While both myocardial and vascular damage contribute to an increase in HGF level, vascular damage is not associated with the increase in VEGF. Vascular endothelial growth factor might be related to left ventricular remodelling in the sub-acute phase of myocardial infarction.

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miodarone has been reported to reduce overall mortality and morbidity in patients with non-ischemic cardiomyopathy, but it has not improved the frequency of sudden cardiac death in such patients. 1,2 It is not clear why this should be, but it is possibly related to the proarrhythmic effects of amiodarone. [3][4][5][6] It was recently reported that the implantable cardioverter defibrillator (ICD) is more effective than antiarrhythmic agents, amiodarone in particular, in preventing sudden cardiac death in patients with left ventricular dysfunction. 7 Some authors have noted that amiodarone can increase the defibrillation threshold. 8,9 Rosenbaum et al showed that microvolt T wave alternans (TWA) is a promising predictor of vulnerability to ventricular tachyarrhythmia. 10 Previous studies have demonstrated that the magnitude of TWA is dependent on heart rate. 11 In addition, Tanno et al have reported that TWA that appears at a rate of less than 100 beats/min is closely related to ventricular tachyarrhythmia. 12 We hypothesized that when the onset heart rate of TWA is lowered after administration of drugs, the risk of the proarrhythmic effects of those drugs is increased. Case ReportA 62-year-old man with dilated cardiomyopathy (DCM) and paroxysmal atrial fibrillation was admitted to hospital in May 1998 because of palpitations caused by sustained ventricular tachycardia (VT), though he had been taking methyldigoxin (0.1 mg/day) and pirmenol (150 mg/day) for 2 years. On physical examination, blood pressure was 78/-mmHg; and pulse rate was 180 beats/min and regular. The electrocardiogram (ECG) showed a wide QRS complex tachycardia exhibiting right bundle branch block and right axis deviation at a rate of 188 beats/min, which was terminated by electrical cardioversion with a 50-J DC shock. The ECG showed conversion to normal sinus rhythm at a rate of 70 beats/min with normal axis and a normal QT interval (QT: 0.44 ms / QTc: 0.48). Chest X-ray showed no sign of pulmonary congestion or cardiomegaly (Fig 1A,B). Laboratory data showed mild elevation of aspartate aminotransferase (60 IU/L), alanine aminotransferase (55 IU/L), and -glutamyl transpeptidase (260 IU/L) because of chronic hepatitis C. Two-dimensional echocardiogram showed a severely hypokinetic left ventricle (LV) the dimensions of which were enlarged (LV end-diastolic dimension: 64.9 mm, LV ejection fraction: 29%).Several forms of sustained VT were induced by programmed ventricular stimulation during an electrophysiologic study. The sustained VTs were hemodynamically unstable, and we had to terminate them with DC cardioversion. An implantable cardioverter defibrillator (ICD) was used because bepridil could not prevent sustained VT. Ten days after the implantation, the VT reappeared and was terminated with 10 J cardioversion. Metoprorol (5 mg/day) was administered in addition to bepridil. However, the VT reccurred and the ICD discharged twice 2 weeks later. Bepridil was then replaced with amiodarone (200 mg/day) and 3 weeks later, an incessant form of VT appear...

While both myocardial and vascular damage contribute to an increase in HGF level, vascular damage is not associated with the increase in VEGF. Vascular endothelial growth factor might be related to left ventricular remodelling in the sub-acute phase of myocardial infarction.

We evaluated the extent of reperfusion injury (RI) following successful coronary intervention quantitatively and non-invasively using technetium-99m