Hypertension
Hypertensive Heart Disease – Diagnosis, Prognostic Value and Changes During Antihypertensive Treatment, Left Ventricular Structure and Function
Kristian Wachtell Department of Cardiology, The Heart Centre, Rigshospitalet, Copenhagen
Abstract
Hypertensive heart disease is prevalent and during the last decade it has been determined that patients with left ventricular (LV) hypertrophy have increased cardiovascular morbidity and mortality. However, many have doubted the effectiveness of LV mass assessment because it is difficult to measure, and there were no data showing a relation between reduced LV mass and improvement in LV systolic and diastolic function and improved cardiovascular outcome. However, improvements to echocardiographic equipment have made it possible to measure LV mass with the same precision as for aortic valve replacement. Reduction of LV hypertrophy, independent of the simultaneous blood pressure reduction, is associated with large improvements in cardiovascular morbidity and mortality. A reduction in LV mass by 25g/m2 leads to a 34% reduction in cardiovascular mortality. Time-varying analyses showed 66% associated risk reduction in cardiovascular mortality if patients with LV hypertrophy were treated to limits of LV mass. Hypertension causes impaired LV systolic function by increased afterload and LV hypertrophy. Normal estimations of LV ejection fraction tend to overestimate LV systolic function; however, improvement of LV systolic function by antihypertensive treatment leads to an improvement of cardiovascular morbidity and mortality. Furthermore, even though there is significant improvement in LV diastolic function during antihypertensive treatment, this occurs more slowly compared with the treatment effects on LV systolic function, and diastolic function does not, compared with LV systolic function, translate into improvement in cardiovascular morbidity and mortality. The perspective of finding cardiac target organ damage is used not only to classify the cardiovascular risk of patients, but also to indicate to the treating physician that specific treatment is needed.
Keywords Hypertension, hypertrophy, left ventricular, systolic function, diastolic function, cardiovascular morbidity and mortality
Disclosure: The author has no conflicts of interest to declare. Received: 16 December 2009 Accepted: 16 May 2010 Citation: European Cardiology, 2010;6(2):23–31 Correspondence: Kristian Wachtell, Department of Cardiology, The Heart Centre, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. E:
kristian@wachtell.net
Left ventricular (LV) hypertrophy is a form of pre-clinical cardiac disease that may be induced by either pressure or volume myocardial overload, as well as genetic factors and a variety of other stimuli. Pressure overload, as exemplified by aortic stenosis, and volume overload, as exemplified by regurgitant aortic or mitral valve disease or chronic anaemia, initiates growth of cardiac myocytes and increase in connective tissue without notable derangements in the interstitial architecture. As a result, myocyte shortening may translate into efficient ventricular contraction with preserved diastolic properties. In hypertensive patients, there is often a combination of pressure and volume overload resulting in a mixture of myocyte elongation, needed to accommodate a higher ventricular chamber volume, and myocyte thickening, stimulated by the greater afterload.1,2
LV hypertrophy is a cardinal manifestation of pre-clinical cardiovascular disease3
stroke and cardiovascular death in patients with hypertension4 members of the general population5 angiographic coronary artery disease.6
that strongly predicts myocardial infarction, in
and in patients with or without The risk of death or non-fatal
complications is increased two- to four-fold in the presence of LV hypertrophy, independently of age, gender and other risk factors.4–6 Further risk stratification may be obtained by characterisation of LV geometrical patterns.4
Longitudinal studies in hypertensive patients7–9 © T O UCH BRIEFINGS 2010
and the general population10
have reported that individuals in whom
LV hypertrophy regressed had lower rates of subsequent morbidity/ mortality than those in whom LV mass increased. As a result, prevention or reversal of hypertensive LV hypertrophy has been widely accepted as a desirable goal. However, until recently, available studies relating to changes in echocardiographic LV mass or electrocardiographic indices in terms of prognosis have suffered from relatively small sample sizes, incomplete knowledge of blood pressure and treatment during follow-up and variably incomplete analyses.11 Furthermore, it was uncertain how best to reverse hypertensive LV hypertrophy because most published studies have been relatively small and commonly have been of short duration, lacked comparative agents, had un-blinded reading of echocardiograms or were performed in non-representative populations.12
Larger trials have not been definitive because of confounding effects of concomitant non-drug therapy, high subject drop-out or absence of LV hypertrophy before therapy.13,14
More recently, the Losartan
Intervention For Endpoint reduction in hypertension (LIFE) trial enrolled hypertensive patients with electrocardiographic LV hypertrophy in a prospective, double-blind, randomised study large enough (n=9,193) to determine whether a greater reduction in morbid events is achieved by either use of losartan compared with the
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