Motohiro Nakao

Enhancement of J–ST-Segment Elevation by the Glucose and Insulin Test in Brugada Syndrome

NOGAMI, A., et al.: Enhancement of J–ST‐Segment Elevation by the Glucose and Insulin Test in Brugada Syndrome. The effects of glucose and insulin on J–ST‐segment elevation were evaluated in seven men (mean age 45 ± 10 years) with Brugada syndrome. Six patients had been reanimated from VF and one patient had experienced syncope. The effects of intravenous (1) pilsicainide 50 mg, (2) glucose 50 g, and (3) glucose 50 g plus regular insulin 10 IU on the precordial ECG leads were examined. Pilsicainide significantly enhanced J‐ST elevation in all patients and induced VF in 1 patient. A significant accentuation of the abnormal J‐ST configuration was observed in all patients at a mean of 51 ± 40 minutes after glucose and insulin infusion. Changes in blood glucose and serum potassium concentration were 111 ± 158 mg/dL and −0.30 ± 0.48 mEq/L , respectively. These changes were not directly related to the ECG changes. Glucose infusion without insulin caused a subtle increase in J‐ST elevation. In conclusion, the administration of glucose and insulin safely unmasked or accentuation the J–ST‐segment elevation in Brugada syndrome. Blood glucose and insulin concentrations may be factors modulating the circadian or day‐to‐day ECG variations in this syndrome. (PACE 2003; 26[Pt. II]:332–337)

Prognostic Utility of Myocardial Blood Flow Assessed by N-13 Ammonia Positron Emission Tomography in Patients With Idiopathic Dilated Cardiomyopathy

Previous studies in patients with idiopathic dilated cardiomyopathy (IDC) have suggested that myocardial perfusion is impaired and spatially heterogeneous in such cases. Our objective was to identify any association between an abnormality in myocardial perfusion and the prognosis of patients with IDC. We collected data on N-13 ammonia positron emission tomography (PET) studies performed in 26 patients with IDC (9 nonsurvivors, 17 survivors) and in 8 normal control subjects. Regional myocardial blood flow (rMBF) was quantified using N-13 ammonia positron emission tomography and the Simple flow model. The spatial heterogeneity of myocardial perfusion was assessed by calculating the coefficient of variance of rMBF. Mean rMBF of the survivors was significantly lower (0.54 +/- 0.13 ml/min/g) than that of control subjects (0.66 +/- 0.06 ml/min/g) (p = 0.03 vs control), but did not differ significantly between nonsurvivors (0.58 +/- 0.15 ml/min/g) and control subjects. The coefficient of variance of rMBF was significantly higher in nonsurvivors than in either survivors or control subjects (0.24 +/- 0.08 vs 0.15 +/- 0.08, p = 0.007, and 0.16 +/- 0.05, p = 0.03, respectively). The probability of 3-year survival (Kaplan-Meier method) was 33.0% in subjects whose coefficient of variance of rMBF was above the median compared with 90.0% in subjects whose coefficient of variance of rMBF was below the median (p = 0.01). The probability of 3-year survival did not differ among subjects whose mean rMBF was above versus below the median (61.5% vs 62.9%, respectively). The results suggest that the prognosis of patients with IDC is associated with the spatial heterogeneity of myocardial perfusion, not with initial absolute rMBF.

Usefulness of implantable loop recorder in a patient with syncope during bathing

A 27‐year‐old man presented to our hospital with a 1‐year‐hisory of repeated syncope, which particularly occurred while bathing or on a hot day. The head‐up tilt test did not induce arrhythmia; however, blood pressure decreased by 39 mm Hg without any symptoms. Given that no bradycardia/tachycardia was induced on electrophysiological study and carotid sinus massage, an implantable loop recorder (ILR) was implanted. After 2 months, syncope again occurred during bathing at midnight. Sinus arrest and a maximum ventricular pause of 10.2 s were documented using the ILR. After pacemaker implantation, the patient had not experienced syncope for 14 months.