Anton P.M. Gorgels

Out-of-hospital cardiac arrest in the 1990s: A population-based study in the Maastricht area on incidence, characteristics and survival

OBJECTIVES We sought to describe the incidence, characteristics and survival of out-of-hospital sudden cardiac arrest (SCA) in the Maastricht area of The Netherlands. BACKGROUND Incidence and survival rates of out-of-hospital SCA in different communities are often based on the number of victims resuscitated by the emergency medical services. Our population-based study in the Maastricht area allows information on all victims of witnessed and unwitnessed SCA occurring outside the hospital. METHODS Incidence, patient characteristics and survival rates were determined by prospectively collecting information on all cases of SCA occurring in the age group 20 to 75 years between January 1, 1991 and December 31, 1994. Survival rates were related to the site of the event (at home vs. outside the home) and the presence or absence of a witness and rhythm at the time of the resuscitation attempt in out-of-hospital SCA. RESULTS Five hundred fifteen patients were included (72% men, 28% women). In 44% of men and 53% of women, SCA was most likely the first manifestation of heart disease. In patients known to have had a previous myocardial infarction (MI), the mean interval between the MI and SCA was 6.5 years, with >50% having a left ventricular ejection fraction >30%. The mean yearly incidence of SCA was 1 in 1,000 inhabitants. Of all deaths in the age groups studied, 18.5% were sudden. Nearly 80% of SCAs occurred at home. In 60% of all cases of SCA a witness was present. Cardiac resuscitation, which was attempted in 51% of all subjects, resulted overall in 32 (6%) of 515 patients being discharged alive from the hospital. Survival rates for witnessed SCA were 8% (16 of 208 subjects) at home and 18% (15 of 85 subjects) outside the home (95% confidence interval 1% to 18.8%). CONCLUSIONS The majority of victims of SCA cannot be identified before the event. Sudden cardiac arrest usually occurs at home, and the survival of those with a witnessed SCA at home was low compared with that outside the home, indicating the necessity of optimizing out-of-hospital resuscitation, especially in the at-home situation.

Progress in the understanding of cardiac early afterdepolarizations and torsades de pointes: time to revise current concepts

Time for primary review 19 days. Afterdepolarizations are oscillations of the transmembrane potential that depend on the preceding action potential (AP) for their generation and can give rise to new APs when they reach a critical threshold for activation of a depolarizing current. This form of abnormal impulse generation is called ‘triggered activity’ [1]. Two types of afterdepolarizations have been distinguished: delayed (DADs) and early afterdepolarizations (EADs). DADs have been defined as “oscillations in membrane potential that occur after repolarization of an action potential” [2]. EADs are generated during the AP and have been defined as “oscillations at the plateau level of membrane potential or later during phase 3 of repolarization” [2]. Depending on the level of the membrane potential at which they are generated, EADs can trigger new APs that may appear as ectopic beats on the ECG. EADs can also augment electrical heterogeneity in regions of neighboring myocardium, which can lead to the formation of new APs via electrotonic interaction between areas that are still inexcitable and those that have already recovered from refractoriness [3]. Although the latter mechanism is reentrant rather than triggered activity, the occurrence of EADs is of pivotal importance for arrhythmogenesis under these circumstances. The clinical significance of EADs lies in their capacity to provide both the trigger (premature ectopic beats) and the substrate (electrical heterogeneity with nonuniform repolarization and refractoriness) for the initiation and perpetuation of torsades de pointes. In this article, we discuss the evidence for a new concept of EAD formation, which includes an important role for cytoplasmic-[Ca2+]-dependent mechanisms, as schematically illustrated in Fig. 1. As a background, we will first review the recent literature on cellular Ca2+ homeostasis. Then, we introduce the classical view on EAD formation with a discussion of the … * Corresponding author. Tel.: +31-43-3875093; fax: +31-43-3875104 p.volders{at}cardio.azm.nl

