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 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.     

Influence of residual myocardial ischaemia on induced ventricular arrhythmias following a first acute myocardial infarction.

OBJECTIVES: The purpose of this study was to assess the possible effect of residual myocardial ischaemia on induced ventricular arrhythmia during programmed ventricular stimulation in survivors of a first acute myocardial infarction. BACKGROUND: Most deaths after hospital discharge for acute myocardial infarction are sudden and presumably arrhythmic. Sudden cardiac death results from a dynamic interaction of structural abnormalities and transient triggering factors. The role of myocardial ischaemia as a trigger for ventricular arrhythmias remains unclear. We hypothesized that residual myocardial ischaemia after a first acute myocardial infarction is a potent trigger for sustained ventricular tachyarrhythmias, particularly in the presence of an abnormal myocardium. METHODS AND RESULTS: In this prospective study, programmed electrical stimulation, coronary angiography and dipyridamole-thallium-201 scintigraphy single-photon emission computed tomography were performed in 90 consecutive survivors of a first acute myocardial infarction. Patients, divided in two groups - group 1 with induced ventricular tachyarrhythmia (n=24) and group 2 without induced ventricular tachyarrhythmia (n=66) - were compared regarding residual myocardial ischaemia. The two groups were comparable in terms of mean left ventricular ejection fraction, infarct size and location, gender ratio, peak creatine kinase value, and extent of coronary disease. Residual myocardial ischaemia was detected in 32 patients: 15 (42.5%) belonged to group 1 and 17 (25.7%) to group 2. There was a statistically significant difference between the two groups regarding the presence and the extent of residual myocardial ischaemia (P<0.05). CONCLUSION: Residual myocardial ischaemia, revealed by dipyridamole-thallium-201 scintigraphy following a first acute myocardial infarction, might contribute to electrical instability evaluated by programmed ventricular stimulation.     

Effects of methylprednisolone on ventricular arrhythmias during acute myocardial ischaemia.

The effects of methylprednisolone (50 mg.kg-1) on the incidence of ventricular tachycardia and fibrillation and on ventricular fibrillation threshold were studied during acute coronary occlusion in anaesthetised dogs. Ventricular tachycardia and/or ventricular fibrillation occurred in 11 of the 16 animals (69%) both before and after methylprednisolone pretreatment. The mean ventricular fibrillation threshold of 10 dogs was 10.1 +/- 1.8 mA before methylprednisolone and it increased slightly to 13.3 +/- 2.3 mA after the drug. This difference was not statistically significant (P greater than 0.2).     

Propranolol therapy for ventricular arrhythmias 2 months after acute myocardial infarction

Treatment of premature ventricular complexes with propranolol was studied in 32 patients 2 months after an uncomplicated acute myocardial infarction. All patients had more than 30 premature ventricular complexes/hour averaged over 24 hours, with bigeminy, couplets, multifocal complexes or ventricular tachycardia. Twenty-four hour ambulatory electrocardiographic monitoring and treadmill testing were performed during a control, a treatment and a second control period. The average dosage of propranolol was 160 mg daily. Treadmill testing and ambulatory electrocardiographic monitoring showed a significant decrease in complexity and frequency of premature ventricular complexes with propranolol treatment when the two control periods were compared (p < 0.01 for frequency). During treatment with propranolol 56 percent of patients had 70 percent or greater suppression and 13 (41 percent) had 90 percent or greater suppression of premature ventricular complexes; the median percent reduction was 80 percent. The frequency of premature ventricular complexes also decreased from the first to the second control period (p < 0.05). No patient died suddenly in the 6 month follow-up period.It is concluded that propranolol effectively suppresses premature ventricular complexes after acute myocardial infarction, reducing both frequency and complexity. No sudden death occurred in this high risk population with complex ventricular arrhythmias. Premature ventricular complexes did not tend to increase with time early after acute myocardial infarction in the patients treated with propranolol. Ambulatory electrocardiographic monitoring should be considered for routine evaluation of patients 3 to 8 weeks after acute myocardial infarction and should be followed by antiarrhythmic therapy when complex premature ventricular complexes are noted.     

