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Mohammed A. Rafey

Published: May 2013


Definition and Etiology

Normal or optimal blood pressure (BP) is defined as the level above which minimal
vascular damage occurs. There is a continuous, consistent, and independent
relationship between elevated BP and risk of cardiovascular events. This was clearly
demonstrated in a meta-analysis that included 1,000,000 individuals with no history
of vascular disease. Among this group, during 12.7 million person-years at risk,
there were about 56000 deaths categorized as vascular in origin (12000 stroke,
34000 ischemic heart disease, and 10000 other vascular) and 66000 other deaths
at ages 40-89 years.1 Results from this study demonstrated that a BP level lower
than 115/75 mmHg appears to better define optimal BP.1 According to the Joint
National Committee 7 (JNC 7), hypertension is defined as physician office systolic BP
level of 140mmHg and diastolic BP of 90mmHg. The JNC 7 defines normal BP as
a systolic BP <120mmHg and diastolic BP <80mmHg. The gray area between
systolic BP of 120-139 mmHg and diastolic BP of 80-89 mmHg is defined as

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Prevalence and Risk Factors

One in 3 Americans over the age of 18 years suffers from hypertension. The
prevalence is higher among older individuals, women and non-Hispanic blacks.
Despite the increase in prevalence, recent data from the National Health and
Nutrition Examination Survey (NHANES) demonstrate an improvement in blood
pressure control (50%) among Americans with hypertension.3 However, the blood
pressure control rate remains suboptimal in people who have serious comorbid
conditions such as chronic kidney disease. In a survey of patients with chronic
kidney disease, BP control was found to be just 13.2%.4 On a global level,
hypertension is a greater problem, with 13.5% of all deaths attributed to BP-related
diseases. Individuals in lower economic strata are disproportionately afflicted with

The prevalence of hypertension increases progressively with age. Results from the
Framingham study demonstrate that among middle-aged and elderly persons, the
residual lifetime risk of developing hypertension is 90%.6 In the majority of patients
(95%), hypertension is primary or idiopathic; there is no identifiable risk factor. The
remainder of these patients have hypertension caused by renovascular disease,
primary aldosteronism, etc.

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Pathophysiology and Natural History

The role of altered salt excretion by the kidney as a central mechanism in the
development of hypertension was proposed by Arthur C. Guyton.7 According to Dr.
Guyton's hypothesis, there is impaired excretion of sodium ions by tubular epithelial
cells in the kidney. To maintain salt and water homoeostasis, the body adopts a
pressure-natriuresis approach that ultimately leads to an elevation in BP. Animal
studies and studies evaluating Mendelian forms of syndromes that manifest as
hypertension and hypotension, such as Bartter's syndrome and Liddle's syndrome,
have provided insight into the pathophysiology of hypertension.8 These data
confirm that the basic problem in conditions leading to alteration in BP lies in the
genetic alteration of sodium transport in renal epithelial cells. Several factors
including aging, sympathetic overactivity, toxins, and a low nephron number have
been proposed as factors that could ultimately damage the renal tubules and alter
epithelial cells, resulting in defective sodium excretion.

In addition, several new conditions that can cause hypertension have been
identified. The metabolic syndrome, with insulin resistance and elevation in insulin
levels, leads to increased sympathetic activity and hypertension. In patients with
obstructive sleep apnea, activation of the sympathetic and renin angiotensin
systems has been defined as a possible mechanism for elevation in BP.

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A detailed history and physical examination is essential for identif