous limbic seizures in genetically epilepsy-prone rats may lead secondarily to a reduction in hippocampal [3H]vinylidene kainic acid binding sites.

Overall risk of left ventricular hypertrophy secondary to systemic hypertension.

Stratification of risk for cardiovascular events is a fundamental aspect of the assessment of hypertensive patients. The assessment of left ventricular (LV) hypertrophy is an important component of such stratification. The low prevalence of LV hypertrophy on the electrocardiogram (less than 3%) in patients with borderline or mild hypertension limits the utility of the electrocardiogram for stratification of risk in such patients. The high sensitivity (roughly 10-fold greater) and specificity of echocardiography for detection of LV hypertrophy and assessment of the severity and the various forms of such hypertrophy have prompted critical evaluation of the risk associated with such LV hypertrophy. Initial information suggesting considerable risk associated with echocardiographically detected increases in LV mass suggests significant clinical and public health importance of this tool. Further detailed cost-benefit analyses are needed to aid in assessing the role of echocardiography in the evaluation of patients with borderline and mild hypertension.

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.

Echocardiographically determined left ventricular structural and functional correlates of complex or frequent ventricular arrhythmias on one-hour ambulatory electrocardiographic monitoring.

The associations between 6 echocardiographic measurements and ventricular arrhythmias on 1-hour ambulatory electrocardiograms were evaluated in 3,348 subjects of the Framingham Heart Study who were free of symptomatic coronary artery disease, congestive heart failure and valvular heart disease and were not receiving diuretic drugs or other blood pressure or cardiac medications. Age-adjusted estimates of association between echocardiographic measurements of left ventricular (LV) structure and function and complex or frequent (Lown grade 2 or greater) ventricular arrhythmia were computed using logistic regression. In this bivariate model only LV internal diameter (systolic and diastolic) and fractional shortening were associated with arrhythmia in both sexes (p less than 0.01). When all variables were entered into a multivariate model, only age and systolic LV internal diameter remained independently associated with arrhythmia (p less than 0.001). Thus, LV chamber size and function are important predictors of risk for ventricular arrhythmia. Systolic LV internal diameter, which reflects both functional and structural information, is the only measurement independently predictive of arrhythmia risk in persons free of apparent heart disease.

"Malignant" hypertrophic cardiomyopathy: identification of a subgroup of families with unusually frequent premature death.

Eight families were identified in which premature cardiac death due to hypertrophic cardiomyopathy occurred with unusual frequency. A total of 69 first degree relatives in the eight families were studied; 41 relatives had evidence of hypertrophic cardiomyopathy and 31 (75 per cent) died of their heart disease. Eighteen of these 31 patients were less than 25 years of age at the time of death. Death was sudden and unexpected in 23 of the 31 patients; in 15 of these 23 patients sudden death was the initial manifestation of cardiac disease. The remaining eight patients (seven were from two families) died after a chronic cardiac illness characterized by congestive heart failure, atrial fibrillation or thromboembolic events. Hence, premature cardiac death occurs frequently in certain families with hypertrophic cardiomyopathy. Such deaths are usually sudden, often occur in previously asymptomatic subjects and are common in children and young adults. These findings suggest that some families may manifest an unusually virulent expression of hypertrophic cardiomyopathy. Although this study cannot establish the precise prevalence with which "malignant" hypertrophic cardiomyopathy occurs, such families appear to be uncommon.

Prognostic significance of 24 hour ambulatory electrocardiographic monitoring in patients with hypertrophic cardiomyopathy: a prospective study.

The prevalence and prognostic significance of ventricular arrhythmias identified on 24 hour ambulatory electrocardiographic monitoring was prospectively assessed in 99 patients with hypertrophic cardiomyopathy. In the absence of antiarrhythmic therapy, high grade ventricular arrhythmias (grade 3 and above) were common; that is they were identified in 66 percent of the patients, including 19 percent with episodes of asymptomatic ventricular tachycardia. Clinical outcome was assessed 3 years after the initial 24 hour ambulatory electrocardiogram. Of the 84 patients who did not undergo ventricular septal myotomy-myectomy, 6 died suddenly or experienced cardiac arrest, 1 died of progressive congestive heart failure and the other 77 have survived without a cardiac catastrophe. The prevalence rate of sudden death or cardiac arrest during the follow-up period was the same (3 percent) in patients with high grade arrhythmias other than ventricular tachycardia (1 of 37) as in those with no or low grade arrhythmias (1 of 29). However, the occurrence of a sudden cardiac catastrophe was significantly more common in patients with asymptomatic ventricular tachycardia of brief duration on 24 hour electrocardiography (4 [24 percent] of 17) than in patients without ventricular tachycardia (2 [3 percent] of 66) (p less than 0.02). In summary, (1) high grade ventricular arrhythmias are commonly found on continuous 24 hour electrocardiography monitoring in patients with hypertrophic cardiomyopathy; and (2) although sudden death is relatively uncommon in patients with high grade ventricular arrhythmias other than ventricular tachycardia (annual mortality rate 1 percent), the finding of ventricular tachycardia on 24 hour electrocardiography identifies a subgroup of patients at high risk for sudden death (annual mortality rate 8.6 percent). Although no conclusions can be drawn regarding the impact of therapy, our findings suggest that 24 hour electrocardiographic monitoring should be performed in patients with hypertrophic cardiomyopathy and that it may be reasonable to initiate antiarrhythmic therapy if ventricular tachycardia is identified.

