Hyperglycaemia has been convincingly shown to be associated with increased occurrence of atherosclerosis [1±4]. Epidemiological studies found that patients with Type II (non-insulin-dependent) diabetes mellitus have a two-to four-fold increased relative risk of cardiovascular disease (CVD) in comparison to nondiabetic subjects [3]. Poorly controlled Type II diabetic patients have a higher risk than patients with good glycaemic control [1,4]. Furthermore, there is evidence that non-diabetic plasma glucose levels are also continuously associated with CVD [5±7], though this relationship has not been confirmed for only moderate degrees of hyperglycaemia [8±10]. So far, Diabetologia (1998) 41: 706±712

Arrhythmogenic right ventricular dysplasia is a structural heart disease characterized by fibrofatty degeneration of right ventricular myocardium and arrhythmias of right ventricular origin. The aim of this study was to characterize endocardial right ventricular activation by electroanatomic mapping as a guide for catheter ablation in patients with arrhythmogenic right ventricular dysplasia. Electroanatomic mapping and entrainment procedures were performed in 5 patients with arrhythmogenic right ventricular dysplasia. Endocardial mapping during ventricular tachycardia demonstrated a focal activation pattern with radial spreading of activation from a site of earliest ventricular activation in all directions. Right ventricular activation time (127 +/- 34 ms) was markedly shorter than tachycardia cycle length (415 +/- 92 ms). The site of earliest ventricular activation was found in an aneurysmal outflow tract (n = 2), at the border of aneurysms near the tricuspid annulus (n = 2), and at the apex of the right ventricle (n = 1). Entrainment mapping criteria of these areas of earliest endocardial activity were consistent with exit sites of a reentrant circuit in an area of abnormal myocardium. Fractionated potentials were found 61 +/- 29 ms before the onset of the QRS complex at these sites. Catheter ablation rendered the "clinical" ventricular tachycardia noninducible in four patients but "nonclinical" faster ventricular tachycardias were inducible in three patients. During the follow-up of 7 +/- 3 months after ablation, the frequency of therapies in 4 patients with an implantable cardioverter defibrillator decreased from 49 +/- 61 episodes per month before ablation, to 0.3 +/- 0.5 episodes per month after ablation (P < 0.05). Electroanatomic mapping during ventricular tachycardia facilitates localization of exit sites in relation to aneurysms in diseased right ventricle and may guide catheter ablation in patients with arrhythmogenic right ventricular dysplasia.

Use of CF catheters in PVI has a beneficial effect on procedural parameters, probably by improving efficacy of transmural lesion formation.

Slow conduction in diseased myocardium close to the LAF or in the middle and inferior aspects of the LV septum may represent the diastolic pathway of VT involving the LAF.

Repetitive reinitiation of BBRT and interfascicular tachycardia by ventricular pacing from the ICD electrode should be considered as a mechanism of VT storm refractory to ICD therapy in patients with a pre-existing conduction delay within the His-Purkinje system.