One of the most interesting questions in the field of human hypertension is the apparent paradox of coronary heart disease. Coronary risk is related in a linear fashion to the prevailing blood pressure, 1 and the incidence of coronary heart disease in the hypertensive population is higher than in the normotensive population. Nevertheless, modern antihypertensive treatment, which is very successful in reducing mortality from stroke and congestive heart failure, has much less of a robust effect on the reduction of coronary morbidity and mortality. 2-3 Many explanations for this discrepancy have been offered. Maybe the treatment was started too late and the blood pressure reduction was not sufficiently aggressive to protect the coronaries. The majority of controlled trials used antihypertensive drugs that increase coronary risk by their effect on electrolytes, blood lipids, and glucose, and this could have offset the positive effect of blood pressure reduction. 4 Finally, too drastic a blood pressure lowering in a subset of patients in clinical trials may have been deleterious: the so-called J-curve effect. In this review, I will marshall evidence for yet another interpretation of the coronary heart disease paradox in hypertension. Some of the coronary morbidity in hypertension may not be a direct consequence of blood pressure elevation. Hypertension is a complex syndrome in which blood pressure elevation is only one sign of multiple underlying pathophysiological abnormalities. In their own right, and somewhat independently of blood pressure level, many of these abnormalities contribute to the development of coronary heart disease as well as to poorer coronary outcomes in hypertension. It will also be suggested that increased sympathetic activity, which is present in a large proportion of patients with hypertension, is the common link among many of the" non-pressure-related" coronary risk factors in hypertension.