Comparative study of exercise-induced ventricular arrhythmias in normal subjects and patients with documented coronary artery disease.

The incidence, types and patterns of emergence of treadmill exercise induced ventricular arrhythmias were studied in 482 subjects with and without coronary heart disease. All subjects were free of premature ventricular complexes at rest and were classified into groups on the basis of their clinical status. In Group 1A were 141 patients with chest pain and normal coronary arteriograms and in Group IB 144 age-matched subjects free of clinical evidence of heart disease. Group II consisted of 197 patients with chest pain and arteriographically documented coronary artery disease. Patients in Group IA and II exercised to at least 85% of their predicted maximal heart rate or until chest pain occurred. Subjects in Group IB underwent maximal exercise testing. The total incidence of exercise-induced ventricular arrhythmias was 16% in Group IA, 44% in Group IB and 29% in Group II. However, when exercise heart rate at the time of appearance of ventricular arrhythmias was taken into account the incidence of exercise-induced ventricular arrhythmias up to a heart rate of 130/min was 27% in the patients with documented coronary artery disease (Group II) compared with rates of 9 and 6%, respectively, for Groups IA and IB (P less than 0.001). The incidence rates of multifocal ventricular premature complexes, ventricular tachycardia and ventricular premature complexes at a rate of more than 10/min were also significantly greater at submaximal heart rates in the patients with coronary disease. Patients with three vessel coronary artery disease and abnormal left ventricular wall motion had a significantly greater incidence of exercise-induced ventricular arrhythmias. The incidence of exercise-induced ventricular arrhythmias in patients with coronary disease and a positive S-T segment response was not significantly increased.     

Exercise and the Risk of Sudden Cardiac Death

Sports activity may precipitate acute fatalities in both adults and young competitive athletes with concealed heart diseases. However, the risk-benefit ratio of physical exercise differs among these two age groups. In adolescents and young adults, competitive physical exercise is associated with a significant increase of the risk of sudden death. Sports is not "per se" cause of the enhanced mortality in this age group; rather, it acts as a trigger of cardiac arrest in those athletes who are affected by silent cardiovascular conditions, mostly cardiomyopathy, premature coronary artery disease and congenital coronary anomalies, which predispose to life-threatening ventricular arrhythmias during physical exercise. In adults, on the other hand, physical activity can be regarded as a "two-edged sword": vigorous exertion increases the incidence of acute coronary events in individuals who did not exercise regularly, whereas habitual physical activity reduces the overall risk of myocardial infarction and sudden coronary death by preventing development of coronary artery disease and progression of coronary atherosclerotic lesions.     

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.     

Diagnostic and prognostic significance of exercise-induced premature ventricular complexes in men and women: a four year follow-up

Two hundred eighty patients (197 men and 83 women) with normal rest electrocardiograms and no history of prior myocardial infarction were referred for evaluation of chest pain. It was found that exercise-induced premature ventricular complexes had a lower sensitivity, specificity, positive predictive value and negative predictive value in predicting significant coronary artery disease than exercise-induced ST segment depression greater than or equal to 1 mm. The incidence of exercise-induced premature ventricular complexes was not significantly different in patients with no significant coronary artery disease, single vessel disease or multivessel disease. The site of origin of exercise-induced premature ventricular complexes was not helpful in predicting the presence or severity of coronary artery disease. At a mean follow-up period of 47.1 months, exercise-induced premature ventricular complexes did not predict coronary events (cardiac death or nonfatal myocardial infarction) in men or women.     

Ventricular arrhythmias and Q-Tc interval during stress-ECG

Q-T prolongation is well-known to be related to ventricular arrhythmias in a number of clinical circumstances. The purpose of this study was to determine whether heart rate corrected Q-T interval (QTc) may indicate susceptibility to ventricular arrhythmias during stress testing. QTc was determined at rest, during submaximal and maximal bicycle work load in normals and patients with remote myocardial infarction, documented coronary artery disease (CAD) and in a group of patients with different cardiac diseases and premature ventricular beats during exercise testing (PVC). Ventricular arrhythmias were graded according to Lown. Q-Tc interval significantly increased in all groups of those patients having complex ventricular arrhythmias (Lown greater than or equal to III). In patients with ischemic S-T segment depression during stress testing, QTc was only lengthened if complex ventricular arrhythmias were present. Q-Tc lengthening in stress testing is assumed to be associated with occurrence of ventricular premature beats rather than ischemia. There is evidence that abnormal repolarization due to imbalance of the autonomic nervous system induces ventricular arrhythmias. Monitoring of Q-Tc interval during stress testing is warranted and may be useful to predict future cardiac events such as sudden cardiac death.     

