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Consequences of Hypertension

Monday, Dec 10 2007

  

Hypertension is a known risk factor for cardiovascular and cerebrovascular diseases. The presence of hypertension raises the risk for coronary heart disease twofold, the risk of a stroke at least threefold, the risk of peripheral artery disease twofold, and the risk of congestive heart failure fourfold (Kannel, 1996). Elevated risk for both cardiovascular and cerebrovascular disease among persons with hypertension holds true for both men and women and after controlling for other major disease risk factors like smoking and high serum cholesterol (Pooling Project Research Group, 1978). Although it may be logical to conclude that the elevated risk for these diseases is from ruptured aneurysms or hemorrhagic events, the vast majority of these disease consequences are actually the result of the underlying physiological condition of atherosclerosis.

Atherosclerosis involves the gradual depositing of plaque on the inner walls of blood vessels that results in a restricted (ischemic) or blocked (infarcted) blood flow. Obviously, if blood flow is blocked in the coronary arteries, a myocardial infarction (heart attack) occurs; if blood flow is blocked in the cerebrovasculature, a stroke occurs. The process of atherosclerosis begins early in life, as our blood vessels are coated with fats (lipids) in our bloodstream. Over time, these fatty streaks harden and turn into plaques, particularly for those of us who regularly consume diets high in saturated fats.

The presence of toxins in our bloodstream (for example, nicotine and carbon monoxide from smoking tobacco) or elevated arterial pressures appears to cause these plaques to crack, resulting in what might be called an intracellular injury. Additionally, the injury can promote a chronic inflammatory response that is mediated by immune system functioning (Schonbeck and Libby, 2004). As with other bodily injuries, the circulatory system responds by sending platelets to the site of the injury to clot it, preventing any loss of blood. The so-called scab, aggravated by the inflammatory response, extends from the internal cellular wall into the blood vessel, obstructing the normal flow of blood.

If the injury recurs, more platelets are dispatched to the site, resulting in an even larger blockage of blood flow. In brief, then, it appears that high blood pressure promotes atherosclerosis and, indirectly, cardiovascular and cerebrovascular diseases, by causing regular injuries to the cellular lining of the blood vessels of the circulatory system. As one might imagine, these injuries are more likely to occur at locations where arterial pressure is highest and blood flow turbulence the greatest, like the coronary arteries, aorta, and bifurcation of the carotid arteries.

If this isn’t bad enough, hypertension appears to have some other rather unpleasant consequences for the body’s other organs. For example, chronic high blood pressure has been documented to have detrimental effects on the ventricles of the heart (particularly the left ventricle), the microvasculature of the kidneys, and the blood vessels in the retina. Because the effects of blood pressure upon these organs are so well known, they are termed the target organs, and damage to them is referred to as target organ (or end organ) damage.

In the hydraulic water-pumping system described earlier, continuous pump action at higher pressures results in greater wear on the pump itself than pumping at lower pressures. The same consequence occurs to the heart. Unlike a mechanical pump, the heart responds to the demand to circulate blood at a chronic elevated blood pressure level by becoming stronger and enlarged. Unfortunately, the increase in muscle mass that results from this response, called left ventricular hypertrophy, places the heart at greater risk for malfunction (Kannel, Gordon, and Offutt, 1969). Presumably, left ventricular hypertrophy is associated with increased cardiovascular disease because the increased muscle mass infringes upon the volume of the left ventricle, resulting in lowered blood capacity of the ventricle associated with the greater oxygen requirements of the coronary arteries supplying the heart (Messerli and Aepfelbacher, 1995). Basically, this suggests that the enlarged heart uses more than its share of the body’s blood resources, pumps less efficiently, and is placed at risk for myocardial infarction, congestive heart failure, or ventricular dysrhythmias (Messerli and Aepfelbacher, 1995). Physicians routinely test for left ventricular hypertrophy in patients with chronic problems with hypertension using electrocardiography or echocardiography, as the presence of left ventricular hypertrophy creates a substantially elevated risk for subsequent cardiovascular disease.

Chronic elevations in blood pressure also result in damage to the microvasculature of the kidney, in peripheral arteries, and in the retina.

Damage to the blood vessels in the kidneys results in an increased secretion of albumen into the blood-stream, which can easily be detected through routine blood work. Although originally used for assessing kidney functioning among diabetic patients, measures of albumen have also been shown to be useful for determining the degree of target organ damage from hypertension (Cirillo et al., 1998).

In contrast to the indirect measurement strategies needed to detect vascular damage in the kidneys, vascular problems can be directly observed in the retina. The retina represents the only organ in the body in which blood vessels can be observed directly without removing surrounding tissue. The physician can examine optic fundi simply by looking into the patient’s eye during a routine physical examination.

Although this method provides a gross estimate of damage to the vasculature of the retina, recent technological advancements in retinal photography represent a more objective approach to examining this form of target organ damage (Olson et al., 2003). Like measures of left ventricular hypertrophy, assessment of vascular damage in both kidney and retina is highly correlated with blood pressure level (Cirillo et al., 1998; Perloff, Sokolow, and Cowan, 1991).

Chronic hypertension has also been shown to affect the elasticity of the vasculature itself (Franklin, 1995). As described earlier, the vessel wall of the artery constricts and dilates in response to alterations in blood flow in an effort to regulate blood pressure. As such, healthy artery walls are elastic. Aging, however, is associated with increased arterial stiffness, particularly in conjunction with elevated blood pressures (Franklin, 1995). With the advent of more sophisticated noninvasive methods for examining vessel responsiveness using ultrasound techniques, essential hypertension has been shown to be associated with lesser dilation of femoral arteries, indicating direct alterations in vascular elasticity (Trieber et al., 1975).

Finally, in addition to vascular changes, several subtle cognitive deficits have been associated with essential hypertension, including psychomotor response slowness (Light, 1975; Waldstein et al., 1996), poor visual recognition (Shapiro et al., 1982), and below average performance on tasks measuring attention, memory, and abstract reasoning (Franceschi et al., 1982; Wilkie and Eisdorfer, 1976). Although significant differences exist on these measures of cognitive processing between hypertensive and normotensive patients, they are typically small in magnitude, do not affect quality of life and work performance, and most likely go unnoticed by hypertensive patients and their family members. Nevertheless, recent research has shown that these cognitive deficits were associated with reduced blood flow to the right hemisphere of hypertensive’s brains during working memory tasks (Jennings et al., 1998). Even though these cognitive deficits are associated with altered cerebral blood flow, these deficits appear to be reversible if stable blood pressure control is achieved with treatment (Miller et al., 1984), indicating that the cognitive deficits are likely to be the result of the elevated blood pressures of hypertensive patients.

Larkin, K. T., and Zayfert, C.
Published with assistance from the foundation established in memory of Amasa Stone Mather of the Class of 1907, Yale College.

References
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Revision date: March 9, 2010
Last revised: by Dr. Kristen Shed, M.D.

Provided by Armina Hypertension Association

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