Therapeutic hypothermia for acute myocardial infarction and cardiac arrest

This report focuses on cardioprotection and describes the advantages and disadvantages of various methods of inducing therapeutic hypothermia (TH) with regard to neuroprotection and cardioprotection for patients with cardiac arrest and ST-segment elevation myocardial infarction (STEMI). TH is recommended in cardiac arrest guidelines. For patients resuscitated after out-of-hospital cardiac arrest, improvements in survival and neurologic outcomes were observed with relatively slow induction of TH. More rapid induction of TH in patients with cardiac arrest might have a mild to modest incremental impact on neurologic outcomes. TH drastically reduces infarct size in animal models, but achievement of target temperature before reperfusion is essential. Rapid initiation of TH in patients with STEMI is challenging but attainable, and marked infarct size reductions are possible. To induce TH, a variety of devices have recently been developed that require additional study. Of particular interest is transcoronary induction of TH using a catheter or wire lumen, which enables hypothermic reperfusion in the absence of total-body hypothermia. At present, the main methods of inducing and maintaining TH are surface cooling, endovascular heat-exchange catheters, and intravenous infusion of cold fluids. Surface cooling or endovascular catheters may be sufficient for induction of TH in patients resuscitated after out-of-hospital cardiac arrest. For patients with STEMI, intravenous infusion of cold fluids achieves target temperature very rapidly but might worsen left ventricular function. More widespread use of TH would improve survival and quality of life for patients with out-of-hospital cardiac arrest; larger studies with more rapid induction of TH are needed in the STEMI population.     

Sinus arrest in acute myocardial infarction

The results are given of a 4-year prospective study regarding the occurrence, clinical pattern, and treatment of sinus arrest in patients with acute myocardial infarction. The arrhythmia was observed in 32 of 1665 patients. The detection rate increased from below 1 per cent in the first year to 5 per cent in the last due to better facilities for monitoring. All patients except one had inferior infarction. Paroxysmal atrial fibrillation was observed in 12, corresponding to a frequency approximately similar to that previously reported in patients with sinus arrest unrelated to myocardial infarction. Syncope due to sinus arrest occurred in 7 and hypotension in 19 patients. Small doses of isoprenaline given intravenously were usually effective in restoring normal heart rate, but pacemaker therapy was necessary in 3 patients.     

Sinus arrest in acute myocardial infarction

The results are given of a 4-year prospective study regarding the occurrence, clinical pattern, and treatment of sinus arrest in patients with acute myocardial infarction. The arrhythmia was observed in 32 of 1665 patients. The detection rate increased from below 1 per cent in the first year to 5 per cent in the last due to better facilities for monitoring. All patients except one had inferior infarction. Paroxysmal atrial fibrillation was observed in 12, corresponding to a frequency approximately similar to that previously reported in patients with sinus arrest unrelated to myocardial infarction. Syncope due to sinus arrest occurred in 7 and hypotension in 19 patients. Small doses of isoprenaline given intravenously were usually effective in restoring normal heart rate, but pacemaker therapy was necessary in 3 patients.     

Electrophysiologic studies in survivors of late cardiac arrest after myocardial infarction

Nine patients resuscitated from life-threatening ventricular arrhythmias (VA) within 3 months of an acute myocardial infarction (AMI) underwent electrophysiologic studies (EPS) with clinical follow-up for at least 12 months. Neither reinfarction, drug therapy, nor electrolyte imbalance was a precipitating factor. VA was induced by ventricular pacing in six of nine patients. Five patients were prescribed empiric drug therapy, while the four other patients had repeated EPS to select optimal drug therapy. One patient remained unstable and died of VA in the hospital. No patient was discharged and successfully maintained on a drug known to prevent induction of VA, yet only two patients (25%) had a further recurrence of VA, one fatal. Our findings suggested that either drug therapy that is determined empirically or found not to suppress the induction of VA during EPS can be associated with a successful outcome in some of these patients, or the natural history of VA after myocardial infarction is that they are self-limiting in the absence of a new ischemic event.     

Time-dependent predictors of primary cardiac arrest in patients with acute myocardial infarction