Early sustained ventricular arrhythmias complicating acute myocardial infarction

Objective

Sustained ventricular arrhythmias complicate 2% to 20% of acute myocardial infarctions (MIs) and are associated with increased in-hospital mortality. However, it remains unclear whether successful mechanical revascularization improves outcomes in these patients. The objective of this analysis was to identify predictors of sustained ventricular arrhythmias after acute MI and to determine the influence of successful revascularization on in-hospital mortality.

Methods

We conducted a retrospective cohort study of all patients who underwent percutaneous coronary intervention for acute MI in New York State between 1997 and 1999.

Results

Of the 9015 patients who underwent percutaneous coronary intervention for acute MI, 472 (5.2%) developed sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) before revascularization. After multivariable adjustment, independent predictors of sustained VT/VF included cardiogenic shock (odds ratio [OR], 4.10; 95% confidence interval [CI], 3.20-5.58; P <.001), heart failure (OR, 2.86; 95% CI, 2.24-3.67: P <.001), chronic kidney disease (OR, 2.58; 95% CI, 1.27-5.23; P = .009), and presentation within 6 hours of symptom onset (OR, 1.46; 95% CI, 1.18-1.81; P = .001). Patients with sustained VT/VF had greater in-hospital mortality (16.3% vs 3.7%, P <.001). Although successful percutaneous coronary intervention was associated with decreased in-hospital mortality in patients with VT/VF (P <.001), patients with sustained VT/VF and successful revascularization experienced increased mortality compared with patients without sustained ventricular arrhythmias (P <.001).

Conclusion

Among patients undergoing percutaneous coronary intervention for acute MI, sustained VT/VF remains a significant complication associated with a 4-fold increased risk of in-hospital mortality. Early mortality is reduced after successful percutaneous coronary intervention, but remains elevated in this high-risk group.     

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.     

Nocturnal hypoxaemia after myocardial infarction: association with nocturnal myocardial ischaemia and arrhythmias.

OBJECTIVE--To document the trend in arterial hypoxaemia and electrocardiographic abnormalities on the second to sixth nights after acute myocardial infarction. PATIENTS--Nineteen consecutive patients with acute myocardial infarction who were monitored continuously during the night (minimum 2300-0700) with a Holter tape recorder and a pulse oximeter. Fifteen patients were monitored for five nights, one patient for four nights, one patient for three nights, and two patients for two nights. RESULTS--Five patients had > 30 episodic oxygen desaturations of > or = 5% during the nights of monitoring and many patients had episodes with oxygen desaturations to < 80% ranging from 46% to 61% (from 7/15 to 11/18 patients) during the nights of monitoring. Constant hypoxaemia was found in 11-13% (2/15) of the patients. Simultaneous episodic hypoxaemia and episodic tachycardia was seen in 9/17 (52%) patients on the second night, 11/18 (61%) on the third, 7/15 (46%) on the fourth, 8/15 (53%) on the fifth, and 5/15 (33%) on the sixth night. Simultaneous episodic hypoxaemia and ST deviation was seen in 5/17 (29%) patients on the second night, 3/18 (16%) on the third, 4/15 (26%) on the fourth, in no patients on the fifth, and in 3/5 (20%) on the sixth night. Simultaneous occurrence of episodic hypoxaemia and arrhythmias (supraventricular, ventricular ectopy, and atrioventricular blockade) was seen in 5/17 (29%) on the second night, 4/18 (22%) on the third, 4/15 (26%) on the fourth, 2/15 (14%) on the fifth, and in no patients on the sixth night. Overall, simultaneous occurrence of episodic hypoxaemia and electrocardiographic abnormalities (episodic tachycardia, ST deviations, and arrhythmias) was seen in 11/17 patients (64%) on the second night, 13/18 (72%) on the third, 10/15 (66%) on the fourth, 8/15 (53%) on the fifth, and 7/15 (46%) on the sixth night. One patient who died of cardiogenic shock had simultaneously occurring episodic hypoxaemia and nonsustained ventricular fibrillation on the night before she died. CONCLUSION--Episodic and constant hypoxaemia are common during the first week after acute myocardial infarction. Episodic hypoxaemia was associated with electrocardiographic abnormalities in most patients. Thus, episodic nocturnal hypoxaemia may be particularly detrimental to the infarcted myocardium in the early phase after infarction; special attention should therefore be directed towards oxygenation in this group of patients.     

