Ruben F. Lewin

Amiodarone-induced polymorphous ventricular tachycardia

Five cases of amiodarone-induced polymorphous ventricular tachycardia (torsade de pointes) are presented. All patients had recurrent syncope or dizziness due to polymorphous ventricular tachycardia and in all cases the QT interval was prolonged. In two cases hypokalemia was present at the time the arrhythmia was first recorded, but in both cases polymorphous ventricular tachycardia persisted despite correction of the electrolyte imbalance. Standard treatment for polymorphous ventricular tachycardia (isoproterenol, ventricular pacing, or both) was successful in all patients, however, therapy had to be continued for 5 to 10 days, most probably because of the long elimination half-life of amiodarone.

Echocardiographic evaluation of patients with systemic sarcoidosis

Echocardiographic evaluation of 42 patients with sarcoidosis disclosed 13 patients (group A) with abnormalities compatible with sarcoid heart involvement such as thickening or thinning of the septum (eight patients), pericardial effusion (four patients), and increased end-diastolic dimension of the left ventricle with decreased systolic function (three patients). The remaining 29 patients (group B) were diagnosed as having normal echocardiograms. The clinical data revealed no statistically significant difference between the groups regarding age, sex, chest x-ray stage, activity, and previous heart disease. Group A patients had older clinical onset of the disease (52 vs 83 months; p less than 0.05) and higher incidence of ECG abnormalities than group B patients. There were no statistically significant differences between the groups regarding two-dimensional echocardiographic internal dimensions of both ventricular chambers. The radionuclear right ventricular ejection fraction was low in both groups and the left ventricular ejection fraction was depressed in group A patients (p less than 0.01). As observed in pathologic studies, the septum is a target structure which can be characterized echocardiographically. Screening suspected sarcoid heart disease involvement is important to characterize patients with a relatively high risk of clinical cardiac abnormalities such as complete atrioventricular block, ventricular arrhythmias, congestive heart failure, and sudden death.

Efficacy of intravenous amiodarone in the management of paroxysmal or new atrial fibrillation with fast ventricular response

We tested the efficacy of intravenous amiodarone (5 mg/kg) in slowing ventricular response and/or restoring sinus rhythm in 26 patients with paroxysmal or new atrial fibrillation with fast ventricular response. There were 16 men and 10 women with ages ranging from 35 to 84 years, mean 63 years. Intravenous amiodarone initially slowed the ventricular response in all patients from 143 +/- 27 to 96 +/- 10 beats/min (P less than 0.001). Twelve patients (46%) reverted to sinus rhythm within the first 30 min (range 5 to 30 min, mean 14 +/- 9 min). One patient reverted to atrial flutter after 10 min and 40 min later to sinus rhythm. Six patients (23%) converted to sinus rhythm after 2 to 8 hr and in these 6 cases, the initial slowing in ventricular response obtained with amiodarone persisted until conversion. Seven patients (27%) did not convert to sinus rhythm following amiodarone administration and they required further medical therapy to slow the ventricular response and/or to convert to sinus rhythm. No serious side effects from drug administration were noted. Intravenous amiodarone appears as a highly effective medication in the conversion or control of new onset atrial fibrillation with fast ventricular response.

Advanced early and late atrioventricular block in acute inferior wall myocardial infarction

Seventy-six patients with acute inferior acute myocardial infarction (AMI) and advanced atrioventricular (AV) block are described. According to pre-established ECG criteria and time of appearance of the advanced AV block, patients were divided into two groups. The early block group consisted of 31 patients who developed advanced AV block during the hyperacute ECG stage of AMI. Advanced AV block in these patients was characterized by early appearance, short duration, third-degree type block, poor response to atropine, and increased need for pacemaker therapy. The late block group consisted of 45 patients who developed advanced AV block during subsequent ECG stages of AMI. Advanced AV block in these patients was characterized by late appearance, longer duration, second-degree type block, positive response to atropine, and diminished need for pacemaker therapy. Morbidity and mortality also differed between both groups. Patients with early block had more syncope (32% vs 2%, p less than 0.0001), more left heart failure (36 vs 7%, p less than 0.005), and more cardiogenic shock (39% vs 2%, p less than 0.001) than patients with late block. The mortality rate in the early block group was high (23%) and similar to that reported in the literature, whereas the mortality rate in the late block group was low (7%, p less than 0.05) and similar to the mortality rate reported for acute inferior AMI without advanced AV block. These data identify a subgroup of patients with acute inferior AMI and advanced AV block, which accounts for the high mortality rate reported in this group of patients.

Unstable angina: The significance of ST segment elevation or depression in patients without evidence of increased myocardial oxygen demand

We evaluated 46 patients with unstable angina (UA), who showed no significant changes in heart rate, blood pressure, and double product (as evidence of increased oxygen demand) during episodes of chest pain. Coronary angiography was performed in all patients during the same hospitalization. Of 26 patients with UA and ST depression (group A), 10 had left main coronary artery disease (CAD) and eight had left main equivalent CAD. Of 20 patients with UA and ST elevation (group B), only one had left main CAD and one had left main equivalent CAD. All patients in group A had ST depression in leads V4 and V5, and all patients in group B had ST elevation in leads V2 and V3. The presence of ST depression in leads V4 and V5 in UA patients without evidence of increased oxygen demand may be suggestive of significant left main or left main equivalent CAD. Therefore, coronary angiography is recommended during the same hospitalization.

