Out-of-hospital cardiac arrest: Causes according to autopsy and electrocardiography - Analysis of 781 patients with neither hospital care nor prescribed medication during the preceding two years.

BACKGROUND: There is a knowledge gap regarding aetiology of and potential for predicting out-of-hospital cardiac arrest (OHCA) among individuals who are healthy before the event. AIM: To describe causes of OHCA and the potential for predicting OHCA in apparently healthy patients. METHODS: Patients were recruited from the Swedish Register of Cardiopulmonary Resuscitation from November 2007 to January 2011. Inclusion criteria were: OHCA with attempted CPR but neither dispensed prescription medication nor hospital care two years before the event The register includes the majority of patients suffering OHCA in Sweden where cardiopulmonary resuscitation (CPR) was attempted. Medication status was defined by linkage to the Swedish Prescribed Drug Register. Cause of death was assessed based on autopsy and the Swedish Cause of Death Register. Prediction of OHCA was attempted based on available electrocardiograms (ECG) before the OHCA event. RESULTS: Altogether 781 individuals (16% women) fulfilled the inclusion criteria. Survival to 30 days was 16%. Autopsy rate was 72%. Based on autopsy, 70% had a cardiovascular aetiology and 59% a cardiac aetiology. An ECG recording before the event was found in 23% of cases. The ECG was abnormal in 22% of them. CONCLUSION: Among OHCA victims who appeared to be healthy prior to the event, the cause was cardiovascular in the great majority according to autopsy findings. A minority had a preceding abnormal ECG that could have been helpful in avoiding the event.

Conventional and dedicated atrial overdrive pacing for the prevention of paroxysmal atrial fibrillation: the AFTherapy study.

AIMS: This investigation was conducted to determine the effectiveness of several conventional overdrive pacing modalities (single rate and rate responsive pacing at various lower rates) and of four dedicated preventive pacing algorithms in the suppression of paroxysmal atrial fibrillation (AF). METHOD AND RESULTS: In this multi-centre, randomized trial, 372 patients with drug-refractory paroxysmal AF were enrolled. Patients received a dual-chamber pacing device capable of delivering conventional pacing therapy as well as dedicated AF prevention pacing therapies and to record detailed AF-related diagnostics. The primary endpoint was AF burden, whereas secondary endpoints were time to first AF episode and averaged sinus rhythm duration. During a conventional pacing phase, patients were randomized to single rate or rate-responsive pacing with lower rates of either 70 or 85 min(-1) or to a control group with single rate pacing at 40 min(-1). In the subsequent preventive pacing phase, patients underwent pacing at a lower rate of 70 min(-1) with or without concomitant application of four preventive pacing algorithms. A substantial amount of data was excluded from the analysis because of atrial-sensing artefacts, identified in the device-captured diagnostics. In the conventional pacing phase, no significant differences were found between various lower rates and the control group receiving single rate pacing at 40 min(-1) or between single rate and rate-responsive pacing. Patients receiving preventive pacing with all four therapies enabled had a similar AF burden compared with patients treated with conventional pacing at 70 min(-1) (P = 0.47). CONCLUSIONS: The results do not demonstrate a significant effect of conventional atrial overdrive pacing or preventive pacing therapies. However, the observations provided important information for further consideration with respect to the design and conduct of future studies on the effect of atrial pacing therapies for the reduction of AF.

Acute effects of lignocaine, procainamide, metoprolol, digoxin and atropine on human myocardial refractoriness.

The acute intravenous effects of therapeutic doses of procainamide, lignocaine, metoprolol, digoxin and atropine on the monophasic action potentials (MAP) and effective refractory periods of the right ventricle (VERP) were studied in 48 healthy volunteers. Procainamide prolonged the VERP in the apex region. Lignocaine shortened the MAP duration at 90% repolarisation. Metoprolol did not affect any of the measured variables in spite of a significant decrease in heart rate. Digoxin produced a significant increase in the VERP at the outflow tract, but not in the apex region and the MAP variables did not change. Following atropine, the VERP at both recording sites decreased but the MAP signal was unaffected. In summary, the effects of procainamide, lignocaine, metoprolol and digoxin were in good agreement with previous studies in normal ventricular muscle cells in vitro. In addition, the findings following atropine, digoxin and procainamide are indicative of a parasympathetic innervation of the endocardial surface of the right ventricle.

