Bretylium Tosylate in the Management of Refractory Ventricular Fibrillation

Nine patients who had recurrent ventricular fibrillation following acute myocardial infarction or angina were given bretylium tosylate in a dose of 5 mg./kg. intramuscularly every eight hours after other measures had proved ineffective. Provided the patients were not in shock or in heart failure, there was a considerable reduction in the episodes of ventricular fibrillation.A second group of nine patients who developed recurrent ventricular fibrillation following open heart surgery were given bretylium intravenously, which controlled the arrhythmia in every instance.Bretylium did not completely abolish ventricular premature beats but the latter did not initiate ventricular fibrillation even when they occurred on the T wave.     

Late potentials in an ovine model of acute transmural myocardial infarction.

The development of slow conduction during the first hours of acute transmural myocardial infarction (ATMI) was studied by signal-averaged electrocardiograms (SAE) in 19 adult anesthetized sheep. SAEs were recorded before and after intravenous infusions of lidocaine and bretylium were begun and 10, 30, and 60 min after ATMI produced by ligation of the left anterior descending and second diagonal coronary arteries. Four sheep died promptly of ventricular tachyarrhythmias; two others developed sustained ventricular arrhythmias, which precluded additional data. Biphasic changes in QRS duration, root mean square voltage of the terminal 40 ms of the QRS complex, and duration of terminal low-amplitude (less than 30 microV) signal were observed. Peak changes in conduction occurred 30 min after infarction and regressed toward baseline thereafter. At 30 min, all animals developed late potentials, which were defined as signals that exceeded both after-drug QRS duration and duration of terminal low-amplitude signal less than 30 microV by more than two standard deviations. At 60 min, only 3 of 13 (23%) animals had late potentials. Conduction is slowest 30 min after ATMI in sheep but may not be related to development of ventricular arrhythmias. In five of six sheep (83%), ventricular arrhythmias occurred within 15 min of infarction before peak slowing was observed by SAE.     

Reduction of ventricular arrhythmias by early intravenous atenolol in suspected acute myocardial infarction.

The effect of intravenous atenolol on ventricular arrhythmias in acute myocardial infarction was assessed in 182 patients admitted within 12 hours of the onset of chest pain. Ninety-five patients were randomised to receive 5 mg intravenous atenolol followed immediately by 50 mg by mouth and 50 mg 12 hours later, then 100 mg daily for 10 days; 87 patients served as controls. The treated patients had significantly fewer ventricular extrasystoles; 58 control patients (67%) had R-on-T extrasystoles compared with only 25 treated patients (26%) (2p less than 0.0001); repetitive ventricular arrhythmias were detected in 64 control patients (74%) and 55 treated patients (58%) (2p less than 0.05). Heart rate was significantly reduced from 77 +/- 1 beats/min at entry to 65 +/- 1 beats/min (2p less than 0.001) in the first hour after intravenous atenolol, and in addition the rate was significantly different from that in the control group. There was no difference in the incidence of heart failure, but fewer patients in the treated group received other antiarrhythmic agents or digoxin. These results show that early intravenous atenolol prevents ventricular arrhythmias in suspected acute myocardial infarction.     

Late ventricular potentials--a new risk factor for cardiac arrhythmias in recent myocardial infarction

The study involved 150 patients with recent myocardial infarction. Ventricular lat potentials were registered in these patients during the first 48 hours and repeated in the third week. Ventricular late potentials were found in 31 patients (21%) in the first 48 hours, and in 27 out of 134 patients (20%) before the release from the hospital. Comparing potentials registration in the acute and late phase of the myocardial infarction it was found that ventricular late potentials occurred in 6 and disappeared in 4 patients. Stable ventricular tachycardia was significantly more frequent (p less than 0.001) within the first 48 hours in patients with ventricular late potentials than those without them (19% vs 3%). Ventricular late tachycardia (over 48 hours) was more frequent (p less than less than 0.001) in patients with ventricular late potentials (21% vs 1%). Premature ventricular excitations of Lown class 2-5 were also more frequent (p less than 0.001) in the group of patients with ventricular late potentials than those without these potential (81% vs 24%) when registered with a 24-hour Holter ECG in the third week following myocardial infarction. Antiarrhythmic drugs did not produce the regression of ventricular late potentials. Non-invasive registration of ventricular late potentials helps to select patients with life-threatening ventricular arrhythmias following the acute myocardial infarction.     

