No abstract

While the combined ischaemic and electrical trauma caused by repeated episodes of ventricular fibrillation and defibrillation during the implantation of a cardioverter-defibrillator did not cause any systolic dysfunction, diastolic filling was significantly impaired.

Addition of the Cardiac Support Device to conventional cardiac surgery, or applied alone, is safe and simple. The device seems to reverse ventricular dilatation and improve functional capacity and well-being of heart failure patients with dilated cardiomyopathy. Further studies will delineate what patient population will best benefit from passive containment surgery using the CorCap Cardiac Support Device.

The implanted cardioverter defibrillator represents an alternative therapy for patients with drug-refractory malignant ventricular arrhythmias. Implantation and testing of the device requires that ventricular fibrillation be evoked and converted, thus providing a situation in which cardiovascular haemodynamics can be studied. In this study we have evaluated the effects of electrically induced ventricular fibrillation, followed by defibrillation, on coronary sinus blood flow and cardiac outflow of endothelin- and neuropeptide Y-like immunoreactivity (-LI) and of noradrenaline. Twelve patients were studied during implantation of a defibrillator. Ventricular fibrillation was induced and terminated after 17 +/- 1 s 5 +/- 1 times in each patient. In six patients coronary sinus blood flow was measured continuously. Plasma samples were obtained from four of these patients and another six patients, from the coronary sinus, radial artery and central vein before and during fibrillation and at two time points ( < 30 s and 5 min). Basal coronary sinus blood flow decreased to 38% at 14 +/- 2 s of ventricular fibrillation. Immediately following defibrillation there was a short-lasting increase in coronary sinus blood flow to 244% and a significant increase in the levels of neuropeptide Y-LI (146%) and noradrenaline (158%) in the coronary sinus while endothelin-LI remained unchanged (97%). Neither fibrillation nor defibrillation evoked any changes in the peripheral arterial and venous levels of endothelin-, neuropeptide Y-LI or noradrenaline. It is concluded that coronary sinus blood flow is markedly reduced during fibrillation and that restoration of normal impulse activity is followed by short-lasting hyperaemia. There was no evidence for effects on the vascular endothelium as assessed by endothelin levels.