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There is overwhelming evidence that hypertension plays a role in the development of coronary atherosclerosis. Furthermore, there is abundant evidence that the treatment of hypertension reduces the development of the adverse consequences of coronary artery disease (CAD) including myocardial infarction and heart failure.
There are data from 22,672 patients with stable CAD who were enrolled in the ProspeCtive observational LongitudinAl RegIstry oF patients with stable coronary arterY disease (CLARIFY) registry that included patients from 45 countries who were treated for hypertension. The primary outcome was the composite of cardiovascular death, myocardial infarction, or stroke. Increased systolic blood pressure (SBP) of 140 mm Hg or more and diastolic blood pressure (DBP) of 80 mm Hg or more were each associated with increased risk of cardiovascular events. Blood pressure (BP) targeted to less than 140 mm Hg systolic and less than or equal to 80 mm Hg diastolic is suggested.
The principle of utilizing a single drug that would address hypertension and angina pectoris has led to guideline recommendations for the use of beta-blockers or calcium channel blockers (CCBs). Some recommendations prefer beta-blockers as the first choice based on the greater amount of data on cardio protection for beta-blockers that arises from the use of beta-blockers in myocardial infarction. The use of either agent as first-line therapy has also gained credibility because of the lower antihypertensive efficacy of beta-blockers in older individuals who are usually in the age group with a greater prevalence of patients with CAD. Other antihypertensive agents can be utilized for hypertension management except for hydralazine, which has the potential to produce a reflex tachycardia and potentially precipitate myocardial ischemia.
Coronary (artery) blood flow (CBF) usually occurs during diastole and is dependent on or determined by myocardial perfusion pressure (MPP), which is a function of (1) DBP, (2) the degree of coronary stenosis, which determines MPP distal to the stenosis, and (3) the resistive properties of the coronary vascular bed. The myocardium exerts an extravascular pressure on the intramural coronary vasculature to reduce CBF. Coronary artery resistance is affected by circulating neurohumoral factors and the autonomic nervous system, as well as factors released by circulating elements such as platelets.
The presence of CAD leading to coronary artery narrowing or stenosis reduces CBF significantly after the degree of stenosis exceeds 80%. Myocardial (oxygen) demands influence symptoms so that increased physical exercise will increase myocardial oxygen requirements in excess of the ability of the stenotic artery to increase myocardial blood flow, producing myocardial ischemia or angina pectoris.
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