Effect on prognosis of abolition of exercise-induced painless myocardial ischemia by medical therapy.

During exercise radionuclide ventriculography, many patients with coronary artery disease exhibit painless myocardial ischemia defined as an abnormal left ventricular ejection fraction response without accompanying angina. To see if complete suppression of such exercise-induced painless ischemia by anti-ischemic medication implies a better prognosis in medically treated coronary artery disease, 34 patients underwent repeat testing at 4 weeks receiving regular conventional therapy that rendered angina no worse than class I. With such therapy, painless ischemia was abolished in 12 patients (group I) and persisted in 22 (65%, group II). Both groups were similar in age, number of diseased vessels, proportion with previous myocardial infarction, exercise ejection fraction, and degree of exercise-induced painless ischemia at baseline. At 9 months, adverse events had occurred in 11 patients (2 patients with myocardial infarction, 4 with unstable angina, 2 with angioplasty and 3 with bypass surgery). Only 1 of 12 patients (8%) in group I had experienced events compared with 10 of 22 (45%) in group II (chi-square, 5.4; p less than 0.025; 95% confidence interval, 12 to 61%). Thus, the relative risk of adverse events in patients whose painless ischemia was abolished was only 18% of that in patients in whom it was persistent. These results suggest that (1) the abolition of exercise-induced painless ischemia by conventional symptom-dictated medical therapy confers a better short-term prognosis in medically treated coronary artery disease, and (2) therapeutic efficacy may need to be assessed by titration against ischemia and not against angina.     

Long-term effect of inducible silent ischaemia on left ventricular systolic function

Silent myocardial ischaemia is readily detected by exercise radionuclide ventriculography in patients with coronary artery disease. In those who remain asymptomatic and event-free, it is not known whether silent ischaemia which is inducibledespite anti-ischaemic medication exerts an insidious detrimental effect on left ventricular function. To study this, 34 medically treated patients (mean age 57; 26 men) underwent prospective measurement of left ventricular ejection fraction (LVEF) during rest and exercise radionuclide ventriculography without interruption of anti-ischaemic medication at baseline and 12 months later.There was no significant mean (standard deviation, 95% confidence interval) deterioration from baseline to 12 months in LVEF at rest (50% v 49%, SD 5; 95% CI=–3 to+1), peak exercise (44% v 45%, SD 8; 95% CI=–1 to + 4) and the change in LVEF from rest to exercise (–6% v – 4%, SD 7; 95% CI=–1 to + 5).Thus, in coronary artery disease patients who remain asymptomatic and event-free on medical therapy, silent myocardial ischaemia which is readily inducible at baseline despite medication does not leadper se to deterioration of left ventricular systolic function at rest or exercise over 12 months.     

Prognostic implications of symptomatic versus asymptomatic (silent) myocardial ischemia induced by exercise in mildly symptomatic and in asymptomatic patients with angiographically documented coronary artery disease

Patients with coronary artery disease (CAD) may undergo periods of reversible myocardial ischemia without experiencing angina. To study the prognostic implications of "silent" myocardial ischemia induced by exercise, exercise electrocardiography and radionuclide angiography were performed in 131 consecutive patients with CAD, preserved left ventricular (LV) function at rest and mild or no symptoms during medical therapy. All patients who died during medical therapy were in the subgroup of patients with 3-vessel CAD in whom exercise-induced ischemia developed, which was characterized by both a decrease in LV ejection fraction and ST-segment depression. Patients in whom angina pectoris developed during exercise (54% of all patients) had a greater prevalence of this combined ischemic response to exercise than patients without angina (61% vs 27%, p less than 0.001) and also a greater prevalence of left main or 3-vessel CAD (59% vs 25%, p less than 0.001). However, when inducible ischemia was demonstrated, risk stratification and prognosis were the same whether the ischemic episode was symptomatic or silent. Among patients having both a reduction in ejection fraction and a positive ST-segment response, the likelihood of significant left main narrowing (13% vs 26%), 3-vessel CAD (56% vs 51%) and death during subsequent medical therapy (16% vs 9%) was similar in patients with silent compared to those with symptomatic ischemia. These data indicate that patients in whom angina develops during exercise have a greater prevalence of high-risk coronary anatomy and of inducible ischemia than patients without angina. However, once inducible ischemia is documented, the symptomatic response to exercise appears irrelevant for prognostic or risk stratification considerations.     