Lack of relation between venous plasma total catecholamine concentrations and ventricular arrhythmias after acute myocardial infarction.

Electrocardiographic tracings were recorded continuously to monitor ventricular tachycardia and R-on-T and R-on-apex-T ventricular premature beats, and repeated estimations of venous plasma total catecholamine concentrations were carried out in 26 patients admitted to a coronary care unit with acute myocardial infarction. No relation existed between the increased catecholamine concentrations found in these patients and the incidence of ventricular arrhythmias occurring six to 48 hours after the onset of symptoms.     

Late ventricular fibrillation following successful resuscitation from postinfarction cardiogenic shock with intraaortic balloon pumping

Early ventricular fibrillation occurs in approximately 5% of patients admitted for acute myocardial infarction. Although late ventricular fibrillation (> 48 hours postinfarction) may occur in stable patients, it occurs more commonly when severe left ventricular power failure is present. We have encountered late ventricular fibrillation in three of 42 (7%) patients treated with intraaortic balloon pumping (IABP) for profound cardiogenic shock secondary to myocardial infarction. These patients progressed to our hemodynamic Class A prior to weaning, and were thought to be stable prior to IABP removal. They were the only ones who expired after achieving Class A status. The episodes of late ventricular fibrillation occurred after the patients had been successfully weaned from IABP and were free of arrhythmias. This experience suggests that prolonged antiarrhythmic therapy may be indicated for postinfarction patients who have had ventricular dysrhythmias during IABP support.     

急性心肌梗死伴新发束支传导阻滞的临床意义

目的:观察急性心肌梗死伴新发左、右束支传导阻滞的临床特点,评价束支阻滞对急性心肌梗死预后的影响。方法:对上海交通大学附属第一人民医院心内科重症监护室2010年1月1日到12月31日收治的197例急性心肌梗死患者的病历资料进行回顾性分析,根据束支传导阻滞有无及类型分为左束支传导阻滞组(12例),右束支传导阻滞组(19例)和对照组(无束支传导阻滞的急性心梗,166例)。分析和比较三组患者的基线资料,心梗部位、Killip分级、恶性室性心律失常、左室射血分数LVEF、病变血管数量、梗死相关冠脉、住院天数及病死率、实验室检查(BNP,心肌损伤标志物峰值)。结果:LBBB组AMI患者的恶性心律失常发生率明显高于对照组(P=0.007),LVEF明显低于RBBB组和对照组(P值分别为0.020、0.045),梗死相关动脉以LAD多见。结论:急性心梗伴束支传导阻滞往往提示病情严重,预后不良,急性心梗合并左束支阻滞较合并右束支阻滞病情更严重。     

Intravenous tissue plasminogen activator and size of infarct,left ventricular function,and survival in acute myocardial infarction.

