Transient myocardial ischaemia after acute myocardial infarction.

The prevalence and characteristics of transient myocardial ischaemia were studied in 203 patients with recent acute myocardial infarction by both early (6.4 days) and late (38 days) ambulatory monitoring of the ST segment. Transient ST segment depression was much commoner during late (32% patients) than early (14%) monitoring. Most transient ischaemia (greater than 85% episodes) was silent and 80% of patients had only silent episodes. During late monitoring painful ST depression was accompanied by greater ST depression and tended to occur at a higher heart rate. Late transient ischaemia showed a diurnal distribution, occurred at a higher initial heart rate, and was more often accompanied by a further increase in heart rate than early ischaemia. Thus in the first 2 months after myocardial infarction transient ischaemia became increasingly common and more closely associated with increased myocardial oxygen demand. Because transient ischaemic episodes during early and late ambulatory monitoring have dissimilar characteristics they may also have different pathophysiologies and prognostic implications.     

Transient ischaemia after acute myocardial infarction: relationship to exercise ischaemia

To study the implications of transient myocardial ischaemia following acute myocardial infarction we compared ambulatory ST segment monitoring with exercise treadmill testing in 170 patients (mean age 58 years) at 4-8 weeks after admission. Ambulatory monitoring detected transient ischaemia (265 episodes; 249 (94%) silent) in 53/170 patients (31%) which was less frequent than ischaemia during exercise testing (90 patients; 53%) (P less than 0.0001). However, patients displaying transient ambulatory ischaemia (i) achieved less total exercise (248.7 +/- 17.2 vs 318.7 +/- 14.1 s; means +/- SEM) (P less than 0.006), (ii) developed exercise ST deviation earlier (172.4 +/- 14.3 vs 244.8 +/- 16.2 s) (P less than 0.0004) and (iii) had more widespread exercise ischaemia (3.8 +/- 0.3 vs 2.5 +/- 0.2 ECG leads) (P less than 0.005). Positive ambulatory ST segment monitoring was infrequently found (12/80 patients; 15%) in the presence of a negative exercise test but did identify the majority of patients (9/11 patients; 82%) with easily provoked exercise ischaemia and hence strongly positive exercise tests. These data suggest a limited role for routine 24 h ambulatory monitoring after myocardial infarction for the diagnosis of ongoing ischaemia but raise the possibility of an important place for this test in prognosis and risk stratification.     

Transient myocardial ischaemia after acute myocardial infarction does not induce ventricular arrhythmias.

OBJECTIVE--To see whether transient myocardial ischaemia on ambulatory monitoring after myocardial infarction is associated with ventricular arrhythmias. DESIGN--A prospective study. SETTING--The coronary care unit, general medical wards, and cardiorespiratory department of a major teaching hospital. PATIENTS--203 consecutive patients without specific exclusion criteria admitted with acute myocardial infarction. INTERVENTIONS--24 hour ambulatory electrocardiographic monitoring for ventricular arrhythmias and ST depression both early (mean 6.3 days after infarction, n = 201) and late (mean 38 days, n = 177). MAIN OUTCOME MEASURES--Episodes of myocardial ischaemia were identified during ambulatory monitoring by transient ST depression of > or = 1.0 mm lasting for > or = 30 s. Ventricular arrhythmias were single extrasystoles, couplets, or ventricular tachycardia. RESULTS--All ventricular arrhythmias were significantly more frequent in late than early monitoring. The arrhythmias included couplets (in 83/174 (48%) v 49/200 (25%) of patients, p = 0.0000028) and ventricular tachycardia (29/174 (17%) v 15/199 (8%), p = 0.0064). Patients with ST depression (29 early; 56 late), compared with those without ischaemia, did not experience a significant increase in single extrasystoles, couplets (31% v 23% early; 47% v 48% late), or ventricular tachycardia (3% v 8% early; 18% v 16% late). Even patients with frequent (> or = 3 episodes), and deep (> or = 1.5 mm) or prolonged (> or = 20 min) ST depression had no increase in arrhythmias. CONCLUSIONS--Ventricular arrhythmias after myocardial infarction are not associated with transient myocardial ischaemia during daily activities. This study does not support the belief that to abolish silent ischaemia would reduce the incidence of sudden death due to uncontrollable ventricular arrhythmias after myocardial infarction.     

