Pharmacological analysis of established ventricular fibrillation.

1. The effects of anti-arrhythmic drugs on the power spectrum of established ventricular fibrillation induced by endocardial electrical stimulation, have been studied in greyhounds anaesthetized with sodium pentobarbitone (35 mg kg-1, i.v.). 2. In dogs receiving no drug, initial recording of ventricular fibrillation showed a dominant frequency of 9.9 +/- 0.7 Hz (lead II) and 10.0 +/- 0.6 Hz (endocardium). After 3.3 min the frequency had fallen to 4.0 +/- 0.4 Hz in lead II, but remained high in the endocardium (10.7 +/- 0.5 Hz). 3. Lignocaine significantly reduced the dominant frequency for fibrillation recorded from lead II at (0-80 s), and for endocardial fibrillation at (0-200 s). 4. Pretreatment with propranolol or bretylium had little effect on the time course of the dominant frequency of fibrillation in lead II or the endocardium. 5. Verapamil prevented the fall in frequency seen in lead II after 80 s in the no drug group. A significantly higher frequency was maintained in both lead II (14.7 +/- 0.9 Hz) and the endocardium (14.8 +/- 0.9 Hz) for 3.3 min, compared with the no drug group (P less than 0.01). 6. Activation of fast sodium channels may determine the rapid frequency of the initial stages of ventricular fibrillation. The rapid fall in dominant frequency in lead II after fibrillation for 80 s can be prevented by calcium channel blockade and may be due to intracellular accumulation of calcium.     

Factors determining success and energy requirements for cardioversion of atrial fibrillation: revised version.

Factors thought to affect the success of and energy requirements for cardioversion of atrial fibrillation were studied in 80 (49 male, 31 female) patients aged 21-88 (mean 61.5 years). Transthoracic impedance was measured in advance of the countershock using a 30 kHz low amplitude AC current passed through self-adhesive ECG/defibrillator pads (diameters 8 and 12 cm) applied to the chest in the antero-posterior (AP) position in 57 patients and the anteroapical (AA) position in 23 patients. Mean transthoracic impedance for all patients was 69.3 +/- 16 (SD) ohms (range 39-131 ohms), but transthoracic impedance was significantly greater in the AA than the AP position (75.4 +/- 13 vs. 66.7 +/- 16 ohms, p = 0.02). Initial energy was 50 J (delivered) and was gradually increased to a maximum of 360 J if required. Cardioversion was successful in 73 of 80 (91.2 per cent), and low energy shocks (< or = 200 J) were successful in 45 of 80 (56.2 per cent) patients. Using single factor analysis, sex, left atrial enlargement, electrode pad positions, aetiology of atrial fibrillation, presence of left ventricular failure, and prior treatment with verapamil or beta-adrenergic blockers were not significant determinants of cardioversion success or success of low energy shocks but prior treatment with digoxin was, both for cardioversion success and success at low energies. In patients with transthoracic impedance < or = 70 ohms, low energy shocks were more often successful (33 of 50, 66 per cent) than in patients with transthoracic impedance > 70 ohms (12 of 30, 40 per cent), p = 0.04. Using univariate analysis, cardioversion success with low energy shocks was not only significantly associated with prior treatment with digoxin but also with the duration of atrial fibrillation (24 hours to less than one month and one month to three years) and for shocks of < or = 100 J, with prior treatment with amiodarone. Multifactorial linear regression analysis selected, in rank order, only duration of atrial fibrillation of 24 hours to less than one month and one month to three years as significant predictors of both cardioversion success irrespective of shock strength, and success of low energy shocks.     

Management of recurrent ventricular tachyarrhythmias associated with Q-T prolongation

Eleven patients with acquired prolongation of the Q-Tc interval and recurrent ventricular tachyarrhythmias were studied. Five patients required 5 to 44 direct current shocks to correct prolonged ventricular tachyarrhythmias, and five were given at least two antiarrhythmic agents in an attempt to control the arrhythmias. In 4 of the 11 patients, when thioridazine, diuretic drugs and antiarrhythmic agents were withdrawn and hypokalemia or hypocalcemia corrected, ventricular tachyarrhythmias did not recur. The Q-Tc interval normalized in 2 to 3 days. Ventricular tachyarrhythmias were recurrent in the remaining seven patients, despite withdrawal of the drugs that caused the Q-Tc prolongation, attempted correction of hypokalemia when present and the administration of antiarrhythmic agents to four of the seven. All antiarrhythmic agents were then withdrawn in this group.