STUDY OBJECTIVE--To assess effect of intravenous recombinant tissue type plasminogen activator on size of infarct, left ventricular function, and survival in acute myocardial infarction. DESIGN--Double blind, randomised, placebo controlled prospective trial of patients with acute myocardial infarction within five hours after onset of symptoms. SETTING--Twenty six referral centres participating in European cooperative study for recombinant tissue type plasminogen activator. PATIENTS--Treatment group of 355 patients with acute myocardial infarction allocated to receive intravenous recombinant plasminogen activator. Controls comprised 366 similar patients allocated to receive placebo. INTERVENTION--All patients were given aspirin 250 mg and bolus injection of 5000 IU heparin immediately before start of trial. Patients in treatment group were given 100 mg recombinant tissue plasminogen activator over three hours (10 mg intravenous bolus, 50 mg during one hour, and 40 mg during next two hours) by infusion. Controls were given placebo by same method. Full anticoagulation treatment and aspirin were given to both groups until angiography (10-22 days after admission). beta Blockers were given at discharge. END POINT--Left ventricular function at 10-22 days, enzymatic infarct size, clinical course, and survival to three month follow up. MEASUREMENTS AND MAIN RESULTS--Mortality was reduced by 51% (95% confidence interval -76 to 1) in treated patients at 14 days after start of treatment and by 36% (-63 to 13) at three months. For treatment within three hours after myocardial infarction mortality was reduced by 82% (-95 to -31) at 14 days and by 59% (-83 to -2) at three months. During 14 days in hospital incidence of cardiac complications was lower in treated patients than controls (cardiogenic shock, 2.5% v 6.0%; ventricular fibrillation, 3.4% v 6.3%; and pericarditis, 6.2% v 11.0% respectively), but that of angioplasty or artery bypass, or both was higher (15.8% v 9.6%) during the first three months. Bleeding complications were commoner in treated than untreated patients. Most were minor, but 1.4% of treated patients had intracranial haemorrhage within three days after start of infusion. Enzymatic size of infarct, determined by alpha hydroxybutyrate dehydrogenase concentrations, was less (20%, 2p = 0.0018) in treated patients than in controls. Left ventricular ejection fraction was 2.2% higher (0.3 to 4.0) and end diastolic and end systolic volumes smaller by 6.0 ml (-0.2 to -11.9) and 5.8 ml (-0.9 to -10.6), respectively, in treated patients. CONCLUSION--Recombinant tissue type plasminogen activator with heparin and aspirin reduces size of infarct, preserves left ventricular function, and reduces complications and death from cardiac causes but at increased risk of bleeding complications4+     

Clinical Experience with Dextro-Alprenolol

Experience with dextro-alprenolol in nine patients has shown that it is relatively ineffective in treating arrhythmias associated with acute myocardial infarction. Marginal effectiveness in the control of ventricular ectopic beats after myocardial infarction is outweighed by an appreciable hypotensive effect with risk of infarction. The drug was ineffective in the management of supraventricular arrhythmias.     

Effect of intravenous infusion of insulin in diabetics with acute myocardial infarction.

Diabetes mellitus is associated with a high mortality after myocardial infarction. To see whether this may be decreased by improved diabetic control the effect of an insulin infusion regimen was studied in patients with acute myocardial infarction. From April 1982 to April 1983, 33 diabetics were admitted with acute myocardial infarction. Those being treated with diet alone or oral hypoglycaemic drugs continued with this unless control was poor, when they were changed to a "sliding scale" regimen of subcutaneous insulin injections thrice daily. Those already receiving insulin were maintained on thrice daily subcutaneous injections. From April 1983 to April 1984, 29 diabetics had acute myocardial infarction. Those receiving treatment with oral hypoglycaemic drugs or insulin were changed to continuous intravenous infusion of insulin, the aim being to maintain the blood glucose concentration at 4-7 mmol/I (72-126 mg/100 ml). Those being treated with diet alone continued with this if blood glucose concentrations were acceptable. Total mortality fell from 42% in the first year to 17% in the second (p less than 0.05). Over the same period mortality among non-diabetic patients with myocardial infarction did not change significantly. There was a significant fall in cardiac arrhythmias (expressed as the percentage of patients in whom arrhythmias were recorded) from 42% to 17% (p less than 0.05). The most significant fall in the incidence of complications occurred in those who had been receiving oral hypoglycaemic drugs on entry to the study (87% to 50%, p less than 0.05).     

