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Biomedical subjects

R B Bestetti

Publications and source records attributed to R B Bestetti.

At least 55 records · Page 3Linked to original sources
PubMed1989

The ajmaline test as a method to disclose latent experimental Chagas' heart disease.

Forty-one chronically T. cruzi-infected male adult albino rats with normal resting ECG were submitted to the ajmaline test (1 mg/kg body weight injected into the dorsal vein of the penis). Twenty-one similar noninfected animals served as controls. Ajmaline induced the following ECG alterations in control rats: A decrease in heart rate, an increase in heart rate, an increase in P-wave duration, an increase in PR interval, lengthening of the QRS complex, and left axis deviation in 33%, 28%, 14%, 90%, 100%, and 33% of the animals, respectively. Ajmaline evoked similar alterations in 29 of 41 (71%) T. cruzi-infected rats. However, 12 of 41 (29%) infected rats showed ECG changes of a magnitude not seen in controls: P-wave enlargement, first-degree AV block, lengthened QRS complex, and first-degree AV block plus lengthened QRS complex in 7%, 12%, 14%, and 4% of the animals, respectively. Microscopical lesions were not found in control rats. However, 22 of 41 (53%) infected rats were found to have the following pathological lesions: mononuclear cell infiltrate, necrosis, myocyte vacuolization, and interstitial fibrosis in 56%, 39%, 29%, and 7% of the animals, respectively. By comparing the ECG changes evoked by ajmaline not seen in controls with the concomitant pathological lesions, the ajmaline test was found to have 54% sensitivity, 100% specificity, and 100% positive predictive value. Thus, the ajmaline test appears to be useful for unmasking myocardial disease and therefore may be considered a potential method for the full characterization of the indeterminate form of Chagas' disease in experimental animals.

Ajmaline↗
PubMed1989

Fatal outcome associated with autopsy proven myocardial bridging of the left anterior descending coronary artery.

Two patients with myocardial bridging of the left anterior descending coronary artery associated with myocardial infarction are described. One of them died from acute cerebral emboli related to cardiac thrombosis in a left ventricular aneurysm. The other died suddenly while sleeping. Both patients were found to have a very long myocardial bridging of the left anterior descending coronary artery as well as patches of fibrosis in the left anterior descending coronary artery territory. Marked left ventricular hypertrophy was also found in the patient who died suddenly. No other cardiac abnormality was observed in either patient. These cases, together with those previously reported, suggest that myocardial bridging of the left anterior descending coronary artery can no longer be considered a benign coronary anomaly.

Adult↗
PubMed1989

Impending myocardial infarction in a patient with marked left ventricular hypertrophy and normal coronary arteriogram--a case report.

A middle-aged woman with long-term uncontrolled arterial hypertension developed a clinical picture of impending myocardial infarction. A normal coronary arteriogram was obtained. However, left heart catheterization showed a marked increase in left ventricular end-diastolic pressure, while left angiocardiography revealed marked left ventricular hypertrophy. She was successfully treated with a beta-blocking and calcium-antagonist agent. The present case shows that an impending myocardial infarction may occur in patients having normal coronary arteriogram but with left ventricular hypertrophy secondary to arterial hypertension.

Angiocardiography↗
PubMed1989

[Transient atrioventricular conduction disorder: a potential cause of sudden death in myocarditis due to varicella. A case report].

The case of a patient with varicella skin lesions presenting with heart failure at 4 years of age is described. A transitory atrioventricular conduction disturbance due to myocardial impairment was documented during hospital stay. Despite the clinical improvement with conventional therapy, the patient died from respiratory failure due to a lung infection but with an almost normal electrocardiogram. Necropsy showed myocardial lesions compatible with acute myocarditis. A possible viral specific affinity for the conduction system of the heart is suggested and judged to be a potential cause of death in this disease. Since the actual incidence of varicella myocarditis associated to an atrioventricular conduction disturbance is unknown it seems prudent that every patient with varicella infection should have a cardiac examination during the acute phase of the disease. As the diagnosis of subclinical myocarditis depends essentially on an electrocardiogram, we believe this method should be employed routinely during the acute phase in order to assess myocardial involvement in this disease, which may be a cause of sudden death.

