Review articleTarget organ involvement in hypertension: a realistic promise of prevention and reversal
Section snippets
Hypertensive heart disease
A constellation of structural, functional, and endothelial pathophysiologic mechanisms that effect coronary hemodynamics and ventricular function explain the clinical outcomes caused by hypertensive heart disease. Structural alterations associated with hypertension that directly impact on coronary blood flow include vascular compression by the hypertrophied LV, increased wall thickening of the coronary arterioles that increase the wall:lumen ratio, and luminal obstruction from atherosclerotic
Effects of hypertension on the heart
Until recently, the only major cardiac involvement in hypertension that was considered in any depth clinically was LVH [29]. Indeed, LVH is considered an extremely important epidemiologic risk factor that underlies CHD, even more than the height of arterial pressure [9], [30], [31]. The precise mechanisms associated with this increased risk now seem to be appearing [9], [28]; but whether the risk of LVH per se is diminished by the antihypertensive therapy that reduces ventricular mass
Effects of aging on hypertension
Perhaps the most striking alterations involving left and right ventricular hemodynamics changes with age were demonstrated in the author's experimental SHR studies involving 20- to 65-week-old SHRs with ischemia of the hypertrophied LV and the nonhypertrophied right ventricle. Moreover, it was of particular interest that the ischemic changes of both ventricles also occurred in normotensive age- and gender-matched WKY rats [33]. Specifically, in that study, the author demonstrated reduced left
Apoptosis
Still more recently, a relatively new pathophysiologic phenomenon has been related to the problem of hypertensive heart disease: the alteration of programmed cellular death or apoptosis of the ventricle [26], [27], [28]. Programmed cellular death is in striking contrast to the cellular death achieved by sudden ischemia, such as that produced by acute vascular occlusion with myocardial infarction. The process of apoptosis seems to be initiated when a locally produced agent (eg, angiotensin)
Therapeutic intervention
Adverse changes in coronary hemodynamics have been related to progressive hypertensive disease and aging, and are manifested by normal or reduced resting blood flow and increased vascular resistance and impaired coronary flow reserve [14], [15], [16], [17], [18], [19], [33]. In addition to LVH, important other structural and functional coronary vascular changes occur in hypertension. These include a thickened arteriolar wall of hypertensive vascular disease clearly manifested in the coronary
Endothelial dysfunction in hypertension
Endothelial dysfunction complicates hypertension-related hemodynamic changes [19], [20], [21], [22], [23], [24], [25]. This alteration is distinctly different from the classical abnormality of hypertensive arteriolar disease. It also occurs in a number of other clinical conditions (eg, aging, menopause, tobacco smoking, hypertension, diabetes mellitus, obesity, atherosclerosis, hyperlipidemia, hyperhomocysteinemia, and cardiac failure). Moreover, a number of differing but disease-specific
Renal involvement in hypertension
End-stage renal disease also continues to increase in patients with essential hypertension, particularly in black patients and in patients with diabetes mellitus. Because hypertension is exceedingly common in diabetes, hypertension should be considered as the major contributor to the development of ESRD [50].
The renal and glomerular hemodynamic changes characteristic of ESRD include afferent arteriolar constriction that diminishes total renal blood flow and blood flow to the glomerulus and
Summary
The major message from this discussion is that the end points from hypertensive disease (stroke, CHD, and hypertensive emergencies) are now preventable. Cardiac failure and ESRD, however, two exceedingly common end points from long-standing hypertension, remain as major disabilities and causes of death. The former is the most common cause of hospitalization in industrialized societies; hypertension and diabetes mellitus are the most common causes of the latter. The mechanisms of risk of these
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Cited by (26)
Hypertensive Crises
2014, Hospital Medicine ClinicsCitation Excerpt :A second effect of the hypertrophy is that the newly thickened ventricle can cause coronary compression and decreased luminal blood flow. Concomitant atherosclerosis worsens the wall-to-lumen ratio, further decreases coronary flow reserve, and leads to coronary ischemia.24 In certain cases, despite increasing wall tension, the left ventricle cannot hypertrophy enough to overcome the acute increase in systemic vascular resistance.
Hypertension Crisis in the Emergency Department
2012, Cardiology ClinicsCitation Excerpt :This increased LV mass can also cause some degree of coronary artery compression, leading to decreased luminal blood flow.3 Preferred agents in treating patients with hypertensive emergencies with evidence of ischemia include nitrates that can lower LV preload and improve coronary blood flow as well as β-blockers that can reduce heart rate, decrease afterload, and improve diastolic coronary perfusion.16 Hydralazine should be avoided, as it can induce a reflex tachycardia and increase cardiac work.
Mentors, role models, and matters of the heart
2007, Journal of the American Society of HypertensionAccelerated NaCl-induced hypertension in taurine-deficient rat: Role of renal function
2006, Kidney InternationalHypertensive crisis: Hypertensive emergencies and urgencies
2006, Cardiology ClinicsCitation Excerpt :Thirdly, hypertension can increase the epicardial coronary wall thickness, which increases the wall-to-lumen ratio and decreases coronary blood flow reserve. Concomitant atherosclerosis worsens the wall-to-lumen ratio, further decreases coronary flow reserve, and leads to coronary ischemia [38]. Acute rise in blood pressure also results in endothelial injury at the level of the coronary capillaries.
Aortic stiffness and flow-mediated dilatation in normotensive offspring of parents with hypertension
2012, Cardiology in the Young