Arterial counterpulsation in continuing myocardial ischaemia after acute myocardial infarction

Twenty-six patients underwent arterial counterpulsation for refractory heart failure without shock complicating acute myocardial infarction. Patients were divided into a group of 12 with continuing myocardial ischaemia, evidenced by anginal pain associated with abnormal ST segment elevation, and a group of 14 without continuing ischaemia. Clinical features (apart from pain) and prognostic indices were similar in the two groups when counterpulsation was started but short- and long-term results were different. Hospital survival was 92 per cent (11/12) and 43 per cent (6/14), respectively, in the groups with and without ischaemia and four-year survival was 73 per cent and 7 per cent. Counterpulsation is of greatest value in acute infarction when used to relieve myocardial ischaemia.     

Arterial counterpulsation in continuing myocardial ischaemia after acute myocardial infarction.

Twenty-six patients underwent arterial counterpulsation for refractory heart failure without shock complicating acute myocardial infarction. Patients were divided into a group of 12 with continuing myocardial ischaemia, evidenced by anginal pain associated with abnormal ST segment elevation, and a group of 14 without continuing ischaemia. Clinical features (apart from pain) and prognostic indices were similar in the two groups when counterpulsation was started but short- and long-term results were different. Hospital survival was 92 per cent (11/12) and 43 per cent (6/14), respectively, in the groups with and without ischaemia and four-year survival was 73 per cent and 7 per cent. Counterpulsation is of greatest value in acute infarction when used to relieve myocardial ischaemia.     

Socioeconomic differentials in recurrent ischaemia and mortality after acute myocardial infarction

OBJECTIVE—To examine the influence of socioeconomic deprivation on case fatality following acute myocardial infarction.
DESIGN—Prospective cohort observational study.
SETTING—General hospital.
PATIENTS—1417 white and south Asian patients admitted with acute myocardial infarction between January 1988 and December 1996, and classified by the Carstairs socioeconomic deprivation score of the enumeration district of residence.
MAIN OUTCOME MEASURES—30 day and one year survival.
RESULTS—There was little variation across deprivation groups in age, sex, or smoking status, though a higher proportion of patients from more deprived enumeration districts were diabetic and of south Asian origin, and a higher proportion of them developed Q wave infarction and left ventricular failure. There was no appreciable variation in clinical treatment with deprivation. Patients from more deprived enumeration districts had a higher risk of recurrent ischaemic events (death, recurrent myocardial infarction, or unstable angina) over the first 30 days: event free survival (95% confidence interval (CI)) of the most deprived quartile was 0.79 (95% CI 0.74 to 0.83) compared with 0.85 (95% CI 0.80 to 0.88) in the least deprived quartile. The unadjusted hazard ratio corresponding to an increase from the 5th to 95th centile of the deprivation distribution was 1.54 (95% CI 1.02 to 2.32), and 1.59 (95% CI 1.03 to 2.44) after adjustment for age, sex, racial group, diabetes, acute treatment with thrombolysis and aspirin, and left ventricular failure. Survival from 30 days to one year, however, did not show a socioeconomic gradient (hazard ratio adjusted for the same variables was 1.07 (95% CI 0.68 to 1.70)).
CONCLUSIONS—In patients hospitalised with acute myocardial infarction, there is a strong association between early recurrent ischaemic events and socioeconomic deprivation that is not accounted for by clinical presentation or treatment. This association appears to be attenuated over time.


     

Exercise-induced symptomatic ischaemia predicts a poor long-term prognosis after acute myocardial infarction

STUDY OBJECTIVES: To evaluate the long-term prognostic significance of symptomatic ischaemia during exercise testing performed 3 weeks after acute myocardial infarction (AMI). DESIGN: A prospective study with long-term follow-up. SETTING: A Cardiac Rehabilitation Clinic in a University Hospital. SUBJECTS: A total of 446 patients were allowed to perform exercise testing 3 weeks after AMI and followed for 72 +/- 20 months. MEASUREMENTS AND RESULTS: Patients were divided into three groups according to whether they had no ECG evidence of ischaemia during exercise testing (334 patients), silent ischaemia (90 patients) or symptomatic ischaemia (22 patients). Cardiac death was significantly more frequent in patients with symptomatic ischaemia when compared with silent ischaemia (31.8% vs. 7.8%, P < 0.01) or when compared with no ischaemia (31.8% vs. 10.2%, P < 0.01). The three groups had a low cardiac mortality during the first 48 months of follow-up. The prognosis of patients with symptomatic ischaemia worsens markedly thereafter. The results of exercise testing did not predict recurrence of myocardial infarction. Coronary revascularization was performed in 34.4% of those without ischaemia, 47.8% of those with silent ischaemia and 45.5% of those with symptomatic ischaemia (P < 0.01). CONCLUSIONS: Patients with symptomatic ischaemia have a good prognosis during the first 4 years of follow-up. Their prognosis worsens thereafter as opposed to patients with or without silent ischaemia. This high-risk group of patients with symptomatic ischaemia deserves optimal management including revascularization when appropriate.     