Chickenpox↗
PubMed1989

[3H]-acetylcholine release from rat atria in chronic chagasic cardiopathy.

Isolated superfused rat atria release [3H]-acetylcholine when depolarized with 57 mM potassium. The depolarization-induced [3H]-acetylcholine overflow was significantly reduced in atria from chronically T. cruzi-infected rats with electrocardiographically characterized cardiopathy. This fact suggests the occurrence of functional alterations of cardiac parasympathetic control in these animals, probably related to cardiac ganglion cell destruction.

Acetylcholine↗
PubMed1988

The usefulness of the resting electrocardiogram for characterizing acute Chagas' heart disease in the rat.

The present experiment was undertaken to characterize the resting electrocardiogram of rats in the acute stage of experimental T. cruzi infection. One-hundred-and-eighty-seven newly-weaned male albino rats were infected intraperitoneally with 1000 parasites/g body weight. Thirty-two similar but non-infected rats served as controls. Groups of eight randomly chosen rats were killed on day 8, and on days 15, 18, 22, 25 and 29 after infection. Groups of 8 control rats were killed on days 8, 15 and 22. Electrocardiographic changes were observed in 25 of 48 (52%) infected rats. P wave abnormalities indicating atrial chamber dilatation, QRS axis deviation, QRS complex changes compatible with left ventricular hypertrophy or myocardial damage, increased PR interval and ventricular repolarization alteration were detected in 24, 27, 18, 10, and 6% of infected rats, respectively. A mononuclear cell infiltrate and pseudocysts of amastigote forms of T. cruzi were found in 91, and 56% of infected animals, respectively. The sensitivity and the positive predictive value of the electrocardiographic changes were 66, 91, and 96%, respectively. Thus, the resting electrocardiogram is a reliable method for detecting myocardial lesions in the rat with acute Chagas' heart disease.

Animals↗
PubMed1988

An unusual case of Budd-Chiari syndrome--a case report.

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.

Adult↗
PubMed1987

Myocardial bridging of coronary arteries associated with an impending acute myocardial infarction.

A 57-year-old woman developed severe substernal chest pain radiating to the left arm accompanied by pallor and marked diaphoresis. These symptoms appeared at rest, lasted 45 minutes, and terminated spontaneously. The patient had been treated for mild hypertension during the last 6 months. An ECG tracing obtained at the beginning of treatment was unremarkable. However, an ECG tracing recorded shortly after the end of the symptoms showed T-wave inversion in all anterior leads. Coronary arteriography was then performed and showed no fixed obstructive coronary artery disease. Nonetheless, a lengthened and constricted myocardial bridging of both the left anterior descending coronary artery and its major diagonal branch was detected. Also, the left anterior descending coronary artery was observed to be very short, terminating before the cardiac apex. The left ventricle was hypertrophied. The patient was treated with a beta-blocking agent which eliminated all symptoms. An ECG tracing obtained about three months after the onset of the clinical picture was normal. Our findings suggest that marked myocardial ischemia at rest does occur in patients having myocardial bridges under special circumstances, such as lengthened and constricted myocardial bridging of a short coronary artery which supplies a hypertrophied ventricle. This anomaly should be taken into account as a possible cause of a threatened myocardial infarction, which may be successfully treated with a beta-blocking agent.

Coronary Vessel Anomalies↗
PubMed1987

Chronic Chagas' heart disease presenting as an impending myocardial infarction: a case favoring the neurogenic pathogenesis concept.

