Painless Ischemia Research Articles

Characteristics of transient ischaemic episodes in patients with silent and symptomatic exercise-induced myocardial ischaemia.

To evaluate transient ischaemic episodes during daily life in patients with coronary artery disease and exercise-induced myocardial ischaemia, 38 patients underwent ambulatory ST-segment monitoring over 48 h. Sixteen patients had painless ischaemia during exercise and occasional angina, and 12 patients had symptomatic ischaemia and frequent angina during daily life. Ten patients with proven coronary artery disease but normal exercise electrocardiograms served as controls. The extent of coronary artery lesions and the prevalence of myocardial infarction were similar in all groups. ST-segment monitoring revealed 817 min and 98 episodes of ST depression in 13/16 patients of the asymptomatic group and 111 min and 21 episodes in 5/12 patients of the symptomatic group (P less than 0.03). Subjective scores for physical activity during Holter monitoring were significantly higher in the first group than in the second. The majority of ischaemic episodes in both groups was asymptomatic. No ischaemic ST changes occurred in control patients. Results indicate a higher frequency of transient ischaemic episodes related to a higher level of physical activity in patients with silent ischaemia than in patients with symptomatic exercise-induced ischaemia.

Silent Myocardial Ischemia: An Update

Silent myocardial ischemia is diagnosed by several different techniques and has been documented in all the anginal syndromes. In addition to other factors, its presence may be related to increased pain threshold and increased pain tolerance. Although some patients with painless ischemia may have less extensive coronary artery disease, cumulative evidence indicates that silent myocardial ischemia does not necessarily signify a lesser degree of cardiac ischemia or a less severe coronary abnormality. As judged by ambulatory monitoring studies, it shows circadian variation; occurs more frequently than symptomatic ischemia; and appears to depend, in large part, on activation of the sympathetic nervous system. Frequent silent ischemic events during ambulatory monitoring are worrisome because they reflect the disease "activity" of single or multiple coronary atherosclerotic lesions. Thus, there may be a direct association between the severity of ischemia seen during Holter monitoring, the extent of underlying coronary artery disease or disease activity, and prognosis. When diagnosed by exercise testing, silent myocardial ischemia may be associated with significant coronary involvement. In this regard, patients with three vessel coronary disease, impaired left ventricular function, and silent ischemia during stress testing should benefit from coronary revascularization. Compared with symptomatic patients, other evidence suggests that patients with exercise-induced asymptomatic ischemia have at least the same or perhaps even a worse outlook; this may be related to the lack of symptoms that would prompt evaluation and therapy. Awareness of the possibility of silent myocardial ischemia and use of commonly available tests, both to establish its presence and severity and to guide treatment, are emerging as new clinical goals. Further data, however, are necessary to determine how vigorously this should be pursued in different patient subgroups. In association with unstable angina or post-myocardial infarction, the added risk of silent myocardial ischemia warrants a more aggressive approach.

Demonstration of exercise-induced painless myocardial ischemia in survivors of out-of-hospital ventricular fibrillation

To ascertain if myocardial ischemia is the mechanism of out-of-hospital ventricular fibrillation (VF), left ventricular (LV) function was assessed at rest and during submaximal exercise in 15 patients who survived out-of-hospital VF. They were separated into asymptomatic (9 patients, group A) and symptomatic (6 patients, group S) groups for a history of angina or myocardial Infarction. Both groups had significant (at least 70% diameter stenosis) coronary artery disease. At catheterization no patient had angina during exercise, but 12 of 15 had ST depression or Increased ST depression (group A, 1.9 ± 1.4 mm; group S, 1.1 ± 1.2 mm) and 11 had abnormal wall motion. From rest to exercise, patients in group S had increased LV end-diastolic pressure (from 21 ± 9 to 37 ± 11 mm Hg, p = 0.0092) and volume (from 100 ± 25 to 107 ± 26 ml/m 2, p = 0.006), with no significant change in LV ejection fraction (from 40 ± 13 to 42 ± 12%). In group A LV end-diastolic pressure increased from 19 ± 4 to 31 ± 8 mm Hg (p = 0.001), but neither end-diastolic volume nor ejection fraction changed significantly (from 83 ± 13 to 92 ± 23 ml/m 2 and from 55 ± 13% to 46 ± 13%, respectively). Thus, patients with coronary artery disease who survive out-of-hospital VF may have evidence of myocardial ischemia during exercise without pain. Painless ischemia may have a role In out-of-hospital VF.