Prognostic significance of silent myocardial ischaemia during maximal exercise testing after a first acute myocardial infarction

Clinical, exercise, and angiographic variables, and long-termfollow-up were compared in patients, who, during maximal Bruceexercise testing after a first acute myocardial infarction (AMI),had positive responses to exercise testing (n = 116, 38% of303) with (n % 23, group I) or without (n = 93, group II) angina.Group I patients more often (52 vs 19%, P < 0.001) had ahistory of pre-infarction angina. Group II had a greater proportion(75 vs 52%, P < 0.05) of inferior wall AMI, whereas groupI had a greater proportion (30 vs 19%, P < 0.01) of non-Qwave AMI. Total exercise duration was significantly (P <0.01) longer in group II (7.6 ± 3.2 vs 5.5 ± 3.1min). Maximal exercise heart rate (144 ± 22 vs 133 ±21, beats . min^–1 P < 0.05 was also higher in groupII. A greater proportion of group II patients (37 vs 9%, P <0.05) had single-vessel disease, whereas multivessel diseasewas more common (91 vs 63% P < 0.03) in group I. Left ventricularfunction was similar in both groups. During follow-up (48 ±22 months) the incidence of cardiac death (group I, 3.3%, groupII, 4.8%), of recurrent infarction (group I, 4.8%, group II3.3%), and of revascularization procedures (group I, 28.5%,group II, 19.8%) were similar in both groups. Although asymptomaticexercise-induced ischaemia was associated with better exerciseperformance and less extensive coronary disease than symptomaticischaemia, it had the same long-term prognostic implications.     

Magnetic resonance imaging of acute myocardial ischaemia and infarction

Recent developments in cardiac magnetic resonance imaging (MRI) have led to tremendous breakthroughs in the imaging of acute myocardial ischaemia and infarction. Hardware and acquisition sequences have improved image quality while simplifying cardiac examinations. Cine-MRI allows for accurate time-resolved imaging of global and segmental left ventricular (LV) function with high spatial resolution. Dynamic multislice MRI of myocardial perfusion is now widely available allowing for the detection of microvascular obstruction after myocardial infarction (MI) or adding significant diagnostic value over usual clinical and biological markers after non ST elevation coronary syndromes. Direct high-resolution MRI of MI is well standardized with important clinical implications for the diagnosis of myocardial viability. In addition, stress cardiac MRI enables time-resolved analysis of myocardial perfusion under pharmacological stress, or accurate assessment of regional LV function during dobutamine cine-MRI for detection of myocardial ischaemia and/or viability. Non-invasive MR coronary angiography is beyond the scope of this article.     

Early reactivation of ischaemia after abrupt discontinuation of heparin in acute myocardial infarction.

Intravenous heparin after thrombolytic therapy for acute myocardial infarction is an effective, widely used treatment. Six cases of acute myocardial infarction are reported with early disease reactivation following the abrupt discontinuation of heparin infusion three days after alteplase thrombolysis and concomitant aspirin therapy. Immediate reinfusion of heparin resulted in regression of symptomatic ischaemia in all six patients. The activated partial thromboplastin time values, determined four hours before the discontinuation of heparin therapy, were within the therapeutic range in five of the six patients, and no difference was found in the values obtained one hour after the reinfusion of heparin (P = 0.065).     

Unfavourable left ventricular remodelling in patients with dobutamine-inducible ischaemia after acute myocardial infarction.