Association of echocardiographic left ventricular mass with body size, blood pressure and physical activity (the Framingham Study).

Left ventricular (LV) hypertrophy has been found to predispose to increased cardiovascular morbidity and mortality. To assess the clinical correlates and potential determinants of LV mass, the relation of echocardiographically determined LV mass to a variety of clinical parameters was examined in a general population. From 1979 to 1983 Framingham Heart Study participants underwent routine evaluation including medical history, physical examination and M-mode echocardiography. LV mass was determined using an anatomically validated formula that incorporates measurements of LV wall thickness and LV internal diameter. The study population consisted of 2,226 men and 2,746 women (mean age 51 years, range 17 to 90). Age, height, systolic blood pressure and body mass index (a measure of obesity) were statistically significant and independent correlates of LV mass in both sexes (p less than 0.001). In men under age 50, leisure-time physical activity was associated with LV mass (p less than 0.05), but this was not observed in women. Results from multivariate analyses in which body mass index and subscapular skinfold thickness were included suggest that lean body mass is correlated with LV mass. Maintenance of ideal body weight and normal blood pressure, weight reduction in obese persons and blood pressure control in hypertensive patients may contribute to the primary and secondary prevention of LV hypertrophy and its sequelae. Clinical interpretation of echocardiograms should include consideration of the correlates of LV mass to gain better insight into the pathogenesis of LV hypertrophy.

Echocardiographic criteria for left ventricular hypertrophy: the Framingham Heart Study.

Of 6,148 original cohort and offspring subjects of the Framingham Heart Study who underwent routine evaluation, a healthy group of 347 men (aged 42 +/- 12 years) and 517 women (aged 43 +/- 12 years) was identified to develop echocardiographic criteria for left ventricular (LV) hypertrophy. Healthy subjects were defined as normotensive, receiving no cardiac or antihypertensive medications, nonobese and free of cardiopulmonary disease. Echocardiographic criteria (in accordance with the American Society of Echocardiography convention) for LV hypertrophy, based on mean plus 2 standard deviations for LV mass, LV mass corrected for body surface area and LV mass corrected for height in this healthy sample are, respectively: 294 g, 150 g/m2 and 163 g/m in men and 198 g, 120 g/m2 and 121 g/m in women. Criteria based on LV mass/height result in higher prevalence rates of LV hypertrophy than LV mass/body surface area while still correcting for body size. The prevalence of LV hypertrophy in the entire study population (using LV mass/height criteria) is 16% in men and 19% in women. Until outcome guided criteria for LV hypertrophy are developed, application of sex-specific criteria based on a healthy population distribution of LV mass offer the best approach to echocardiographic diagnosis of LV hypertrophy.

Electrocardiographic estimate of left ventricular mass versus radiographic cardiac size and the risk of cardiovascular disease mortality in the epidemiologic follow-up study of the First National Health and Nutrition Examination Survey.

The prognostic value of a left ventricular (LV) mass index (g/m2) estimated from an electrocardiographic model and radiographic estimates of the relative heart volume (ml/m2) and cardiothoracic ratio for predicting the risk of cardiovascular disease mortality were investigated using Cox regression analysis to adjust for age, systolic blood pressure and history of heart attack in 1,807 men (1,609 white, 198 black) and 2,143 women (1,884 white, 259 black). The study population (ages 35 to 74 years at baseline) was followed from 5 to 12 years (average 9.5 years) for cardiovascular disease mortality. LV mass index and relative heart volume were independent predictors of cardiovascular disease mortality among white men. All 3 cardiac size estimates were independent predictors for cardiovascular disease mortality among white and black women. When LV mass index was used as a dichotomized variable to indicate the presence or absence of LV hypertrophy, the age-adjusted relative risk of cardiovascular disease mortality was 2.48 (95% confidence interval 1.77 to 3.46) for white men, 3.03 (1.49 to 6.16) for black men, 1.86 (1.21 to 2.87) for white women and 2.05 (0.83 to 5.05) for black women. The corresponding prevalence of LV hypertrophy was 15.4% for white men, 36.6% for black men, 20.1% for white women and 17.4% for black women. It is concluded that the electrocardiographic estimate of LV mass index can identify a substantially larger fraction of persons at increased risk for cardiovascular mortality than conventional electrocardiographic criteria for LV hypertrophy and that LV mass index estimated by electrocardiogram is a valuable supplement to radiographic cardiac size estimates in epidemiologic applications.

Risk of ventricular arrhythmias in left ventricular hypertrophy: the Framingham Heart Study.

The association of ventricular arrhythmias with left ventricular (LV) hypertrophy was examined in 6,218 participants in the Framingham Heart Study. Electrocardiographic (ECG) LV hypertrophy was present in 171 subjects and echocardiographic hypertrophy was detected in 869. Echocardiographic LV hypertrophy was associated with increased risk for each of 6 ventricular arrhythmia grades in men (relative risk up to 8.9, p less than 0.01), and 4 of 6 grades in women (p less than 0.05). Similarly, men with ECG LV hypertrophy were at increased risk for 4 of 6 arrhythmia grades (p less than 0.05). However, owing to low prevalence ECG LV hypertrophy was not associated with arrhythmia in women. After adjustment for age, sex, systolic blood pressure, valvular heart disease, angina pectoris and acute myocardial infarction, the association of echocardiographic but not ECG LV hypertrophy with ventricular arrhythmia remained significant (p less than 0.001). Thus, echocardiographic LV hypertrophy is more prevalent and more sensitive for ventricular arrhythmias than ECG LV hypertrophy.