The clinical challenge of preventing sudden cardiac death immediately after acute ST-elevation myocardial infarction

Unfortunately, of all patients experiencing acute myocardial infarction (MI), usually in the form of ST-elevation MI, 25–35% will die of sudden cardiac death (SCD) before receiving medical attention, most often from ventricular fibrillation. For patients who reach the hospital, prognosis is considerably better and has improved over the years. Reperfusion therapy, best attained with primary percutaneous coronary intervention compared to thrombolysis, has made a big difference in reducing the risk of SCD early and late after ST-elevation MI. In-hospital SCD due to ventricular tachyarrhythmias is manageable, with either preventive measures or drugs or electrical cardioversion. There is general agreement for secondary prevention of SCD post-MI with implantation of a cardioverter defibrillator (ICD) when malignant ventricular arrhythmias occur late (>48 h) after an MI, and are not due to reversible or correctable causes. The major challenge remains that of primary prevention, that is, how to prevent SCD during the first 1–3 months after ST-elevation MI for patients who have low left ventricular ejection fraction and are not candidates for an ICD according to current guidelines, due to the results of two studies, which did not show any benefits of early (<40 days after an MI) ICD implantation. Two recent documents may provide direction as to how to bridge the gap for this early post-MI period. Both recommend an electrophysiology study to guide implantation of an ICD, at least for those developing syncope or non-sustained ventricular tachycardia, who have an inducible sustained ventricular tachycardia at the electrophysiology study. An ICD is also recommended for patients with indication for a permanent pacemaker due to bradyarrhythmias, who also meet primary prevention criteria for SCD.     

Thrombolytic therapy vs primary percutaneous intervention after ventricular fibrillation cardiac arrest due to acute ST-segment elevation myocardial infarction and its effect on outcome

The aim of this study was to evaluate the effect of thrombolytic therapy on neurologic outcome and mortality in patients after cardiac arrest due to acute ST-elevation myocardial infarction and to compare this with those in patients treated with primary percutaneous coronary intervention (PCI). We retrospectively examined patients after they had ventricular fibrillation cardiac arrests. To assess the effect of thrombolysis and PCI on outcome, we used odds ratios and their 95% confidence intervals and logistic regression modeling. Thrombolysis was applied in 101 patients (69%) and PCI in 46 patients (31%). More patients who received thrombolysis had favorable functional neurologic recovery (cerebral performance category 1 and 2) and survived to 6 months compared with patients with primary PCI (P = .38 and P = .13, respectively). In patients with cardiac arrest due to ST-elevation myocardial infarction, it may be acceptable to use thrombolysis as a reperfusion strategy. This applies especially in hospitals where immediate PCI is not available.     

Coronary Artery Bypass Grafting and Defibrillator Implantation in Patients with Ventricular Tachyarrhythmias and Ischemic Heart Disease

In patients with sustained ventricular tachyarrhythmias and myocardial ischemia due to multivessel coronary artery disease, it remains unclear whether revascularization is enough to control the arrhythmias or whether additional implantation of a defibrillator is indicated. We therefore reviewed our clinical strategy of performing both bypass surgery and implantation of a defibrillator in patients with syncopal ventricular tachycardia or fibrillation and significant multivessel coronary artery disease. We retrospectively reviewed the outcome of 18 patients with malignant ventricular tachyarrhythmias, significant multivessel coronary artery disease, and signs of myocardial ischemia who underwent both bypass surgery and defibrillator implantation. Data on these patients were compared to data from 232 other defibrillator patients with respect to baseline clinical variables, cardiac events, and mortality during follow-up. Except for underlying pathology, no other important differences in baseline characteristics were noted between the study patients and the other defibrillator patients. The cumulative occurrence of shocks during follow-up was comparable in both groups (66% vs 67%). The cumulative survival from all-cause mortality was 94% in the study patients and 78% in the others (P = NS). Pre- and postoperative electrophysiological testing was not useful to predict arrhythmia recurrences. In this population of patients with ventricular tachyarrhythmias and ischemia due to multivessel coronary artery disease, bypass surgery alone would not have prevented recurrences of arrhythmias. An excellent survival and a high incidence of shocks after both bypass surgery and defibrillator implantation were observed.     

Management of cardiac patients after thrombolytic therapy

Early thrombolytic therapy has significantly reduced morbidity and mortality through preservation of myocardium in patients with acute transmural myocardial infarction. Indications for emergent or early coronary angiography and possible angioplasty are generally limited to ongoing infarction and/or recurrent ischemia. Patients remaining clinically stable require risk stratification. Coronary angiography and revascularization with angioplasty or coronary bypass surgery is important for patients with exercise-induced ischemia. Patients with left ventricular dysfunction, poor or no exercise performance and/or advanced age are at higher risk for subsequent coronary events and thus warrant a more aggressive diagnostic approach.     