Immediately on the establishment of overdrive ventricular or atrioventricular sequential pacing in these patients, ventricular tachyarrhythmias were abolished. No breakthrough ventricular tachyarrhythmias occurred during temporary pacing. Temporary pacing was required for an average of 10 days and the Q-Tc interval normalized an average of 5 days from the onset of pacing. Three patients required a permanent pacemaker, one because of chronic complete heart block, one because of the sick sinus syndrome, and one because of frequent ventricular ectopic complexes complicating ischemic heart disease. All 11 patients survived their period of hospitalization.     

Chronic Q fever endocarditis.

Eight patients with chronic Q fever endocarditis were treated with tetracycline for up to 40 months. In addition, five of these patients received co-trimoxazole. Six patients had prosthetic valves. Two patients who had Q fever endocarditis on their native valves required valve replacement because of haemodynamic difficulties: in only one did the Q fever endocarditis contribute to the haemodynamic difficulty. One patient died. It is suggested that medical treatment is continued until clinically and haematologically there is no evidence of endocarditis and the Q fever phase 1 antibody titre is less than 200. No recurrence of Q fever endocarditis has been detected in three of our patients who have now stopped treatment.     

Cardiac injury with damped sine and trapezoidal defibrillator waveforms

To assess defibrillator-induced cardiac damage, 49 anaesthetized greyhounds received either no shocks (control group) or five shocks from a defibrillator delivering one of five waveforms (Lown, Edmark, Belfast damped sine waveforms: 5 and 20 ms trapezoidal waveforms). At 3 days the hearts of the 36 surviving dogs were examined for macroscopic damage. The Belfast and Edmark waveforms caused significantly more damage (mean 21.1 +/- SEM 2.9 g and 16.0 +/- 3.7 g) respectively than the Lown waveform (3.5 +/- 1.3 g) P less than 0.01. The 20 ms trapezoid caused significantly more damage (8.1 +/- 3.1 g) than the 5 ms pulse (0.7 +/- 1.3 g) P less than 0.05). The ventricular ectopic counts per minute were not significantly different in the three sine wave and 20 ms trapezoidal groups at 24 and 48 h (P greater than 0.05), but at 2 and 72 h were significantly greater in the Belfast and Edmark groups than in the Lown group (2 h, Belfast P less than 0.01, Edmark P less than 0.05: 72 h P less than 0.05). At 15 min there was more right chest ST-segment elevation in the Belfast than in the Lown, Edmark and 20 ms trapezoid groups (P less than 0.01), while left chest ST elevation was greater in the Belfast and Edmark than in the Lown (P less than 0.05) and 20 ms trapezoid groups (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of nifedipine on enzymatically estimated infarct size in the early phase of acute myocardial infarction

In a double blind placebo controlled trial, 434 patients with suspected myocardial infarction were randomised to treatment with nifedipine (n = 217) or placebo (n = 217) within six hours from the onset of chest pain. During the treatment period of 48 hours, a 10 mg capsule containing nifedipine or placebo was given sublingually every four hours for 24 hours, then orally every four hours for the next 24 hours. Acute myocardial infarction was confirmed in 295 patients (146 in the nifedipine group and 149 in the placebo group). The median delay time to intervention with nifedipine in patients with acute myocardial infarction was 111 minutes. Infarct size was assessed by the estimation of release of creatine kinase isoenzyme MB and creatine kinase from blood samples taken every four hours for 48 hours. The total mean (SEM) creatine kinase MB released was 406.4 (27.2) IU/l in the nifedipine group and 345.7 (20.5) IU/l in the placebo group. Total mean (SEM) creatine kinase released was 2749.6 (165.1) IU/l in the nifedipine group and 2698.4 (145.9) IU/l in the placebo group. In hospital mortality was similar for both the nifedipine and placebo groups (6.6% and 5.8% respectively). Treatment with nifedipine in the early phase of acute myocardial infarction seems to have no effect on enzymatically measured infarct size.     

Long-term survival of a patient with left ventricular free wall rupture without surgical repair

This report describes the case of a patient who developed postinfarction left ventricular free wall rupture and cardiac tamponade. He was managed conservatively, made a successful recovery, and is alive and asymptomatic 10 months after the index episode. Only 17 cases in which the patients survived subacute rupture of the ventricular free wall over the long term without surgical repair have been reported in the literature.