Silent myocardial ischemia

Silent myocardial ischemia seems a relatively frequent manifestation of coronary insufficiency. The practice of more and more sophisticated tests to detect myocardial ischemia shows that it is a relatively frequent pathological occurrence. It occurs in patients with an abnormality or a transient or constant failure of the alarm system, represented by pain during the ischemia. It is an heterogenous picture which may take the appearance of a completely silent ischemia (the metabolic, hemodynamic and electrical consequences of ischemia being the only symptoms of coronary insufficiency, demonstrated by the presence of severe, angiographic or anatomical, stenoses); of a silent transient ischemia (with alternance of symptomatic and silent episodes or with silent episodes after myocardial infarction); of myocardial necroses without pain or ischemic myocardiopathies. It is the consequences of either an ischemia which is too moderate to reach the pain threshold, or a severe ischemia in patients presenting alterations of the transmission system and of the perception of pain. It has metabolic, hemodynamic and anatomical consequences which may lead to necrosis or degeneration and fibrosis of the myocardium. The prognosis of a painless disease is difficult to make but it does not seem to be as poor as the one of the usual forms of ischemic cardiopathies. Medical treatment is mandatory, and surveillance of its efficacy must be systematic using the techniques of detection of the ischemia.     

Silent myocardial ischemia

Silent myocardial ischemia has emerged from a subject of mainly research interest to one with important clinical implications for practicing physicians. Although the pathophysiologic mechanisms responsible for the absence of pain are still not clear, it is apparent that episodes of silent myocardial ischemia are frequent and occur in many patients with coronary artery disease; episodes occur both in asymptomatic and symptomatic patients; episodes are detectable by various noninvasive and invasive techniques; and episodes appear to have important prognostic implications when combined with the extent of anatomic disease and degree of left ventricular dysfunction. It is expected the rapidly accumulating prognostic data, especially in patients after infarctions and patients with unstable angina, will have a profound effect on the way physicians treat their patients with coronary artery disease.     

Silent myocardial ischemia after acute myocardial infarction.

Silent ischemia after myocardial infarction has definite prognostic significance but should be interpreted within the context of other prognostic indicators. The rationale for therapeutic intervention is based on the prognostic implications of silent ischemia and the potentially deleterious effect of repeated episodes of ischemia on the integrity of the left ventricle. We measured parameters of ischemia in 20 patients who showed asymptomatic ischemic ST-T changes on exercise testing in the early phase after myocardial infarction. After diltiazem administration, a reduction of exercise-induced ST-T depression from 2.3 +/- 0.8 to 0.7 +/- 0.6 mm (p less than 0.01) occurred, and regional wall-motion score at exercise, determined by radionuclide angiography, improved significantly (p less than 0.02). These and other observations warrant further studies in which the duration, severity and frequency of the ischemic episodes should be quantified and correlated with prognosis after myocardial infarction.     

Silent myocardial ischemia in unstable angina and acute myocardial infarction. Prospective clinical study

To establish the prevalence and characteristics of silent myocardial ischemia in patients with unstable angina and acute myocardial infarction and its possible correlation with coronary artery lesions; two groups patients were studied, fifteen with unstable angina and fifteen with acute myocardial infarction. In all patients a continuous 24 hours ECG recording was made with a solid state microprocessor for ST variation analysis, and all underwent coronary arteriography and ventriculography, the severity of coronary heart disease was determined by Gensini scoring system and the coronary angiography morphology was studied. In 86% patients with unstable angina ischemic ST changes were found, 90% of these episodes were silent. There were 66% of the patients with acute myocardial infarction and ST ischemic changes of these 75% were silent. There was no correlation with the ischemic myocardium score index, nor with the angiographic morphology or the heart rate. Therefore it can be said that myocardial ischemia is a result not only of anatomic factors but of many others such as vasoconstriction, endothelial, myocardial, systemic and hemorheological alterations.     