Long-term prognosis of vasospastic angina without significant atherosclerotic coronary artery disease

Long-term prognosis of 90 patients with vasospastic angina without significant coronary artery disease (less than 50% reduction in luminal diameter) was examined for a mean follow-up period of 4 years. All patients had episodes of angina at rest and were treated with calcium antagonists. One patient developed myocardial infarction and 2 died suddenly during the follow-up period. In the patient with myocardial infarction, there was an abrupt worsening of angina prior to the infarction despite therapy with a calcium antagonist. One of the sudden death patients discontinued his calcium antagonist before his death. Of the sudden death patients, one had ventricular tachycardia and the other had a complete atrioventricular block during an anginal attack. The incidence of such serious arrhythmias was higher (p less than 0.01) in sudden death patients (2/2) than that in survivors (6/88). The treatment with calcium antagonists reduced the severity and frequency of angina in all patients. These results suggest that long-term prognosis of vasospastic angina without significant coronary artery disease is good as characterized by the low incidence of myocardial infarction and death and the favorable response to treatment with calcium antagonists.     

Evaluation of cardiac arrhythmias by exercise testing.

Exercise testing is an important noninvasive method for the exposure of arrhythmias. It provides complementary information to that obtained from ambulatory monitoring or electrophysiologic testing. By producing a number of important physiologic changes, especially activation of the sympathetic nervous system and an increase in circulating catecholamines, exercise testing provides a more complete assessment. On continuous monitoring, exercise-induced ventricular premature beats may be found in up to 34% of healthy subjects, in 60 to 70% of those with heart disease and in all patients who have experienced sustained ventricular tachycardia. Couplets or nonsustained ventricular tachycardia can be found during exercise in 0 to 6% of healthy subjects, in 15 to 31% of patients with heart disease and in 75% of those with sustained ventricular tachycardia. Even in patients with heart disease, there is only a small risk of inducing sustained ventricular tachycardia or ventricular fibrillation during exercise. The prognostic relevance of exercise-induced ventricular arrhythmias in patients with coronary artery disease or cardiomyopathy has not been clearly established. There appears to be an increased risk, however, in patients with ventricular premature beats as well as ST-segment depression or in patients with repetitive forms of ventricular arrhythmias during exercise which cannot be medically controlled. In healthy subjects, exercise-induced ventricular premature beats are of no prognostic relevance. In particular, for patients in whom arrhythmias are induced by exercise, exercise testing should be used to assess the effectiveness of antiarrhythmic drug treatment. Importantly, serious cardiac toxicity, often not observed at rest or during routine activities, may become apparent during exercise testing. It should be a standard part of arrhythmia assessment and management.     

Functional changes of ventricular late potentials by provocation with increase of heart rate. Evaluation during atrial pacing.

