[Silent myocardial ischemia and nitrates].

Silent ischaemia (SI), generally identifiable as a transient abnormality of ECG, not accompanied by angina or equivalent clinical symptoms, is a common finding in patients suffering from coronary heart disease before and after myocardial infarction, or after surgical coronary revascularization or angioplasty. SI per se is considered to be a serious independent cardiovascular risk factor. From a pathophysiological point of view, SI is intimately related to myocardial oxygen imbalance, in which the demand, both at rest and during effort, exceeds the supply, essentially due to coronary arteriosclerosis or arterial spasm, or both, alongside other neuroendocrine and clotting factors which contribute to the final clinical picture. The absence of large-scale prospective studies prevents a rigorous assessment of whether the currently available anti-ischaemic treatments modify the cardiovascular prognosis related to the presence of SI. Long-acting nitrates, as well as beta-blockers and type L calcium channel blockers exert a beneficial effect on the total ischaemic load, improving not only the clinical profile of angina patients and their exercise tolerance, but also, in most published series, considerably decreasing the number of silent ischaemic events. Today's medical challenge therefore consists of determining whether the reduction of SI by means of anti-ischaemic drugs is accompanied by a proportional reduction of overall morbidity and mortality attributable to this process. As the asymptomatic nature of this type of ischaemia prevents evaluation on the basis of clinical data, it specialized analyses are necessary, such as stress ECG, Holter monitor, TEP, or Thallium 201 myocardial scan, and especially prognostic follow-up, in order to establish the real efficacy of drugs therapy. Coronary videoangiography and the various myocardial revascularization techniques can be applied when the ischaemia cannot be controlled clinically, and when a significant reduction of total ischaemic load is not obtained. In situations of pre-infarction ischaemia, some studies show that the use of nitrate vasodilators reduces the total ischaemic load, improving the clinical course of the disease and significantly reducing the total number of silent ischaemic episodes, although their secondary preventive action remains to be demonstrated. The anti-ischaemic action is more obvious for events triggered by physical effort (ergometry) than for those observed during Holter monitoring, which confirms that multiple mechanisms are responsible for inducing ischaemia and that circadian variability also depends on many factors, which is why the choice of an anti-ischaemic drug must be based on a thorough knowledge of the pathophysiological mechanisms which induce ischaemia and the anatomical and functional setting in which it develops. It has been clearly shown that nitrate vasodilators not only exert a beneficial action in terms of the control of painful or silent ischaemic events, but that they are also useful as coadjuvant therapy in the presence of signs of ischaemic ventricular dysfunction.