The Asymptomatic Cardiac Ischemia Pilot (ACIP) study: Design of a randomized clinical trial,baseline data and implications for a long-term outcome trial

Objectives. The primary objectives of the Asymptomatic Cardiac Ischemia Pilot were 1) to compare the 12-week efficacy of three treatment strategies to suppress cardiac ischemia, and 2) to assess the feasibility of a prognosis trial in patients with asymptomatic cardiac ischemia.Background. Cardiac ischemia has been associated with increased morbidity and mortality. However, most cardiac ischemia is asymptomatic, and although therapeutic strategies ranging from no medication to revascularization are being used to treat ischemia, no prospective study evaluating different treatment strategies has been reported.Methods. Patients with angiographically documented coronary artery disease and ischemia on exercise and ambulatory electrocardiogram (ECG) in 11 clinical units were randomized to receive angina-guided medical therapy, angina-guided plus ambulatory ECG ischemia-guided medical therapy or revascularization (coronary angioplasty or bypass surgery). Patients were also randomized to receive either diltiazem plus isosorbide dinitrate or atenolol plus nifedipine when possible. After anti-ischemic medication adjustment to control angina, blinded medication was adjusted in the medical therapy groups to eliminate ischemia in the ischemia-guided group. The primary outcome was the absence of ischemia at 12 weeks. Follow-up was scheduled for 1 year.Results. A total of 1,959 patients were screened by ambulatory ECG monitoring; 982 (49%) had asymptomatic ischemia, and 618 (65%) were enrolled in the study. Most patients were men, were >60 years old and had two or more ischemic episodes, early positive exercise tests and multivessel disease.Conclusions. Design and baseline data for a pilot study of ischemia treatment strategies are described.     

Evaluation of left ventricular contractility indexes for the detection of symptomatic and silent myocardial ischemia

This study evaluated the role of left ventricular (LV) ejection fraction and systolic blood pressure (BP) to end-systolic volume ratio to detect symptomatic and silent myocardial ischemia. The sensitivity and diagnostic accuracy of these contractility indexes were compared with angina and ST depression during exercise. Thirty consecutive patients referred for chest pain performed symptom-limited bicycle exercise and had coronary angiography within 3 months. Twenty-two had angiographically significant coronary artery disease and 8 had normal coronary anatomy. Systolic BP was measured by sphygmomanometry; LV ejection fraction and end-systolic volume were obtained by nuclear ventriculography. Normal values for contractility indexes were defined as LV ejection fraction greater than 52% at rest and increment of greater than or equal to 5% during exercise, and systolic BP to end-systolic volume ratio greater than 2.2 mm Hg/ml at rest and greater than 3.0 mm Hg/ml during exercise. The sensitivity of systolic BP to end-systolic volume ratio to identify patients with coronary artery disease at rest was 71 vs 33% for LV ejection fraction. During exercise, each contractility index had a sensitivity of 95% and there was a combined sensitivity of 100%. This compares with 71% for ST depression and 48% for exercise-induced angina. Thus, 52% had no angina and 36% of them were also silent by electrocardiography. Among the patients with symptomatic ischemia, 20% had no ST-segment depression. Measurement of contractility indexes enhanced the detection of silent myocardial ischemia and provided information on LV function vital to prognosis and management of patients with coronary artery disease.     

Prognostic value of total ischemic burden in patients with stable ischemic heart disease.

