Prediction of Arrhythmic Events After Acute Myocardial Infarction Using Two Methods for Late Potentials Recording

One hundred consecutive patients recovering from an acute myocardiai infarction underwent, prior to home discharge, signal-averaged electrocardiography (ECG), left ventriculography. and 24-hour Holter ECG recording. The signal-averaged ECG was recorded and analyzed using two procedures: the orthogonal bipolar XYZ lead configuration with a bidirectional filter: and a precordial unipolar lead configuration with a uonrecursive digital filter. An abnormal signal-averaged ECG was seen in 40% of patients with the XYZ system and in 30% of patients in the precordial method, abnormal ejection fraction (< 40%) in 24% of patients and high grade ectopy activity in 22%. During the 24-month follow-up period, 12 patients (12%) had an arrhythmic event defined as either sudden death (11 patients) or sustained ventricular tachycardia (1 patient). Neither the signal-averaged ECG with the XYZ configuration, the abnormal ejection fraction, nor the high grade ectopy were able to statistically predict a higher arrhythmic event rate. The signal-averaged ECG with the precordial configuration was able to statistically predict a higher arrhythmic event rate, P < 0.03; odds ratio = 3.96. The combination of the orthogonal XYZ configuration signal-averaged ECG with the ejection fraction (P < 0.01, odds ralio = 7.33), or with ejection fraction and Holter monitoring (P < 0.06. odds ratio = 6.17) was able to predict a higher arrhythmic event rate. The combination of the precordial configuration signal-averaged ECG with the ejection fraction (P < 0.002, odds ratio = 14.4), or with ejection fraction and Holter monitoring (P < 0.06. odds ratio =10) was able to better predict a higher arrhythmic event rate. The combination of a normal or abnormal signal-averaged ECG and ejection fraction gave a sensitivity, specificity, positive, or negative value prediction of arrhythmic events of 60%, 90.6%, 37.5%, and 96%, respectively. It must be emphasized that the number of arrhythmic events during the 2-year follow-up was small and further study is required to determine the true predictive value of each method for arrhythmic events.     

Oral and Intravenous Amiodarone for Atrial Fibrillation-Flutter

Amiodrone is a benytfuran derivative with class III anti arrhythmic effects. It has also been reported to convert atrial fibrillation and flutter to sinus rhythm and is highly effective for the prevention of atrial fibrillation (especially of the paroxysmal form) with an overall efficacy in the range of 70–50%. This high degree of efficacy was obtained in a majority of patients who had already failed various conventional anti arrhythmic agents. The mechanism of arrhythmia termination by intravenous amiodarone is not clear. The slowing in ventricular response, which most probably improves cardiac hemodynamics, has an indirect salutary effect. Despite the fact that none of the published reports on intravenous amiodarone used a placebo control group, these studies suggest that intravenous amiodarone has an important role in the acute treatment of atrial fibrilation with fast ventricular response.     

Alternating Wenckebach Periods in Acute Inferior Myocardial Infarction: Clinical, Electrocardiographic, and Therapeutic Characterization

We report on twelve patients with alternating Wenckebach periods (AWP) occurring during an acute inferior myocardial infarction (AIMI). There were nine males and three females, with a mean age of 61 years (range, 43 to 75). AWP appeared during the first 48 hours of the AIMI in 10 patients and on the fourth day of hospitalization in two patients. AWP occurred spontaneously in nine patients and following the administration of atropine in the remaining three patients. Mean systolic blood pressure significantly decreased during AWP as compared to the period preceding or following the bradyarrhythmia (93 ± 42 mmHg vs 123 ± 37 mmHg, p < 0.02). Killip functional class was significantly higher during AWP as compared to the period preceding or following the bradyarrhythmia (2.1 ± 1.2 vs 1.5 ± 0.8, p < 0.02). Pacemaker therapy was initiated prophylactically in two patients, because of syncope in six, because of hemodynamic deterioration in two, and for syncope and hemodynamic deterioration in two. Three patients died in cardiogenic shock despite pacemaker therapy. No evidence of right ventricular infarction was seen in the patients.
Atropine administration during AWP significantly increased the sinus rate and significantly decreased the ventricular rates and the systolic blood pressure. In addition, three patients developed long bouts of paroxysmal AV block. Isoproterenol administration improved AV conduction in one patient, caused no change in two patients and induced non-sustained ventricular tachycardia in three patients.
In conclusion, AWP occurring during AIMI is a symptomatic bradyarrhythmia associated with hemodynamic deterioration. Drug therapy for this bradyarrhythmia is usually ineffective and sometimes paradoxical responses are observed. Pacemaker therapy is usually needed to correct symptoms and the worsening hemodynamic status. We recommend prophylactic pacemaker implantation in patients developing AWP during AIMI.     

