Cesar A. Conde

Clinical, electrophysiologic and hemodynamic profile of patients resuscitated from prehospital cardiac arrest.

Abstract Of 352 prehospital cardiac arrest patients studied during a three year period, the initial mechanism recorded by rescue personnel was ventricular fibrillation in 220 (62 per cent), ventricular tachycardia in 24 (7 per cent) and bradyarrhythmias or asystole in 108 (31 per cent). Early survival was best in the group with ventricular tachycardia (16 of 24 patients resuscitated and survived hospitalization—67 per cent); the prognosis was worst in the group with bradyarrhythmias asystole (nine of 108 admitted to the hospital alive—none survived hospitalization); and 51 of 220 patients with ventricular fibrillation (23 per cent) were resuscitated and survived subsequent hospitalization, a significantly better outcome than previously reported for ventricular fibrillation. Central nervous system damage accounted directly or indirectly for 28 of 48 in-hospital deaths (59 per cent), and hemodynamic abnormalities for 31 per cent. Only five in-hospital deaths (10 per cent) were primary arrhythmic. The majority of survivors had evidence of left ventricular hemodynamic abnormalities (mean left ventricular end-diastolic pressure=17.80 ± 8.99 mm Hg; mean cardiac index=2.62 ± 0.72 liters/min/m 2 ; mean ejection fraction=38.58 ± 17.55 per cent), but approximately one third of the surviving patients had normal left ventricular function. Early in-hospital electrophysiologic data demonstrated persistent, drug-resistant complex ventricular arrhythmias during the first 72 hours; but intracardiac electrophysiologic studies elicited specific patterns only in patients with ventricular tachycardia, whose arrhythmias were reproducible in five of six patients studied. The risk of recurrent ventricular fibrillation in the first 72 hours was predicted better by coexistent conducting system abnormalities, than by the persistent ventricular arrhythmia alone. We conclude that the electrical mechanism of prehospital cardiac arrest provides early prognostic information, that early survival rates are improving and that one third of the discharged survivors have normal indices of left ventricular function. The presence of conducting system abnormalities identifies a subgroup at high risk for in-hospital recurrent ventricular fibrillation.

Antiarrhythmic drug therapy in survivors of prehospital cardiac arrest: comparison of effects on chronic ventricular arrhythmias and recurrent cardiac arrest.

We studied the long-term effects of membrane-active antiarrhythmic agents on chronic ventricular arrhythmias in patients who have survived prehospital cardiac arrest. Among 16 patients treated with a dose-adjusted, plasma level-monitored antiarrhythmic regimen, eight have survived for longer than 12 months eight have had recurrent cardiac arrests (RCAs). Monthly Holter monitor tapes (HIM) recorded during the 4 months before the eight RCAs were compared with monthly HM tapes matched for time of entry duration of follow-up in the eight patients who did not have RCAs. Transient or persistent complex ventricular ectopic depolarizations (VEDs) have been recorded on 47 of the 63 monthly HM tapes (75%). The difference between VEDs in the RCA patients (mean 153 VEDs/hr, median 19 VEDs/hr) VEDs in the patients who have not had RCA (mean 122 VEDs/hr, median 8 VEDs/hr) was not significant (p ≥ 0.2); nor was there a predictable relationship between therapeutic plasma levels of antiarrhythmic agents the frequency complexity of chronic asymptomatic VEDs (therapeutic levels mean 104 VEDs/hr, median 6 VEDs/hr; subtherapeutic levels – mean 184 VEDs/hr, median 21 VEDs/hr). Differences were not significant (p ≥ 0.1). In contrast, all eight RCA patients had unstable plasma levels (21 of 31 determinations subtherapeutic) while six of the eight patients who have not had RCA had consistently therapeutic levels (p ≤ 0.01). Thus, adequate plasma levels of antiarrhythmic agents may protect against RCA, despite failure to suppress VEDs predictably. The apparent dissociation between predictable suppression of chronic VEDs protection against RCA suggests that clinical effectiveness of these agents may not be best measured by their effect on chronic VEDs.

Long-term survival after prehospital cardiac arrest: Analysis of outcome during an 8 year study

We analyzed long-term follow-up data accumulated during an 8 year study of survivors of prehospital cardiac arrest. All patients included in this study were primary entrants via community-based rescue systems; patients who were tertiary referrals (survivors of cardiac arrest from other hospitals) were not included in this analysis. In the group of 61 patients entering our study between 1975 and 1980, with a follow-up to 1983, there have been a total of 24 deaths (39%). Sixteen of the 24 deaths were the result of recurrent cardiac arrest; eight were nonsudden cardiac deaths or noncardiac deaths. The mean duration from entry to death in the nonsurvivors was 27.5 +/- 19.7 months, and the time from the index event to last follow-up in the long-term survivors was 59.9 +/- 19.4 months. Life table analysis demonstrated a 10% rate of recurrence of cardiac arrest in the first year, with a 5% per year rate in each of the subsequent 3 years. Left ventricular ejection fractions at entry were not significantly different between survivors (mean = 45.3 +/- 13.6%) and nonsurvivors (mean = 37.6 +/- 12.6%), and the severity of ejection fraction abnormality at entry did not correlate with time to death in the nonsurvivors. However, ejection fraction was significantly lower in patients who died from causes other than recurrent cardiac arrest than in those who died of cardiac arrest (24.5 +/- 9.1% vs 42.7 +/- 9.2%; p less than .002).(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial infarction due to coronary atherosclerosis in three young adults with systemic lupus erythematosus

Three patients, 24, 24 and 25 years of age, with systemic lupus erythematosus had signs of myocardial infarction. Two had serial electrocardiographic changes indicative of infarction without any cardiac symptoms. The third patient had clinical evidence of an acute massive myocardial infarction, which was proved at autopsy to be due to coronary atherosclerosis. This case is presented in detail and the association between systemic lupus erythematosus and myocardial infarction is reviewed. It is postulated that the relation between lupus erythematosus and coronary atherosclerosis is more than coincidental.