Silent myocardial ischemia. Contribution of coronarography

Coronary angiography enables to determine the true frequency of silent myocardial ischemia (SMI) and specify its prognostic value. Three types of populations are studied. First, patients who are completely asymptomatic and without any past history. The prevalence of coronary disease in this group depends on the age and varies between 2 and 12 p. cent. Then patients with a known coronary insufficiency (past history of myocardial necrosis, for instance). After infarction, in 100 patients evaluated, 50 are asymptomatic and, however, half of them present a SMI. Among those, coronary angiography discloses pluritruncular lesions in half of the cases. And finally, patients with diffuse myocardial disease. 14 p. cent of primary myocardiopathies are of ischemic origin, with diffuse coronary lesions and a severe prognosis.     

Silent myocardial ischemia during mastication

Ambulatory outpatient monitoring of patients with angina suggests a different view of myocardial ischemia than is conventionally obtained from in-hospital tests. Multiple episodes of ST segment depression occur, and the majority of these disturbances are not associated with symptoms. Recently, studies of regional myocardial perfusion using the technique of positron emission tomography with rubidium 82 have confirmed the ischemic nature of these silent ST changes. Furthermore, activities of everyday life such as mental stress or cold exposure seem to provoke both symptomatic and asymptomatic ischemia, as judged by ST depression and reduced cation uptake. This report presents an unusual case of silent myocardial ischemia observed during the chewing of food.     

Silent ischemia after myocardial infarct

The Framingham study demonstrated that 25% of all episodes of acute myocardial infarction (AMI) do not present clinical symptoms, and are later recognized in a routine ECG. Silent ischaemia is frequently found after acute myocardial infarction, and has been identified in 25-60% of the patients according to the results of different studies and the different criteria employed for diagnosis. Silent ischaemia after AMI, as well as angina, is related with the presence and extent of severe coronary lesions located in the infarct related coronary artery or in other vessel not responsible for the acute episode of necrosis. The prognostic significance of silent ischaemia after AMI has not been well established. In some studies the painless ST segment depression during an exercise test soon after AMI presented the same prognostic value that the ST segment depression accompanied by angina, but in others the symptomatic episodes were a better predictor of major events and long term survival after the infarct. Several studies employing ambulatory ECG monitoring (Holter) also seem to indicate that the painless and transient episodes of ST segment depression identify a group of patients with worse prognosis, but in these studies the patients were selected, introducing a clear bias in the results of these investigations. Finally, asymptomatic transient perfusion defects in thallium studies clearly identify a group of high risk patients with a higher incidence of complications and higher mortality rate than the patients with negative thallium studies. The efficacy of anti-ischaemic drugs or myocardium revascularization procedures, including surgery, has not been studied in patients with silent ischaemia after acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Silent myocardial ischemia: diagnosis, clinical significance and management

With the inception of continuous ECG monitoring with high-fidelity reproduction of the ST-segment, silent myocardial ischemia has been regarded with increasing importance in the detection and management of coronary artery disease. With the aid of a variety of invasive and noninvasive methods, the validity of ST-segment depression as indicative of myocardial ischemia, even in the absence of symptoms, has been adequately documented. In completely asymptomatic subjects with positive evidence of silent ischemia in the exercise ECG or Holter monitoring, the risk of developing a future manifestation of coronary artery disease may be up to ten-fold higher than in individuals with negative tests In patients with established coronary artery disease, concomitant use of continuous ECG monitoring and exercise testing, methods which complement each other rather than being mutually exclusive, a substantial number of patients with otherwise typical angina pectoris may be found to have silent ischemic episodes. An adequate differentiation between those with symptomatic and those who are asymptomatic based on characterization with respect to age, sex, hypertension, coronary anatomy, etc., has not been successful. Patients with silent ischemia during exercise may also exhibit more episodes of silent ischemia during daily activities and up to 75% of ischemic episodes may be asymptomatic. In general, however, silent ischemia during exercise appears more common than silent ischemia only during daily activities. In the latter case, since there is usually no increase in heart rate, the pathophysiology is regarded as dissimilar from that associated with exercise-induced ischemia. While the presence of silent ischemia appears quite common in patients after acute myocardial infarction, its occurrence, to date, has not been confirmed to carry additional risk, whereas in unstable angina, the association of silent ischemia is indicative of a higher probability of subsequent cardiac events.     