Holter monitoring in assessment of angina pectoris

Holter monitoring of ST-segment changes is a unique method of studying the character of transient myocardial ischemia that occurs during ordinary daily life. The electrocardiographic signal is a reliable marker of ischemia in defined populations of patients with angina and coronary disease, but should be interpreted with caution outside of these groups. Detailed studies in patients with chronic stable angina have shown that transient ischemia is frequently silent and prolonged, and may occur without evidence of physical exertion. Analysis of underlying changes in regional myocardial perfusion using rubidium-82 and positron tomography has shown that a decrease in myocardial perfusion (supply) is involved in the genesis of many episodes of ischemia during daily life. Clinical trials have shown that drugs that affect demand and supply are efficacious against both painful and painless ischemia and that combinations of agents can provide useful benefits. There is, however, marked natural variability in disease activity despite “stable” symptoms, which must be taken into account in individual patient assessment and the rational design of clinical trials. Ambulatory monitoring permits quantitation of previously unrecognized myocardial ischemia, and treatment can thus be assessed in terms of ischemic activity during everyday life rather than on data obtained during brief hospital visits. An active approach to the detection and monitoring of transient ischemia with and without pain will be necessary if prospective clinical research shows that treatment of silent myocardial ischemia can prevent myocardial damage and improve prognosis.

Role of coronary artery spasm in symptomatic and silent myocardial ischemia

The revival of the concept of coronary spasm has stimulated research into coronary artery disease. Observations in patients with variant angina have substantially contributed to the appreciation of painless myocardial ischemia. However, the presence or absence of pain during ischemic episodes is not related to the cause of ischemia, because painless ischemia can be observed in variant angina (caused by spasm), in effort-induced angina (caused by increased myocardial demand) and in myocardial infarction (caused by thrombosis). Continuous monitoring initially of patients with variant angina and subsequently of patients with unstable and stable angina proved that often painful and painless ischemic episodes are caused by a transient impairment of regional coronary blood flow rather than by an excessive increase of myocardial demand. The transient impairment of coronary flow appears to be caused by dynamic stenosis of epicardial coronary arteries. This most often occurs at the site of atherosclerotic plaques encroaching on the lumen to a variable extent. Dynamic stenosis can be caused by 1) "physiologic" increase of coronary tone, as in stable angina, 2) spasm, as in variant angina, and 3) thrombosis, usually in combination with "physiologic" changes in tone or with spasm, or both, as in unstable angina. The mechanisms of spasm, as typically observed in variant angina, are different from those of "physiologic" increase of tone; they appear to be related to a local alteration that makes a segment of coronary artery hyperreactive to a variety of constrictor stimuli causing only minor degrees of constriction in other coronary arteries. The nature of this abnormality, which may remain stable for months and years, is yet unknown.

Transient asymptomatic S-T segment depression during daily activity

The significance of asymptomatic episodes of ischemic type S-T segment depression was studied in 20 patients with coronary heart disease. Continuous 10 hour electrocardiographic recordings accompanied by detailed daily diaries of activity and symptoms were obtained periodically during a mean time of 16 months. All patients had ischemic type S-T depression associated with angina pectoris during treadmill exercise. Measurements of heart rate, S-T depression and exercise level at the onset of angina obtained during repeated controlled exercise tests at the start of each study period were compared with the measurements recorded during daily activity. After 2,826 hours of recording, 411 transient epidsodes of ischemic type S-T depression were noted during usual daily activity. Only 101 (25 percent) of these episodes were associated with angina. The remaining episodes were unrelated to other symptoms or to posture. All occurred at heart rates significantly lower than those observed at the onset of angina during exercise testing. Of these episodes of asymptomatic S-T depression, 72 percent occurred only at rest or during very light activity such as slow walking or sitting. Nitroglycerin administered hourly significantly reduced the frequency of these episodes, thus supporting the concept that they represent painless ischemia. Because the episodes of asymptomatic ischemic type S-T depression occurred more frequently than angina during usual daily activity and were evident at heart rates and activity levels well below those expected to evoke ischemia, they may be caused by factors other than those that cause angina.