Prediction of terminal atrial myocardial repolarisation from incomplete phase 3 data.

The duration of the monophasic action potential (MAP) carries prognostic antiarrhythmic information when the recording is done during sinus rhythm (SR) after DC conversion of atrial fibrillation (AF). This study analyses whether it is possible to predict MAP duration during sinus rhythm by analysing the atrial MAP during AF, even though complete myocardial repolarisation is never reached during this arrhythmia. We have therefore evaluated the estimated duration of the action potential (AP) and MAP by exponential extrapolation of phase 3 data. (1) AP studies were done on 11 human atrial myocardial specimens. Resting membrane potential (RMP) and AP duration were better identified when more data obtained during repolarisation were used for prediction. Thus the predicted RMP deviated on average by -0.4% of AF amplitude from the real RMP level when data to 90% repolarisation were used for extrapolation. AP duration at 90% repolarisation correlated well with the real AP duration (r = 0.88) at this level of data aquisition. (2) Continuous recording of atrial MAPs was done in 15 patients during AF and in 12 of these during SR after DC conversion. Resting myocardial repolarisation level during AF, RP(EST), and estimated MAP duration, MAPD(EST), could be calculated by exponential extrapolation in 12 patients. The actual repolarisation during fibrillation reached below 90% of the RP(EST) level in eight patients and below 70% in all 12. The MAP duration during SR could be predicted with increasing precision when data closer to the RP(EST) were used for calculation of MAPD(EST). Thus MAPD(EST) correlated well with SR MAP duration when data reaching at least 90% of RP were used (r = 0.85).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular block progression in patients with bifascicular block assessed by repeated electrocardiography and a bradycardia-detecting pacemaker.

Syncope may be due to intermittent high-degree atrioventricular (AV) block, but a cause-relation is sometimes difficult to prove. Diagnostic methods with high predictive value proven by instruments for safe and sensitive follow-up are needed. A bradycardia-detecting pacemaker was used in patients with bifascicular block, who had been the subjects of pharmacologic stress testing of the His-Purkinje system. Thirty-seven patients were included, of whom 26 had experienced at least 1 syncopal episode of suspected bradycardia origin, and 11 had previously documented transient high-degree AV block. The electrophysiologic study included injection of disopyramide 2 mg/kg (up to 150 mg) over 5 minutes. A positive test result was defined as spontaneous or pacing-induced His-Purkinje high-degree AV block after drug or a drug-induced HV prolongation of > or = 50%. Patients were followed an average 63 months with repeated electrocardiography and a diagnostic pacemaker (n = 23). Altogether, 24 patients had a significant bradycardia diagnosed by either or both methods. The sensitivity and positive predictive values were: HV interval > or = 70 ms at baseline, 47% and 88%; a positive disopyramide test result, 75% and 80%; and HV interval > or = 70 ms or a positive disopyramide test result, 93% and 74%, respectively. Thus, the diagnostic pacemaker is a safe and sensitive tool for evaluating the information obtained at electrophysiologic study, and pharmacologic stress testing with disopyramide has an informative value in patients with bifascicular block and syncope when results at baseline are inconclusive.

Göteborg Metoprolol Trial: effects on arrhythmias.

During the initial hospitalization, ventricular fibrillation (VF) developed in 6 metoprolol-treated patients (0.9%) vs 17 placebo-treated patients (2.4%) after inclusion in the study (p = 0.035). There were 6 episodes of VF in the metoprolol group compared with 41 episodes in the placebo group (p less than 0.001). During the same period, 14 metoprolol-treated patients had treated ventricular tachycardia vs 26 placebo-treated patients (p = 0.076). Similar favorable results were found when the incidence of severe ventricular arrhythmias during the first rehospitalization within the 3-month double-blind treatment period was analyzed.

Incidence of sudden death after radiofrequency ablation of the atrioventricular junction for atrial fibrillation.

