Hypertension and Aging

Sep 04 2011

By Michelle S. Cotroneo, Ph.D., Scientific Advisor

Hypertension is commonly referred to as high blood pressure. Blood pressure is the force exerted by the blood on the arterial walls. It is measured in millimeters of mercury, and consists of two parts, a top number (systolic) and a bottom number (diastolic). Systolic refers to the pressure during contraction of the heart, where blood is pumped out into the arteries. Diastolic is the pressure when the heart relaxes and fills with blood. Hypertension is usually asymptomatic. If left untreated, it can lead to stroke, heart attack, kidney disease and other problems.

The criteria for a diagnosis of hypertension defined by the Seventh Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure are as follows:

1. Blood pressure readings are taken after the patient has been seated quietly for 5 minutes.

2. The blood pressure cuff is the correct size and the arm is elevated with support to be level with the heart.

3. The patient must refrain from smoking, exercising, or consuming caffeine 30 minutes prior to the measurement.

4. Elevated blood pressure on two readings (average) per visit on two or more visits is suggested for diagnosis of hypertension.

The committee also classified blood pressure readings for adults:

Classification

Systolic and Diastolic Readings

Normal

<120 systolic and <80 diastolic

Prehypertension

120–139 systolic or 80–89 diastolic

Stage 1 Hypertension

140–159 systolic or 90–99 diastolic

Stage 2 Hypertension

>160 systolic or >100 diastolic

Chobanian AV, Bakris GL, Black HR, et al. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42:1206–52.

The likelihood of having hypertension increases with age; it is estimated that more than 50% of people 65 and older have hypertension (American Geriatric Society). There are many contributing factors in the etiology of developing hypertension with aging. Many are due to physiologic changes that occur in the arteries that result in loss of elasticity. These include collagen accumulation and crosslinking, thinning of the elastic vessel components, calcium buildup and a decrease in smooth muscle cells (1). These structural changes are most evident in large arteries, like the aorta (2). The resulting thickening and a loss of elasticity leads to a decreased ability of the artery to respond to changes in blood flow occurring as the heart pumps. The impaired ability of the arteries to expand when blood is pumped out of the heart will elevate systolic blood pressure. Elevations in systolic blood pressure are now thought to be associated with adverse outcomes, such as stroke and heart attack.

Age-related hypertension is also related to salt-sensitivity, which tends to increase in aging. Approximately 60% of individuals with hypertension are physiologically sensitive to sodium intake. These individuals will have an increased blood pressure response to sodium, compared with those who are not sensitive. This is thought to be related to a decrease in the ability of the kidney to clear sodium from the body (3). Excess sodium retention may be due to decreased functioning of cellular sodium-potassium pumps (4) or an increase in substances that inhibit the action of sodium pumps (5). In some individuals, salt sensitivity may be due to inherited gene mutations. In women, decreased estrogen production after menopause is thought to increase salt sensitivity (6).

Hypertension is commonly treated with antihypertensives. However, lifestyle factors can be modified to lower blood pressure in hypertensive people.

1. Dao HH, Essalihi R, Bouvet C, et al. Cardiovasc Res 2005; 66: 307–17.

2. Mitchell GF, Parise H, Benjamin EJ, et al. Hypertension 2004; 43: 1239–45.

3. Epstein M, Hollenberg NK. J Lab Clin Med 1976; 87: 411–7.

4. Zemel MB, Sowers JR. Am J Cardiol 1988; 61(16): 7H–12H.

5. Anderson DE, Fedorova OV, Morrell CH, et al. Am J Physiol Regul Integr Comp Physiol 2008; 294: R1248–54.

6. Colylewright M, Reckelhoff JE, Ouyang P. Hypertension 2008; 51: 952–9.

Posted under: Cardiovascular diseases, Hypertension.

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Coronary Artery Disease: A Beastly Cad

Feb 17 2010

By Michelle S. Cotroneo, Ph.D., Scientific Advisor

Coronary artery disease (CAD) is a narrowing or blockage of the arteries leading to the heart. It is the leading cause of mortality in the United States. This condition can reduce blood flow to the heart, which can lead to angina (pain). Complete blockage of the vessels can lead to death of heart muscle (heart attack).

CAD results from the formation of plaques in the lining of the arterial walls, a condition referred to as atherosclerosis. Plaques are composed of fat, cholesterol, cellular waste products, calcium, platelet clumps, and fibrin. Their accumulation over time leads to narrowing of the blood vessels and potential clot formation.

Factors known to increase risk of CAD include hypertension, diabetes, hypercholesterolemia, hyperlipidemia, smoking, sedentary lifestyle, high blood levels of the amino acid, homocysteine, and obesity. Other lifestyle factors, such as excess alcohol consumption, sleep apnea, and stress can also contribute to the development of CAD. Most of these factors can be managed or changed.

Non-modifiable risk factors are family history and age. The incidence of cardiovascular diseases, including CAD, increases with age. Men develop coronary artery disease at a younger age than women. However, the incidence for CAD in women increases following menopause, eventually becoming equal to that in men. This is thought to be due to the loss of the protective effects of estrogen on the arteries.

Why is age is a risk factor for cardiovascular disease?

Age-related changes in the arteries may play a role in the development of CAD. Arterial walls stiffen and thicken with age, losing their elasticity and ability for expansion to accommodate blood flow, resulting in hypertension. Understanding the cellular mechanisms behind vascular aging is the subject of a vast number of research studies.

Oxidative stress and inflammatory processes occurring in the endothelial cells have been hypothesized to contribute to CAD by promoting atherosclerosis. The formation of reactive oxygen species (ROS), such as peroxide, in aging endothelial cells activates the production of inflammatory cytokines and depletes nitric oxide (NO) levels. Nitric oxide has protective functions, including the prevention of platelet aggregation and control of inflammatory signaling pathways. The increase in inflammatory cytokines, coupled with a reduction in vasculoprotective NO can result in dysfunction or death of the endothelial cells.

Interestingly, comparative biologists have provided insight into the underlying cellular mechanisms of aging by comparing species with a short lifespan with those having longer ones. Existing comparisons support the theory that oxidative stress and production of ROS contribute to aging, and that vasculoprotection are predicted to occur with a reduced and/or delayed onset of production of ROS and increased defense mechanisms (Ungvari Z, et. al, Front Biosci. 2008, 13:5056-70). Ongoing and future biomedical research will continue to shed light on the relationship between vascular aging and coronary artery disease. Clinical research, such as the VALIDATE Study (ClinicalTrials.gov identifier: NCT00246493) will aid in understanding why age is such an important risk factor for the development of coronary artery disease.

Posted under: Cardiovascular diseases.

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