植入型心律转复除颤器在心肌梗死后心脏性猝死中的研究进展

心脏性猝死(SCD)是由各种心脏因素引起的意外死亡,通常发生在症状出现后1 h内。冠心病和急性心肌梗死是SCD的主要病因。植入型心律转复除颤器是预防SCD最有效的措施,有效提高了心肌梗死后SCD高危患者的生存率,成为SCD一级预防的标准治疗方法。近年来,在临床上的应用有了新进展。现综述SCD的流行病学、心肌梗死后SCD的发生机制和心律转复除颤器在心肌梗死后SCD中的应用进展。     

静息心电图对心肌梗死后猝死的预警意义

猝死是全球关注的健康问题,其中心脏性猝死是心肌梗死后患者死亡的重要原因。大部分心肌梗死后心脏性猝死的高危患者都可以通过普通检查发现,从而有效的预防。现通过对标准12导联心电图相关指标的分析,预测心肌梗死后患者的猝死风险,以提高临床诊治水平。     

Arrhythmia Profile and Sudden Death After Myocardial Infarction and Cardiac Arrest

Incidence of sudden death and arrhythmia pattern were studied using ambulatory monitoring in 40 patients resuscitated < 24 hours (n = 26, Group I) or 4–12 weeks (n = 14, Group II) after myocardial infarction. Forty patients with myocardial infarction and no resuscitation served as controls (Group III). Ambulatory ECGs were recorded with an average of 2 months (Recording 1) and 28 months (Recording 2) after myocardial infarction. Incidence of sudden death was significantly higher in Group II (43%) than in Group I (15%) or Group III (8%) (p < 0.01). In Recording 1, there were no significant differences in the incidence of premature ventricular beats and complex arrhythmias (couplets or salvos) between survivors and sudden death patients in Groups I, II and III, whereas in Recording 2 the mean incidence of premature ventricular beats and complex arrhythmias was significantly higher in survivors in Group II than in Group I or Group III (p < 0.05). In addition, in survivors in Group II, incidence of premature ventricular beats and complex arrhythmias was significantly higher in Recording 2 than in Recording 1 (p < 0.05). Our data show that the risk of sudden death is high in patients with cardiac arrest 4–12 weeks after myocardial infarction. Repeated studies using ambulatory monitoring are helpful in estimating the risk of sudden death in patients with myocardial infarction and cardiac arrest.     

Alcohol Use, Myocardial Infarction, Sudden Cardiac Death, and Hypertension

Studying coronary risk factors, this article concludes that: regular use of alcohol may protect against major coronary events; regular use of three or more drinks daily is a probable risk factor for hypertension; the relations of alcohol use to coronary disease, hypertension, and cardiomyopathy are disparate.     

Characteristics of the Circadian Rhythm of Heart Rate Variability in Patients with Sudden Cardiac Death after Myocardial Infarction

Background: Sudden cardiac death (SCD) after myocardial infarction, most commonly caused by ventricular fibrillation, is closely associated with autonomic nervous tone. However, the mechanism of SCD and its association with autonomic nervous tone and the circadian rhythm of this tone remain obscure. We examined the characteristics of autonomic nervous tone in patients with SCD using heart rate variability (HRV) analysis. Methods: HRV was analyzed by spectral and nonspectral methods in 46 postinfarction patients, including 6 patients who experienced SCD (SCD[+]) and 40 survivors (SCD[—]). The circadian rhythm of HRV was assessed by a nonlinear least squares method combined with the maximum entropy method (MEM) using data from 24-hour ambulatory ECGs. The mean follow-up period was 27 ± 12 months. Results: Midline estimating statistic of rhythm and the amplitude of the high frequency (HF) component in the SCD(+) group were lower than those in the SCD(—) group, and differences of the circadian rhythm of the HF component between the SCD(+) group and the SCD(—) group were observed. Conclusions: A decreased HF component indicating diminished parasympathetic nervous activity was the strongest independent predictor of SCD. These results suggest that postinfarction patients whose parasympathetic nervous activity is low and whose circadian changes are small may be susceptible to SCD.     

Circadian Pattern of QT/RR Adaptation in Patients with and Without Sudden Cardiac Death after Myocardial Infarction

