The population samples of the FINMONICA project carried out in different regions in Finland in 1992 showed that the prevalence of elevated BP (≥ 160/95 mmHg or the use of antihypertensive medication) was 26–31% and 19–21% in men and women aged 25 to 64 years, respectively (Nissinen et al. 1994). In Finland, 440 207 subjects were entitled to a special refund of antihypertensive medication at the end of 1993. A new classification of adult blood pressure based on its impact on cardiovascular disease was provided by NIH in 1997 (Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, 1997). In this classification, the optimal blood pressure with respect to cardiovascular risk is SBP < 120 mm Hg and DBP < 80 mm Hg. Persons with stage I (mild) hypertension have SBP 140–159 mm Hg or DBP 90–99 mm Hg based on the average of two or more readings taken at each of two or more visits after an initial screening. Persons with stage II hypertension have SBP 160–179 mm Hg or DBP 100–109 mm Hg. Persons with stage III hypertension have SBP ≥ 180 mm Hg or DBP ≥ 110 mm Hg. Based on these definitions, as many as 43 million people in the United States have hypertension or are taking antihypertensive medication, which accounts for approximately 24% of the adult population. The recommendations of the Second Task Force of European and Other Societies on coronary prevention, including evaluation and treatment of high blood pressure, were issued in 1998 (Wood et al. 1998).
Non-fatal and fatal CVD events, including CHD and stroke, as well as renal disease and all-cause mortality, increase progressively with higher levels of both SBP and DBP. However, unawareness of elevated BP and inadequate control of hypertension are frequent. Kastarinen et al. (2000) found that 6.8% of hypertensive men aged 25–64 years were untreated and unaware of their hypertension, 9.4% were aware but untreated, and 12.3% were treated with drugs, while 71.5% of men were normotensive in 1997. The corresponding prevalences in women were 2.9%, 5.8%, 10.1% and 81.2% in 1997. During 1982–1997, the proportion of subjects not aware of their hypertension decreased consistently for both sexes.
The proportion the adult population having hypertension or taking antihypertensive medication varies with (1) race, being higher in blacks (32.4%) and lower in whites (23.3%) and Mexican Americans (22.6%); (2) age, because in the industrialized countries, systolic BP continues to rise throughout life, whereas diastolic BP rises until age 55 to 60 years, and thus the greater increase in the prevalence of hypertension is mainly due to systolic hypertension; (3) geographic patterns, because hypertension is more prevalent in the southeastern United States; (4) gender, because hypertension is more prevalent in men (though menopause tends to abolish this difference); and (5) socioeconomic status, which is an indicator of lifestyle attributes and inversely related to the prevalence, morbidity and mortality rates of hypertension (Carretero & Oparil 2000).
Essential, primary, or idiopathic hypertension is defined as high BP without secondary causes, such as renovascular disease, renal failure, pheochromocytoma, aldosteronism, or other causes of secondary hypertension or mendelian forms (monogenic). Essential hypertension accounts for 95% of all cases of hypertension. However, essential hypertension is a heterogeneous disorder, with different subjects having different causal factors that lead to high BP. In most patients, one or several of these causes can be recognized and modified in order to reduce the future CVD risk.
The most important independent risk factors for the development of hypertension have been shown to be age (multiple regression coefficient 0.58 in men and 0.75 in women) and subscapular skinfold as a measure of obesity (multiple regression coefficient 0.28 in men and 0.37 in women) (Kannel 1990). Future hypertensives tend to evolve from the upper end of the normal blood pressure distribution. Hence, initial BP is actually the best single predictor of the future hypertension incidence. However, a fat person is at an increased risk of future hypertension regardless of his/her initial BP. Baseline BP explains no more than 20% of the hypertension-obesity-incidence relationship. Attributable risk estimates, using an obesity threshold of 1 cm subscapular skinfold, suggest that 78% of hypertension in men, as opposed to 65% in women, is directly attributable to adiposity. In the Framingham study (Ashley & Kannel 1974), it was estimated that each 10% weight gain is associated with a 6.5 mmHg increase in systolic BP. The mechanism by which obesity raises BP is not fully understood, but increased BMI is associated with an increase in plasma volume and cardiac output. BP in obese adolescents is sodium-sensitive, and fasting insulin is a predictor of this sensitivity Rocchini et al. 1989). This sensitivity has been suggested to be due to the combined effect of hyperinsulinemia, hyperaldosteronism and increased activity of the sympathetic nervous system (Carretero & Oparil 2000). Other potentially modifiable risk factors that increase BP have been shown to be insulin resistance, high alcohol intake, high salt intake (in salt-sensitive patients), stress, low potassium intake and low calcium intake. Furthermore, many of these factors are additive, such as obesity and alcohol intake. The influence of genes on BP has been suggested by family studies, pedigree and twin studies. BP variability attributed to all genetic factors varies from 25% in pedigree studies to 65% in twin studies. Additionally, genetic factors also influence behavioral patterns, which might lead to BP elevation. Mutations in at least 10 genes have been shown to raise BP through a common pathway by increasing or decreasing salt and water reabsorption by the nephron (Lifton 1996).
Hypertensive vascular disease appears to affect mainly the small arteries and arterioles. The major features are thickening of the muscular layers and proliferation of the intima, often with some hyaline changes in the arterial wall and hyperplasia of the elastic layers. Disruption of the intima with thrombus formation is not usually seen in benign hypertension. All the manifestations of hypertensive vascular disease appear to be direct consequences of the elevated intra-arterial pressure (Doyle 1991). In the pathogenesis of atherosclerosis, the main factor appears to be the disturbances of lipoprotein metabolism, particularly the elevated levels of LDL cholesterol.
There is powerful evidence to link blood pressure to clinical cardiovascular pathology. Hypertension predisposes both sexes to ischemic infarction of the myocardium and in both elderly and young age groups. Hypertension, for reasons which are unclear, appears to predispose particularly to silent or atypical myocardial infarctions. In hypertensive men and women 35% and 45% of infarctions, respectively, go unrecognized (Kannel 1990). Although diastolic elevations are accorded more importance than systolic increases, there is no evidence to show that major cardiovascular sequelae would be more closely linked to diastolic than systolic blood pressure. Indeed, in elderly subjects with systolic hypertension, the risk of CVD was unrelated to the concurrent diastolic blood pressure. In diastolic hypertensives, on the other hand, concurrent systolic pressure was highly predictive. Isolated systolic hypertension is associated with a greater than twofold risk of CVD. The probability of developing CVD is directly related to the degree of elevation of BP in both sexes at all ages without any obvious threshold level (Taylor 1987).
Lipid and lipoproteins are fundamental to the atherosclerotic process and greatly affect the impact of hypertension on the pace of atherogenesis. Among nonsmokers, the differences in risk per 10 000 person-years between the highest and lowest cholesterol quintiles ranged from 7.6 for those with diastolic BP less than 76 mm Hg to 19.6 for those with diastolic BP 92 mm Hg or greater (Neaton et al. 1992). The protective effect of HDL cholesterol is at least equally strong as the atherogenic influence of LDL cholesterol.