急性心肌梗死静脉溶栓治疗和心电监护的体会

目的探讨静脉溶栓治疗和心电监护对急性心肌梗死（AMI）的疗效。方法全部病例均符合WHO规定的AMI诊断标准,治疗均给予尿激酶（UK）100U～150万U,加生理盐水100ml,静脉点滴,30min滴完。同时给予心电监护,以期能及时发现患者存在的各种心律失常。结果本组72例中,均无牙齿出血、消化道出血及出血性脑卒中等并发症的发生,1例出现静脉穿刺部位皮肤瘀斑;所有患者均好转出院。结论静脉溶栓治疗和心电监护对急性心肌梗死（AMI）的疗效可靠,值得在基层医院使用。     

Shock Following Myocardial Infarction: A Clinical Survey of 140 Cases

All admissions for acute myocardial infarction to a metropolitan general hospital over a 10-year period have been reviewed. One hundred and forty patients developed complications meeting the criteria for cardiogenic shock. The mortality rate in this group of patients was 83%. The mortality rate in 95 patients who received treatment with intravenous noradrenaline was no different from that in 45 patients who did not receive this type of therapy (p = >0.8). Patients dying from cardiogenic shock were younger than those dying of other complications. Autopsy study of this group of shocked patients revealed a significantly lower incidence of previous healed myocardial infarction (p = <0.01).A decline in the annual incidence of cardiogenic shock was noted over the decade surveyed. It is suggested that this may be due to the earlier and more frequent use of intravenous noradrenaline. Despite the reduction in the incidence of shock, the annual mortality rate from myocardial infarction has remained unaltered.     

High incidence of cardiovascular complications in pheochromocytoma

Excess of catecholamines in pheochromocytoma is usually accompanied with classical symptoms and signs. In some cases, severe cardiovascular complications (e. g., heart failure, myocardial infarction) may occur. We performed a retrospective analysis focused on the incidence of cardiovascular complications (classified as follows: arrhythmias, myocardial involvement or ischemia and atherosclerosis, cerebrovascular impairment) before the establishment of diagnosis of pheochromocytoma among 145 subjects treated in our hospital. Cardiovascular complications occurred in 28 subjects, but these subjects did not differ significantly from subjects without complications in age, gender, body mass index, paroxysmal symptoms, symptom duration, tumor dimension, catecholamine secretory phenotype, and incidence of hypertension or diabetes mellitus. Arrhythmias occurred in 15 subjects (2 arrhythmia types in 2 subjects): atrial fibrillation in 9 subjects, supraventricular tachycardia in 3 cases, and ventricular tachycardia in 2 patients. Significant bradycardia was noted in 3 cases. Five subjects presented with heart failure with decreased systolic function (takotsubo-like cardiomyopathy found in 2 cases). One subject suffered from hypertrophic obstructive cardiomyopathy. Seven subjects presented with non-ST-segment elevation myocardial infarction, 2 patients with ST-segment myocardial infarction, and 1 subject underwent coronary artery bypass grafting. Two subjects suffered from significant peripheral atherosclerosis. Among cerebrovascular complications, transient ischemic attack was found in 3 cases, 2 subjects suffered from stroke, and subarachnoidal bleeding occurred in 1 patient. One subject suffered from diffuse neurological impairment due to multiple ischemic white matter lesions. These data show relatively high incidence of cardiovascular complications (19.3%) in subjects with pheochromocytoma. Early diagnosis is mandatory to prevent severe complications in pheochromocytoma.     

Risk-benefit stratification as a guide to lidocaine prophylaxis of primary ventricular fibrillation in acute myocardial infarction: an analytic review.

Early investigators suggested that ventricular fibrillation without heart failure in acute myocardial infarction was reliably preceded by warning arrhythmias, and that suppression of such arrhythmias with intravenous lidocaine could avoid the need for resuscitation. While the efficacy and safety of lidocaine have been substantiated, the reliability of warning arrhythmias as predictors for primary ventricular fibrillation has not. We present data showing that the risk of primary ventricular fibrillation is most dependent on the patient''s age and the interval since the onset of his symptoms, rather than on the presence of warning arrhythmias. We have estimated that lidocaine prophylaxis would have to be given to about 12 patients in the highest risk group (patients under age 50 and within six hours of the onset of symptoms), compared to about 400 patients in the lowest risk group (patients above age 70 and more than 24 hours since the onset of symptoms), to prevent one episode of primary ventricular fibrillation in each group. We propose that these risk stratifications, as adapted to the conditions in specific hospitals, provide the most rational approach to lidocaine prophylaxis of primary ventricular fibrillation.     

