From Left Ventricular Hypertrophy to Congestive Heart Failure: Management of Hypertensive Heart Disease

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Other than age, left ventricular hypertrophy (LVH) is the most potent predictor of adverse cardiovascular outcomes in the hypertensive population, and is an independent risk factor for coronary heart disease, sudden death, heart failure and stroke. Although directly related to systolic blood pressure, other factors including age, sex, race, body mass index and stimulation of the renin-angiotensin-aldosterone and sympathetic nervous systems play an important role in the pathogenesis of LVH. LVH involves changes in myocardial tissue architecture consisting of perivacular and myocardial fibrosis and medial thickening of intramyocardial coronary arteries, in addition to myoctye hypertrophy. The physiologic alterations which occur as a result of these anatomical changes include disturbances of myocardial blood flow, the development of an arrhythmogenic myocardial substrate and diastolic dysfunction. The latter is directly related to the degree of myocardial fibrosis and is the hemodynamic hallmark of hypertensive heart disease. When diastolic dysfunction is present, left ventricular end-diastolic pressure increases out-of-proportion to volume and may be elevated at rest or with exertion leading to clinical heart failure. At least one third of heart failure patients in the United States can be considered to have heart failure related to diastolic dysfunction. Compared to heart failure patients with systolic dysfunction, diastolic heart failure patients are more likely to be older, female, and to be hypertensive at the time of presentation. Although it has been assumed that LVH may lead to systolic dysfunction, evidence is lacking that LVH resulting from hypertension is a major risk factor for systolic heart failure independent of coronary artery disease. Treatment of hypertension greatly attenuates the development of LVH and significantly decreases the incidence of heart failure. In patients with established LVH, regression is both possible and desirable and results in a significant reduction in adverse clinical endpoints.

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Incidence and Prevalence

Criteria used to define LVH both by electrocardiogram (ECG) and echocardiography are not uniform and vary substantially among studies. Estimates of left ventricular mass (LVM)are conventionally indexed to body size, yielding a value for LVM index (LVMI) in grams per square meter if corrected for body surface area or grams per meter if corrected for height. Hammond et al3 has suggested that 134 g/m2 in men and 110 g/m2 in women are suitable LVMI threshold values for defining LVH in a

Factors in LVH Development

Left ventricular hypertrophy is an adaptive response of the myocardium to increased cardiac workload; its development normalizes wall tension and is thought to preserve systolic ventricular function. The incidence of LVH is directly related to the level of systolic BP.20, 21, 22, 23, 24 The relationship between the age-adjusted prevalence of LVH, as determined by echocardiography and average systolic BP in the Framingham study, is shown in Fig 1. Although a linear relationship to BP is

Structural Alterations

The myocardium is an elastic network of myocytes enmeshed in a collagen matrix that connects the myocytes and supporting coronary vasculature (Fig 2).31

The cardiac anatomical changes that accompany chronic elevation of systolic and diastolic BP are commonly referred to by the term left ventricular hypertrophy. It is important to keep in mind, however, that the remodeling process, which accompanies hypertension, consists of a range of changes in tissue architecture, which include perivacular and

Prevention

Treatment of hypertension greatly attenuates the development of LVH and heart failure. In a meta-analysis by Moser and Herbert66 reviewing major hypertension trials conducted over a 20-year period and involving more than 48 000 subjects, ECG-LVH was reduced by about one third and heart failure by 52%. The type of heart failure—systolic vs diastolic—was not specified. It is likely that these figures underestimate the potential of aggressive antihypertensive therapy. Target BPs in many of these

Summary

Left ventricular hypertrophy is an adaptive response of the heart to hypertension, which results in changes in myocardial structure that greatly increase the risks of cardiovascular mortality, sudden death, coronary heart disease, heart failure, and stroke. Ischemia, ventricular arrhythmias and diastolic dysfunction are the functional components of hypertensive heart disease. Myocardial fibrosis appears to be the most important structural alteration in its development. Although elevated BP is

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