BACKGROUND: Standard methods fail to reveal late potentials in 20 to 30% of patients with ventricular arrhythmias after myocardial infarction. However, these patients may develop transient delayed ventricular activation during increases in heart rate. METHODS AND RESULTS: Atrial pacing was performed, at the rates of 100 min-1 and 120 min-1, in 50 patients after myocardial infarction. Twenty-six patients had a history of documented, sustained ventricular tachycardia, 12 had a history of ventricular fibrillation and 12 no history of ventricular arrhythmias. The low-noise surface electrocardiogram was analysed before and during atrial pacing in the time and frequency domains. Fifteen of 26 patients with ventricular tachycardia, four of 12 with ventricular fibrillation and three of 12 without ventricular arrhythmias experienced late potentials during sinus rhythm. Atrial pacing led to a shift of 26 +/- 15 ms of preexistent late potentials into the ST segment, this being greater in patients with anterior infarctions and to an increase in magnitude in patients with inferior infarctions. In patients without late potentials during sinus rhythm, atrial pacing provoked late potentials in eight of 11 patients with ventricular tachycardia, in four of eight patients with ventricular fibrillation and in one of nine patients without ventricular arrhythmias. Low amplitude signals (LAS) were increased in patients after inferior and filtered QRS in patients after anterior infarction. In 10 patients without cardiac disease no late potentials were detectable in the time and frequency domain either at rest or during increased heart rate. CONCLUSIONS: Increase in heart rate may unmask late potentials in patients prone to malignant ventricular arrhythmias. Therefore, functional late potential analysis with non-invasive clinical stress tests, i.e. exercise tests, should be performed only with an adequate rate response. This might identify patients at risk of malignant ventricular arrhythmias otherwise not identified with conventional late potential analysis.     

The incidence, significance and prognosis of arrhythmias in acute myocardial infarction.

Concepts of the incidence, significance and prognosis of almost all cardiac arrhythmias during acute myocardial infarction have changed greatly in the last 15 years. In some cities facilities are available to reach patients in the very earliest phases of ischaemia or infarction. As previously suspected but now confirmed, ventricular fibrillation occurs commonly at this time and depending on whether ischaemia or infarction is the basis of its occurrence, has a variable long-term prognosis. In the coronary care unit ventricular arrhythmias are more frequent than was originally believed and current research suggests that they have little if any predictive value in defining individuals who would develop ventricular fibrillation. Such events, however, appear related to the severity of myocardial or coronary artery disease. Similarly, asystole and heart block in acute myocardial infarction are important causes of mortality through their association with severe underlying disease. Other cardiac arrhythmias are not infrequent in acute myocardial infarction. They may carry an immediate prognostic implication for the patient but rarely have long-term implications. Autonomic nervous system disturbances may underlie many arrhythmias occurring particularly in the earliest phases of infarction.     

Prognostic value of resting and submaximal exercise radionuclide ventriculography after acute myocardial infarction in high-risk patients with single and multivessel disease

In patients who survive the acute phase of myocardial infarction, those with multivessel coronary artery disease generally have a worse prognosis than those with single-vessel disease. However, some patients with significant multivessel stenoses have a good prognosis, whereas some with a significant single-vessel stenosis have a poor prognosis. Thus, although definition of coronary anatomy may be helpful, it is a not a fail-safe prognosticator. In this retrospective analysis, the association of abnormalities at rest and during submaximal exercise testing with radionuclide ventriculography after acute myocardial infarction with major cardiac complications (death, recurrent infarction, severe angina or congestive heart failure) in the ensuing 6 months was assessed in patients with single and multivessel disease. Coronary angiography and submaximal exercise testing with radionuclide ventriculography were performed within 3 months of each other in 42 patients. Eleven of the 16 patients with single-vessel coronary stenosis had major cardiac complications. The subsequent course of these 16 patients was correctly predicted by left ventricular ejection fraction (LVEF) ≤ 0.40 in 8 patients, by LVEF < 0.55 in 7 patients, by failure of LVEF to increase by 0.05 units in 13 patients, and by an increase in left ventricular end-systolic volume index (LVESVI) during exercise >5% above baseline in 11 patients. Of the 26 patients with multivessel coronary artery disease, 24 had major cardiac complications. The subsequent course of these 26 patients was correctly predicted in 13 by LVEF ≤ 0.40, in 20 by LVEF < 0.55, in 25 by a failure of LVEF to increase by 0.05 units during exercise, and in 20 by an increase in LVESVI by > 5% during exercise. Thus, submaximal exercise testing with radionuclide ventriculography may provide valuable prognostic information concerning the occurrence of major cardiac events after myocardial infarction not only in patients with multivessel disease, but also in those with single-vessel disease. Exercise-induced abnormalities of left ventricular function may have greater prognostic importance than the delineation of coronary arterial anatomy or the assessment of residual left ventricular function at rest.     