Patients with stable coronary artery disease commonly have transient myocardial ischemia with or without experiencing angina, but the prognostic implications of this "total ischemic burden" is still a matter of debate. We studied 112 consecutive patients with coronary artery disease, normal left ventricular function at rest and exercise-induced myocardial ischemia, a 24-hour ambulatory EKG was performed after drug withdrawal. The mean exercise duration was 572 +/- 192 seconds, with an ischemic threshold (ST depression = 1 mm) of 390 +/- 190 seconds). By Holter monitoring 30 patients had no ischemia and 82 (73%) had a total of 332 episodes of ST segment changes, the majority of which were asymptomatic (242/332, 73%). Among 82 patients with transient myocardial ischemia, 44 (54%) had only asymptomatic episodes. Nine patients (11%) complained of angina coincident to ST changes. Twenty-nine patients (35%) had both painful and painless ST segment alterations. All patients were prospectively followed-up while on conventional medical therapy. During a mean follow up of 25 +/- 10 months cardiac events occurred in 31 patients; there were 5 cardiac deaths, 3 non-fatal myocardial infarctions, 2 hospitalization for unstable angina and 21 revascularization procedures (PTCA or CABG). By multivariate analysis the number of stenotic vessels on coronary angiography was predictive of the events during the follow-up (p = 0.03), while other demographic, clinical, ergometric and angiographic variables were not influential. Event-free survival was similar for all subsets of transient myocardial ischemia (silent, symptomatic, or none).(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of nifedipine and isosorbide dinitrate when added to maximal propranolol therapy in stable angina pectoris

A study was performed to compare isosorbide dinitrate and nifedipine as adjunctive therapy in 14 patients with coronary artery disease and stable angina pectoris taking maximal beta-blocking drugs. Drug titration phases ensured maximal therapy of propranolol, isosorbide or nifedipine. The combination of nifedipine and propranolol was more effective than the combination of isosorbide and propranolol in reducing angina and increasing exercise capacity (323 vs 416 seconds, p less than 0.005) during exercise treadmill testing. Nifedipine produced a greater reduction in systolic blood pressure at submaximal exercise than isosorbide. Global and regional ejection fraction at rest and exercise was assessed with radionuclide ventriculography. The substitution of nifedipine for isosorbide depressed the global ejection fraction at rest (0.61 to 0.56 p less than 0.05) and produced a slight improvement in exercise ejection fraction (0.47 to 0.51, difference not significant). The decrease in ejection fraction from rest to exercise was 0.14 to 0.04 with nifedipine (p less than 0.005). The benefit of nifedipine compared with isosorbide occurred in regions with marked exercise-induced ischemia. In patients treated with maximal beta-blocking therapy, nifedipine is an effective alternative to isosorbide as a combination agent with propranolol. The salutary effects of nifedipine included afterload reduction with exercise and possible improvements in coronary blood supply.     

Determinants of ventricular arrhythmias in mildly symptomatic patients with coronary artery disease and influence of inducible left ventricular dysfunction on arrhythmia frequency

To determine the relation among ventricular arrhythmias, prognostic factors and reversible ischemia in coronary artery disease, 131 drug-free, minimally symptomatic patients were studied by radionuclide angiography and 24 hour Holter electrocardiographic monitoring. High grade ventricular arrhythmias (couplets, salvos of premature ventricular complexes and R on T phenomenon) were observed in 33 patients (25%) and were related to lower rest and exercise ejection fraction, greater number of stenotic coronary arteries and higher prevalence of regional wall motion abnormalities at rest (all p less than or equal to 0.1). Among patients with subnormal rest ejection fraction, high grade arrhythmias occurred with greater prevalence in those with reversible left ventricular dysfunction (reduction in ejection fraction) during exercise compared with those with a normal ejection fraction response (59 versus 23%, p less than 0.05), a relation observed principally in patients with multivessel disease. These data indicate that in minimally symptomatic patients with coronary artery disease, arrhythmias are related to both extent of disease and severity of regional and global ventricular dysfunction and are most prevalent in patients with ventricular dysfunction and evidence of inducible ischemia, factors indicating poor long-term prognosis during medical therapy.     

