Messerli F H, Schmieder R
Drugs. 1986;31 Suppl 4:192-201. doi: 10.2165/00003495-198600314-00023.
The heart adapts to increasing afterload, such as that which occurs in arterial hypertension, with an increase in wall thickness in order to bring wall stress back to normal. As a consequence, concentric left ventricular hypertrophy ensues. Hypertension as well as advancing age has been shown to be associated with an increase in posterior wall thickness. Accordingly, the prevalence of left ventricular hypertrophy becomes very high in the elderly and may occur in more than 50% of elderly hypertensive patients. Left ventricular hypertrophy is not merely a physiological process serving to compensate for the increased afterload. The Framingham study has indicated that patients with left ventricular hypertrophy are at an increased risk of sudden death and other cardiovascular morbidity and mortality. The risk for sudden death is 5 to 6 times higher in patients with left ventricular hypertrophy than in those without, regardless of levels of arterial pressure. By Holter monitoring of these patients it has been shown that those with left ventricular hypertrophy have a prevalence of premature ventricular contractions that is 40 to 50 times higher than those patients without left ventricular hypertrophy. In addition, patients with left ventricular hypertrophy rated substantially higher with regard to Lown's classes than those without. These data indicate that left ventricular hypertrophy is common, particularly in the elderly, and predisposes to ventricular ectopy, higher grade arrhythmias, and sudden death. Clearly, these considerations have to be taken into account when selecting antihypertensive therapy inasmuch as hypokalaemia, hypomagnesaemia, and other electrolyte shifts predisposing to ventricular arrhythmias must be scrupulously avoided.