Predictors of survival and sudden death in patients with stable severe congestive heart failure due to ischemic and nonischemic causes: a prospective long term study of 200 patients

This prospective study of 200 stable outpatients with New York Hospital Association (NYHA) class III congestive heart failure on maximal medical therapy was done to determine which factors affect survival, to record the incidence of sudden death, and to identify prognostic features which characterize patients at high risk of sudden death. Congestive heart failure was due to coronary artery disease in 151 patients (76%). After an average follow-up of 40 months, 96 patients (48%) had died: 30 (15%) suddenly, 41 (22%) of low output, and 25 (13%) of other causes. Of the 30 patients dying suddenly 12 had autopsies, and acute myocardial infarction was found in nine. Of the 41 patients dying of low output 15 had autopsies, and recent myocardial infarction was found in five. Nine of the 25 patients dying of other causes died of acute myocardial infarction. Multivariate stepwise analysis revealed that severity of ventricular arrhythmias (modified Lown classification), exercise tolerance and left ventricular ejection fraction were the most important determinants of survival. In patients with coronary artery disease, complex ventricular arrhythmias detected by ambulatory Holter monitoring were frequent in all groups and were not clinically useful in predicting which of these patients were at a higher risk of dying suddenly. In contrast, patients without coronary artery disease who died suddenly had a higher incidence of nonsustained ventricular tachycardia and a tendency towards more frequent ventricular arrhythmias in general. The authors conclude that in ambulatory patients with stable NYHA class III heart failure, the severity of ventricular arrhythmias is a predictor of survival.(ABSTRACT TRUNCATED AT 250 WORDS)     

S-T segment elevation during exercise: Electrocardiographic and arteriographic correlation in 38 patients

The clinical significance and underlying mechanisms of S-T segment elevation during exercise were evaluated by correlating the exercise-induced S-T elevation with the coronary arteriograms and left ventriculogram in 38 patients. Of these, 37 (97 percent) showed significant coronary artery disease; 71 percent of these had proximal lesions. Of 27 patients with old myocardial infarction manifested in the electrocardiogram at rest, 25 had significant coronary artery disease and a ventricular aneurysm. All 11 patients with no previous myocardial infarction in the electrocardiogram at rest had significant coronary artery disease but only 2 (18 percent) had a ventricular aneurysm. One patient had a ventricular aneurysm without coronary artery disease. The sites of S-T elevation correctly localized the area of ventricular aneurysm of 30 (91 percent) of 33 instances and the area of the compatible diseased vessels in 38 (95 percent) of 40 instances.Our data suggest that (1) S-T elevation during exercise in the absence of a pattern of previous myocardial infarction in the electrocardiogram at rest indicates significant proximal coronary artery disease without ventricular aneurysm, whereas in the presence of such a pattern it is indicative of both ventricular aneurysm and significant proximal coronary artery disease; (2) the sites of S-T elevation accurately identify the location of ventricular aneurysm and the compatible diseased vessels; and (3) ischemia and abnormal wall motion may independently or additively underlie the mechanism for S-T elevation during exercise.     

Hyperkinetic ventricular arrhythmia during the treadmill test in chronic ischemic heart disease

Aim of this study was to evaluate the pattern of onset and the characteristics of ventricular arrhythmias (VA) observed during treadmill test (TT) in patients with chronic ischemic heart disease (CIHD). Two groups of patients with CIHD were retrospectively compared: group A consisted of 120 consecutive patients with premature ventricular beats (PVBs) either isolated (greater than 2/min) or repetitive during exercise, or maximal exercise, or recovery; group B consisted of 140 consecutive patients without PVBs during TT. The two groups were comparable in mean age, male/female ratio, incidence of previous myocardial infarction, of previous coronary artery by-pass graft or of percutaneous transluminal coronary angioplasty. There were no significant differences between the two groups regarding the parameters evaluated during TT: duration of exercise, maximal heart rate, heart rate-systolic blood pressure product as well as in the percentage of positive tests for acute myocardial ischemia (51.6% vs 40.7%). In the two subgroups of patients who underwent coronary arteriography and left ventricular angiography (24/120 and 23/140 patients respectively) no differences were found in the number and distribution of critical coronary stenosis and of dyskinetic or akinetic areas. In both groups A and B the QTc interval at maximal exercise was significantly longer than its value at rest (p less than 0.001), but there was no relevant difference between the two groups. In group A patients with VA during maximal exercise (n = 60) showed a higher prevalence of complex VA (class Lown greater than or equal to 3) compared to the others (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of coronary artery spasm in ischemic heart disease. Therapeutic implications

