Treatment of silent myocardial ischemia

Long-term studies regarding the effect of treatment on prognosis are lacking, but the adverse implications suggested for silent ischemia support aggressive management. Treatment of silent ischemic episodes is possible utilizing a large variety of agents. Optimal detection and quantitation methods are still being developed, but guidelines for treatment should be similar to those for treatment of symptomatic ischemia.     

Angiography of silent myocardial ischemia]

From March 1986 through October 1987, elective diagnostic coronary angiography was performed in 1,542 consecutive patients. Among them, silent myocardial ischemia was investigated based on the histories in their medical questionnaires, the results of exercise stress tests and the presence of significant coronary artery stenosis. Exercise-induced silent myocardial ischemia was documented only in 3% in the non-infarction group, and in 2.1% of those with significant coronary stenosis. However, asymptomatic post-infarction patients comprised 33%. With regard to the extent of coronary artery disease in the non-infarction group, one-, two- and three-vessel disease accounted for 42%, 29% and 29%, respectively (NS). However, one-vessel disease was predominant among the asymptomatic post-infarction patients (p < 0.01). Among the non-infarction group, those with asymptomatic coronary stenosis had a relatively high incidence of diabetes mellitus (p < 0.01), but such a difference was not significant among the asymptomatic post-infarction patients. Among the post-infarction group, many of those who had chest pain during exercise showed redistribution on exercise thallium scintigraphy. Angioplasty was performed in most of the patients in the asymptomatic group, but its long-term effects are yet unknown.     

Psychological ramifications of silent myocardial ischemia

The diagnosis of silent myocardial ischemia is increasing as a result of the widespread use of noninvasive screening techniques. Primary physicians and consulting cardiologists are often unsure how to approach patients with this disorder because its natural history is unknown. There is continuing controversy over proper treatment. This uncertainty, combined with the paradox of having serious heart disease without symptoms, often leads to psychological stress in patients and their families. In a pilot study designed to evaluate the psychological impact of the diagnosis of silent myocardial ischemia, 15 patients were studied. In general, patients and spouses were surprised and concerned by the diagnosis, but most felt that their physicians had been supportive in explaining the problem to them. Because patients trusted their physicians, they not only changed their lifestyles markedly in regard to exercise and diet but also underwent medical or surgical treatment as recommended. Public awareness of the disorder was generally believed to be almost nonexistent. This pilot study provides insight into a subgroup of patients with potentially serious psychological problems and the clinical implications for their physicians.     

Holter monitoring and silent myocardial ischemia

Angina is not a very sensitive indicator of myocardial ischaemia. In patients with coronary disease 75 percent of ischaemic episodes are asymptomatic. Holter monitoring enables such silent episodes to be detected in daily life, this method becoming more sensitive when pursued for several days. The procedure is facilitated by a new generation of Holter recorders fitted with microprocessors that digitalize electrocardiograms. Silent episodes occur in the same circumstances as painful episodes, with a peak of incidence between 6 a.m. and noon, but they are often somewhat shorter. In patients with stable angina, as in those with unstable angina and after infarction, silent ischaemia is of poor prognosis. Holter monitoring therefore is useful in patients with known coronary disease to identify subjects at risk and to evaluate the effectiveness of anti-ischaemic treatments.     

Psychological stress and silent myocardial ischemia

Episodes of transient myocardial ischemia during daily life were investigated in 30 patients on two separate occasions, by ambulatory Holter ST monitoring. The first occasion was at a time of uncertainty in the patients' lives, when the results of coronary angiography and the need for surgery were to be discussed. The second was at a later date, when there had been time to adjust to the decision-making process. There were 515 episodes of myocardial ischemia of which 174 were associated with pain and 341 were asymptomatic. Silent ischemia was significantly more frequent during the first period of monitoring compared to the second (p less than 0.02). Patients who had more silent ischemia on the first occasion also entered more self reports of "emotional upset" (tension, worry, etc.,) in their diaries compared to the second occasion. The level of urinary cortisol was taken as a measure of uncertainty and worry, and was significantly higher on the first occasion (p less than 0.03). Differences in urinary noradrenaline excretion were taken as a measure of subjective stress. Patients who excreted more noradrenaline on the first compared to the second occasion had significantly more silent ischemia (p less than 0.007) and longer total ischemic time (p less than 0.01). We suggest that psychological stress may exacerbate myocardial ischemia which is frequently painless.     

Beta-adrenergic blockers in silent myocardial ischemia

Factors contributing to the development of exercise-induced painful ischemia, such as actions of the central nervous system and catecholamines, have been well identified, but the mechanisms by which nonexercise-related silent episodes of ischemia are provoked are unknown. Possible mechanisms receiving much study in recent years are those having the potential to influence the myocardial oxygen supply-demand relation. Beta-adrenergic receptor stimulations, by increasing myocardial oxygen demand through augmentation of heart rate and contractility (beta 1), may mediate responses that cause ischemia or perpetuate ischemic episodes induced by other means. Other receptors (beta 2) may mediate coronary and peripheral vascular constriction, limiting myocardial oxygen supply and further increasing myocardial oxygen demand. Studies have investigated the effect of beta blockade on ischemic episodes in patients with a variety of clinical forms of coronary heart disease. Beta blockade has been shown to reduce the frequency and duration of silent and painful ischemic episodes in patients with effort angina and rest angina. The data suggest that heart rate and perhaps other changes observed with use of beta blockade play an important role in silent ischemia; heart rate at specific times throughout the day, particularly in the late A.M., and the increase in heart rate seen in conjunction with silent ischemic episodes are all decreased with administration of beta blockade. Results of a recent study focusing only on silent ischemia showed that beta-blocker treatment with metoprolol, compared with placebo, significantly reduced total silent ischemic time (frequency and duration of episodes) in all periods examined.     