无痛性心肌缺血与炎症

尽管疼痛阈值的个体差异可部分解释痛觉的差异性,但日常活动或者劳累、情绪激动后的无痛性心肌缺血（silent myocardial ischemia,SMI）的确切发生机制尚不明确。部分研究者提出疼痛缺失的原因是预警机制的缺陷,强调患者之间疼痛敏感性的差异。也有学者认为可能与中枢神经系统和外周神经末梢的病理改变相关。     

Silent myocardial ischemia: Recent developments

Silent myocardial ischemia is now in its fourth decade of recognition as a clinical syndrome within the spectrum of coronary artery disease. Prior decades have seen important research into the pathophysiology, detection, prevalence, prognosis, and therapy of this syndrome. More recent developments have continued to add data to each of these areas, with particular emphasis on the comparative value of various diagnostic procedures and the effect of therapy on prognosis. While controversy still exists concerning proper screening guidelines for the asymptomatic population, there is a growing consensus that some form of stress testing in high-risk individuals (ie, those with multiple coronary risk factors) is appropriate.     

Silent versus symptomatic dipyridamole-induced ischemia after myocardial infarction: clinical and prognostic significance.

The prevalence and prognostic significance of silent myocardial ischemia were prospectively assessed in 217 patients (mean age 57 +/- 9 years, 83% male) recovering from a first uncomplicated acute myocardial infarction and undergoing a dipyridamole echocardiography test before hospital discharge. Clinical, angiographic, exercise electrocardiographic (ECG) and dipyridamole echocardiographic variables were also examined. Of the 217 patients, 89 had no echocardiographically proved dyssynergy after dipyridamole, whereas 128 had dipyridamole-induced wall motion abnormalities that were silent in 94 (Group I) and symptomatic in 34 (Group II). There was no intergroup difference with respect to dipyridamole time (i.e., the time from onset of the test to frank dyssynergy: 7 +/- 3 vs. 8 +/- 3 min; p = NS); prevalence of inferior myocardial infarction (69% vs. 71%; p = NS); ischemic ECG changes during the test (83% vs. 71%; p = NS); diabetes (8.5% vs. 6%; p = NS); ongoing medical therapy; multivessel disease (57% vs. 56%; p = NS); and baseline left ventricular ejection fraction (57 +/- 13% vs. 57 +/- 10%; p = NS). There was also no significant difference between Group I and Group II with respect to wall motion score index at peak dipyridamole effect (1.77 +/- 0.39 vs. 1.78 +/- 0.36; p = NS). Patients were followed up for 24 +/- 4 and 25 +/- 5 months, respectively (p = NS). Life table analysis revealed no difference in unstable angina, reinfarction and death between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Silent ischemia: clinical relevance

Myocardial ischemia can occur without overt symptoms. In fact, asymptomatic (or silent) ST-segment depression during ambulatory electrocardiogram monitoring occurs more often than symptomatic ST-segment depression in patients with coronary artery disease. Initial studies documented that silent ischemia provided independent prediction of adverse outcomes in patients with known and unknown coronary artery disease. The ACIP (Asymptomatic Cardiac Ischemia Pilot Study) enrolled patients in the 1990s and found that revascularization was better than medical therapy in reducing silent ischemic episodes and possibly cardiovascular (CV) events. However, the more recent COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation) trial found similar CV event rates between patients treated with optimal medical therapy alone and those treated with optimal medical therapy plus percutaneous revascularization. Therefore, in the current era, medical therapy appears to be as effective as revascularization in suppressing symptomatic ischemia and preventing CV events. COURAGE was not designed to evaluate changes in the frequency of silent ischemia. Therefore, silent ischemia may persist despite current-era treatment and might still identify patients with increased risk of CV events. Also, silent ischemia is likely to occur frequently in heart transplant patients with denervated hearts and coronary allograft vasculopathy, and future study aimed at improving the management of silent ischemia in this population is warranted. Additionally, future research is warranted to study the effect of newer medical therapies such as ranolazine or selected use of revascularization (for example, guided by fractional flow reserve) in those patients with persistent silent ischemia despite optimal current-era medical therapy.