Correlation between blood pressure response to sub maximal exercise and left ventricular hypertrophy

Abstract

There is currently no consensus on the definition of normal BP (blood pressure) increase during physical activity and thus of the exaggerated BP response to exercise. A hypertensive response to exercise (HRE) is frequently observed in individuals without hypertension or other cardiovascular disease. However, mechanisms and clinical implication of HRE is not fully explained. Endothelial dysfunction and increased afterload contribute to development of HRE. From neurohormonal aspects. Studies showed that excess stimulation of sympathetic nervous system and augmented rise of angiotensin II seems to be important mechanism in HRE [1]. However, evidences for efficacy and outcomes of treatment of HRE to submaximal exertion in individuals without hypertension or low grade hypertension is scarce and therefore warrants further studies. Presents small cohort of patients a total of 38 women and 46 men, aged 52±8 years, without evidence of cardiovascular disease, with a mean resting BP of 142±7/75±7 mmHg had their BP measured at rest and during submaximal treadmill exercise. LV mass was measured using trans thoracic echocardiography. For the majority of the subjects on the initial evaluation we discovered echocardiographic evidence of concentric hypertrophy. Among the resting and exercise BP indices, sub maximal SBP was the strongest correlate of LV mass  (r=0.40, P<0.04). In multivariate analysis, maximal SBP was independently associated with LV mass an concentric LV hypertrophy, after adjustment for lean body mass and gender. Subaximal exercise SBP is a modest but still independent predictor of LV remodeling (grade and type of LV geometry) in population with prehypertension, I and II grade hypertension. These results raise the possibility that the SBP response to sub maximal exercise is an early marker of developing
LV hypertrophy.