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)     

Ventricular arrhythmias in ischemic heart disease

Ventricular arrhythmias remain the leading cause of death from coronary artery disease. This review summarizes current thinking in several areas relating to the pathophysiology, prognosis, and therapy of ventricular arrhythmias associated with acute and chronic coronary artery disease syndromes. The experimental basis of arrhythmias in the setting of acute myocardial ischemia and chronic myocardial infarction is described, stressing the important pathophysiologic differences between these two conditions. The effects of the autonomic nervous system as a key modulator of ischemic arrhythmogenesis are discussed. Insights, derived from endocardial mapping studies, into the nature of ventricular tachycardia in humans with chronic myocardial infarction are described, including implications for risk stratification and therapy to prevent arrhythmia recurrence. Current therapeutic principles are discussed in the management of ventricular arrhythmias associated with coronary artery disease, including pharmacologic approaches, surgical and catheter ablation, and automatic implantable cardioverting and defibrillating devices.     

Prognostic implications of asymptomatic ventricular arrhythmias: the Framingham Heart Study.

OBJECTIVE: To evaluate the prevalence and prognostic significance of asymptomatic complex or frequent ventricular premature beats detected during ambulatory electrocardiographic (ECG) monitoring. DESIGN: Cohort study with a follow-up period of 4 to 6 years. SETTING: Population-based. PARTICIPANTS: Surviving patients of the original Framingham Heart Study cohort and offspring of original cohort members (2727 men and 3306 women). MEASUREMENTS: One-hour ambulatory electrocardiography. RESULTS: The age-adjusted prevalence of complex or frequent arrhythmia (more than 30 ventricular premature complexes per hour or multiform premature complexes, ventricular couplets, ventricular tachycardia, or R-on-T ventricular premature complexes) was 12% (95% Cl, 11% to 13%) in the 2425 men without clinically evident coronary heart disease and 33% (Cl, 24% to 42%) in the 302 men with coronary heart disease. The corresponding values in women (3064 without disease and 242 with disease) were 12% (Cl, 11% to 13%) and 26% (Cl, 9% to 43%). After adjusting for age and traditional risk factors for coronary heart disease in a Cox proportional hazards model, men without coronary heart disease who had complex or frequent ventricular arrhythmias were at increased risk for both all-cause mortality (relative risk, 2.30; Cl, 1.65 to 3.20) and the occurrence of myocardial infarction or death from coronary heart disease (relative risk, 2.12; Cl, 1.33 to 3.38). In men with coronary heart disease and in women with and without coronary heart disease, complex or frequent arrhythmias were not associated with an increased risk for either outcome. CONCLUSIONS: In men who do not have clinically apparent coronary heart disease, the incidental detection of ventricular arrhythmias is associated with a twofold increase in the risk for all-cause mortality and myocardial infarction or death due to coronary heart disease. The preventive and therapeutic implications of these findings await further investigation.     