Sudden death and silent myocardial ischemia

Recent research indicates that silent myocardial ischemia may play a role in sudden cardiac death. To what extent treatment can reduce occurrence of silent ischemia remains to be assessed. Three classes of silent ischemia patients are identified: type 1--totally asymptomatic; type 2--post myocardial infarction; and type 3--noninfarcted with both silent ischemia and angina. An index of prognostic risk (PR), showing the percent of adverse events attributable to silent ischemia, is calculated to measure the potential impact of successful treatment of silent ischemia on population mortality. Type 1 individuals' PR is estimated at a low 3.8%, suggesting that screening the general asymptomatic population would be unproductive. Type 2 patients exhibit an 80% PR. We lack the empirical information to estimate type 3 patients' PR, but silent ischemia is a recognized adverse prognostic factor in the subgroup exhibiting unstable angina. These results suggest that successful treatment of silent ischemia might favorably influence coronary artery disease patient outcomes.     

Indications for treatment of silent myocardial ischemia

Summary A rational approach to treatment of silent myocardial ischemia is based on an appreciation of those factors influencing prognosis in the three types of patients that clinicians see with this disorder: those who are totally asymptomatic (type 1), those who are asymptomatic following myocardial infarction (type 2), and those who have angina and silent myocardial ischemia (type 3). Prognosis in type 1 and type 2 patients is generally good, except when triple vessel or left main disease is present. Risk factor modification and anti-ischemic medication should be employed in these patients, with serious consideration given to revascularization procedures. The latter approach is less controversial in type 3 patients who have frequent episodes of silent myocardial ischemia, especially if high dose anti-ischemic agents fail.     

Role of beta-endorphins in silent myocardial ischemia

The reason for the absence of pain perception in silent myocardial ischemia is unknown. A role of increased endorphinic activity in patients with silent ischemia has been postulated. To further investigate this hypothesis, 10 men with documented coronary artery disease and previous positive electrocardiographic findings during exercise without anginal pain were studied. Six healthy volunteers served as control subjects. The protocol included 2 bicycle exercise tests, the first test serving as baseline and the second performed after administration of naloxone, a specific opiate antagonist. Plasma beta-endorphin levels were measured by radioimmunoassay in both tests at rest, at peak exercise level and after recovery. All patients underwent thallium-201 scintigraphy after coronary vasodilation to provide an additional independent marker of ischemia. All patients showed stress-induced reversible perfusion abnormalities. No patient reported pain after naloxone application. Exercise duration, blood pressure and heart rate were not significantly altered by naloxone. Plasma beta-endorphin levels ranged from 18 +/- 6 pg/100 microliters (mean +/- standard deviation) at rest to 22 +/- 6 pg/100 microliters during exercise in the patient group and from 20 +/- 5 to 27 +/- 9 pg/100 microliters in the control subjects. Thus, there was no significant increase of plasma beta-endorphins during exercise or after naloxone administration, nor was there any difference observed between patients and control group. These data support the view that endorphinic activity does not play an essential role in the pathophysiology of silent myocardial ischemia.     

The incidence of silent myocardial ischemia]

Retrospectively evaluated was the patient population of the years 1982 to 1988 which underwent ergometric investigations concerning the appearance of silent myocardial ischaemias. In 256 reactions of exercise ischaemia of patients with definitive coronary disease in 47 cases angina pectoris appeared (18.4%). Reactions of ischaemia in a large area of the breast wall showed, compared with a small area of ischaemia, a significantly higher proportion of symptomatic episodes (34.3% vs 13.0%, P less than 0.05). Ergometric exercises lying below the norm of age were more frequently accompanied by symptomatic ischaemias than ischaemic reactions, which only appeared in a good area of performance (26.0% vs 11.4%, P less than 0.05). In addition to this more anginose complaints were found in patients, whose ischaemic reaction was accompanied by an insufficient frequency response (28.1% vs 9.8%, P less than 0.05).     

Role of nitrates in silent myocardial ischemia

Assessment of systemic and coronary hemodynamics, myocardial metabolic and mechanical function and scintigraphic and electrocardiographic studies has provided ample evidence for the existence of asymptomatic silent myocardial ischemia in both acute and chronic coronary artery syndromes. There is growing evidence to suggest that a primary decrease in coronary blood flow, resulting from increased coronary arterial resistance, is the principal cause for spontaneous symptomatic and asymptomatic myocardial ischemia in these patients. The precise mechanism for increased coronary arterial resistance has not been clarified, and it is likely to be different in different angina syndromes but similar for both symptomatic and asymptomatic myocardial ischemia. Since nitroglycerin and nitrates can decrease coronary arterial tone and coronary artery resistance, as well as myocardial oxygen requirements, these agents have the potential to relieve episodes of silent myocardial ischemia in patients with coronary artery syndromes.     