Guidelines for the use of intravenous thrombolytic agents in acute myocardial infarction. Ontario Medical Association Consensus Group on Thrombolytic Therapy.

A consensus group convened under the auspices of the Ontario Medical Association produced guidelines for the use of intravenous thrombolytic agents in acute myocardial infarction. The guidelines, updated to December 1988, include the following points. 1) Any hospital that routinely accepts the responsibility for looking after patients with acute myocardial infarction could offer thrombolytic therapy if monitoring facilities are available and if the staff are experienced in the treatment of cardiac rhythm disturbances. 2) Before treatment, all patients must be carefully screened for factors predisposing to hemorrhagic complications. 3) A physician should be clearly designated as responsible for the care of the patient receiving an infusion and be available in the event of problems. 4) For the two approved agents the usual dosages are as follows: streptokinase, 1.5 million units given over 1 hour; and tissue-type plasminogen activator (tPA), 100 mg over 3 hours, delivered as 60 mg in the first hour (of which 6 to 7 mg should be given as a bolus in the first 1 to 2 minutes) and then an infusion of 20 mg/h over the next 2 hours. 5) Intravenous thrombolytics should be considered for any patient with presumed acute myocardial infarction, as suggested by prolonged chest pain or other appropriate symptoms and typical electrocardiographic changes. Expeditious treatment is critical, since myocardial necrosis occurs within hours. 6) Emergency angiography is indicated for patients with hemodynamic compromise and no apparent response to streptokinase or tPA and in those with recurrent chest pain suggestive of acute myocardial infarction despite an apparent response to intravenous thrombolysis. Angiography before discharge is recommended for patients with postinfarction angina or evidence from noninvasive testing of significant residual ischemic risk. 7) There is insufficient evidence to choose between streptokinase and tPA on the basis of the two most important outcome measures: patient survival and myocardial preservation. More conclusive evidence comparing tPA, streptokinase and another promising agent, acylated plasminogen-streptokinase activator complex, will be available in 1989-90.     

Survival in acute myocardial infarction; factors observed in 318 patients

Factors influencing survival in a group of 318 cases of acute myocardial infarction were analyzed. The mortality rate for the entire series was 41 per cent. Among the men it was 39.5 per cent; among women, 44.4 per cent. The mortality rate increased with the age of the patient. Twenty-six per cent of all deaths occurred within the first 24 hours, 44 per cent within 72 hours, and 71 per cent within the first week following hospital admission. Increased mortality rate was associated with previous history of congestive failure, myocardial infarction, hypertension or cardiomegaly. As to circumstances immediately preceding an infarction, the only ones that seemed to be related to a high mortality rate were hemorrhage and the postoperative state. Not only the presence but the degree of shock, congestive failure, cyanosis and dyspnea adversely influenced chances for survival. Duration, location, radiation and number of attacks of pain did not appear to be associated with extraordinary mortality rates. Anterior was slightly more common than posterior infarctions, and the mortality rate was much higher. Thromboembolic complications and certain disorders of rhythm and of conduction definitely worsen prognosis. Comparison of average mortality data as reported in different studies on acute myocardial infarction is improper and misleading because of the great differences between the kinds of patients included in various series reported upon. A standard method of grading the severity of acute myocardial infarction would help toward sounder comparisons.     

