Hypertension is a major public health problem in the United States and many countries worldwide. Since the American Heart Association/American College of Cardiology has reduced threshold for diagnosis of hypertension and treatment targets to systolic blood pressure (BP) of 130 mm Hg and diastolic BP of 80 mm Hg, prevalence of hypertension in the United States has risen to at 47%. Similarly, prevalence of resistant hypertension (failure to achieve BP control despite three or more medications that included inhibitors of renin-angiotensin system, calcium channel blockers, and a diuretic) has increased to 20% among treated population. When the risk is calculated over lifetime, the burden of hypertension in middle-aged men and women is enormous. Eight to nine out of 10 normotensive women or men older than 55 years are expected to develop hypertension in the next 20 years. Thus, complete understanding of basic pathophysiologic mechanisms and treatment strategies is one crucial step in improving hypertension control.
PATHOPHYSIOLOGY & ETIOLOGY
Pathophysiology of primary hypertension is complex and heterogeneous. At least one or more of the mechanisms involved in BP regulation, such as vascular, neural, renal, and hormonal mechanisms, contribute to development of primary hypertension. Accordingly, therapy often requires more than one antihypertensive agent or approach to tackle hypertension in the majority of patients.
Systemic vascular resistance and cardiac output are two major determinants of BP. Thus, augmented peripheral vasoconstriction at the level of resistance vessels may lead to hypertension in the presence of normal cardiac output. More recently, large arterial stiffness has been shown to contribute to elevated systolic BP. In many epidemiologic studies, systolic BP increases with age both in men and women. However, after the fifth decade of life, systolic BP continues to increase while diastolic BP starts to fall, causing the pulse pressure to widen. Normally, elasticity of aorta helps absorb pressure during systole, and the elastic recoil of the aorta helps maintain BP during diastole. The loss of aortic elasticity causes BP to rise excessively during systole and decrease markedly during diastole. Furthermore, the aortic pulse wave travels at much faster speed in the stiff artery, and the reflected wave from the peripheral sites further amplifies the systolic BP in the central aorta. Although diastolic BP is traditionally thought to be the most important predictor of cardiovascular risk, ...