Silent ischaemia and hypertension.

For many years now, silent ischaemia has been recognized as a distinct clinical entity, and its relevance in different patient groups has been established. However, a number of basic questions have not been answered. In explaining the pathophysiology of silent ischaemia, factors affecting both the demand and the supply side are now being recognized. With the exception of certain well-defined groups, it is not clear why some patients are mostly symptomatic, while other patients are predominantly asymptomatic. There appear to be many factors influencing the ischaemic pain threshold. Studies investigating the prevalence of silent ischaemia show a remarkably high prevalence of silent ischaemia in different patient groups. Patients with hypertension but without coronary artery disease form a specific and vulnerable high-risk population that is particularly prone to silent ischaemia. Since changes at the macrovascular level are not responsible, various factors negatively influencing either cardiac supply or demand have been investigated. A reduced coronary reserve is central in explaining the increased prevalence of silent ischaemia in hypertensives. Left ventricular hypertrophy renders meaningful detection of ST segment changes difficult, but a possible solution dealing with this problem is offered by applying more stringent criteria in terms of minimal ST depression in the definition of ischaemia. The treatment of silent ischaemia is largely the same as for angina pectoris, but whether therapy should be directed at elimination of all ischaemic episodes or only of symptomatic episodes depends on further prospective work addressing this question.