Severe exercise-induced ischemia does not identify high risk patients with normal left ventricular function and one- or two-vessel coronary artery disease

Objectives. This study was conducted to determine whether severe exercise-induced ischemia identifies high risk patients with a normal left ventricular ejection fraction and one- or two-vessel coronary artery disease.Background. Severe ischemia during exercise radionuclide angiography has been shown to identify high risk patients among certain other patient subsets.Methods. Four hundred twenty patients with left ventricular ejection fraction ≥50% and one- or two-vessel disease underwent exercise radionuclide angiography within 3 months of coronary angiography. Patients were treated initially with revascularization (n = 140) or medical therapy (n = 280) at the discretion of their physicians. Patients treated with revascularization were more likely to have angina by history, a positive exercise electrocardiogram, a lower exercise ejection fraction, two-vessel disease and proximal left anterior descending coronary artery disease. Two hundred sixty-four of the 280 patients given medical therapy who had complete follow-up data formed the study group. Outcome was compared between patients with (n = 56) and without (n = 208) severe exercise-induced ischemia, defined by previously published criteria (work load ≤600 kg-m/min, ST segment depression ≥1 mm and decrease in ejection fraction with exercise).Results. During follow-up, there were 30 initial cardiac events (12 cardiac deaths and 18 nonfatal myocardial infarctions). There was no difference in the 5-year event-free survival rate: 91% in patients with and 87% in patients without severe ischemia (p = 0.89). There was no association between event-free survival and severe ischemia (χ²= 1.41, p = 0.24). The study had approximately 80% power at α = 0.05 to detect a 25% decrease in event-free survival in the group with severe ischemia. In addition, there was no association between severe ischemia and outcome if late revascularization was included as an event or if the total mortality rate (overall survival) was analyzed.Conclusions. Severe exercise-induced ischemia fails to identify a high risk subgroup among patients with normal left ventricular function and one- or two-vessel disease who are treated initially with medical therapy.     

Relation of severity of symptoms to prognosis in stable angina pectoris

To determine if severity of angina is related to the extent of coronary artery disease (CAD) or prognosis, 341 patients were evaluated by a systematic physician-administered angina questionnaire at entry into a large-scale randomized study of medical vs surgical treatment of stable angina pectoris. Severity of angina was numerically scored; scores were based on frequency of pain, rest pain, amount of daily medication, and level of daily activity. Severity scores were separated into mild, moderate and severe groups of approximately equal numbers and correlated with (1) number of coronary arteries narrowed, (2) presence of left main CAD, (3) ejection fraction less than 50%, (4) abnormalities of left ventricular function, (5) 3-vessel CAD with abnormal left ventricular function, (6) increased heart size by chest x-ray, (7) a noninvasive measure of prognosis, and (8) mortality. Severity of angina was not significantly related to any of the above variables except for the presence of left main CAD (p = 0.046) and increased heart size by chest x-ray (p = 0.001), both of which had low prevalence rates. Severity of angina at baseline was not related to 7-year survival in patients treated medically or surgically. Severity of angina at baseline, however, did predict 1- to 2-year survival in medically treated patients. Similarly, the severity of angina at 1 year and severity at 5 years predicted survival in the subsequent 4 years in the medical group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of coronary arterial bypass surgery on exercise-induced ventricular arrhythmias. Long-term follow-up of a prospective randomized study.

The effect of coronary arterial bypass surgery on exercise-induced ventricular arrhythmias and their relation to sudden death was examined in 102 patients with stable angina pectoris randomly assigned to medical and surgical therapy (54 and 48 patients, respectively). Symptom-limited treadmill tests were performed at entry and at 1 and 5 years. The surgical group demonstrated significant improvement in exercise performance at 1 year compared with the medical group, and at 5 years exercise-induced ischemia as evidenced by S-T depression and exertional angina remained substantially decreased in the surgical group with little change in the medical group. However, the frequency and severity of exercise-induced ventricular arrhythmias in each group remained unchanged at 1 and 5 years from those at entry. Similar results were obtained from an evaluation of ventricular arrhythmias in the electrocardiogram at rest. With the exception of exercise-induced ventricular tachycardia and fibrillation, no relation was found between ventricular arrhythmias and sudden death. Coronary bypass grafting does not decrease the frequency or severity of exercise-induced or resting ventricular arrhythmias. In patients with stable angina pectoris, with the exception of ventricular tachycardia and fibrillation, exercise-induced ventricular arrhythmias are poor predictors of sudden death. The data suggest that exercise-induced ventricular arrhythmias may not be related to ischemia but to other effects of exercise such as cardiac stimulation by catecholamines or other factors.     

