Silent myocardial ischemia can be defined as the situation during which a discrepancy occurs between O2 consumption and supply, resulting in tissue metabolic, electrical and functional alterations typical of myocardial ischemia, all in the absence of pain. This situation can be transient (transient ischemic attack) or irreversible, culminating in necrosis (silent myocardial infarction). Silent ischemia is the form of myocardial ischemia most widely studied in recent years. Many results from these studies are definitive [1-8] while others are still controversial [9, 10]. There is a general consensus on the high prevalence of silent myocardial ischemia (2/3 of all transient attacks are silent) [1-8], on the similarity of the electrical, mechanical and hemodynamic changes, both in silent or symptomatic myocardial ischemia [1, 5, 7, 11-14], and finally, on the prognosis which has been found to be the same in either symptomatic or asymptomatic patients [8, 10, 15-16]. In a previous report of our group, among patients with effort angina , exercise-induced myocardial ischemia was silent in 43% of cases and this figure was similar to that found by other authors [15,16]. Patients with and without symptoms did not differ in respect to sex, age, prevalence of previous myocardial infarction, hypertension, diabetes and severity of coronary artery disease. Although patients with silent ischemia exercised longer, the rate pressure product at ischemic threshold (= 1 mm ST depression) was similar between symptomatic and asymptomatic patients . The clinical outcome of patients with silent exercise-induced myocardial ischemia did not differ from the outcome of patients with exercise-induced myocardial ischemia associated with chest pain, even when patients were grouped according to the number of diseased coronary vessels [8-16]. Still uncertain is the pathophysiological interpretation of the presence or absence of pain. It is not clear whether the absence of pain is related exclusively to the intensity of the ischemic stimulus or to a defect in the conduction and modulation of pain. In previous reports of our group, using a dental pulp stimulation test , pain threshold has been found to be higher in patients with silent exercise-induced myocardial ischemia. Such a result supports the hypothesis of a defective anginal warning system . The role of endogenous opioids, particularly beta-endorphins and meta-enkephalins, is not completely understood despite many studies have been carried out regarding their action in pain modulation [19-23]. In patients with effort angina we found that plasma levels of beta-endorphins were higher in those patients who are silent during myocardial ischemia induced by physical exercise . The absence of pain in acute myocardial ischemia induced by a primary reduction in blood supply has been studied only in the clinical setting of variant angina [5, 25, 26, 28]. Percutaneous transluminal coronary angioplasty (PTCA) may provide a suitable model to induce transient myocardial ischemia by a primary reduction in coronary blood flow in man [13, 27]. The aim of the present study was to investigate the prevalence and the characteristics of silent ischemia during PTCA and to investigate its correlation with exercise-induced silent ischemia and clinical history of angina. The possible role of beta-endorphins was also analyzed.
|Number of pages||11|
|Journal||Advances in Cardiology|
|Publication status||Published - 1990|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine