Exercise Bp Case Study

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Exercise BP is an important marker of CV events that are associated with incident HTN,12-16 myocardial infarction,17,18 stroke,19 and CV mortality20,21 in individuals without overt CHD. It has been reported that individuals characterized by elevated exercise BP may account for 5%15 to 40%17 of individuals at high risk of CV events. Understanding the vascular and clinical correlates of exercise BP response to moderate exercise may provide mechanistic insights into the development of HTN, left ventricular hypertrophy (LVH), and CV events. However, predictors of exercise BP have not been well characterized in ambulatory individuals in the community.
Group of individuals with a hypertensive exercise BP response are frequently characterized by limited exercise tolerance, LVH, and impaired left ventricular diastolic function,22 which have been attributed to abnormalities in vascular function despite limited data to support this claim.

Mechanism explaining exaggerated blood pressure:
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Endothelial dysfunction (ED) is a compromised physiologic state associated with numerous chronic diseases and health conditions including HTN, CHD, congestive heart failure, peripheral artery disease, diabetes mellitus, and chronic kidney disease.23 ED promotes apotosis24 leading to arterial stiffening25 that reduces the ability of the vasculature to buffer the increase in SBP generated by left ventricular ejection.26 ED is characterized by reduced bioavailability of vasodilators, particularly nitric oxide (NO), and/or increased vasoconstrictors such as endothelin.27 The resultant imbalance between vasodilation and vasoconstriction leads to an impairment in endothelium dependent vasodilation

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