To understand predictors of cardiac arrest early in acute myocardial infarction (AMI), for the Thrombolytic Predictive Instrument, we developed a multivariable regression model predicting primary cardiac arrest using time-dependent variables based on a case-control study of emergency department (ED) patients with AMI: 65 cases with sudden cardiac arrest and 258 without cardiac arrest. Within the first hour of AMI symptom onset, adjusting for age, systolic blood pressure, serum potassium, and infarct size, increased risk of cardiac arrest was associated with electrocardiographic prolonged QTc interval and a greater sum of ST-segment elevation. After 1 hour, the effect of ST-segment elevation was much reduced and the effect of the QTc interval was reversed, so prolonged QTc appeared protective. Accordingly, for patients presenting 30 minutes after chest pain onset, compared with a QTc of 0.44, the risk for cardiac arrest for patients with QTc of 0.50 was more than doubled (odds ratio [OR] 2.20, 95% confidence intervals [CI] 1.17 to 4.13), whereas for those presenting after an hour, it was much lower (e.g., at 1.5 hours, OR 0.21, 95% CI 0.06 to 0.73). Patients presenting 30 minutes after chest pain onset with a sum of ST elevation of 20 mm had a threefold higher risk than patients with a sum of ST elevation of 5 mm (OR 3.37, 95% CI 1.83 to 6.20). However, if presenting 1.5 hours after chest pain onset, the risk was barely elevated (OR 1.18; 95% CI 1.09 to 1.29). Thrombolytic therapy was protective, halving the odds of cardiac arrest (OR 0.51, 95% CI 0.27 to 0.93). Thus, the relation of prolonged QTc interval and substantial ST segment elevation to cardiac arrest in AMI may be obscured because patients with these risks are more likely to die soon after AMI onset, before ED presentation, and are thereby unavailable for study. Those with prolonged QTc or substantial ST elevation who survive the initial 1.5-hour period are those less susceptible to these risks.     

Cardiopulmonary bypass in a model of acute myocardial infarction and cardiac arrest

Cardiopulmonary bypass (CPB) reperfusion has demonstrated improved resuscitation rates in ventricular fibrillation cardiac arrest models. To investigate the effectiveness of CPB reperfusion in an ischemic cardiac arrest setting, simulating the clinical scenario of myocardial ischemia preceding sudden cardiac death, we developed a canine model of acute myocardial infarction followed by ventricular fibrillation. Sixteen dogs were randomly assigned to two groups. Group 1 (eight) had ventricular fibrillation induced without left anterior descending coronary artery occlusion. Group 2 (eight) had a thrombogenic copper coil placed in the left anterior descending artery and showed ECG evidence of acute myocardial infarction before induction of ventricular fibrillation. CPR commenced after eight minutes of ventricular fibrillation. Epinephrine 0.05 mg/kg and NaHCO3 1.0 mEq/kg were administered at ten minutes. CPB was begun at 12 minutes and continued for one hour. Myocardial ischemic and necrotic areas were determined in four-hour survivors by dual histochemical staining. All animals were resuscitated; all eight group 1 and six of eight group 2 animals survived to four hours. With the onset of CPB, coronary perfusion pressures increased significantly by 68.6 +/- 31.8 (SD) mm Hg in group 1 and 56.2 +/- 34.6 mm Hg in group 2 over those obtained with CPR (P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)     

急性心肌梗塞合并心脏骤停的急救治疗分析

目的：探讨急性心肌梗塞合并心脏骤停的急救方法,分析疗效。方法选取以往10例急性心肌梗塞合并心脏骤停的患者,回顾当时的急救治疗过程,通过对心电的检测情况、早期电击除颤情况、电击除颤时所用药物以及用药的方法和途径进行分析,讨论急救治疗的有效方法,提高复苏成功概率。结果通过对10例患者进行急救,利用电击除颤的方法,观察心电变化情况,进行合理药物治疗,10例患者都得到了及时的抢救,复苏成功,血压得到控制,心跳频率恢复平稳状态,心律逐渐变为窦性。经过后期治疗有9例患者成功出院,有1例患者由于突发性心脏病去世。结论及时观察心电的变化情况,做到早发现,早进行急救,进而成功的救助患者生命,再加上急救之后的护理干预,确保每一个患者顺利康复出院。     

Frequency of hypokalemia after successfully resuscitated out-of-hospital cardiac arrest compared with that in transmural acute myocardial infarction

To evaluate the prevalence of hypokalemia in out-of-hospital cardiac arrest, the initial serum potassium and arterial pH values were reviewed from 138 consecutive patients resuscitated from cardiac arrest. For comparison, the same variables were reviewed for 62 consecutive patients who had transmural acute myocardial infarction (AMI) without cardiac arrest. The mean serum potassium level was lower after resuscitation from cardiac arrest (3.6 +/- 0.6 mEq/liter) than during AMI (3.9 +/- 0.5 mEq/liter) (p less than 0.005). The incidence of hypokalemia (potassium less than 3.5 mEq/liter) was greater in patients sustaining cardiac arrest (41%) than in patients who had AMI without cardiac arrest (11%) (p less than 0.001). Hypokalemia was common after cardiac arrest regardless of the occurrence of AMI at the time of arrest. Hypokalemia after cardiac arrest was independent of arterial pH, epinephrine or bicarbonate therapy during resuscitation, or prior therapy with diuretic drugs, digoxin or propranolol. In 10 patients with marked hypokalemia, the serum potassium level returned to normal rapidly (16 hours) during the hospitalization even though only 29% of the predicted potassium requirement was infused before its normalization. Thus, hypokalemia is prevalent immediately after out-of-hospital cardiac arrest, whereas it is uncommon in AMI in the absence of cardiac arrest. The cause and electrophysiologic consequences of this hypokalemia are unknown; in most cases, it is apparently caused by a shift of potassium from the intravascular compartment rather than a total body depletion of potassium.     