丹参红花提取物干预对急性心肌梗死后心室重构的影响

目的：探讨丹参红花提取物干预对急性心肌梗死后心室重构的影响。方法选择 ST 段抬高型急性心肌梗死患者90例,随机分为丹参红花提取物组和对照组各45例,两组均在发病后6小时内行急诊经皮冠状动脉介入治疗(PCI),两组在手术前、后给予抗血小板聚集、抗凝、调脂、β受体阻断剂及血管紧张素转化酶抑制剂(ACEI)等常规药物治疗;丹参红花提取物组在常规药物治疗的基础上,于 PCI 术当天加用丹参红花提取物治疗。结果治疗24周末,丹参红花提取物组左心室舒张末内径(LVEDD)、左心室收缩末内径(LVESD)、左心室舒张末期容积(LVEDV)、左心室收缩末期容积(LVESV)较对照组相比明显降低(P <0.01),左心室射血分数(LVEF)较对照组明显升高(P <0.01),未发生严重不良事件。结论丹参红花提取物可以干预心肌梗死后的心室重构,其机制可能是通过一种复杂的多因素参与的调节机制综合获得。     

ST-segment resolution and prognosis after facilitated versus primary percutaneous coronary intervention in acute myocardial infarction: a meta-analysis

Background  

Complete ST-segment resolution (STR) is associated with favorable prognosis in ST-elevation myocardial infarction (STEMI). The optimal reperfusion strategy in patients with STEMI presenting early after symptom-onset is still a matter of debate. So far, there are only a few studies comparing the effect of facilitated and primary percutaneous coronary intervention (PCI) on early myocardial reperfusion assessed by STR. The objective of this meta-analysis was, therefore, to evaluate the extent of early STR and subsequent prognosis in facilitated versus primary PCI.     

Percutaneous coronary intervention and the no-reflow phenomenon

No-reflow during percutaneous coronary intervention (PCI) is observed most commonly during saphenous vein graft intervention, rotational atherectomy and primary PCI for acute ST-elevation myocardial infarction. The contributions of distal embolization and ischemia/reperfusion injury to the pathogenesis of no-reflow vary in these settings, as does prevention and management. Prevention of no-reflow in these high-risk groups is the best treatment strategy, employing antiplatelet agents, vasodilators and/or mechanical devices to prevent distal embolization. Once mechanical factors are excluded as a cause for reduced epicardial flow, the treatment of established no-reflow is mainly pharmacologic, since the obstruction occurs at the level of the microvasculature. Compared with patients in whom no-reflow is transient, refractory no-reflow is associated with a markedly increased risk of 30-day mortality.     

急性心肌梗死再灌注心律失常124例分析

目的 :探讨再灌注心律失常的临床特点。方法 :分析 168例急性心肌梗死急诊经皮冠状动脉介入治疗 ,冠状动脉再通后心律失常的发生情况。结果 :12 4例 (73 8% )发生再灌注心律失常 ,其中 69例 (5 5 6% )为室性心律失常 ,7例(5 6% )发生室颤或持续性室性心动过速 ,3 6例 (2 9% )发生加速性室性自主心律。 5 1例 (4 1 1% )发生缓慢性心律失常 ,且均发生在下 /后壁梗死患者。结论 :再灌注心律失常发生率高 ,应引起警惕。加速性室性自主心律和缓慢性心律失常为予示再灌注的较可靠的临床指征     

Fibrinolytic therapy in patients with ST-elevation myocardial infarction

ST-elevation myocardial infarction (STEMI) is related to acute occlusion of a coronary artery by a fibrin-rich thrombus. Early reperfusion in STEMI reduces infarct size and improves prognosis. Acute reperfusion may be achieved with percutaneous coronary intervention (PCI) and/or fibrinolytic agents. When performed in a timely manner, primary PCI is the preferred method of reperfusion; however, due to logistic reasons, including lack of PCI-capable hospitals and delay in the first medical contact-to-balloon time, this simplified approach lacks universal applicability. Due to clinical efficacy and the ease of administration, fibrinolysis is still an important reperfusion modality in patients with STEMI who cannot have primary PCI within guideline-recommended time. This review focuses on the role of fibrinolysis in patients with STEMI.     