Out-of-hospital cardiac arrest-the relevance of heart failure. The Maastricht Circulatory Arrest Registry

AIMS To describe the incidence and aetiology of heart failure in out-of-hospital sudden circulatory arrest (SCA) in the Maastricht area of the Netherlands. METHODS All cases of SCA were studied in the age group 20 to 75 years between 1 January 1997 and 31 December 2000. Demographic characteristics, aetiology and clinical features, related to heart failure were studied. RESULTS Four hundred and ninety-two patients were included (72% men), mean age of 62+/-10. The yearly incidence of SCA was 9.2/10,000 inhabitants. Sudden death represented 19% of all deaths, occurring in the same time period. In 52% of the men and 59% of women, SCA was the first manifestation of heart disease. In the SCA group with a cardiac history overt heart failure was present in 26% of the cases, the time interval between the first heart failure episode and SCA being 4.3+/-6.3 year. In the heart failure group the majority had previously been in a poor functional class and LVEF. Concerning aetiology, of the SCA group, 77% were known with CAD and 72% with an old MI. Also in the group with a LVEF >50% CAD was the most frequent cause. CONCLUSIONS There is an increased risk of SCA at poorer pump function and most SCA victims with previous heart failure are in a poor functional class SCA. However heart failure is seen in only a minority of the SCA population. CAD is by far the most common cause of SCA.

Familial Sudden Death Is an Important Risk Factor for Primary Ventricular Fibrillation A Case-Control Study in Acute Myocardial Infarction Patients

Background— Primary ventricular fibrillation (VF) accounts for the majority of deaths during the acute phase of myocardial infarction. Identification of patients at risk for primary VF remains very poor. Methods and Results— We performed a case-control study in patients with a first ST-elevation myocardial infarction (STEMI) to identify independent risk factors for primary VF. A total of 330 primary VF survivors (cases) and 372 controls were included; patients with earlier infarcts or signs of structural heart disease were excluded. Baseline characteristics, including age, gender, drug use, and ECG parameters registered well before the index infarction, as well as medical history, were not different. Infarct size and location, culprit coronary artery, and presence of multivessel disease were similar between groups. Analysis of ECGs performed at hospital admission for the index STEMI revealed that cumulative ST deviation was significantly higher among cases (OR per 10-mm ST deviation 1.59, 95% CI 1.25 to 2.02). Analysis of medical histories among parents and siblings showed that the prevalence of cardiovascular disease was similar between cases and controls (73.1% and 73.0%, respectively); however, familial sudden death occurred significantly more frequently among cases than controls (43.1% and 25.1%, respectively; OR 2.72, 95% CI 1.84 to 4.03). Conclusions— In a population of STEMI patients, the risk of primary VF is determined by cumulative ST deviation and family history of sudden death.

Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction

OBJECTIVES The study assessed the value of the electrocardiogram (ECG) as predictor of the left anterior descending coronary artery (LAD) occlusion site in relation to the first septal perforator (S1) and/or the first diagonal branch (D1) in patients with acute anterior myocardial infarction (AMI). BACKGROUND In anterior AMI, determination of the exact site of LAD occlusion is important because the more proximal the occlusion the less favorable the prognosis. METHODS One hundred patients with a first anterior AMI were included. The ECG showing the most pronounced ST-segment deviation before initiation of reperfusion therapy was evaluated and correlated with the exact LAD occlusion site as determined by coronary angiography. RESULTS ST-elevation in lead aVR (ST elevation(aVR)), complete right bundle branch block, ST-depression in lead V5 (ST depression(V5)) and ST elevation(V1) > 2.5 mm strongly predicted LAD occlusion proximal to S1, whereas abnormal Q-waves in V4-6 were associated with occlusion distal to S1 (p = 0.000, p = 0.004, p = 0.009, p = 0.011 and p = 0.031 to 0.005, respectively). Abnormal Q-wave in lead aVL was associated with occlusion proximal to D1, whereas ST depression(aVL) was suggestive of occlusion distal to D1 (p = 0.002 and p = 0.022, respectively). For both the S1 and D1, inferior ST depression > or = 1.0 mm strongly predicted proximal LAD occlusion, whereas absence of inferior ST depression predicted distal occlusion (p < or = 0.002 and p < or = 0.020, respectively). CONCLUSIONS In anterior AMI, the ECG is useful to predict the LAD occlusion site in relation to its major side branches.

Reproducible Induction of Early Afterdepolarizations and Torsade de Pointes Arrhythmias by d -Sotalol and Pacing in Dogs With Chronic Atrioventricular Block

It has been well established that antiarrhythmic drugs can also have proarrhythmic effects such as torsade de pointes (TdP) arrhythmias. It was the purpose of this study to create an animal model with a high incidence of reproducible TdP that occurs under clinically relevant circumstances. Experiments were performed in anesthetized dogs that had been in chronic atrioventricular block for 9 +/- 6 weeks. TdP inducibility was attempted using different pacing modes before and after the administration of 2 mg/kg d-sotalol. In some experiments, endocardial monophasic action potentials were recorded. d-Sotalol increased the cycle length of the idioventricular rhythm (1475 +/- 460 to 1730 +/- 570 ms, P < .01) and the QT time (390 +/- 65 to 480 +/- 85 ms, P < .01). In 10% of the experiments, spontaneous TdP occurred after d-sotalol. The incidence of pacing-dependent TdP was 52% (P < .01). In the inducible group, the cycle length of idioventricular rhythm and QT time were significantly longer despite equal percentage increases in these parameters after d-sotalol in both groups. The pacing modes consisting of more than one frequency change had a higher TdP induction rate (P < .05). Reproducibility of TdP induction (three times or more using the same pacing train) remained present for approximately 60 minutes after d-sotalol and was greater than 90% within the same animal over weeks. TdP induction was related to the presence of early afterdepolarizations on the monophasic action potential recordings: five of six in the inducible group versus two of six in the nonresponders. Inducibility could be further increased to 89% when a second bolus of d-sotalol was administered to noninducible dogs. On the other hand, decreasing QT time by faster basic pacing or administration of isoproterenol, or MgSO4 prevented TdP induction. This effect of MgSO4 coincided with the disappearance of early afterdepolarizations. Our animal model shows a high incidence of reproducible acquired TdP arrhythmias, allowing study of the mechanism and treatment of TdP. TdP induction was related to the combination of a slow ventricular rate, the prolongation of QT time, a sudden induced rate change that often required two or more cycle length changes, and the presence of early afterdepolarizations.

Value of the 12-lead electrocardiogram at hospital admission in the diagnosis of pulmonary embolism

In 49 consecutive patients (27 men and 22 women, age range 44 to 86 years) presenting with acute symptoms and with subsequently proven pulmonary embolism, and without previous lung disease, the 12-lead electrocardiograms obtained at hospital admission were reviewed in a blinded fashion to identify electrocardiographic features suggestive of right ventricular overload. Pulmonary embolism was considered probable in 37 patients (76%), from the presence of > or = 3 of the following abnormalities: (1) incomplete or complete right bundle branch block (n = 33); which was associated with ST-segment elevation (n = 17) and positive T wave (n = 3) in lead V1; (2) S waves in leads I and aVL of > 1.5 mm (n = 36); (3) a shift in the transition zone in the precordial leads to V5 (n = 25); (4) Q waves in leads III and aVF, but not in lead II (n = 24); (5) right-axis deviation, with a frontal QRS axis of > 90 degrees (n = 16), or an indeterminate axis (n = 15); (6) a low-voltage QRS complex of < 5 mm in the limb leads (n = 10); and (7) T-wave inversion in leads III and aVF (n = 16) or leads V1 to V4 (n = 13), which occurred more often in patients with symptoms for > 7 days. In the 12 patients with normal electrocardiograms at admission, serial electrocardiograms revealed diagnostic features of embolism in an additional 3 patients. Two-dimensional Doppler echocardiography at admission revealed tricuspid valve regurgitation and an increased right ventricular end-diastolic diameter in all cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia

Efficacy of procainamide and lidocaine in terminating spontaneous monomorphic ventricular tachycardia (VT) was assessed in a randomized parallel study. Patients with acute myocardial infarction and those with poor hemodynamic tolerance of VT were excluded. Procainamide 10 mg/kg was given intravenously with an injection speed of 100 mg/min, and lidocaine was administered at an intravenous dose of 1.5 mg/kg in 2 minutes. Fourteen patients were randomized to lidocaine and 15 to procainamide. Termination occurred in 3 of 14 patients after lidocaine and in 12 of 15 patients after procainamide (p <0.01). Procainamide stopped 8 of 11 VTs not responding to lidocaine, and lidocaine stopped 1 of 1 not responding to procainamde. Of a total of 41 VT episodes, 4 of 15 responded to lidocaine and 20 of 26 to procainamide (p <0.01). Because of VT recurrences, 16 patients could be studied repeatedly with drugs given in the reversed order. This resulted in a total of 55 trials of 79 drug injections. Lidocaine terminated 6 of 31 VTs and procainamide 38 of 48 (p <0.001). The protocol was stopped in 4 cases because of adverse effects. A comparison of the QRS width and QT interval before and at the end of the injection revealed significant lengthening of these values after procainamide but no change after lidocaine. In conclusion, procainamide is superior to lidocaine in terminating spontaneously occurring monomorphic VT.

Did prognosis after acute myocardial infarction change during the past 30 years? A meta-analysis

Much effort has been spent to improve survival after acute myocardial infarction. To investigate how effective this effort has been, a meta-analysis was performed of studies published between 1960 and 1987 concerning mortality after acute myocardial infarction. Thirty-six studies were analyzed. They were classified with respect to deaths in the hospital and at 1 month and the 5-year mortality rate starting at hospital discharge. Mortality was assessed from all studies by comparing studies from different institutions with use of identical inclusion criteria (externally controlled studies) and by analyzing studies reporting on changes in mortality in two or more comparable patient cohorts admitted to the same institution at different time periods (internally controlled studies). Reports on clinical trials (for example, thrombolytic therapy, beta-adrenergic blockade) in acute myocardial infarction were excluded. Average overall in-hospital mortality decreased from 29% during the 1960s to 21% during the 1970s and to 16% during the 1980s. The externally controlled studies also showed a declining trend: from 1960 to 1969, 32%, from 1970 to 1979, 19% and from 1980 to 1987, 15%. The 1-month overall mortality rate decreased from 31% during the 1960s to 25% during the 1970s and 18% during the 1980s externally controlled studies. Most internally controlled studies also showed significant improvement in in-hospital and 1-month survival. In contrast, 5-year mortality after hospital discharge did not significantly decrease (33% from 1960 to 1969 and 33% from 1970 to 1979). It is concluded that in the prethrombolytic era, short-term prognosis after acute myocardial infarction has improved since 1960.(ABSTRACT TRUNCATED AT 250 WORDS)

Use of ajmaline in patients with the Wolff-Parkinson-White syndrome to disclose short refractory period of the accessory pathway

Ajmaline given intravenously produced complete anterograde block in the accessory pathway of 32 of 59 patients with the Wolff-Parkinson-White syndrome. An electrophysiologic investigation performed 1 day later revealed that failure of ajmaline to produce complete anterograde block in the accessory pathway corresponded to a short refractory period of this pathway (less than 270 ms). The use of ajmaline intravenously is advanced as a reliable and rapid procedure for identifying those patients with the Wolff-Parkinson-White syndrome who have a short refractory period of the accessory pathway and are possible at risk of circulatory insufficiency or sudden death if atrial fibrillation supervenes.