Tobe Tobe - Academia.edu (original) (raw)

Papers by Tobe Tobe

American Journal of Kidney Diseases, 1999

The hemolytic uremic syndrome (HUS) is known to have several causes, including infectious disease... more The hemolytic uremic syndrome (HUS) is known to have several causes, including infectious diseases, drugs, pregnancy, and malignant disease. We report a patient who developed acute renal failure attributable to HUS in the course of Capnocytophaga canimorsus bacteremia. Acute tubular necrosis as well as HUS should be considered as a cause of acute renal failure in the setting of Capnocytophaga canimorsus bacteremia. 1999 by the National Kidney Foundation, Inc.

American Journal of Cardiology, 1991

American Journal of Cardiology, 1993

Atthough a number of studies have shown that the htcidence of late potentials is lower after thro... more Atthough a number of studies have shown that the htcidence of late potentials is lower after thrombolytic therapy, it is not known whether this is paralleled by fewer atrhythmic events during ion&term foiiow+rp. in patients with first acute myocardiai hrfarction, filtered QRS duration was sigdflcantiy shorter when treated with streptoW nase (95 + 11 ms, n = 53) than when treated with conventional therapy (66 f 12 ms, n = 77, p <0.05). The iowanpiitude si~i (D& was shorter after thrombolysis (26 f 11 vs 22 +-12 ms, p ~0.02). Terminal rootmean-square voltage did not dir significantly (412 24 vs 35 f 23 pV)

International Journal of Cardiology, 1994

In a series of 171 consecutive survivors of acute myocardial infarction, the predictive value of ... more In a series of 171 consecutive survivors of acute myocardial infarction, the predictive value of late potentials and QTc prolongation was prospectively assessed. QT intervals were measured in lead Vz, corrected QT (QTc) was calculated using Bazett's equation (cut-off value 440 ms). Late potentials were considered to be present when all of the three signal-averaged electrocardiographic variables were abnormal (i.e. QRS > 114 ms, D4,, > 38 ms, and Va< 20 pV). Complete follow-up was obtained (mean 13 f 6 months, range 6-24 months). Six percent of the patients had an arrhythmic event (i.e. sustained ventricular tachycardia or sudden death). The relative risk of late potentials for arrhythmic events was 7.7 (P < 0.02). The relative risk of QTc > 440 ms was 1.1 (NS). In a multivariate analysis, the addition of QTc prolongation did not significantly improve the prognostic value of late potentials alone. It is concluded that late potentials are predictive of arrhythmic events after myocardial infarction, but the presence of concomitant QTc prolongation does not worsen the prognosis.

Basic Research in Cardiology, 1991

Exogenous bradykinin was administered to pigs in which an experimental infarction was evoked by i... more Exogenous bradykinin was administered to pigs in which an experimental infarction was evoked by ischemia and reperfusion. Ischemia (45 min) was induced in a closed-chest model with a balloon catheter in the left anterior descending artery, reperfusion by deflating and removing the balloon. The pigs were treated with saline (n = 11) or bradykinin (0.1 mg/kg in 30 min) infusion (n = 10) during the last 15 min of the ischemic period and the first 15 min of reperfusion. During ischemia, heart rate increased in the saline group to 120 ± 9 % of the initial value (p < 0.05) and in the bradykinin group to 155 ± 13 % (p < 0.05). After reperfusion, the rate-pressure product was increased in both groups. The increase of arterial creative kinase levels was significantly less in the bradykinin-treated group. However, the catecholamine and purine levels were increased, as was the plasma renin activity when compared with the saline group. Two weeks after the infarction, six pigs had died in each group. In three out of five surviving saline-treated pigs and one out of four surviving bradykinin-treated pigs, a sustained ventricular tachyarrhythmia was inducible after programmed electrical stimulation. In conclusion, although systemically administered bradykinin caused a temporary increase in myocardial ischemia, it did reduce the (enzymatic indices of) infarct size. Therefore, the beneficial effects, previously found for ACE-inhibitors might at least partially be related to the potentiation of endogenous bradykinin.

Journal of Cardiovascular Pharmacology, 1992

Journal of The American College of Cardiology, 1992

The purpose of this study was to determine the incidence of late potentials and their relation to... more The purpose of this study was to determine the incidence of late potentials and their relation to QT prolongation in a family with a high incidence of sudden death during sleep at a young age and bradycardia-dependent QT prolongation (n =9) and to compare the findings with those in consanguineous family members without QT prolongation (n =13). Six (67%) of the 9family members with From the

Journal of Cardiovascular Pharmacology, 1991

In this study, the effect of bradykinin or saline infusion during ischemia and reperfusion on ele... more In this study, the effect of bradykinin or saline infusion during ischemia and reperfusion on electrical stability, 2 weeks after myocardial infarction, was assessed. Acute myocardial infarction was induced in 21 pigs by a transluminal occlusion of the left coronary artery with a catheter balloon, inflated for 45 min. Bradykinin was administered by a 30-min infusion that started after 30 min of coronary occlusion and was continued until 15 min after reperfusion. Although creatine kinase levels in bradykinin-treated animals were significantly lower (p less than 0.001), 2 week survival was not different between groups. In survivors, the filtered QRS (ventricular deflection) duration (detected using signal-averaged electrocardiography) was significantly prolonged in saline-treated pigs, whereas in bradykinin-treated pigs this prolongation was prevented. The terminal voltage of the QRS complex was significantly lower in saline-treated pigs than in bradykinin-treated pigs. These two parameters signify an improved electrical stability after bradykinin treatment. Refractory periods in saline-treated hearts were longer than in bradykinin-treated hearts (106 +/- 10% vs. 95 +/- 13%, p less than 0.05). Also, current thresholds in the infarct border zones showed a greater variance in saline-treated hearts (p less than 0.001), pointing toward more tissue heterogeneity of the infarct border zone. Programmed electrical stimulation showed a trend toward reduced inducibility of sustained ventricular tachycardia in bradykinin-treated hearts. Therefore, bradykinin improves electrical stability weeks after experimental myocardial infarction.