Background: Abnormalities in the adaptation of the QT interval to changes in the RR interval may facilitate the development of ventricular arrhythmias. Methods: This study sought to evaluate the dynamic relation between the QT and RR intervals in patients after acute myocardial infarction. The study population consisted of 14 patients after myocardial infarction (age 60 ± 7 years, 12 men) who died suddenly (SCD victims) within 1 year after the myocardial infarction and 14 pair-matched age, sex, left ventricular ejection fraction, infarct site, thrombolytic therapy) patients who remained event-free after myocardial infarction (Ml survivors) for at least 3 years. Fourteen normal subjects were studied as controls (age 55 ± 9 years, 11 men). QT and RR intervals were measured on a beat-to-beat basis automatically with a visual control from 24-hour ambulatory ECGs using Reynolds Pathfinder 700. Mean hourly values of the QT/RR slope (QT =α+βRR) and corrected QT interval at 1000 ms of RR interval (QT_1s) were derived for each subject using an inhouse program (QT_1s=α+1000β). The dynamics of the QT/RR slope and QT_1s were assessed on the basis of hourly mean values. The circadian rhythm of ventricular repolarization (QT_1s and QT/RR slope) was examined by harmonic regression analysis. Results: There was a trend towards a significant difference in 24-hour mean value of QT_1s between study groups (408 ± 26 ms vs 381 ± 43 ms and 386 ± 22 ms, P = 0.06), and a significant difference was found between SCD victims and normal subjects (408 ± 26 vs 386 ± 22 ms, P = 0.02). The QT_1s differed significantly between study groups (P = 0.038) only during the day time (09:00–19:00 hour), when QT_1s was significantly longer in SCD victims than in normal subjects (409 ± 33 vs 380 ± 27 ms, P = 0.02) and tended to be longer than in Ml survivors (409 ± 33 vs 379 ± 42 ms, P = 0.08). The 24-hour mean value of QT/RR slope was significantly different between study groups (P = 0.04), with a significantly steeper slope in SCD victims than in normal subjects (0.15 ± 0.07 vs 0.09 ± 0.02, P = 0.008). During day time, the QT/RR slope differed significantly between study groups (P = 0.04), while the difference was less marked at night (P = 0.08). The slope was significantly steeper in SCD victims than in normal subjects during both day and night (P < 0.05). A marked circadian variation of QT_1s was observed in normal subjects, which was blunted in Ml survivors and SCD victims. Conclusions: Abnormal repolarization behaviors, characterized by longer QT_1s and impaired adaptation of QT to variations in RR intervals, were found in SCD victims. Hence, lethal ventricular tachyarrhythmias might be provoked by the altered repolarization dynamics in patients after myocardial infarction. A.N.E. 1999;4(3):286–294     

Four-year Incidence of Myocardial Infarction and Sudden Coronary Death in Twelve Finnish Population Cohorts

ABSTRACT. Suhonen O, Reunanen A, Aromaa A, Knekt P, PyÖrÄlÄ K. (Research Institute for Social Security, Social Insurance Institution, Helsinki, Finland.) Four-year incidence of myocardial infarction and sudden coronary death in twelve Finnish population cohorts. The incidence of myocardial infarction (MI) and sudden coronary death in four years was studied in 6510 men and 5800 women, aged 30–59 years, derived from 12 Finnish population cohorts constituting the invited population to a prospective study. The incidence of all fatal coronary events in four years was 13.0/1000 in men and 1.8/1000 in women. The incidence of sudden coronary death was 7.8/1000 in men and 0.7/1000 in women. The incidence of non-fatal MI was 22.2/1000 in men and 7.3/1000 in women. Coronary mortality was significantly higher in non-participants in the initial survey than in participants. The incidence of MI was highest in men from eastern Finland (North Karelia), intermediate in men from central and western Finland and lowest in men from southwestern Finland. There were no significant regional differences in the incidence of MI in women. The incidence of MI in this study was in good agreement with that recorded in the myocardial community registers.     

Prognostic Value of Standard Electrocardiographic Parameters for Predicting Major Adverse Cardiac Events after Acute Myocardial Infarction

Background: The prognostic value of electrocardiographic (ECG) variables in predicting major adverse cardiac events (MACEs) after acute myocardial infarction (AMI) in the era of modern therapy is unclear. This study was conducted to evaluate the prognostic significance of ECG parameters in predicting 1‐year MACEs for AMI patients. Methods: Between January 2006 and January 2008, 529 AMI patients were included. ECG variables were analyzed from the ECG taken on discharge day. The 1‐year MACEs were defined as death, nonfatal MI, and revascularization including repeat percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). Mean follow‐up duration was 360 ± 119 days. Results: Of these patients, 497 (94%) patients provided complete follow‐up data (355 males; 67 ± 12 years old). The rate of 1‐year MACEs was 16%. In univariate analysis, heart rate, corrected QT interval, left ventricular (LV) hypertrophy, voltage (SV₁+ RV₅), lateral ST‐depression (V_5–6 or I, aVL), pathologic Q wave (V_1–4, V_5–6), ST‐elevation (V_1–4, V_5–6 or I, aVL), and T‐wave inversion (V_1–4, V_5–6, or I, aVL) had a significant association with 1‐year MACEs. In the Cox regression hazard model, lateral ST‐depression (hazard ratio [HR] 2.260, 95% confidence interval [CI] 1.204 to 4.241, P = 0.011) and corrected QT interval (HR 1.007, 95% CI 1.002 to 1.011, P = 0.004) were independent predictors of 1‐year MACEs. After adjustment for all risk variables, lateral ST‐depression (HR 3.781, 95% CI 1.047 to 13.656, P = 0.042) was the only ECG variable that independently predicted 1‐year MACEs. Conclusion: Lateral ST‐depression on discharge day ECG is an independent predictor of 1‐year MACEs after AMI. Ann Noninvasive Electrocardiol 2011;16(1):56–63     

