Surgical cure of the Wolff-Parkinson-White syndrome--a comparison of two techniques.

Curative arrhythmia surgery for patients with symptomatic Wolff-Parkinson-White syndrome (WPW) was first performed in South Africa in November 1987. Pre-operatively all patients were symptomatic despite medical therapy, and 32% were assessed as being at risk for sudden death. The first 9 patients (November 1987 to December 1989) underwent either epicardial or localised endocardial surgical dissections, and a cure was obtained in 66%. Aberrant atrioventricular conduction recurred in 2 patients, 3 degrees atrioventricular heart block occurred in 2 patients, and there was 1 postoperative death in a patient who had undergone simultaneous coronary artery bypass grafting. In contrast, a standardised endocardial technique was used in the subsequent 10 patients. Surgical cure was obtained in all 10 patients (P < 0.01). However, 1 patient required reoperation 24 hours after the first procedure because of early postoperative recurrence due to initial incorrect pathway localisation. This was successful. There were no deaths, and no patient developed atrioventricular heart block. In view of the excellent surgical results, arrhythmia surgery should be considered in select WPW patients who either have refractory symptoms or are at risk for sudden death. Furthermore, this reliable surgical technique provides an essential back-up should alternative interventional procedures such as percutaneous radiofrequency ablation fail.

Normal left ventricular function does not protect against propafenone-induced incessant ventricular tachycardia.

Propafenone is a class Ic anti-arrhythmic agent with mild beta-blocking properties which has recently become available in South Africa. We have used the drug in 3 patients with sustained monomorphic ventricular tachycardia not due to ischaemic heart disease. All had normal left ventricular function; 1 had Wegener's granulomatosis and 2 had arrhythmogenic right ventricular dysplasia. In the latter 2, propafenone provoked incessant monomorphic ventricular tachycardia which persisted for more than 24 hours despite repeated efforts at termination. The morphology was similar to the patients' spontaneous ventricular tachycardia, but the rate was slower and the QRS complexes broader, consistent with propafenone's marked ability to slow intraventricular conduction. It is postulated that incessant tachycardia results from perpetuation of re-entry due to marked conduction slowing produced by the drug. Previous reports have suggested that this is most likely to occur in patients with poor left ventricular function, but our experience indicates that those with normal left ventricular function are also at risk, particularly if the substrate for re-entry is present. Propafenone, like all other powerful anti-arrhythmic agents, may provoke life-threatening arrhythmias and should be used with great caution after due consideration of the indications, even in patients with normal left ventricular function.

Surgery for the Wolff-Parkinson-White syndrome. The Groote Schuur Hospital experience.

Surgical division of accessory atrioventricular (AV) connections has been performed on 9 patients with the Wolff-Parkinson-White (WPW) syndrome at Groote Schuur Hospital. All patients had symptomatic paroxysmal tachycardia. The indication for surgery in 5 patients was poor control on antiarrhythmic drugs. Surgery was performed on a 15-year-old boy to prevent lifelong dependence on drugs, although his atrial fibrillation (ventricular rate greater than 300/min) was controllable with sotalol 1,280 mg daily. The remaining 3 patients required cardiac surgery for other indications and therefore their accessory pathways (APs) were divided concurrently. The AP was localised by pre-operative endocardial mapping and intra-operative epicardial mapping. There were 4 posteroseptal, 3 left free-wall and 2 right free-wall pathways. An endocardial approach was used to divide the pathways. All 5 free-wall APs were successfully divided without complications or recurrence. However, 1 patient with paroxysmal atrial fibrillation and severe unstable angina due to coronary artery disease died unexpectedly 10 days after 4-vessel coronary bypass grafting and division of a posteroseptal AP. Postoperative complications occurred in a further 2 patients with posteroseptal APs. One patient developed complete heart block and is now asymptomatic with a DDD pacemaker, while the other had recurrence of retrograde bypass conduction postoperatively, but is now successfully controlled on sotalol. Therefore 7 of the 8 survivors are free of recurrence of tachycardia on no anti-arrhythmic drugs after a mean follow-up of 14.3 months. New insights into the surgical technique, particularly for division of posteroseptal pathways, can be expected to improve the outlook.

Comparative activities of combinations of acyclovir, vidarabine or its 5'-monophosphate, and cloned human interferons against herpes simplex virus type 2 in human and mouse fibroblast cultures.

Human interferon-alpha A/D (Bgl), an alpha-hybrid cloned interferon, displays activity in both human and mouse cell lines. We measured the effects of this interferon in double and triple combinations with acyclovir, vidarabine or its 5'-monophosphate against herpes simplex virus type 2 in mouse and human fibroblasts. A 75% cytopathic effect reduction assay employing a modified checkerboard technique was used. Results in human fibroblasts were compared with those obtained when recombinant human interferon-alpha 2 was substituted for the hybrid. Combinations of the hybrid interferon and nucleoside antiviral agents evoked comparable synergistic isobolograms and fractional inhibitory concentration indices in human and mouse cells versus herpes simplex virus type 2. Similar interactions were found when human interferon-alpha 2 was substituted. Uninfected cells treated with the tested combinations showed no toxicity. These data suggest that combinations of recombinant human interferon-alpha A/D (Bgl) and nucleosides in mouse models of herpes infection deserve study.

Comparative activities of selected combinations of acyclovir, vidarabine, arabinosyl hypoxanthine, interferon, and polyriboinosinic acid-polyribocytidylic acid complex against herpes simplex virus type 2 in tissue culture and intravaginally inoculated mice.

The effects of double and triple combinations of acyclovir (ACV), adenine arabinoside (ara-A), arabinosyl hypoxanthine, or interferon on herpes simplex virus type 2 in mouse embryo fibroblasts were measured. These in vitro data were compared with results obtained in mice infected intravaginally with herpes simplex virus type 2 and treated intraperitoneally with low- and high-dose combinations of ACV, ara-A, or polyriboinosinic-polyribocytidylic acid(poly-L-lysine)carboxymethylcellulose complex [poly IC(LC)], an interferon inducer. Although all double combinations and one triple combination evoked synergistic reactions in vitro, results did not necessarily predict in vivo observations. In vivo synergy was observed when combinations of ACV and ara-A and low doses of ara-A-ACV-poly IC(LC) were used. However, toxicity was seen with full-dose nucleoside-poly IC(LC) doublets. The full-dose ACV-ara-A combination completely prevented progression beyond vaginitis, with all animals surviving. The ara-A-ACV results observed in mice, together with in vivo data of others, suggest that this combination might prove clinically useful for certain herpes simplex virus type 2 infections.