AIMS: Aim of the study was to assess the role of early inducible ischaemia for determining left ventricular remodelling in patients with acute myocardial infarction. METHODS AND RESULTS: In 179 consecutive patients with first myocardial infarction the occurrence of new wall motion abnormalities during dobutamine stress echocardiography at discharge was related to the left ventricular volume changes at 6 months. Left ventricular end-diastolic and end-systolic index volumes (mL/m(2)) were echocardiographically detected at discharge and at 6 months and the relative changes were calculated. The study population consisted of 105 patients without and 74 patients with inducible ischaemia; of these, 46 patients had > or =4 ischaemic segments. At 6 months, the end-diastolic index volume increased in patients with inducible ischaemia compared to patients without (+7.5+/-11.2 vs -0.1+/-10.2 mL/m(2); P=0.0049) and final mean end-diastolic volume was greater in patients with inducible ischaemia than without (70.8+/-16.0 vs 61.1+/-17.0 mL/m(2); P=0.0012). The end-systolic volume increased at 6 months in patients with inducible ischaemia and it decreased in patients without (+2.8+/-8.6 vs -1.4+/-7.8 mL/m(2); P=0.021). At the multivariate analysis, inducible ischaemia in > or =4 segments (odds ratio=6.43), the wall motion score index at the peak of dobutamine infusion (odds ratio=1.14) and the end-systolic index volume at discharge (odds ratio=1.06) were independent predictors of subsequent left ventricular end-diastolic index volume increase > or =15 mL/m(2). CONCLUSION: In patients with first myocardial infarction the presence and the severity of inducible ischaemia, as detected by dobutamine stress echocardiography at discharge, indicates an unfavourable left ventricular remodelling.     

Determinants of left ventricular systolic function after acute myocardial infarction: the role of residual myocardial ischaemia

BACKGROUND: Left ventricular systolic function (LVSF) is one of the major determinants of survival after acute myocardial infarction (AMI). Some factors such as the infarct size and localization, and the patency of the infarct-related artery are known determinants of LVSF. However, the long-term effect of myocardial ischaemia on LVSF has been poorly studied in clinical settings. OBJECTIVES: To assess the acute and long-term effects of myocardial ischaemia on LVSF in patients recovering from an AMI. METHODS: A cohort of 74 patients recovering from AMI was studied. Myocardial ischaemia was detected by means of ambulatory electrocardiogram (ECG) monitoring at recruitment (4+/-2 days after AMI), exercise ECG test and stress echocardiography at discharge (7+/-4 days after AMI). LVSF was studied by means of two-dimensional echocardiography at recruitment, at discharge, and at 1, 3, 6 and 12 months after AMI. RESULTS: Patients with myocardial ischaemia on ambulatory ECG monitoring and stress echocardiography had worse LVSF at recruitment than those without ischaemia. The presence of myocardial ischaemia on ambulatory ECG monitoring was an independent determinant of LVSF at recruitment together with infarct localization and size (assessed by creatine kinase MB isoenzyme (CK-MB) levels). Patients with signs of myocardial ischaemia on ambulatory ECG monitoring and stress echocardiography had a progressive left ventricular dysfunction compared with those without ischaemia. CONCLUSIONS: Residual ischaemia is an independent determinant of LVSF after AMI and its presence implied a progressive worsening of the LVSF. Because left ventricular systolic dysfunction is a major determinant of survival after AMI, its precursors, among them residual myocardial ischaemia, should be identified. Treatment of ischaemia is known to be associated with improved prognosis and improved LVSF.     

Thrombolysis significantly reduces transient myocardial ischaemia following first acute myocardial infarction.

In order to investigate whether thrombolysis affects residual myocardial ischaemia, we prospectively performed a predischarge maximal exercise test and early out-of-hospital ambulatory ST segment monitoring in 123 consecutive men surviving a first acute myocardial infarction (AMI). Seventy-four patients fulfilled our criteria for thrombolysis, but only the last 35 patients included received thrombolytic therapy. As thrombolysis was not available in our Department at the start of the study, the first 39 patients included were conservatively treated (controls). No significant differences in baseline clinical characteristics were found between the two groups. In-hospital atrial fibrillation and digoxin therapy was more prevalent in controls (P less than 0.05). During exercise, thrombolysed patients reached a higher maximal work capacity compared with controls: 160 +/- 41 vs 139 +/- 34 W (P less than 0.02). Thrombolysis resulted in a non-significant reduction in exercise-induced ST segment depression: prevalence 43% vs 62% in controls. However, during ambulatory monitoring the duration of transient myocardial ischaemia was significantly reduced in thrombolysed patients: 322 min vs 1144 min in controls (P less than 0.05). Thrombolysed patients reached a higher heart rate during transient ischaemic episodes: 114 +/- 17 vs 93 +/- 11 b.min-1 in controls (P less than 0.001). In conclusion, thrombolytic therapy administered for a first AMI significantly reduces the burden of transient myocardial ischaemia. This may explain the improvement in myocardial function during physical activities, which was also observed in this study.     