T波峰-末间期对急性心肌梗死并发室性心律失常的预测价值

目的:探讨T波峰-末间期(Tp-Te间期)和Tp-Te间期离散度(Tp-Ted)对急性心肌梗死并发室性心律失常的预测价值。方法:选择我院2013年5月至2014年5月收治的140例确诊急性ST段抬高型心肌梗死(STEMI)患者,按照心律失常类型分为室性心动过速组,室性早搏组以及无室性心律失常组。分析并比较各组患者心电图Tp-Te间期及Tp-Ted的变化情况。结果:急性期FPG、Tp-Te、Tp-Ted高于恢复期,差异有统计学意义(P0.05);急性期与恢复期之间TG、CHOL、LDL-C、K+、Na+水平差异无统计学意义(P0.05)。无室性心律失常组与室性心动过速组及室性早搏组比较,Tp-Te和Tp-Ted更低,差异有统计学意义(P0.05);室性早搏组和室性心动过速组比较,Tp-Te和Tp-Ted更低,差异有统计学意义(P0.05)。结论:Tp-Te间期和Tp-Ted可用于区分急性心肌梗死患者室性心律失常类型。     

Effects of intravenous magnesium in suspected acute myocardial infarction: overview of randomised trials.

OBJECTIVE--To investigate the effect of intravenous magnesium on mortality in suspected acute myocardial infarction. DESIGN--Systematic overview of all available randomised trials in which patients were allocated to receive either intravenous magnesium or otherwise similar treatment without magnesium. SETTING--Coronary care units of several hospitals. PATIENTS--1301 patients in seven randomised trials. MAIN OUTCOME MEASURE--Short term mortality. RESULTS--Considering the seven trials collectively there were 25 (3.8%) deaths among 657 patients allocated to receive magnesium and 53 (8.2%) deaths among 644 patients allocated control, generally during hospital follow up. This represents a 55% reduction in the odds of death (p less than 0.001) with 95% confidence intervals ranging from about one third to about two thirds. 70 of 648 patients allocated magnesium compared with 109 of 641 controls had serious ventricular arrhythmias, suggesting that magnesium reduces the incidence, though the definition varied among trials. Other adverse effects were rare in the limited number of patients for whom this data were available. CONCLUSION--Despite the limited number of patients randomised this overview suggests that intravenous magnesium therapy may reduce mortality in patients with acute myocardial infarction. Further large scale trials to confirm (or refute) these findings are desirable.     

Effect of Heparin on Serum Free-fatty-acids,Plasma Catecholamines,and the Incidence of Arrhythmias following Acute Myocardial Infarction

The effect of intravenous heparin in a therapeutic dosage on cardiac arrhythmias in patients with indubitable acute myocardial infarction was investigated. The value of serum free-fatty-acids (F.F.A.s) and plasma catecholamines in the prediction of patients vulnerable to serious arrhythmias was also studied.Heparin produced a significant rise in F.F.A., maximal within 10 minutes of injection, but did not increase the incidence of cardiac arrhythmias.No relationship was found between the incidence of arrhythmias and the initial levels of F.F.A. or adrenaline. No correlation was obtained between F.F.A. and plasma catecholamine levels. Heparin did not have a consistent effect on plasma catecholamines. Initial control plasma noradrenaline concentrations, however, were found to be significantly correlated with the incidence of subsequent arrhythmias. It is suggested that the level of plasma noradrenaline may be a valuable predictive guide to those patients likely to develop significant arrhythmias after acute myocardial infarction.     

Initial Heparin Therapy in Acute Myocardial Infarction

The administration of heparin during the first 48 hours following acute myocardial infarction is widely practised. Heparin treatment is also recommended for acute coronary insufficiency on the grounds that it may prevent development of an impending myocardial infarction. These measures had been accepted without support of a controlled clinical trial. By random selection, 101 patients hospitalized with a provisional diagnosis of acute myocardial infarction received heparin (100 mg. intravenously every eight hours for 48 hours) and 105 patients were assigned to a control group. Both groups of patients received bishydroxycoumarin (Dicumarol). The mortality in the heparin series was 30% and in the control group, 28%. A significantly large number of the heparin-treated patients developed clinical and laboratory proof of recent myocardial infarction. It is concluded that early intermittent intravenous heparin treatment does not lower the mortality in patients with acute myocardial infarction nor does it prevent impending myocardial infarction in patients with acute coronary insufficiency.