Exercise testing in hypertensive patients for assessing the cardiovascular protective potential of antihypertensive drugs

Abstract

Exercise testing is an established noninvasive tool in cardiology used to diagnose and guide treatment in individuals with suspected or confirmed coronary artery disease. Owing to the wealth of information it provides, exercise testing is also being utilized to evaluate prehypertensive stages, characterize hypertension, assess tolerance to exercise and the efficacy of antihypertensive therapies, and predict target organ damage and cardiovascular risk. The literature on exercise tolerance tests is relatively limited since these studies are difficult to conduct although they represent a valuable test for evaluating the benefits of antihypertensive therapies beyond their blood-pressure-lowering efficacy at rest or during exercise. Such a setting can be immensely useful for the evaluation and for the differentiation of treatments, especially in patients with evident rises in systolic blood pressure and with concomitant diseases, who are at higher risk of stroke. Exercise-induced increase in systolic blood pressure from rest to peak exercise should therefore be used as the primary efficacy variable. There is growing evidence that central pressure is a better predictor for cardiovascular risk than peripheral blood pressure, since this variable takes into account the overall effect of vascular aging and increased arterial stiffness that age and other concomitant diseases may induce. It is also important to include central aortic blood pressure and biomarkers of hypertension and cardiac disease in the overall assessment.

Calcium Homeostasis Is Altered in Skeletal Muscle of Spontaneously Hypertensive Rats

“…It is well recognized that both in animal models and in humans, cardiovascular diseases are often associated with distinct skeletal muscle alterations regarding function and metabolism. 2,3,5,51 In EDL and soleus of SHR animals, a series of muscle alterations were found, indicating a form of mild myopathy. 6,7,11,14 Herein, we demonstrated that hypertension causes a phenotype-dependent dysregulation of skeletal muscle calcium homeostasis.…”