Enhanced release of atrial natriuretic factor during exercise-induced myocardial ischaemia in patients after acute myocardial infarction.

To determine whether acute myocardial ischaemia induced by dynamic exercise can lead to changes in plasma levels of atrial natriuretic factor, we performed symptom-limited bicycle electrocardiographic tests in 20 males with recent acute myocardial infarction and in 8 control males. Ten patients developed exercise-induced myocardial ischaemia and 10 patients did not. There were no significant differences between the two groups with regard to age, site of myocardial infarction, urinary sodium, atrial sizes, radionuclide left ventricular ejection fraction, workload, baseline and peak-exercise heart rate, baseline and peak-exercise rate-pressure product, duration of exercise. Also baseline atrial natriuretic factor concentrations were similar in both groups (ischaemic patients: 34.51 +/- 15.73 pg/ml; nonischaemic patients: 27.17 +/- 8.74 pg/ml, NS), while peak-exercise atrial natriuretic factor concentrations were higher in patients with exercise-induced myocardial ischaemia (112.31 +/- 35.5 pg/ml) than in the others (80.46 +/- 23.43 pg/ml) (P less than 0.05). After 15 minutes of recovery, plasma atrial natriuretic factor levels were still raised only in the ischaemic patients (63.3 +/- 15.44 pg/ml, P less than 0.01), returning to baseline after 30 minutes in both groups. In control subjects, the behaviour of atrial natriuretic factor resembled that of the patients without exercise-induced ischaemia, with a significant increase at peak-exercise (from baseline levels of 23.1 +/- 10.5 pg/ml to peak-exercise levels of 91.3 +/- 14.5 pg/ml, P less than 0.0005) and a rapid return to baseline levels after 15 minutes of recovery (28.5 +/- 10.6 pg/ml, NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiological effects of acute ischaemia on electrically stable myocardial infarction

The purpose of this study was to examine the effects of acute ischaemia superimposed on an electrophysiologically stable, small myocardial infarction, and to determine the mechanisms of induced ventricular arrhythmias, using a canine infarction model. Ten dogs without inducible ventricular tachycardia or fibrillation on the 7th day post-myocardial infarction (Group 1) and 14 control dogs (Group 2) were subjected to 30 min acute ischaemia by occlusion of the proximal left anterior descending artery. The areas of infarcted myocardium ranged from 1.0 to 20.4% (mean 8.9, SD 7.7) of total left ventricular weight. Ventricular arrhythmias were inducible by programmed electrical stimulation in eight of 10 dogs (80%) after acute ischaemia, but in only one of 14 control dogs (7%) (p less than 0.005). In seven of eight Group 1 dogs, epicardial mapping showed that ventricular arrhythmias did not originate from the epicardial region. In one dog, in which there was simultaneous epicardial and endocardial mapping, an endocardial electrogram from the boundary area between infarcted and acutely ischaemic zones recorded continuous fragmented activity. It was thus suggested that re-entry in a relatively isolated endocardial site could be attributed to the induction of ventricular tachyarrhythmias, and that the electrical instability could be significantly enhanced during acute ischaemia when underlying myocardial infarction was present.     

Revascularization after acute myocardial infarction

Objective: To investigate the influence of hospital teaching status and service availability on rates of revascularization following myocardial infarction. Design: Retrospective cohort study based on province-wide hospital discharge abstracts. Setting: All acute care hospitals in Ontario, Canada’s most populous province (9.7 million). Patients: Patients admitted to hospital between April 1, 1991, and September 30, 1991, with a principal diagnosis of acute myocardial infarction. Measurements: The odds of a patient’s having been referred for revascularization (angioplasty or bypass surgery) within six months of a myocardial infarction were calculated based on the type of hospital to which he or she had initially presented, defined as “teaching” or “nonteaching” or as having or not having interventional facilities onsite (cardiac catheterization and/or revascularization). Odds ratios were adjusted for potential confounding variables, and for possible joint effects of teaching status and on-site interventional capabilities. Results: The patients were more likely to have had revascularization (OR 1.79 95% CI 1.47–2.14, p=0.0001) when they had been admitted to a teaching hospital, and independently were more likely to have been referred for revascularization (OR 1.34; 95% CI 1.09–1.66, p=0.0067) when they had been admitted to a hospital with on-site interventional facilities. There was no interaction between teaching status and service availability regarding referral for revascularization. Conclusion: Teaching status is an important determinant of revascularization following acute myocardial infarction and is independent of service availability, which also influences revascularization rates.