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.


     

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.     

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.     

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).     

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)     

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.     

The relationship between myocardial ischaemia and cell death during acute myocardial infarction.

Praecordial mapping of the electrocardiogram (ECG) demonstrated the natural history of ST segment elevation, loss of R and appearance of Q waves in 50 patients suffering uncomplicated anterior myocardial infarction. The results showed that ST segment elevation has a complicated natural history. The loss of R wave electromotive force and development of Q waves were complete by 12 h following the onset of chest pain. This evidence for the loss of viable myocardium was complete before the MB-isoenzyme of creatine kinase (MBCK) was detected in the plasma. Regression analysis of these results showed a direct relationship between the praecordial area of ST segment elevation at 2 h (myocardial ischaemia) and the praecordial area of Q waves at 24 h after the onset of symptoms (cell death). The efficacy of interventions on the natural history of myocardial infarction might be assessed by their effects on the relationship between myocardial ischaemia and cell death.     

Transient abnormal Q waves during acute myocardial infarction.

A 65 years old woman with an acute myocardial infarction, as it was judged by serial enzyme changes, developed transitory Q waves in V2-V4 and II, III and AVF during the attack of chest pain. These Q waves were not present 12 hours later. It is suggested that these changes represent a focal block in the septal fibers of the left bundle system. This defect could explain the transient right precordial Q waves seen in myocardial infarction or ischemia, as well as the fixed Q waves of many patients without septal infarction at autopsy.     

Silent myocardial ischemia after acute myocardial infarction.

Silent ischemia after myocardial infarction has definite prognostic significance but should be interpreted within the context of other prognostic indicators. The rationale for therapeutic intervention is based on the prognostic implications of silent ischemia and the potentially deleterious effect of repeated episodes of ischemia on the integrity of the left ventricle. We measured parameters of ischemia in 20 patients who showed asymptomatic ischemic ST-T changes on exercise testing in the early phase after myocardial infarction. After diltiazem administration, a reduction of exercise-induced ST-T depression from 2.3 +/- 0.8 to 0.7 +/- 0.6 mm (p less than 0.01) occurred, and regional wall-motion score at exercise, determined by radionuclide angiography, improved significantly (p less than 0.02). These and other observations warrant further studies in which the duration, severity and frequency of the ischemic episodes should be quantified and correlated with prognosis after myocardial infarction.     

Prognostic significance of transient myocardial ischaemia after first acute myocardial infarction: five year follow up study.

OBJECTIVE--To assess the five year prognostic significance of transient myocardial ischaemia on ambulatory monitoring after a first acute myocardial infarction, and to compare the diagnostic and long term prognostic value of ambulatory ST segment monitoring, maximal exercise testing, and echocardiography in patients with documented ischaemic heart disease. DESIGN--Prospective study. SETTING--Cardiology department of a teaching hospital. PATIENTS--123 consecutive men aged under 70 who were able to perform predischarge maximal exercise testing. INTERVENTIONS--Echocardiography two days before discharge (left ventricular ejection fraction), maximal bicycle ergometric testing one day before discharge (ST segment depression, angina, blood pressure, heart rate), and ambulatory ST segment monitoring (transient myocardial ischaemia) started at hospital discharge a mean of 11 (SD 5) days after infarction. MAIN OUTCOME MEASURES--Relation of ambulatory ST segment depression, exercise test variables, and left ventricular ejection fraction to subsequent objective (cardiac death or myocardial infarction) or subjective (need for coronary revascularisation) events. RESULTS--23 of the 123 patients had episodes of transient ST segment depression, of which 98% were silent. Over a mean of 5 (range 4 to 6) years of follow up, patients with ambulatory ischaemia were no more likely to have objective end points than patients without ischaemic episodes. If, however, subjective events were included an association between transient ST segment depression and an adverse long term outcome was found (Kaplan-Meier analysis; P = 0.004). The presence of exercise induced angina identified a similar proportion of patients with a poor prognosis (Kaplan-Meier analysis; P < 0.004). Both exertional angina and ambulatory ST segment depression had high specificity but poor sensitivity. The presence of exercise induced ST segment depression was of no value in predicting combined cardiac events. Indeed, patients without exertional ST segment depression were at increased risk of future objective end points (Kaplan-Meier analysis; P < 0.0045). These findings may be explained in part by a higher prevalence of left ventricular dysfunction in patients without ischaemic changes in the exercise electrocardiogram (P < 0.05). CONCLUSION--There seem to be limited reasons to perform ambulatory ST segment monitoring in survivors of a first myocardial infarction who can perform exercise tests before discharge. Patients at high risk of future myocardial infarction or death from cardiac causes are not identified. Ambulatory monitoring and exertional angina distinguish a small subset of patients who will develop severe angina pectoris demanding coronary revascularisation during follow up. Patients without exercise induced ST segment depression comprise a high risk subgroup in terms of subsequent objective end points. The role of ambulatory ST segment monitoring performed in unselected patients immediately after infarction when risk is maximal remains to be clarified.     

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.