Impact of regression of left ventricular hypertrophy on cardiac function in hypertension

• Published in: European heart journal 1992-09, Vol.13 (suppl-D), p.107-110
• Main Authors: Omotoso, A. B., Dunn, F. G.
• Format: Article
• Language: English
• Subjects: Antihypertensive Agents - therapeutic use; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Cardiac Volume - drug effects; Cardiac Volume - physiology; Cardiology. Vascular system; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Diastole - drug effects; Diastole - physiology; diastolic function; Hemodynamics - drug effects; Hemodynamics - physiology; Humans; Hypertension - drug therapy; Hypertension - physiopathology; Hypertrophy, Left Ventricular - drug therapy; Hypertrophy, Left Ventricular - physiopathology; Medical sciences; regression of left ventricular hypertrophy; Systole - drug effects; Systole - physiology; Systolic function; systolic wall stress; Ventricular Function, Left - drug effects; Ventricular Function, Left - physiology
• ISSN: 0195-668X; 1522-9645
• DOI: 10.1093/eurheartj/13.suppl_D.107

It is now established that regression of left ventricular hypertrophy (LVH) occurs following reduction of arterial pressure in patients with hypertension. A number of factors contribute towards this regression, including the fall in blood pressure itself, the drug therapy given, and the pre-existing degree of hypertrophy. LVH is in some senses a beneficial adaptive response in terms of systolic function, and therefore it is important to clarify whether or not regression of hypertrophy is damaging to cardiac function. Overall assessment of these effects has been more difficult because the antihyper tensive drug therapy and the changes in blood pressure also contribute to left ventricular function. Current data indicate that systolic function is maintained both at rest and following exercise but not necessarily improved. In contrast, diastolic function in some but not all studies, has been shown to have been improved Recent information has allayed fears that regression of LVH may cause a deterioration in function if blood pressure is allowed to return to its pretreatment levels. It would appear that in this situation function is maintained both at rest and during exercise. Finally, the assessment of cardiac function following regression of hypertrophy remains a surrogate end-point. The key information required remains the influence of regression of hypertrophy and its alteration in function on morbidity and mortality in patients with hypertension.