Exercise-induced myocardial ischemia in patients with coronary artery disease: lack of evidence for platelet activation or fibrin formation in peripheral venous blood

The hypothesis that exercise-induced myocardial ischemia is associated with abnormal platelet activation and fibrin formation or dissolution was tested in patients with coronary artery disease undergoing upright bicycle stress testing. In vivo platelet activation was assessed by radioimmunoassay of platelet factor 4, beta-thrombo-globulin and thromboxane B2. In vivo fibrin formation was assessed by radioimmunoassay of fibrinopeptide A, and fibrinolysis was assessed by radioimmunoassay of thrombin-increasable fibrinopeptide B which reflects plasmin cleavage of fibrin I. Peripheral venous concentrations of these substances were measured in 10 normal subjects and 13 patients with coronary artery disease at rest and during symptom-limited peak exercise. Platelet factor 4, beta-thromboglobulin and thromboxane B2 concentrations were correlated with rest and exercise catecholamine concentrations to determine if exercise-induced elevation of norepinephrine and epinephrine enhances platelet activation. Left ventricular end-diastolic and end-systolic volumes, ejection fraction and segmental wall motion were measured at rest and during peak exercise by first pass radionuclide angiography. All patients with coronary artery disease had documented exercise-induced myocardial ischemia manifested by angina pectoris, ischemic electrocardiographic changes, left ventricular segmental dyssynergy and a reduction in ejection fraction. Rest and peak exercise plasma concentrations were not significantly different for platelet factor 4, beta-thromboglobulin, thromboxane B2, fibrinopeptide A and thrombin-increasable fibrinopeptide B. Peripheral venous concentrations of norepinephrine and epinephrine increased significantly (p less than 0.001) in both groups of patients. The elevated catecholamine levels did not lead to detectable platelet activation. This study demonstrates that enhanced platelet activation, thromboxane release and fibrin formation or dissolution are not detectable in peripheral venous blood of patients with coronary disease during exercise-induced myocardial ischemia.     

Verapamil in stable effort angina: Effects on left ventricular function evaluated with exercise radionuclide ventriculography

A double blind placebo-controlled study was performed in 12 patients with stable angina pectoris to evaluate the effects of oral verapamil (320 mg/day) on left ventricular function, as measured at rest and during exercise with gated equilibrium radionuclide ventriculography. On verapamil, patients had a lower heart rate-blood pressure product at each work load than with placebo. Anginal threshold increased by 28 ± 19 watts (p < 3.005), and maximal exercise capacity increased by 20 ± 14 watts (p < 0.001) with verapamil, but the rate-pressure product at the onset of angina and at maximal exercise was unchanged. Left ventricular ejection fraction at rest during verapamil therapy was the same as with placebo therapy. On exercise during placebo therapy, the ejection fraction decreased from 40 ± 9 to 35 ± 11 percent (p < 0.025) because end-systolic volume increased disproportionately compared with end-diastolic volume. On exercise during verapamil therapy, the ejection fraction did not decrease (44 ± 8 versus 45 ± 12 percent) and was significantly higher at identical work loads than on placebo because of a smaller increase in end-systolic volume. Oral verapamil is effective treatment for effort angina and may prevent the decrease in left ventricular ejection fraction due to exercise-induced ischemia.     

The effect of coronary artery bypass grafting on left ventricular systolic function at rest: evidence for preoperative subclinical myocardial ischemia

Successful coronary artery bypass grafting (CABG) improves exercise-induced left ventricular (LV) dysfunction in patients with coronary artery disease (CAD), but its potential for improving resting LV function remains controversial. To assess the influence of CABG on LV function at rest, 31 CAD patients without previous myocardial infarction were studied before and 6 months after CABG by radionuclide angiography after all cardiac medicines were withdrawn. No patient had angina or ischemic electrocardiographic changes at rest. In 27 patients with patent bypass grafts, CABG significantly increased LV ejection fraction during exercise (47 +/- 11% before to 63 +/- 9% after operation, p less than 0.001), indicating reduction in exercise-induced LV ischemia. Moreover, LV ejection fraction at rest also increased (55 +/- 9 to 60 +/- 8%, p less than 0.001), with 20 of 27 patients manifesting an increase compared with preoperative values. Eleven of these 20 patients had apparently normal LV function at rest (ejection fraction and regional wall motion) before CABG. LV regional ejection fraction was computed by dividing the LV region of interest into 20 sectors. Regional analysis indicated that improved ejection fraction at rest after CABG occurred in regions developing ischemia during exercise before CABG. In 4 patients with occluded grafts, the ejection fraction at rest was unchanged by CABG globally (59 +/- 8 to 58 +/- 9%, difference not significant) and regionally. Thus, LV global and regional function at rest improved after successful CABG, even in patients with normal global LV ejection fraction and no visually detectable wall motion abnormality before surgery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term prognosis of “variant” angina with medical treatment