Left Ventricular Malposition of a Transvenous Cardioverter Defibrillator Lead: A 3-Year Follow-Up

A case of left ventricular malposition of a transvenous implantable cardioverter defibrillator lead through an atrial septal defect is presented. The patient has been continually anticoagulated with warfarin. A 3-year follow-up has thus far been uneventful.     

Implantation of Cardioverter Defibrillator and Pacemaker Using the Same Pectoral Quadrant

We implanted a cardioverter defibrillator (ICD) together with a pacemaker system in three patients with ventricular tachycardia and bradyarrhythmias. Both systems (ICD and pacemaker) were implanted in the same left pectoral quadrant using a single skin incision and the subclavian and/or the cephalic vein. The ICD was implanted deep to the pectoralis major muscle, the pacemaker was placed subcutaneously in a more medial pocket. There were no technical difficulties during implantation or complications during follow-up.     

Sick Sinus Syndrome in a Patient with Extensive Cardiac Lipomatosis (Sinus Node Dysfunction in Lipomatosis)

We present a case of a 45‐year‐old man with an incidental and longstanding diagnosis of extensive mediastinal and cardiac lipomatosis. Along the years, he had experienced various arrhythmias, mainly bradyarrhythmias, mostly asymptomatic. Recently after documenting a sinus pause of 6 seconds and runs of nonsustained ventricular tachycardias, he underwent an implantation of a cardioverter‐defibrillator. There are many reports of cardiac lipomatosis in the literature, including reports of related ventricular arrhythmias, some of which are fatal. (PACE 2010; 513–515)     

Perforation of the Right Ventricular Free Wall by an Active Fixation Transvenous Cardioverter Defibrillator Lead

A 58-year-old patient with dilated cardiomyopathy underwent implantable cardioverter defibrillator (ICD) implantation. The postoperative course was complicated by perforation of the right ventricular free wall by the active fixation transvenous ICD lead. The type of ICD lead and the type of organic heart disease are apparently important risk factors for perforation.     

Polymorphous Ventricular Tachycardia and Atrioventricular Block

Nine patients are presented who had polymorphous ventricular tachycardia (PMVT) occurring during atrioventricular (AV) block. There were five men and four women with a mean age of 80 +/- 9 years. Five patients had organic heart disease and the remaining four had primary conduction disease (bundle branch block). AV block was complete in four patients (2:1 in three, and paroxysmal in two). The mean ventricular cycle length (of the AV block rhythm) was 1567 +/- 203 ms. The mean QT interval was 0.64 +/- 0.09 s and the mean QTc was 0.51 +/- 0.06 s. When compared to a similar control group with AV block but without PMVT, the ventricular cycle length was similar but the QT and QTc were significantly longer. PMVT was usually of short duration (eight beats to 12 s) and in seven of these nine patients, frequent premature ventricular beats (PVBs) were recorded at various times from the occurrence of PMVT. This is in contrast to the control patients in whom PVBs were detected in one patient only. In conclusion, patients with AV block who develop PMVT usually have longer QT intervals and have detectable PVBs on routine ECGs, unlike similar patients with AV block but without PMVT. In a patient with AV block, a QT interval above 0.60 s and PVBs on the ECG seem to indicate an increased risk for the development of PMVT.