The Belfast experience with resuscitation ambulances

The majority of sudden deaths are due to ventricular fibrillation. In the initiation of ventricular fibrillation, an R on T extrasystole was the most important factor. A late cycle ectopic, ventricular tachycardia and idioventricular rhythm initiated ventricular fibrillation less frequently. An increase or marked slowing of the heart rate were predisposing factors in the initiation of ventricular fibrillation. The first successful correction of ventricular fibrillation outside the hospital was achieved by the Belfast Mobile Coronary Care Unit in 1966. A single shock of 100 or 200 watt seconds (stored) was highly successful in the correction of ventricular fibrillation. The most likely factor in unsuccessful defibrillation is incorrect paddle application. For the correction of ventricular fibrillation during the first hour of the onset of symptoms, ≤ 2DC shocks were required in 41% of patients. Only 8% of patients required more than ten shocks. Smaller portable defibrillators are now available for use by family practitioners. Lidocaine 100 mg intravenously and 300 mg intramuscularly failed to prevent the development of ventricular tachycardia and ventricular fibrillation during the first hour of the drug's administration. Patients who survived ventricular fibrillation that occurred within four hours of the onset of symptoms of myocardial infarction were younger, tended to have had a mild coronary attack, and had the most favorable long-term prognosis. The early control of chest pain, autonomic disturbances, arrhythmias, and hemodynamic disturbance leads to a reduced incidence of cardiogenic shock and hospital mortality.     

Safety of Transvenous Low Energy Cardioversion of Atrial Fibrillation in Patients with a History of Ventricular Tachycardia: Effects of Rate and Repolarization Time on Proarrhythmic Risk

The objective of this study was to assess the safety and efficacy of transvenous low energy cardioversion of atrial fibrillation in patients with ventricular tachycardia and atrial fibrillation and to study the mechanisms ofproarrhythmia. Previous studies have demonstrated that Cardioversion of atrial fibrillation using low energy, R wave synchronized, direct current shocks applied between catheters in the coronary sinus and right atrium is feasible. However, few data are available regarding the risk of ventricular proarrhythmia posed by internal atrial defibrillation shocks among patients with ventricular arrhythmias or structural heart disease. Atrial defibrillation was performed on 32 patients with monomorphic ventricular tachycardia and left ventricular dysfunction. Shocks were administered during atrial fibrillation (baseline shocks), isoproterenol infusion, ventricular pacing, ventricular tachycardia, and atrial pacing. Baseline shocks were also administered to 29 patients with a history of atrial fibrillation but no ventricular arrhythmias. A total of 932 baseline shocks were administered. No ventricular proarrhythmia was observed after well-synchronized baseline shocks, although rare inductions of ventricular fibrillation occurred after inappropriate T wave sensing. Shocks administered during wide-complex rhythms (ventricularpacing or ventricular tachycardia) frequently induced ventricular arrhythmias, but shocks administered during atrial pacing at identical ventricular rates did not cause proarrhythmia. The risk of ventricular proarrhythmia after well-synchronized atrial defibrillation shocks administered during narrow-complex rhythms is low, even in patients with a history of ventricular tachycardia. The mechanism of proarrhythmia during wide-complex rhythms appears not to be related to ventricular rate per se, but rather to the temporal relationship between shock delivery and the repolarization time of the previous QRS complex.     

Percutaneous coronary intervention and the no-reflow phenomenon

No-reflow during percutaneous coronary intervention (PCI) is observed most commonly during saphenous vein graft intervention, rotational atherectomy and primary PCI for acute ST-elevation myocardial infarction. The contributions of distal embolization and ischemia/reperfusion injury to the pathogenesis of no-reflow vary in these settings, as does prevention and management. Prevention of no-reflow in these high-risk groups is the best treatment strategy, employing antiplatelet agents, vasodilators and/or mechanical devices to prevent distal embolization. Once mechanical factors are excluded as a cause for reduced epicardial flow, the treatment of established no-reflow is mainly pharmacologic, since the obstruction occurs at the level of the microvasculature. Compared with patients in whom no-reflow is transient, refractory no-reflow is associated with a markedly increased risk of 30-day mortality.     

New strategies for the management of no-reflow after primary percutaneous coronary intervention

The myocardial no-reflow phenomenon is characterized by a reduced antegrade myocardial blood flow despite an open infarct-related artery in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention. Importantly, no-reflow is known to be associated with unfavorable clinical outcome and prognosis. It is a complex phenomenon and is caused by the variable combination of four pathogenetic components: distal atherothrombotic embolization, ischemic injury, reperfusion injury and susceptibility of coronary microcirculation to injury. As a consequence, appropriate strategies to prevent or treat each of these components are expected to reduce the occurrence of no-reflow. Mechanical and pharmacological approaches performed before, during and after performing myocardial revascularization have been investigated in recent studies, in order to reduce the rate of no-reflow. In this article, we concentrate on the major preventive and therapeutic approaches currently available for the management of the no-reflow phenomenon.     