One hundred thirty-eight patients with “variant angina” were followed up for periods of 2 to 8 years. All patients had a history of angina at rest, and 42 percent also had exertional angina. Normal coronary arteries were found in 9 of the 107 patients who underwent coronary arteriography; the remainder had stenosis greater than 50 percent in diameter of at least one major vessel. Coronary vasospasm was demonstrated in all 37 patients studied with coronary arteriography during angina at rest. Twenty-eight patients had acute myocardial infarction and five patients died within 1 month of admission to hospital. Of the 133 surviving patients, 120 were treated medically and 13 underwent coronary arterial surgery. In the medically treated group, only seven patients died and only four had acute myocardial infarction during the remainder of the follow-up period. Symptoms became less frequent and less severe; approximately 50 percent of the patients remained completely asymptomatic for at least 12 months by the end of the 4th year. Death, acute myocardial infarction and persistence of symptoms were more frequent in those patients with more severe coronary atherosclerotic disease although, even in this group, the overall incidence of death and acute myocardial infarction was small. It is concluded that the prognosis of patients with “variant” angina receiving appropriate medical therapy is reasonably good after the acute phase, even in the presence of severe coronary atherosclerosis.     

Correlation between beta-endorphin plasma levels and anginal symptoms in patients with coronary artery disease

To verify whether beta-endorphin plasma levels influence the presence of anginal symptoms, 74 consecutive male patients were studied. All patients had previously documented coronary artery disease and reproducible exercise-induced myocardial ischemia. Thirty-five patients (Group I) had a history of angina and reported anginal symptoms during exercise stress testing; 39 patients (Group II) were asymptomatic and had documented silent myocardial ischemia during exercise. Baseline beta-endorphin plasma levels were measured in blood samples taken before exercise stress testing and analyzed by beta-endorphin-I125-RIA Kit-NEN (a radioimmunoassay method). The mean baseline beta-endorphin plasma level was 22.5 +/- 19 pg/ml in patients with anginal symptoms compared with 43.7 +/- 28 pg/ml in asymptomatic patients (p less than 0.001). Baseline blood pressure and heart rate-systolic pressure (rate-pressure) product at baseline and at ischemia threshold (1 mm ST segment depression) were similar in the two groups. Group II patients had a longer exercise duration (p less than 0.01), more pronounced ST segment depression (p less than 0.001) and a higher peak rate-pressure product (p less than 0.01). The extent of coronary artery disease, ejection fraction and left ventricular end-diastolic pressure were similar in the two groups. These data suggest that higher baseline beta-endorphin plasma levels may play a role in the decreased sensitivity to pain in patients with silent myocardial ischemia. In addition, different beta-endorphin levels can be associated with a different sensitivity to pain.     

Effect of nitroglycerin on exercise-induced abnormalities of left ventricular regional function and ejection fraction in coronary artery disease. Assessment by radionuclide clineagiography in symptomatic and asymptomatic patients.

