Risk of ventricular arrhythmias in left ventricular hypertrophy: The Framingham Heart Study

Levy, Daniel; Anderson, Keaven M.; Savage, Daniel D.; Balkus, Susan A.; Kannel, William B.; Castelli, William P.

doi:10.1016/0002-9149(87)90305-5

Cited by 377 publications

(144 citation statements)

References 49 publications

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“…Several studies have shown that hypertensive patients with LVH have an increased frequency of premature ventricular ectopic beats and ventricular arrhythmias. [12][13][14][15] In the Framingham Heart Study, echocardiographic evidence of LVH was associated with ventricular arrhythmia independent of conventional cardiovascular risk factors. 12 In untreated hypertensive patients, non-sustained ventricular arrhythmia was observed in up to 5% of patients during 24-h Holter monitoring.…”

Section: Ventricular Arrhythmiamentioning

confidence: 99%

Hypertension and cardiac arrhythmias: a review of the epidemiology, pathophysiology and clinical implications

Yiu

Tse

2008

J Hum Hypertens

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Hypertension is commonly associated with cardiac arrhythmias in patients with and without concomitant cardiovascular disease. Experimental and epidemiological studies have demonstrated potential links between hypertension and atrial and ventricular arrhythmias, although the underlying pathophysiological mechanism remains unclear. Nonetheless, the importance of hypertension as a cause of atrial and ventricular arrhythmias is not well recognized. In particular, the occurrence of left ventricular hypertrophy is a strong predictor for the development of AF, ventricular ectopy and sudden cardiac death. Recent prospective clinical trials reveal that antihypertensive therapy may delay or prevent the occurrence of cardiac arrhythmias and sudden cardiac death in patients with hypertension. Although antihypertensive agents that block the renin-angiotensin-aldosterone system appear to protect against cardiac arrhythmias, this needs to be confirmed by current ongoing clinical trials.

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Section: Ventricular Arrhythmiamentioning

confidence: 99%

Hypertension and cardiac arrhythmias: a review of the epidemiology, pathophysiology and clinical implications

Yiu

Tse

2008

J Hum Hypertens

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“…10 Echo-LVH has also been shown to be associated with increased risk of sudden death, 11 probably via the development of ventricular arrhythmias, 12 which may itself be related to the increased QTc dispersion demonstrated on the electrocardiogram of patients with LVH. 13,14 Echocardiography has thus become the current 'gold standard' for detection of LVH, despite some minor variations in recorded prevalence of LVH when differing echocardiographic diagnostic criteria are employed.…”

mentioning

confidence: 99%

The ECG and left ventricular hypertrophy in primary care hypertensives

Conway

Lip

2001

J Hum Hypertens

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Keywords: ECG; left ventricular hypertrophy; primary care hypertensivesWhilst cardiac hypertrophy is initially a compensatory response to the high blood pressure, the increased muscle mass outstrips its oxygen supply and coupled with the reduced coronary vascular reserve seen in hypertension, results in myocardial ischaemia even with normal coronary arteries. Thus beyond a certain point, left ventricular hypertrophy (LVH) secondary to hypertension becomes a major risk factor for myocardial infarction, stroke, sudden death, and congestive cardiac failure, 1 and this increased risk is in addition to that imposed by hypertension itself. Furthermore, hypertensives with LVH are at increased risk of cardiac arrhythmias (atrial fibrillation, ventricular arrhythmias) and atherosclerotic vascular disease (coronary and peripheral artery disease). 1 Patients with hypertension and LVH should therefore be identified for aggressive management, not only of blood pressure, but of all their cardiovascular risk factors.Epidemiological data regarding prevalence of LVH and the increased risk of cardiovascular mortality and morbidity was initially provided by the Framingham Heart Study more than 30 years ago, which employed ECG criteria to define LVH. 2 Conversely, the association between hypertension and LVH is also well-established, 3 leading to a particularly high cardiovascular risk for the uncontrolled hypertensive via the development of LVH. However, the correlation between blood pressures measured in the clinical environment and left ventricular mass is poor. 4 By contrast, 24-h ambulatory blood pressure monitoring (ABPM) provides a closer correlation between average daytime arterial blood pressure and left ventricular mass. 5 Many different criteria for identifying LVH exist, based on both echocardiographic (echo-LVH) and electrocardiographic (ECG-LVH) features, but there is considerable variation in sensitivity and specificity between these methods. 1,6,7 A commonly used screening test for LVH in hypertensives uses the 12-lead ECG and the Sokolow and Lyon criteria, that is, the sum of the S wave in lead V1 and the R wave in leads V5 or V6 on the ECG Ͼ35 mm, with a sensitivity of 22% and specificity of 79%. Other methods have also been evaluated: 6-9 (i) The Romhilt-Estes Point-Score System of у4 has a sensitivity of 12% and specificity of 87%; (ii) The Cornell system has a sensitivity of 31% and specificity of 87%; (iii) the Sokolow-Lyon Index (RaVL у1.1 mV) has a sensitivity of 18% and specificity of 92%; and (iv) the Rodrigez Padial system has a sensitivity of 82% and specificity of 8% respectively. These figures suggest that most forms of interpreting the ECG with regards to LVH are not useful as a screening tool. This can be marginally improved by multiplying QRS-voltage by QRS-duration, thus increasing the specificity to 96% and sensitivity to about 50%. 6,7 Crudely speaking, the features of LVH on ECG normally mean that true LVH is present, but its absence does not mean that LVH is absent. Nevertheless, the specificit...

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“…3,4 We suggested that the higher supplemental doses, along with a longer duration of use, in other studies 3,4 may have permitted the detection of an effect of supplemental vitamin E. We did not suggest that our findings negate any role of supplemental vitamin E in the prevention of coronary disease; a recent study provides further evidence in support of such a role. 5 Our study has not definitively ruled out the influence of other dietary factors, whether beneficial or detrimental with respect to the risk of coronary heart disease. It is precisely for the reasons presented by Dr. DeGrand that we conducted analyses adjusting for other factors, including meat and other foods and food groups, as we note in our article.…”

Section: The Authors Replymentioning

confidence: 71%

“…5 The medical community would be well advised to respond to the ineffectiveness of studies using one stereoisomer, all-trans -b -carotene, not by abandoning the search but by strongly encouraging the performance of studies using a chemically more rational approach. To the Editor: Beta carotene supplementation failed to reduce the incidence of lung cancer in the Beta-Carotene and Retinol Efficacy Trial (CARET), which used 30 mg of beta carotene per day plus 25,000 IU of retinol, and in the Physicians' Health Study, which used 50 mg of beta carotene every other day.…”

Section: Antioxidant Vitamins Cancer and Cardiovascular Diseasementioning

confidence: 99%

“…This does not, of course, mean that other antioxidant vitamins, such as vitamin E or C, or even very prolonged beta carotene supplementation may not eventually be beneficial in reducing the risk of cancer, especially among poorly nourished persons with low blood levels of beta carotene, 4 or in the secondary prevention of cardiovascular disease. 5 Whether there is a true hazard associated with beta carotene supplementation among current cigarette smokers, a question raised by the ATBC study 3 and the CARET study, 2 will be evaluated by a collaborative overview of the postpublication results of continued follow-up in all the completed trials. If the apparent excess risk observed in those trials is in fact real, it should persist with longer follow-up.…”

Section: The Authors Replymentioning

confidence: 99%

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