Left ventricular hypertrophy in hypertension. Prevalence and relationship to pathophysiologic variables.

Abstract

SUMMARY In less than a decade since development of echocardiographic measurement of left ventricular muscle mass, studies using this technique have provided considerable information about the prevalence and pathophysiology of left ventricular hypertrophy in human hypertension. Increased left ventricular mass has been found in a significant minority of patients with systemic hypertension, with the exact prevalence dependent both on how a population is selected and on the sex, race, and possibly age composition of its members. All published studies have reported that left ventricular hypertrophy is more closely related to blood pressure recorded in the patient's natural setting during normal activity or exercise -whether measured by portable recorder or home manometer -than to blood pressure measured by the physician. In addition, studies indicate that the classic hypertensive abnormalities of concentric left ventricular hypertrophy and increased peripheral resistance are interrelated, while left ventricular hypertrophy is absent in a subgroup of patients with mild essential hypertension who exhibit high cardiac output and evidence of supernormal myocardial contractility. Conversely, the left ventricular functional response to exercise is inversely related to the degree of hypertrophy. High levels of blood viscosity, which would tend to blunt the reduction in peripheral resistance expected during sleep or exercise, have also been associated with left ventricular hypertrophy in patients with essential hypertension. Echocardiographic studies have provided evidence both for and against the hypothesis that activity of the sympathetic or reninangiotensin systems plays a direct role in causing hypertensive cardiac hypertrophy. These findings demonstrate the useful role that echocardiographic assessment of left ventricular structure and function may play in hypertension research. patients with systemic hypertension -being both a J necessary adaptation to pump a normal amount of blood against the increased pressure load and a pathologic manifestation of hypertensive cardiovascular disease. For many years, knowledge of the complex status of the heart in human hypertension advanced slowly because of the lack of suitable means of measuring cardiac anatomy and function in unselected hypertensive patients or of following their natural history. The development over the last decade of accurate echocardiographic methods for detection of LVH and characterization of ventricular contractile performance has catalyzed an explosion of information about the heart in hypertension.

Measured haplotype analysis of the aldosterone synthase gene and heart size

“…The prevalence of echocardiographic LV hypertrophy of 34.3% was similar to the rates found in other populations with hypertension. 26 Almost all the subjects with hypertension were receiving antihypertensive treatment, but no participant was receiving spironolactone, a diuretic that acts by antagonising the effect of aldosterone. The average family size and number of generations per family was seven members (range 3 -27) and two generations (range 2 -4), respectively.…”

The heart in the hypertensive elderly

“…In hypertensive patients irrespective of age, LVH is an adaptation to an increased end systolic wall stress and by thickening of LV walls leads to its normalisation. 2,11 In a stepwise multiple analysis of a very heterogeneous population of 171 hypertensive patients, we demonstrated that age was an independent determinant of posterior and septal wall thickness and of LV mass. 11 Posterior wall thickness increased by about 25% between the 2nd and 7th decade of life, and the ratio of radius to wall thickness declined, indicating LVH of the concentric type.…”

“…Various studies have documented an increase in wall thickness with age in the presence of unchanged chamber volume. [1][2][3] In addition to the increased size of the myocytes, the aging heart is characterised by a high rate of degenerative age-associated findings such as lipid deposition, tubular dilatation and decreased mitochondrial oxidative phosphorylation. 3,4 Concomitantly, the amount of elastic tissue, collagen and fat increases.…”

Impaired atrial synchronicity in patients with metabolic syndrome associated with insulin resistance and independent of hypertension

“…The LV diameter in end diastole, interventricular septum (IVSd) and LV posterior wall thickness in end diastole were measured from the M-mode readings. LV mass (LVM) was calculated by the formula of Devereux 15 and was indexed to the allometric power of height (LVM/Ht 2.7 ).The LV ejection fraction was estimated by the use of a modified version of Simpson's biplane method.…”