The effects of nitroglycerin (TNG) on exercise-induced abnormalities of left ventricular wall motion and ejection fraction are unknown in symptomatic and asymptomatic patients with coronary artery disease (CAD). In the present investigation radionuclide cineangiographic studies were performed in 47 patients with CAD (14 without angina during exercise) and in 25 normal subjects. All CAD patients, including those without symptoms, demonstrated regional wall motion abnormalities during exercise. In all patients, ejection fraction (EF) also responded abnormally to exercise: EF decreased from 48% at rest to 36% during exercise (P less than 0.001). EF increased in all normal subjects from an average of 58% at rest to 71% during exercise (P less than 0.001). In all CAD patients TNG reduced exercise-induced regional wall abnormalities and increased EF attained during exercise from an average of 36 to 48% (P less than 0.001). EF in normal subjects was unchanged by TNG. Thus, exercise can cause abnormalities in left ventricular regional function and ejection fraction in patients with or without symptoms; these abnormalities can be mitigated by prophylactic TNG.     

Global and regional left ventricular ejection fraction abnormalities during exercise in patients with silent myocardial ischemia

Sixteen asymptomatic patients with coronary artery disease and silent myocardial ischemia were studied with exercise radionuclide ventriculography. Radionuclide ventriculograms were analyzed for changes in ejection fraction globally and in three regions. Results were compared with radionuclide ventriculograms in 24 symptomatic patients. Both groups (silent myocardial ischemia and angina) were similar in prevalence of multivessel disease and previous myocardial infarction, as well as in age and sex. Global ejection fraction decreased by 0.06 in both groups during exercise; regional ejection fraction also decreased by similar amounts in the two groups. Furthermore, the percent of regions with normal ejection fraction at rest that demonstrated a decrease during exercise was identical: 19 (60%) of 33 versus 26 (60%) of 46. These exercise radionuclide ventriculographic results suggest that abnormalities in regional and global left ventricular wall motion are similar in patients with coronary artery disease with and without silent myocardial ischemia.     

Exercise echocardiography after stabilization of unstable angina: correlation with exercise thallium-201 single photon emission computed tomography.

The diagnostic usefulness of predischarge exercise echocardiography in 35 patients with unstable angina who responded to medical therapy was correlated with exercise thallium-201 single photon emission computed tomography (TI-SPECT) performed, on the average, three days after the exercise echocardiography. None of the patients had myocardial infarction prior to hospitalization or before TI-SPECT and none had left bundle-branch block on their rest electrocardiogram (ECG). Exercise echocardiography was positive in 21 patients and TI-SPECT in 24. The results of the two techniques were concordant in 28 of 35 patients (agreement = 80%, k = 0.57 +/- 0.14, p less than 0.001). Wall-by-wall comparison of the distribution of exercise-induced wall motion abnormalities with reversible thallium defects showed complete or partial correlation in all of 19 patients in whom both the tests were positive. A positive exercise ECG and positive exercise echocardiography identified 11 of 11 patients with angiographically verified significant coronary artery disease (CAD) and 11 of 12 patients (92%) with positive TI-SPECT. Thus, exercise echocardiography is a valuable addition to routine predischarge exercise test in the noninvasive diagnosis of myocardial ischemia and shows a good correlation with TI-SPECT in detecting and localizing ischemia in patients with unstable angina stabilized on medical therapy.     

Treatment of unstable angina pectoris.

Unstable angina pectoris may be manifested as new-onset angina, a change in the anginal pattern, pain at rest with associated electrocardiographic (ECG) changes, or postinfarction angina. Of these, pain at rest with ischemic ECG changes is known to be associated with the poorest prognosis. The pathogenesis of unstable angina pectoris involves a combination of a fixed atherosclerotic obstruction and a dynamic component related to coronary vasoconstriction, thrombus formation, or both. Long-acting nitrates, inhibitors of platelet aggregation, beta blockers, and calcium antagonists are among the agents that have been shown to be effective in the medical management of unstable angina. A study now in progress is evaluating the routine use of thrombolytic therapy for this indication. Although alleviation of symptoms and prevention of death and myocardial infarction are important therapeutic goals, the overall efficacy of a particular medical therapy can best be assessed by objective evaluation of its ability to control ischemia, using such techniques as exercise scintigraphy and ambulatory ECG monitoring. Cardiac catheterization and revascularization are indicated for patients with unstable angina who continue to experience symptoms or who show evidence of silent ischemia despite medical therapy. A study is under way to determine the advisability of routine revascularization of such patients. Revascularization will provide symptomatic relief in most patients with unstable angina and may prolong survival and improve left ventricular function in certain subsets.