Outcome determinants in cardiac arrest patients secondary to acute myocardial infarction receiving extra-corporeal membrane oxygenation combined with percutaneous coronary intervention therapy

正Objective To investigate the clinical efficacy and outcome determinants in cardiac arrest patients secondary to acute myocardial infarction treated with extracorporeal membrane oxygenation(ECMO)and percutaneous coronary intervention(PCI).Methods The clinical data of27 patients hospitalized from January 2014 to March 2017 in 3 hospitals were retrospectively analyzed.The clinical     

Does overprotection cause cardiac invalidism after acute myocardial infarction?

OBJECTIVE: To determine if overprotection on the part of the patient's family and friends contributes to the development of cardiac invalidism after acute myocardial infarction. DESIGN: Longitudinal survey. SETTING: Nine hospitals in the southwestern United States. SUBJECTS: One hundred eleven patients who had experienced a first acute myocardial infarction. Subjects were predominantly male, older-aged, married, caucasian, and in functional class I. Eighty-one patients characterized themselves as being overprotected (i.e., receiving more social support from family and friends than desired), and 28 reported receiving inadequate support. Only two patients reported receiving as much support as they desired. OUTCOME MEASURES: Self-esteem, emotional distress, health perceptions, interpersonal dependency, return to work. RESULTS: Overprotected patients experienced less anxiety, depression, anger, confusion, more vigor, and higher self-esteem than inadequately supported patients 1 month after myocardial infarction (p < 0.05). Inadequately supported patients were more dependent 4 months after the event. CONCLUSIONS: Overprotection on the part of family and friends may facilitate psychosocial adjustment in the early months after an acute myocardial infarction rather than lead to cardiac invalidism.     

Use of exercise cardiac rehabilitation after acute myocardial infarction.

The purpose of this study was to determine the rate of participation of patients after acute myocardial infarction (AMI) in phase II cardiac rehabilitation with exercise training (ie, exercise cardiac rehabilitation, ECR) in Japan. Forty-six hospitals treating patients with AMI were surveyed for their implementation of phase II ECR after AMI in 1996-98. Of the 46 hospitals, 19 were approved and 27 were not approved for health insurance payment for ECR. A total of 13685 patients with AMI were admitted to the 46 hospitals. There were no differences between approved and non-approved hospitals in the annual number of patients with AMI (Approved, 117+61 vs Non-approved, 86+71 patients per hospital, NS), the rate of performance of emergency coronary angioplasty (63+16 vs 65+20%, NS), or the rate of emergency coronary stenting (31+16 vs 34+22%, NS). However, ECR was performed routinely in 84.2% (16/19 hospitals) of the approved hospitals, but in only 22.2% (6/27 hospitals) of the non-approved hospitals (p<0.001). Although the participation rate of AMI patients in ECR was 21.0% (2875/13685 patients) overall, it was markedly lower in the non-approved hospitals (8.0%, 557/6999 patients) than in the approved hospitals (34.7%, 2318/6686 patients, p<0.0001). Based on the present result, the overall rate of participation of AMI patients in ECR in Japan was estimated at 4.8-11.7%. Despite similar patient volumes and acute phase interventional treatment of AMI between the hospitals approved and not approved for health insurance payment for ECR, ECR was markedly underused in the non-approved hospitals in Japan. To promote ECR for all AMI patients in Japan, the number of hospitals approved for ECR should be substantially increased.     

Brain natriuretic peptide and cardiac rupture after acute myocardial infarction

Cardiac rupture is a fatal complication in the acute stage of myocardial infarction (MI). However, no measures have yet been established to predict it. Herein we describe three MI patients with cardiac rupture in whom plasma brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) concentrations had been serially monitored from the onset of MI to cardiac rupture. In these cases, plasma BNP levels increased without symptomatic and hemodynamic changes and reached their highest level immediately before cardiac rupture, while plasma ANP levels remained unchanged. These cases suggest that the increased plasma BNP concentrations without symptomatic and hemodynamic changes may be a useful marker for predicting cardiac rupture after acute MI.     

Predictors of ventricular fibrillation or cardiac arrest in patients hospitalized for acute myocardial infarction

A community-wide study of patients hospitalized with acute myocardial infarction in metropolitan Baltimore was conducted to examine socio-demographic and clinical characteristics in association with ventricular fibrillation and cardiac arrest (VF/CA). Multivariate analyses revealed that variables significantly associated with occurrence of VF/CA included older age (60 years or older), male sex, and a history of cigarette smoking. These factors allow the identification of subgroups of patients hospitalized with acute myocardial infarction at high risk for the subsequent development of VF/CA, in whom prophylactic therapy and close surveillance are especially recommended.