A 55-year-old Caucasian woman suddenly developed substernal chest pain at rest accompanied by pallor, diaphoresis, nausea, and vomiting. Physical examination was otherwise unremarkable. The resting ECG showed T-wave inversion in all anterior leads which returned to normal 24 h after the onset of the symptoms. The pain was eliminated promptly by sublingual isosorbide dinitrate. "Impending" acute myocardial infarction was diagnosed. Coronary arteriography, however, failed to reveal any change in any major coronary artery but an apical aneurysm of the left ventricle was detected. As the complement-fixation test for Chagas' disease was positive, the diagnosis of chronic Chagas' heart disease was then established. This unusual clinical manifestation of Chagas' disease is thought to be the consequence of a transient imbalance in the cardiac autonomic nervous system, which is considered to play a central role in the pathogenesis of chronic Chagas' heart disease. In addition, the present case may alert clinicians to the thus far neglected atypical chest pain, which is frequently seen in chagasic patients but whose etiology remains obscure.

Chagas Cardiomyopathy↗
PubMed1987

Electrocardiographic changes in T. cruzi-infected rats after the ajmaline test.

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.

Ajmaline↗
PubMed1987

Congenital arrhythmia in a normal newborn.

We describe a case, unique to the best of our knowledge, in which bigeminal supraventricular premature contractions were detected in a normal newborn. These arrhythmias disappeared spontaneously after the twelfth day of life. Since they do not appear to evolve towards paroxysmal supraventricular tachycardia, treatment with antiarrhythmic drugs is not recommended.

Arrhythmias, Cardiac↗
PubMed1987

Ability of the electrocardiogram to detect myocardial lesions in isoproterenol induced rat cardiomyopathy.

Resting electrocardiograms were recorded in 18 male adult rats injected subcutaneously with two doses of isoproterenol (200 mg.kg-1 body weight) 10 days before the animals were submitted to the ajmaline test (1 mg.kg-1 body weight iv). After the ajmaline test all rats were killed and the hearts examined histologically. Electrocardiographic changes were detected at rest in 72% of the isoproterenol injected rats: pathological Q waves, lengthening of the QRS complex, and QRS abnormality were found in 50%, 44%, and 44% of these animals respectively. Ajmaline induced similar changes in both control and isoproterenol treated rats (P wave enlargement (p less than 0.01 and p less than 0.001 respectively), increased PR interval (p less than 0.003 and p less than 0.001 respectively), and increased QaT interval (p less than 0.001 in both groups]. However, ajmaline caused an increase in heart rate only in isoproterenol treated rats (p less than 0.05). A pronounced increase in PR interval, not observed in control rats, was detected in one of five isoproterenol injected rats with a normal resting ECG but showing microscopical cardiac lesions. Apical aneurysm of the left ventricle was found in 16% of isoproterenol injected rats. A mononuclear inflammatory reaction was observed in 13 (72%) of the isoproterenol injected rats and was multifocal in at least three regions of the myocardium in six (46%) and disseminated throughout the myocardium in seven (53%) of these animals. When the electrocardiographic and pathological findings were compared, the ECG changes were found to have a 91% sensitivity, 83% specificity, and 91% positive predictive value.(ABSTRACT TRUNCATED AT 250 WORDS)

Ajmaline↗
PubMed1987

Chronic Chagas' heart disease in the elderly: a clinicopathologic study.

A retrospective study of the medical records of our hospital from 1965 to 1985 was carried out to characterize for the first time chronic Chagas' heart disease in the elderly (more than 70 years old). A total of 25 patients (mean age = 76) were suitable for the study. Congestive heart failure, sudden cardiac death, thromboembolism and atypical chest pain were found in 68, 16, 8 and 8% of cases, respectively. Ventricular premature contractions (60%), right bundle branch block (32%), left anterior hemiblock (28%), atrial fibrillation (28%) and right bundle branch block associated with left anterior hemiblock (20%) were the ECG changes most frequently found. A morphological study was performed on 8 (32%) patients. All of them showed cardiac abnormalities, with apical aneurism being detected in 100% of cases. At autopsy, pulmonary embolism was observed in 3(37%) of these patients who presented with congestive heart failure, ventricular premature contractions and/or intraventricular conduction defect and/or atrial fibrillation. Thus, the characteristics of chronic Chagas' heart disease in the elderly are similar to those found in middle-aged patients. We suggest that these patients are important for the study of the pathogenesis of chronic Chagas' heart disease because they may have less aggressive pathophysiologic mechanisms than middle-aged patients.

Aged↗