Natural history and prognosis of ischemic heart disease

Forty-four cases with myocardial rupture (33 with free wall rupture, 9 with interventricular septal perforation and 2 with papillary muscle rupture), all of which were ascertained by autopsy and/or at surgery, were analyzed. When the following 7 risk factors were actively managed in the acute stage of myocardial infarction, the incidence of myocardial rupture was significantly reduced: a) high blood pressure on admission, b) physical and emotional instability, c) recurrent chest pain, d) aged females, e) no history of angina or myocardial infarction, f) large myocardial infarction on ECG and g) the first 10 days after the attack of myocardial infarction. If cardiogenic shock occurs, surgery should be performed as soon as possible; if not, it should be delayed 3 weeks. The natural history of ischemic heart disease was analyzed in 400 medically-treated patients with significant coronary artery disease. They had been followed up continuously and periodically for more than one year. The prognosis of the patients with 3-vessel disease or left main trunk disease, those with poor left ventricular function (EF less than 30%) and of old age (greater than or equal to 60) and those who had a history of ischemic heart disease was poor. Follow-up study was done in 30 patients with variant angina. They often had life-threatening arrhythmias during attacks (8 ventricular tachycardia or ventricular fibrillation, 8 serious bradyarrhythmia). All patients with variant angina should be treated medically at first, and only patients with organic coronary artery disease and chest pain on effort in spite of the medical treatment should be considered as candidates for AC bypass surgery.     

Submaximal exercise testing early after myocardial infarction. Difficulty of predicting coronary anatomy and left ventricular performance

Impaired left ventricular function and extensive coronary artery disease are important determinants of prognosis after acute myocardial infarction. The ability of clinical and predischarge submaximal exercise test variables to predict multivessel coronary artery disease and impaired left ventricular function was assessed in 62 survivors of acute myocardial infarction. Abnormal exercise blood pressure response and short exercise performance were predictors of multivessel disease, but exercise induced ST segment changes and clinical variables were not. Q wave infarction, high grade Killip classification, and exercise induced ST segment elevation predicted statistically significant impairment of resting left ventricular function, whereas other clinical and exercise test variables did not. Exercise induced ST segment changes were therefore of little value in detecting extensive coronary disease, although exercise induced ST elevation was an indicator of poor resting left ventricular function. Although abnormal exercise haemodynamics may detect extensive coronary artery disease, other physiological markers of reversible myocardial ischaemia are probably necessary to plan optimal management in these patients.     

Submaximal exercise testing early after myocardial infarction. Difficulty of predicting coronary anatomy and left ventricular performance.

Impaired left ventricular function and extensive coronary artery disease are important determinants of prognosis after acute myocardial infarction. The ability of clinical and predischarge submaximal exercise test variables to predict multivessel coronary artery disease and impaired left ventricular function was assessed in 62 survivors of acute myocardial infarction. Abnormal exercise blood pressure response and short exercise performance were predictors of multivessel disease, but exercise induced ST segment changes and clinical variables were not. Q wave infarction, high grade Killip classification, and exercise induced ST segment elevation predicted statistically significant impairment of resting left ventricular function, whereas other clinical and exercise test variables did not. Exercise induced ST segment changes were therefore of little value in detecting extensive coronary disease, although exercise induced ST elevation was an indicator of poor resting left ventricular function. Although abnormal exercise haemodynamics may detect extensive coronary artery disease, other physiological markers of reversible myocardial ischaemia are probably necessary to plan optimal management in these patients.     

Long-term prognosis of Kawasaki disease patients with coronary artery obstruction

Summary The prognosis of coronary artery obstruction was studied in patients with Kawasaki disease. Between May 1973 and December 1987, coronary artery obstruction was diagnosed by coronary angiography in 30 patients (21 males, 9 females), of whom, only 8 (26.7%) had clinical symptoms. One patient died after 9 years of illness. Two complained of frequent chest pain, which disappeared after bypass surgery in one case and spontaneously in the other. Five had symptomatic myocardial infarction. Myocardial ischemia was diagnosed in 31.8% by treadmill stress testing, but was well demonstrated in 85.7% by thallium-201 myocardial tomography. Frequent ventricular premature beats, Wenckebachtype atrioventricular block, and ST-segment depression accompanied by chest pain were recognized by 24-h Holter monitoring. In the past, the methods used to determine the prognosis of Kawasaki disease patients with coronary artery obstruction were not adequate. However, the examinations used in this study revealed an improved ability to determine the prognosis in this disease. Myocardial tomography, in particular, provided a more accurate evaluation of myocardial damage. Ventricular arrhythmias seem to be a serious problem in these patients. Therefore, careful observation using these tests, especially myocardial tomography and Holter monitoring, should be done even if the patients are free of symptoms.