Ventricular Tachycardia and Ventricular Fibrillation in Patients with Short P-R Intervals and Narrow QRS Complexes

Eleven patients with short P-R Intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A-H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P-R and A-H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an expression of the “enhanced A-V conduction” that had been manifested in sinus beats by short P-R and A-H intervals. In clinical settings and physiological conditions proven to be hemodynamicaliy unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R-on-T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studies     

AMI患者在急诊经皮冠状动脉介入治疗中发生心室颤动的救治配合及护理

目的探讨急性心肌梗死（acute myocardial infarction,AMI）患者在急诊行经皮冠状动脉介入治疗（percutaneous coronary intervention,PCI）中并发心室颤动的救治配合和护理要点。方法回顾性分析在急诊实施PCI中发生心室颤动的15例AMI患者的病例资料。结果除1例患者死亡外,1例患者因反复心室颤动经5次电击除颤后恢复窦性心律：9例经1次电击除颤后恢复窦性心律;其余病例均经心前区叩击和胸外心脏按压后恢复窦性心律。结论在AMI患者实施急诊PCI术的过程中,护士做好急救药品及除颤设备的准备,开放高效静脉通路,加强心理护理、心电监护和救治配合是成功抢救心室颤动的重要因素。     

Atrial and Ventricular Vulnerability in a Patient with the Wolff-Parkinson-White Syndrome

An electrophysiologic study was carried out in a patient with the Wolff-Parkinson-White syndrome and a history of spontaneous atrial fibrillation but with no evidence of organic cardiac disease. A single induced premature ventricular depolarization resulted in ventricular tachycardia followed by ventricular fibrillation. Similarly, atrial pacing or premature atrial stimulation resulted in frequent episodes of atrial fibrillation or flutter, The atrial and ventricular effective refractory periods were 180 ms and < 160 ms, respectively, at a driven cycle length of 480 ms. Intravenous administration of procainamide resulted in lengthening of the refractory periods and failure to induce either atriaJ or ventricular arrhythmias with pacing. In most patients with enhanced atrioventricular nodal or accessory atrioventricular nodal bypass, the mechanism of ventricular tachycardia is related to an inordinately rapid ventricular response during supraventricular arrhythmias. In our patient, a unique mechanism was apparent: atrial and ventricular vulnerability to fibrillation was associated with extremely short myocardial effective refractory periods. The relationship of this finding to sudden cardiac death bears further study.     

Outcome after coronary artery bypass surgery and percutaneous coronary intervention in patients with atrial fibrillation and oral anticoagulation

Abstract

Aim. This study was planned to compare the clinical characteristics and outcome of patients on warfarin treatment for atrial fibrillation (AF) undergoing coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI).

Methods. This is a retrospective analysis of 121 patients who underwent isolated CABG and 301 patients who underwent PCI.

Results. PCI patients were older (mean age, 72.9 versus 69.8 years) and more often had prior cardiac surgery (15.9% versus 1.7%) and acute coronary syndrome (53.8% versus 21.5%). CABG patients more often had two- and three-vessel disease (95.0% versus 60.2%) and left main stenosis (32.2% versus 7.0%). The 30-day outcome was similar after PCI and CABG. At 3 years, PCI was associated with lower overall survival (72.0% versus 86.4%, P = 0.006), freedom from repeat revascularization (85.3% versus 98.2%, P < 0.001), freedom from myocardial infarction (83.4% versus 93.8%, P = 0.008), and freedom from major cardiovascular events (57.4% versus 78.9%, P < 0.001). Propensity score adjusted analysis showed that PCI was associated with increased risk of all-cause mortality (P = 0.016, RR 2.166, CI 1.155–4.060), myocardial infarction (P = 0.017, RR 3.161, 95% CI 1.227–8.144), repeat revascularization (P = 0.001, RR 13.152, 95% CI 2.799–61.793), and major cardiac and cerebrovascular complications (P = 0.001, RR 2.347, 95% CI 1.408–3.914). There was no difference in terms of stroke and bleeding episodes at any time point.

