Abstract
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.
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.
Originalsprog | Engelsk |
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Udgivelsessted | Københavns Universitet |
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Vol/bind | 1 |
Udgave | 1 |
Antal sider | 93 |
ISBN (Trykt) | 978-87-994868-0-9 |
Status | Udgivet - 4 nov. 2011 |