This study assesses the incidence of sudden death and classifies the causes of death following radiofrequency ablation of the atrioventricular (AV) junction. We studied 220 patients with paroxysmal (n = 105) or chronic (n = 115) atrial fibrillation (AF) and a mean age of 64 +/- 12 years. These patients were followed 31 +/- 15 months after radiofrequency ablation of the AV junction and pacemaker implantation. In 86 patients, structural heart disease was identified before the procedure. All patients were traced via the Swedish National Civic Registry and Cause of Death Registry. The cause-of-death was classified according to data from death certificates, autopsy protocols, and medical records. Thirty-one patients (mean age 69 +/- 11 years, 16 men) died 15 +/- 15 months (range 0.2 to 60) after the procedure. There were 6 sudden unexplained deaths, 14 cardiovascular deaths, and 11 deaths from noncardiovascular causes. Eleven patients, all with structural heart disease, died suddenly out of hospital 16 +/- 16 months (range 0.2 to 42) after the procedure. In 6 of these there was no obvious cause of death. Three of these 6 patients underwent autopsy, which showed extensive coronary artery disease (n = 1), severe heart failure (n = 1) and cardiac hypertrophy and dilation (n = 1). The remaining 3 all had depressed left ventricular systolic function and a history of congestive heart failure. Five of the patients who died suddenly from cardiovascular causes had autopsies that revealed acute myocardial infarction (n = 4) and massive pulmonary embolism (n = 1).

Torsades de pointes induced by transesophageal atrial stimulation after administration of almokalant.

This case-report describes a patient who developed a torsades de pointes tachycardia after infusion of almokalant, a selective class III antiarrhythmic agent. The patient was studied with transesophageal atrial stimulation because of Wolff-Parkinson-White syndrome. After a base-line procedure during which an orthodromic tachycardia was induced and pace-terminated, almokalant was given intravenously. The corrected QT interval was markedly prolonged despite similar plasma concentration compared to the rest of the studied patients. During the continued pacing protocol several episodes of non-sustained ventricular tachycardia was observed after pacing induced pauses. A sustained orthodromic tachycardia with left bundle branch morphology was induced, and another almokalant infusion was given. At a plasma concentration of approximately 252 nmol/l the corrected QT interval was further prolonged to 680 ms and the patient developed a torsades de pointes tachycardia after a pacing induced pause. The tachycardia degenerated into ventricular fibrillation that required immediate defibrillation. One week later the patient underwent ablation of the accessory pathway. The QT interval was in the absence of preexcitation normal, and programmed electrical stimulation did not reveal any ventricular arrhythmias. Further studies will have to be performed to clarify whether an early and marked QT interval prolongation, such as observed in this patient, will be useful in identifying patients prone for proarrhythmias in relation to therapy with selective class III drugs.

One-year mortality rate after discharge from hospital in relation to whether or not a confirmed myocardial infarction was developed.

Consecutive patients admitted to our hospital with suspected acute myocardial infarction during 21 months were prospectively evaluated. One-year mortality after discharge from hospital was related to whether or not an infarction developed (infarct versus non-infarct patients). Of patients discharged alive after developing an infarct, there was a mortality of 17% (n = 777) versus 12% (n = 1830) (P less than 0.001) for all patients not developing infarction. In a high risk group (any of the following: age greater than or equal to 75 years, previous history of myocardial infarction, diabetes mellitus or congestive heart failure) patients developing infarction had a mortality of 24% (n = 457) versus 17% (n = 1221) for those who did not (P less than 0.001). In a low risk group (none of the high risk criteria), the corresponding mortality was 8% (n = 316) for patients suffering infarction and 3% (n = 603) for those not having infarction (P less than 0.001). The difference in mortality between patients with and without infarction was most marked in women (21% vs 11%; P less than 0.01) and in hypertensives (25% vs 12%; P less than 0.001), but less marked in men (16% vs 13%; NS) and in patients without hypertension (13% vs 12%; NS). Among patients not suffering infarction, mortality was particularly high in those with previous congestive heart failure (23%) and diabetes mellitus (21%).

Effects of digoxin on electrocardiogram in patients with acute atrial fibrillation--a randomized, placebo-controlled study. Digitalis in Acute Atrial Fibrillation (DAAF) Trial Group.