Conclusion. In clinical practice, PCI is the preferred revascularization strategy in these frail patients. Patients selected for CABG have a relatively low operative risk and better mid-term outcome in spite of warfarin treatment. The poor prognosis after PCI may mainly reflect frequent co-morbidities in this patient group.     

Reperfusion strategies in the emergency treatment of ST-segment elevation myocardial infarction

Prompt restoration of blood flow is the primary treatment goal in ST-segment elevation myocardial infarction to optimize clinical outcomes. The ED plays a critical role in rapid triage, diagnosis, and management of ST-elevation myocardial infarction, and in the decision about which of the 2 recommended reperfusion options, that is, pharmacologic and mechanical (catheter-based) strategies, to undertake. Guidelines recommend percutaneous coronary intervention (PCI) if the medical contact-to-balloon time can be kept under 90 minutes, and timely administration of fibrinolytics if greater than 90 minutes. Most US hospitals do not have PCI facilities, which means the decision becomes whether to treat with a fibrinolytic agent, transfer, or both, followed by PCI if needed. Whichever reperfusion approach is used, successful treatment depends on the ED having an integrated and efficient protocol that is followed with haste. Protocols should be regularly reviewed to accommodate changes in clinical practice arising from ongoing clinical trials.     

Comparison of carvedilol and metoprolol in patients with acute myocardial infarction undergoing primary coronary intervention

Summary Background The value of early therapy with beta-blocking agents in acute myocardial infarction (AMI) undergoing reperfusion is not yet well established. Newer beta-blocking agents such as carvedilol offer potential advantages in the setting of ischemia and reperfusion injury. Methods We randomized 100 patients with acute ST-elevation myocardial infarction (STEMI) to receive either 12.5 mg carvedilol or 50 mg metoprolol tartrate orally already before percutaneous coronary intervention (PCI) of the infarct-related artery, uptitrating to a daily target dose of 50 mg carvedilol or 150 mg metoprolol during the first week. Pts. were subjected to left ventricular (LV) angiography just before reperfusion and after 14 days to compare ejection fraction (EF) and regional wall motion abnormalities by quantitative LV analysis. Furthermore, kinetics of cardiac troponin T (cTnT), NT-proANP, NT-proBNP, endothelin, argenine vasopressin, epinephrine and norepinephrine were assessed during the first 12 hours and again at 2 weeks. In addition, reperfusion-induced rhythm abnormalities like VT, triplets, couplets, and bradycardic events were assessed continuously during the first 12 hours starting at reperfusion by Holter analysis. Results Both groups did not differ with respect to onset of pain, target vessel, extent of coronary heart disease, age, gender, rate of stenting or use of a GP IIb/IIIa inhibitor, pre- and postinterventional TIMI flow grade, time course of heart rate or blood pressure. There were neither significant differences in the cardiac and neurohumoral markers nor in the occurrence of arrhythmias between both treatment groups. Within 14 days, EF improved by 5.8±2.0% (mean±SEM) in the metoprolol group and by 5.2±2.1% in the carvedilol group (n.s.). Area of infarction was reduced by 6.1±2.9% in the metoprolol group and by 12.8±3.6% of total LV outline in the carvedilol group (n.s.). Maximum hypokinesia in the central infarcted region was diminished by 0.40±0.11 standard deviation (SD) in the metoprolol group and by 0.34±0.13 SD in the carvedilol group (n.s.). Conclusion In the setting of direct PCI in acute STEMI, administration of carvedilol before reperfusion appears not to be superior to metoprolol with respect to myocardial injury and improvement of global and regional LV function. The study documents equivalent improvement of LV function and similar kinetics of cardiac and neurohumoral markers in pts. with acute STEMI undergoing direct PCI if the pts. were immediately treated with either carvedilol or metoprolol. Thus, superiority of carvedilol in experimental studies did not translate into a clinical benefit.     

Empiric Therapy with β-Blockers

The only class of drugs with significant effects on ventricular fibrillation and sudden death in humans is that of β-blockers. The exact mechanisms for these prophyiactic effects are not knotvn but may be related to both ontiischemic or anliarrhythmic infiuences. It seems reasonable to suggest that one should use a β-blocker with proven effect on total mortality and sudden cardiac death after myocardial infarction as prophylaxis. Therefore, propranolol, timolol. or metoprolol. should be instituted in order to improve prognosis when there are no conlraindications. In addition to possible effects on survival one would aiso expect to reduce the risk for new ischemic events with angina or reinfarction. In contrast, class I antiarrhythmic agents are useful for symptomatic ventricular arrhythmias but there is no proof for any effect on ventricular fibrillation and sudden cardiac death.