Hypertensive Heart Disease - Diagnosis, Prognostic Value and Changes During Antihypertensive Treatment, Left Ventricular Structure and Function

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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.

Disclosure
The author has no conflicts of interest to declare.
Correspondence
Kristian Wachtell, Department of Cardiology, The Heart Centre, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. E: kristian@wachtell.net
Received date
16 December 2009
Accepted date
16 May 2010
Citation
European Cardiology - Volume 6 Issue 2;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
DOI
http://dx.doi.org/10.15420/ecr.2010.6.2.23
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