BACKGROUND: Studies of healthy volunteers or patients in sinus rhythm have indicated that treatment with digoxin produces characteristic changes in the electrocardiogram (ECG). No randomized, placebo-controlled studies are available and no study has investigated the effect on ECG in patients with atrial fibrillation. HYPOTHESIS: In a substudy to a trial comparing the therapeutic effect of intravenously administered digoxin with placebo in patients with acute atrial fibrillation, we investigated these effects as well as the relation between ECG changes and serum concentration of digoxin. METHODS: In all, 167 patients were included. Standard ECGs recorded at baseline, and at 2, 6, 12, and 16 h after randomization were digitized, and changes in RR-intervals, QRS width, ST-segment amplitude at 60 ms after the J point, T-wave amplitude, and QTc interval were calculated. Furthermore, the correlation between the serum concentration of digoxin at 16 h after inclusion and changes on the ECG was analyzed. RESULTS: Compared with placebo, digoxin resulted in an increase in RR-interval (p < 0.0001), a decrease in ST-segment and T-wave amplitude (p = 0.009 and p = 0.002, respectively), and in the QTc interval (p = 0.01). These changes were present 2 h after the first dose, but were more pronounced after 16 h. There was no significant correlation between serum concentration of digoxin and ECG changes at 16 h. CONCLUSION: Compared with placebo, digoxin produces significant changes on ECG in patients with acute atrial fibrillation. The changes are in accordance with previous findings in individuals in sinus rhythm. There was no correlation between serum concentration of digoxin and ECG changes.

Paroxysmal vagally mediated AV block with recurrent syncope.

Paroxysmal complete atrioventricular (AV) block without associated electrocardiographic (ECG) abnormality is not a well recognized entity. A mother and her daughter had recurrent syncopal episodes, but a normal ECG. The episodes were preceded by nausea and vomiting. ECG during these episodes revealed complete heart block. In the mother, one episode was promptly reversed by atropine. Electrophysiological evaluation of the sinus and AV nodal function and atrial and ventricular effective refractory periods before and after autonomic blockade was normal. Provocative manoeuvres failed to induce AV block. Paroxysmal AV block was vagally mediated in one of the patients, as indicated by prompt response to atropine. In the second case, the vagal dependence could not be proved but appears to be the most likely explanation. It thus appears that paroxysmal, vagally mediated complete AV block should be seriously considered in patients with unexplained syncope.

Effects of metoprolol on heart rate in patients with digitalis treated chronic atrial fibrillation.

Adequate control of ventricular rate in patients with chronic atrial fibrillation (AF) may not be achieved with digitalis alone. In the present study the additional effect of two different doses (50 mg and 50 +/- 50 mg) of oral metoprolol, a new selective beta-blocking agent, on ventricular rate in patients with longstanding AF has been studied. A decrease in the mean ventricular rate during rest and during exercise at various work loads was observed after both doses. The effect was more pronounced at the highest work load of 80 W, both after 50 mg (p less than 0.002) and after 50 +/- 50 mg (p less than 0.01) of the drug. A high initial heart rate at rest or during exercise was reduced more by the drug than a lower one. Exercise tolerance was reduced in 2 patients. These results suggest that patients with AF in whom satisfactory control of heart rate cannot be achieved with digitalis alone may benefit from addition of individualized metoprolol therapy.

Arrhythmogenic right ventricular dysplasia presenting with ventricular tachycardia in a father and son.

A father and his son presented with ventricular tachycardia of left bundle-branch block configuration, two years apart. The patients had no clinical signs of right or left ventricular dysfunction. The diagnosis of arrhythmogenic right ventricular dysplasia was based on right ventricular angiographic and radionuclide findings. Microscopic sections obtained at surgery for the ventricular tachycardia in the father revealed abnormal infiltration of fat and focal fibrosis in the right ventricular myocardium, confirming the diagnosis. The importance of thorough evaluation of right and left ventricular function and structure in patients with ventricular tachycardia of right ventricular origin is emphasized. Currently available diagnostic techniques and management are presented.

Prophylactic treatment after electroconversion of atrial fibrillation.