Unstable angina pectoris evolving to acute myocardial infarction: significance of ECG changes during chest pain

We retrospectively evaluated 32 patients with unstable angina (UA) and no evidence of increased oxygen demand during episodes of chest pain (no significant changes in heart rate and blood pressure), who developed an acute myocardial infarction (AMI) during the same hospitalization. Based on the type of ST changes during anginal pain, two groups were defined: Group A included 19 patients who developed ST elevation during AMI; 15 of these 19 patients (79%) were in Killip class I, two were in class II, and there was one patient each in classes III and IV, respectively. Only one of the 19 patients died. Group B included 13 patients who developed ST depression during AMI; nine of these 13 patients were in Killip class IV and the remaining four patients died before they could be evaluated. Ten patients died (77%) (p less than 0.01), seven in electromechanical dissociation and three in cardiogenic shock. Postmortem examination, performed in four patients, revealed total obstruction of the left main coronary artery. It is concluded that patients with UA who, during attacks of chest pain, develop ST depression and no evidence of increased oxygen demand may have a poor prognosis when they develop an AMI. This selected group of high-risk patients appears to need immediate intensive medical care and most probably early surgical treatment.

Multiform accelerated idioventricular rhythm in acute myocardial infarction: Electrocardiographic characteristics and response to verapamil

Thirteen patients with acute myocardial infarction with multiform accelerated idioventricular rhythm (AIVR) occurring during the first 12 hours of monitoring in the coronary care unit are described. This arrhythmia, similar to the more common uniform AIVR, was intermittent, did not cause hemodynamic compromise, and was not related to more serious ventricular arrhythmias. There was no correlation between the bundle branch block pattern of the multiform AIVR and the electrocardiographic location of the myocardial infarction, but there was a perfect correlation between the frontal plane electrical axis of the multiform AIVR and the electrocardiographic location of the myocardial infarction. The presence of fusion beats between the different forms of AIVR suggests multifocality rather than multiformity. Intravenous verapamil (3 to 5 mg bolus) was administered to 6 patients with multiform AIVR in whom the arrhythmias were persistent enough to allow the evaluation of the effect of verapamil on the arrhythmia. Verapamil caused no change in the rate of AIVR in 1 patient, but in a second patient it decreased the rate by 20 beats/min. In 4 patients, verapamil abolished the arrhythmia: in 2 patients carotid sinus pressure (induced sinus slowing) allowed the emergence of the AIVR at a lower rate, and in the remaining 2 patients the arrhythmia was not observed.

Polymorphous Ventricular Tachycardia and Atrioventricular Block

Nine patients are presented who had polymorphous ventricular tachycardia (PMVT) occurring during alrioventricular (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 an the ECG seem to indicate an increased risk for the development of PMVT.

Left and right ventricular function in inferior acute myocardial infarction and significance of advanced atrioventricular block.

Of 139 consecutive patients with a first inferior acute myocardial infarction, 26 (19%) had advanced atrioventricular (AV) block and 113 (81%) did not. All were evaluated by 2-dimensional echocardiography (2-D echo) and radionuclide angiography. Patients with advanced AV block had lower radionuclide left ventricular (LV) ejection fraction (51 +/- 10 vs 58 +/- 11%, p less than 0.01), higher LV wall motion score on 2-D echo (5.6 +/- 2.6 vs 3.1 +/- 2.7, p less than 0.001), lower radionuclide right ventricular (RV) ejection fraction (32 +/- 15 vs 39 +/- 16%, p less than 0.001) and higher RV wall motion score on 2-D echo (3.4 +/- 1.7 vs 1.5 +/- 2, p less than 0.002) than did patients without AV block. The incidence rate of RV dysfunction was higher in patients with advanced AV block (78 vs 40%, p less than 0.02), and the mortality rate was also higher (although not significantly) in patients with advanced AV block (15 vs 6%). In conclusion, patients with inferior acute myocardial infarction and advanced AV block have larger infarct sizes (as seen on radionuclide angiography and 2-D echo) and lower RV and LV function than patients without AV block. This finding may explain the higher mortality rate observed in this group.

Paroxysmal atrial flutter and fibrillation associated with preexcitation syndrome: treatment with ajmaline

Ajmaline was administered intravenously to six patients with the Wolff-Parkinson-White syndrome for the acute management of paroxysmal atrial flutter (three patients) or fibrillation (three patients) with a fast ventricular response (over the accessory pathway). Ajmaline increased refractoriness in the accessory pathway in all three patients with atrial flutter and stopped the flutter in one. The drug completely abolished preexcitation in two of the three patients with atrial fibrillation, decreasing the means ventricular rate of 240 and 300 beats/min to 110 and 180 beats/min, respectively. In the third patient with atrial fibrillation, ajmaline increased refractoriness over the accessory pathway, decreasing the mean ventricular rate of 300 beats/min to 160 beats/min. In two patients ajmaline was continued as an intravenous maintenance infusion until sinus rhythm was restored. It is concluded that ajmaline is an effective drug for the acute management of atrial flutter or fibrillation with a fast ventricular response in patients with the Wolff-Parkinson-White syndrome.