After effective antihypertensive therapy was introduced in the 1950s, we rapidly showed that lowering blood pressure in patients with hypertensive crises saved lives. In the 1960s, the benefit for those with asymptomatic elevations of diastolic blood pressure levels of ≥115 mm Hg was proven and, in the early 1970s, the value for those with diastolic levels ranging from 105 to 114 mm Hg was demonstrated. In the early 1990s, the Systolic Hypertension in the Elderly Program (SHEP) showed benefits for elderly hypertensive patients with isolated systolic hypertension. Because it has been difficult to show that treating hypertensive patients with diastolic elevations from 90 to 99 mm Hg reduces clinical events, metaanalyses were used to pool available clinical trial data to evaluate antihypertensive therapy for such patients. Using this technique, it was clear that active therapy reduced strokes as expected but fell short for coronary artery disease. There are many possible explanations for this “coronary artery disease paradox,” including the misclassification and stratification of hypertensive patients, inadequacy of available trial data, unidentified and identified competing cardiovascular risk factors, and limited selection of the antihypertensive agents used in the trials analyzed, which were exclusively diuretics and β-blockers. This paper will review these possible reasons for the coronary artery disease paradox, concentrating on classification and problems with drug therapy.