Atrial fibrillation is a common arrhythmia. Sinus rhythm can often be restored by electroconversion, but the relapse rate is high. Various antiarrhythmic drugs have been used to maintain sinus rhythm after electroconversion. This article reviews the experience with these drugs and suggests a treatment strategy.

Effects of diltiazem, propranolol, and their combination in the control of atrial fibrillation.

The effect of the combined treatment with propranolol 20 mg tid and diltiazem 60 mg tid in patients with chronic atrial fibrillation treated with digoxin was evaluated. Thirteen patients entered a double-blind, three-phase crossover study. Heart rate was significantly reduced during rest and at maximal exercise (p less than 0.05) during combined treatment compared with treatment with any single drug. No significant changes in maximal work load, exercise time, systolic blood pressure at maximal work load, or subjective sensation of well-being could be demonstrated during combined drug treatment. The RR distribution pattern was unaffected by the addition of propranolol, diltiazem, or their combination to the chronic digoxin treatment. It is concluded that the combination of diltiazem and propranolol has no advantages over any of these drugs singly, in the moderation of heart rate in patients with atrial fibrillation even combined with basic digitalis treatment, and that the intrinsic AV nodal function is unaffected by these drugs or their combination.

A case of arrhythmogenic right ventricular dysplasia with ventricular fibrillation.

A case of repeated attacks of ventricular fibrillation is described. The patient suffered from an arrhythmogenic right ventricular dysplasia (ARVD) documented by right and left ventriculograms and myocardial biopsies obtained during surgical treatment of the arrhythmia. The histological changes were interpreted as being signs of fresh myocardial damage of unknown origin in addition to a replacement of the normal myocardium by adipose and fibrotic tissue. The repeated attacks of ventricular fibrillation in this patient contrast to the arrhythmia spectrum noted in the available literature on ARVD, mostly stable chronic ventricular tachycardias.

[Preventive treatment against recurrence after electric regulation of chronic atrial fibrillation]. / Profylaktisk behandling mot recidiv efter elregularisering av kroniskt förmaksflimmer.

In cases of atrial fibrillation, a common arrhythmia, sinus rhythm can often be restored by electroconversion, though the relapse rate is high. Various anti-arrhythmic drugs have been tried to sustain sinus rhythm after electroconversion. In the article experience with such drugs is reviewed and a treatment strategy suggested.

Analysis of initial rhythm, witnessed status and delay to treatment among survivors of out-of-hospital cardiac arrest in Sweden.

BACKGROUND: The characteristics of patients who survive out-of-hospital cardiac arrest (OHCA) are incompletely known. The characteristics of survivors of OHCA during a period of 16 years in Sweden are described. METHODS: All the patients included in the Swedish Cardiac Arrest Registry between 1992 and 2007 in whom cardiopulmonary resuscitation was attempted and who were alive after 1 month were included in the survey. RESULTS: In all, 2432 survivors were registered. Information on initial rhythm at their first ECG recording was missing in 11%. Of the remaining 2165 survivors, 80% had a shockable rhythm and 20% had a non-shockable rhythm. Only a minority with a shockable rhythm among the bystander-witnessed cases were defibrillated within 5 min after cardiac arrest. This proportion did not change during the entry period. Among survivors found in a non-shockable rhythm, the majority were bystander-witnessed cases and a few had a delay from cardiac arrest to ambulance arrival of <5 min. Of all survivors, more women (27%) than men (18%) were found in a non-shockable rhythm (p<0.0001). During the 16 years in which the register was used for this study, the proportion of survivors found in a shockable rhythm did not change significantly. The cerebral performance categories score indicated better cerebral function among patients found in a shockable rhythm than in those found in a non-shockable rhythm. CONCLUSION: Among survivors of OHCA, a substantial proportion was found in a non-shockable rhythm and this occurred more frequently in women than in men. The proportion of survivors found in a shockable rhythm has not changed markedly over time. Survivors found in a shockable rhythm had a better cerebral performance than survivors found in a non-shockable rhythm. The proportion of survivors who were bystander-witnessed and found in a shockable rhythm and defibrillated early is still remarkably low.