No abstract

No abstract

Fifty-eight chronically T. cruzi-infected rats and 26 control rats were submitted to the ajmaline test (1 mg/kg, i.v. during ECG monitoring) after obtaining the resting ECG. Abnormal ECG tracings were detected in the resting ECG of 26 (44%) infected rats. After ajmaline injection, a decrease in heart rate was observed in control but not in infected rats. P wave enlargement, lengthening of the QRS complex, and increase of the PR as well as the QaT intervals were detected in all animals. Ajmaline induced right axis deviation in 7% of the control rats and left axis deviation in 26% of the controls, as well as in 23% of the T. cruzi-infected rats with abnormal resting ECG. However, after ajmaline injection, 7 (21%) of the 32 infected rats having normal resting ECG presented the following ECG changes not observed in control animals: indeterminate axis (15%), marked increase in PR interval and bizarre QRS complex (3%), and marked decrease in heart rate plus a significant increase in PR interval. These data show that ajmaline induces important ECG changes not only in controls, but also in T. cruzi-infected rats. Furthermore, since severe ECG changes occurred only in T. cruzi-infected rats having normal resting ECG, the ajmaline test can be used to unmask cardiac lesions in experimental chronic Chagas' disease.

A total of 125 rats were infected with the Colômbia strain of T. cruzi (2000 parasites/g) shortly after weaning. Of these, 58 survived the acute phase and were used in the present experiment. Twenty eight similar but not infected rats served as controls. All rats were submitted to the resting ECG When they were 6 months old. Classic and 3 precordial leads were employed in order to record the ECG as completely as possible. Electrocardiographic changes similar to those found in human chronic Chagas' heart disease and not previously described in this model were found in 44% of the T. cruzi-infected rats: left axis deviation (22%), right axis deviation (7%), lengthened and bizarre QRS complex (14%) and abnormal J point elevation (3%). On the basis of these results, we believe that the resting ECG constitutes a valuable tool for studying experimental chronic Chagas' heart disease in rats.

The authors report a rare case of congenital Budd-Chiari syndrome in a twenty-eight-year-old male mongoloid. The patient was submitted to azygous-portal disconnection, because of the syndrome of portal hypertension supposedly due to cirrhosis of the liver. He died of hemorrhage of the liver on the third postoperative day. Autopsy revealed a congenital fibrotic obstruction of all suprahepatic veins, with a wide, round ligament containing a functional umbilical vein, which had been routinely ligated during surgery. An extensive review of the literature showed no similar report. The authors speculate that the inadvertent interruption of the round ligament, which until then had served as a pathway for venous draining of the liver, followed by ligation of the anastomoses between the portal and azygous systems, was the factor that triggered the lethal outcome. Thus, this appears to be the first case of congenital Budd-Chiari syndrome predominantly maintained at the expense of the round ligament of the liver, with a patent vascular branch.