Effects of nicardipine in silent myocardial ischemia

201Tl myocardial scintigraphy was performed in 29 patients with coronary heart diseases and silent myocardial ischemic episodes revealed during a long-term monitoring of ST segment. The painless ST segment depression episodes and long high-amplitude painless ST segment elevations were found to be indicative of a significant severity of pathological processes in the myocardium. A 12-day nicardipine monotherapy produced antianginal and hypotensive effects and contributed to decrease in the frequency, duration, and amplitude of silent ST-segment depressions and in the duration of silent ST-segment elevations.     

Impaired fasting glucose and silent myocardial ischemia

The present study was designed to reveal the incidence of silent myocardial ischemia in asymptomatic elderly patients with impaired fasting glucose. Abnormal perfusion pattern was found in 13 of 48 (27.1%), who were finally considered to have a SMI. The evidence suggests that early and intensive detection may be needed as a part of routine care for this group.     

Effect of diltiazem on silent myocardial ischemia]

Thirty-four patients with coronary heart disease who had silent myocardiac ischemic episodes as evidenced by long-term ECG monitoring were examined. Silent ST-segment elevations and depressions were encountered 2.7- and 4.9-fold as compared to manifest ones. The fact that the CHD patients had silent ST-segment depressions and/or prolonged high-amplitude silent ST-segment elevations suggests a grave severity of abnormal myocardial processes. There was a reduction in the number, duration of silent ST-segment elevations and depression episodes and in the amplitude of silent ST-segment depressions. This may indirectly indicate that the agent affects predominantly coronary blood flow and coronary vascular tone.     

Detection of silent myocardial ischemia in diabetes mellitus

The prevalence of silent myocardial ischemia and its relation to autonomic dysfunction and pain threshold was studied in 58 men with diabetes mellitus and without cardiac symptoms. All patients underwent 48-hour ambulatory electrocardiographic monitoring and exercise testing after assessment of their autonomic function and pain threshold. Silent myocardial ischemia, defined as greater than or equal to 1 mm of ST-segment depression on either exercise testing or ambulatory electrocardiographic monitoring, was corroborated by exercise-induced reversible defect(s) on tomographic thallium scintigraphy. Autonomic function was assessed by heart rate response to: (1) Valsalva maneuver, (2) deep breathing, and (3) upright posture, as well as by diastolic blood pressure response to sustained handgrip and systolic blood pressure response to upright posture. Autonomic dysfunction was defined as greater than or equal to 2 abnormal responses. Pain threshold measurements were performed using electrical cutaneous stimulation of both forearms. Of the 58 diabetic patients, 21 were found to have autonomic dysfunction (36%). Silent myocardial ischemia was detected in 10 patients (17%), and was significantly more frequent in patients with than without autonomic dysfunction (38 vs 5%, p = 0.003). There was no difference in the electrical pain threshold or tolerance in subjects with and without silent myocardial ischemia. It is concluded that silent myocardial ischemia in asymptomatic diabetic men occurs frequently and in association with autonomic dysfunction, suggesting that diabetic neuropathy may be implicated in the mechanism of silent myocardial ischemia.     

糖尿病患者无症状心肌缺血的检出

英国糖尿病（DM）前瞻性研究（UKPDS）及随后的研究发现．DM患者发生心肌梗死与有心肌梗死病史的非DM患者再梗死的机会相当,是冠心病的等危症。DM是引发心血管疾病的强危险因素,Framingham研究随访20年发现,DM患者发生心脑血管疾病（冠心病、间歇跛行、脑梗死）的比例显著高于非DM者。DM血管病变致心血管病及卒中是其主要死因．占总死亡的65％～80％．比非DM者高2～4倍;致心力衰竭（心衰）在男性增加2倍、女性增加5倍^[1]。近年,2型DM已成为我国常见病,且发病率增长迅速,据估计,到2025年我国DM患者将从目前约2千万人猛增到超过4千万人。可见,对2型DM患者的心血管疾病的早期防控势在必行。     

无症状性心肌缺血合并心律失常的临床分析

目的探讨无症状性心肌缺血合并心律失常的主要影响因素及分类。方法对123例发生无症状性心肌缺血老年患者的动态心电图(Holter)结果进行分析。结果其中78例发生无症状性心肌缺血的老年患者合并心律失常,并以激动起源异常多见,而激动传导异常较少;心律失常最常见为室性早搏,24h动态心电图监测中发生无症状性心肌缺血的次数>10次患者心律失常发生率明显增高。结论老年患者发生无症状性心肌缺血合并心律失常以激动起源异常多见,其中室性早搏最常见,多次发生无症状性心肌缺血加重心肌损伤可能是导致发生心律失常的重要原因之一。