Prevention of Sudden Cardiac Death After a First Myocardial Infarction by Pharmacologic or Surgical Antiadrenergic Interventions

Antiadrenergic Interventions and Prevention of Sudden Death after MI. Introduction: Growing evidence points to sympathetic hyperactivity as one critical trigger for life-threatening arrhythmias among postmyocardial infarction patients. Methods and Results: We have evaluated, in a placebo-controlled multicenter study, the efficacy of a β-adrenergic blocking agent (oxprenolol 160 mg) and of a selective left cardiac sympathetic denervation in preventing sudden death in patients with a first and anterior myocardial infarction. Two patient groups were studied. The high-risk group included 144 patients who survived a myocardial infarction complicated by either ventricular tachycardia or fibrillation. The relatively low-risk group included 869 patients whose myocardial infarction did not have these complications; they were allocated only to placebo or oxprenolol. Randomization took place 30 days postmyocardial infarction; mean follow-up was 22 months. In the high-risk group the sudden cardiac death (crude rate) in the placebo subgroup was indeed high (21.3%), and was strikingly reduced to 2.7% and to 3.6% by oxprenolol and by left cardiac sympathetic denervation, respectively (P < 0.05). In the low-risk group the sudden cardiac death (crude rate) in the placebo subgroup was 5.2% and was still reduced by oxprenolol to 1.6% (P < 0.05). The results for total mortality were quite similar to those for sudden death iu both groups. Conclusion: This study, unique for the populations studied and for one of the treatments used, demonstrates that pharmacologic and surgical antiadrenergic interventions significantly reduce sudden cardiac death in postmyocardial infarction patients at high and at low risk. With due consideration to the relatively small size of the high-risk group, it seems reasonable to suggest that left cardiac sympathetic denervation may be considered as a possible alternative for high-risk patients with contraindications to beta blockers. (J Cardiovasc Electrophysiol, Vol 3, pp. 2–16, February 1992)     

Myocardial Viability Detected by Myocardial Contrast Echocardiography—Prognostic Value in Patients after Myocardial Infarction

Objective: This study aimed to assess the role of myocardial contrast echocardiography (MCE) as a predictor of cardiac events and death in patients with acute myocardial infarction (AMI). Methods: Eighty‐six patients underwent primary percutaneous coronary angioplasty for AMI. Segmental perfusion was estimated by MCE in real time at mean 5 days after PCI using low MI (0.3) after 0.3–0.5 ml bolus injection of intravenous Optison. MCE was scored semiquantitatively as: (1) normal perfusion (homogenous contrast effect), (2) partial perfusion (patchy myocardial contrast enhancement), (3) lack of perfusion (no visible contrast effect). A contrast score index (CSI) was calculated as the sum of MCE scores in each segment divided by the total number of segments. The patients were followed up for cardiac events and death. Results: A CSI of >1.68 was taken to be a predictor of cardiac events and death. Death occurred only in patients with CSI >1.68. Patients with CSI >1.68 had a significantly (P = 0.03) higher incidence of cardiac death or cardiac events (75%) compared to those with CSI <1.68 (27%). The absence of residual perfusion within the infarct zone was an independent predictor of death and cardiac events (P = 0.02). Conclusions: The absence of residual myocardial viability in the infarct zone supplied by an infarct‐related artery is a powerful predictor of cardiac events in patients after AMI. (Echocardiography 2010;27:430‐434)     

Myocardial Inflammation and Sudden Death in the Inherited Cardiomyopathies

The best studied of the inherited cardiomyopathies—hypertrophic (HCM), dilated (DCM) and arrhythmogenic (ACM)—present overlapping clinical phenotypes with varying, often unrecognized, risk of sudden death. Risk assessment is informed by patient sex and by the specific disease-causing variant. HCM and arrhythmogenic right ventricular cardiomyopathy (ARVC) remain important causes of sudden death. A phenotype mimicking DCM in patients with inherited ACM is associated with premature sudden death in families with overlapping DCM and ACM phenotypes. The role of inflammation as a determinant of disease development and progression and sudden death is poorly understood but potentially important. Sudden death registries report myocarditis as the cause in 5% to 13%; examination of 30 hearts from victims of ARVC sudden death found focal myocarditis in areas of myocyte necrosis in 20 (67%). The link to specific disease-causing variants remains to be explored, including genetic determinants of the immune response. Clinical and experimental studies support immune- and autoimmune-mediated disease in DCM and ACM. Immunosuppression in biopsy-proven noninfectious myocarditis and inflammatory DCM is a treatment option. Recognition of ACM requires greater focus on distinguishing ACM from DCM. The potential to recognize disease before adverse events and to characterize patients who may benefit from immunosuppression or device therapy highlights the importance of more comprehensive genetic and immunologic characterization of patients with myocarditis and in those with a family history or clinical presentation of an inherited cardiomyopathy. This review will examine from a predominantly clinical perspective the potential importance of myocardial inflammation as a determinant of sudden death in inherited HCM, DCM, and ACM.