Relationship between plasma levels of procainamide, suppression of premature ventricular complexes and prevention of recurrent ventricular tachycardia.

We compared the relationship between plasma levels of procainamide and suppression or prevention of various forms of ventricular arrhythmias in 18 patients, six of whom had premature ventricular complexes (PVCs) during acute myocardial infarction (AMI), six of whom had PVCs in the setting of stable chronic ischemic heart disease (CIHD), and six of whom had recurrent symptomatic ventricular tachycardia (VT) with chronic PVCs between episodes of VT. The mean plasma level of procainamide required for 85% suppression of PVCs in the AMI patients was 5.0 ± 0.5, g/ml, while that required for the CIHD patients was 9.3 ± 0.7 gg/ml (p < 0.05). The mean plasma level required for prevention of spontaneous episodes of symptomatic sustained tachycardia in the VT group was 9.1 ± 3.4, g/ml, while the mean level required for 85% suppression of PVCs in the same patients was 14.9 ± 3.8, g/ml (p < 0.01). In the VT group, PVC frequency was decreased by a nmean of only 36% (range 11-63%) at plasma levels of procainamide sufficient to prevent spontaneous VT. The relationship between plasma levels of procainamide and PVC suppression appears to be different in AMI and CIHD patients; furthermore, a high degree of PVC suppression is not a necessary endpoint of antiarrhythmic therapy when attempting to protect patients against recurrent symptomatic VT.

Transient Q waves in Prinzmetal's angina

Transient abnormal Q waves were seen in two patients with Prinzmetals angina during episodes of chest pain. The Q waves appeared recurrently while the patients had chest pain and disappeared when it subsided, indicating that Q waves suggestive of myocardial infarction can be seen with severe myocardial ischemia without actual necrosis. We describe these two patients, the various conditions in which transient abnormal Q waves have been reported and the theories offered to explain this electrophysiologic finding.

Effectiveness of pacemaker treatment in the bradycardia-tachycardia syndrome

Thirty-one patients with the bradycardia-tachycardia syndrome treated with permanent ventricular pacemakers were studied. All were symptomatic before pacemaker insertion, and their symptoms were not controlled with drug therapy alone. Bradycardia and tachycardia associated with multiple arrhythmias were present in all cases; heart rate was less than 40 beats/min in 58 percent of patients and more than 140 beats/min in 71 percent. Conduction abnormalities were present in 61 percent. After insertion of a demand pacemaker, 27 patients (87 percent) were symptom-free for 1 month to 5 years. Although four patients with a normally functioning pacemaker continued to have recurrent arrhythmia, the presence of a pacemaker facilitated further pharmacologic treatment of the disturbance. Pacemaker insertion has been found to be a satisfactory method of treating the symptoms and preventing the recurrence of arrhythmias in patients with the bradycardia-tachycardia syndrome by allowing the use of digitalis and other antiarrhythmic agents.

Decreased frequency of exercise-induced ventricular ectopic activity in the second of two consecutive treadmill tests.

Two exercise tests were performed with an intervening rest period of 45 minutes in a group of 13 subjects with previously identified exercise-induced ventricular arrhythmias and no resting arrhythmias. Both normal subjects and patients with heart disease were included in the group. The level of stress was equal in both tests as judged by similar rate-pressure products at peak exercise. There was a significant decrease (P < 0.05) in the number of VPCs induced by exercise during and after the second test. When the number of VPCs on test I and test II in the same patients were compared, a regression line fitted the data well (r = 0.92). Analysis of the recovery periods revealed significant (P < 0.01) decreases in systolic blood pressure at one and three minutes post exercise, comparing the second to the first test. The underlying mechanism may be decreased myocardial oxygen demand during the second test as the lowered rate-pressure products during recovery (P < 0.01) reflect. The results of this study indicate that tests of effectiveness of an antiarrhythmic drug should not be based solely on a decrease in the amount or severity of ventricular irritability between two successive exercise tests, one immediately before and the other following administration of the drug.

Disappearance of abnormal Q waves after aortocoronary bypass surgery

Sixty-one patients were selected from 100 consecutive patients under-going aortocoronary artery bypass. The number of vessels diseased as defined by coronary arteriography and the number of bypass grafts were recorded. Review of the preoperative electrocardiograms showed an infarct pattern in 26 of the 61 patients and analysis of the postoperative electrocardiograms revealed loss of abnormal Q waves in 3 of the 26. The pre- and postoperative clinical course of these three patients is analyzed and the extent of their coronary artery disease and number of bypass grafts compared with those of the 23 patients who had persistence of the infarction pattern and the 17 patients who manifested new Q waves. Possible explanations for the disappearance of abnormal Q waves are discussed.

Bacterial endocarditis with ruptured sinus of Valsalva and aorticocardiac fistula.

A case is presented of bacterial endocarditis with a ruptured sinus of Valsalva and formation of an aorticocardiac fistula from the right coronary sinus into the right atrium and right ventricle. The pathologic, clinical and surgical aspects of bacterial endocarditis complicated by a ruptured sinus of Valsalva and an aorticocardiac fistula are analyzed. This complication of bacterial endocarditis is still uncommon, but alertness to its diagnosis makes possible early and successful surgical treatment.