Early mitral regurgitation after acute myocardial infarction does not contribute to subsequent left ventricular remodeling

BACKGROUND: It is well known that mitral regurgitation may lead to left ventricular dilation; however, the relationship between progressive left ventricular dilation after acute myocardial infarction (MI) and mitral regurgitation has not yet been clarified. HYPOTHESIS: This study tested the hypothesis that early mitral regurgitation contributes to left ventricular remodeling after acute MI. METHODS: We prospectively evaluated 131 consecutive patients by serial two-dimensional and Doppler echocardiography on Days 1, 2, 3, and 7, after 3 and 6 weeks, 3 and 6 months, and 1 year following acute MI. Patients were divided into two groups: those with mitral regurgitation in the first week after acute MI (Group 1, n = 34) and those without mitral regurgitation (Group 2, n = 81). RESULTS: Over 1 year, a significant increase in end-diastolic volume index (from 62.1 +/- 12.9 to 70.5 +/- 23.6 ml/m2, p = 0.001) with a strong linear trend (F = 15.1, p < 0.001) was noted. Initial end-diastolic volume index was higher in Group 1 (65.6 +/- 13.3 vs. 60.4 +/- 12.5 ml/m2, p = 0.047), but this difference remained constant throughout the study (F = 1.76, p = NS). Therefore, the pattern of end-diastolic volume changes was similar in both groups during the period of observation. CONCLUSIONS: These data indicate that early mitral regurgitation after acute MI does not contribute to subsequent left ventricular remodeling in the first year 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.     

Cod liver oil does not reduce ventricular extrasystoles after myocardial infarction

Previous work has shown that in experimental animal models a lower incidence of arrhythmias and sudden death was observed if the animals were fed cod liver oil or fish oil. After a 48-h control period starting, on average, 8 days after the onset of symptoms, 18 men who were recovering from acute myocardial infarction were given 20 ml d-1 cod liver oil for 6 weeks, either immediately after the control period, weeks 0-6 (n = 10), or during weeks 6-12 (n = 8). Forty-eight-hour Holter monitoring was carried out before cod liver oil administration and at the end of weeks 6 and 12. The eicosapentaenoic acid content of plasma phospholipids was increased by 230% during cod liver oil administration. However, no significant change was observed in the 24-h prevalence of ventricular extrasystoles or other arrhythmias during the study period. The mean ln number of ventricular extrasystoles was 2.95 +/- 0.51 (+/- SEM) during cod liver oil ingestion and 2.63 +/- 0.30 when not taking cod liver oil.     

急性心肌梗死后左心室重构与室性心律失常的关系

目的 探讨急性心肌梗死（AMI）后左心室（左室）重构与室性心律失常之间的关系.方法 选取84例AMI患者,随机分为两组,A组接受ACEI治疗,B组不接受ACEI或ARB类药物治疗.随访观察梗死后左室收缩末期容积（LVESV）,左室舒张末期容积（LVEDV）、左室重量（LVM）和左室射血分数（LVEF）与室性心律失常发生率之间的关系.结果 AMI 1年后A组LVESV小于B组,LVEF大于B组.A、B两组的LVESV随病程延长而增大,LVEF随病程延长而减低.AMI 2周内发生室性心律失常组的LVM高于未发生组.AMI 6个月和一年后发生心律失常组的LVEDV、LVESV和LVM高于未发生组,未发生组的LVEF高于发生组.发生室性心律失常组的LVEDV、LVESV和LVEF在三个时间点间差异及未发生室性心律失常组的射血分数在三个时间点间差异均有显著性（P＜0.05）.室性心律失常在AMI2周内与LVM;6个月后与LVESV和LVM;1年后与LVEDV和LVESV密切相关.结论 AMI后左室重构是引起室性心律失常重要基质.