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)

Effects of long term metoprolol administration on the electrocardiogram of rats infected with T cruzi.

STUDY OBJECTIVE: The aim of the study was to evaluate the role of beta receptor antagonists in the evolution of experimental Chagas' disease. DESIGN: Rats were infected with T cruzi, 2000 parasites.g-1 body weight, soon after weaning. One group was then given metoprolol, 100 mg.kg-1.d-1, in drinking water. A comparison group received no metoprolol. Two control groups of non-infected rats were also studied, one with and one without metoprolol in the same dose. SUBJECTS: Adult male albino rats were used: 144 were infected with T cruzi and received metoprolol (group IM), 137 were infected and received no metoprolol (group IW), 46 non-infected rats received metoprolol (group CM), and 43 non-infected rats did not receive metoprolol (group CW). MEASUREMENTS and main results--30 d after infection, resting ECG was performed in all surviving rats. (There were 63 deaths in the infected groups and none in the non-infected groups.) Abnormal ECG was found in 20/81 infected rats in group IM and in 30/74 in group IW (p less than 0.05). No ECG changes were found in the non-infected rats. Of rats in group IM with normal resting ECG, 31 continued to take metoprolol (group IMNM), while 30 similar rats did not (group IMNW); in group IM with abnormal ECG, 10 rats continued to take metoprolol (group IMAM), while 10 similar rats did not (group IMAW). Of rats in group IW with normal ECG, 22 were started on metoprolol (group IWNM), while 22 similar rats were not (group IWNW); in group IW with abnormal ECG, 15 rats were started on metoprolol (group IWAM), while 15 similar rats did not (group IWAW). After 120 d and 300 d infection there were no differences in mortality rate and Ajmaline test in any of the matched groups (IMNM X IMNW; IMAM X IMAW; IWNM X IWNW; IWAM X IWAW). After 120 d there was no difference in ECG between the groups, but after 300 d there was a decrease in abnormal ECG in group IWAM (IWAM v IWAW, 0/12 v 5/12, p less than 0.05). No histological differences were found. CONCLUSIONS: Metoprolol decreases the proportion of rats with abnormal resting ECG in both the acute and the chronic stage of T cruzi infection.

Giant aneurysm of the ascending aorta secondary to medial agenesis in infancy.

A 14-month-old infant was found to have a giant aneurysm of the ascending aorta at the time he underwent angiography. At the time of autopsy, a saccular chamber was found to take the place of the aorta. Histologic examination of the aneurysm revealed absence of the medial layer. Thus, medial genesis may be another cause of aneurysm of the ascending aorta.

Absence of Trypanosoma cruzi myocardial infection reactivation in Chagas' heart transplant.

The risk of Trypanosoma cruzi myocardial infection reactivation after immunosuppressive therapy has led to precluding heart transplantation as a therapeutic procedure for patients with end-stage Chagas' heart disease. We report a case of an orthotopic heart transplantation in a 43-year-old critically ill chagasic patient with an uneventful postoperative period. He was treated with azathioprine and cyclosporine to control graft rejection and showed no reactivation of the chagasic infection. One year following surgery, the patient is doing well. Nonsteroidal therapy appears not to reactivate T. cruzi infection in transplant chagasic patients.

Ruptured chordae tendineae of the posterior leaflet of the tricuspid valve as a cause of tricuspid regurgitation following blunt chest trauma.

A 12-year-old boy suffered a blunt chest trauma. Some hours later, a pulsatile bilateral jugular venous distension, a holosystolic murmur heard at the low parasternal border and hepatomegaly were observed. On echocardiography, ruptured chordae tendineae of the posterior leaflet of the tricuspid valve, as well as tricuspid regurgitation were detected. He remained asymptomatic during hospital stay and was discharged home in good condition. Thus, isolated ruptured chordae tendineae of the posterior leaflet of the tricuspid valve is another cause of tricuspid regurgitation following blunt chest trauma.

Beneficial effects of gangliosides on the natural history of acute chagasic myocarditis in rats.

This study was designed to investigate the effects of ganglioside treatment on acutely Trypanosoma cruzi-infected rats with emphasis on the heart. Newly weaned Wistar rats were infected with T. cruzi (Colombian strain, 50,000 parasites/kg body weight injected intraperitoneally). Two groups of 25 infected rats received daily injections of saline or ganglioside (10 mg/kg body weight) intraperitoneally between the 14th and 30th days after infection. Two groups of 10 noninfected rats were similarly treated. On day 31, all surviving rats were killed. Hearts were collected for histopathology and norepinephrine assay. An arbitrary score for myocardial microscopic lesions was used to characterize each heart wall. Mortality was recorded throughout the experimental period. Seven of 25 (28%) ganglioside-treated and 14 of 25 (56%) saline-treated rats died spontaneously (p = 0.02). The histological score was 5.4 ± 3.2 for ganglioside-treated and 7.9 ± 3.0 for saline-treated rats (p < 0.05). No difference was detected in myocardial norepinephrine content. Thus, ganglioside treatment decreases mortality and myocardial inflammation in acute chagasic myocarditis in rats.

Cardiomyopathy in rats with Walker 256 tumor: The potential role of microvascular disease in its genesis.

Considering that diffuse abnormalities of myocardial microcirculation with transient ischemia have been suggested to play a role in the genesis of myocytolytic necrosis, characteristic lesion of dilated or congestive cardiomyopathies, and the bloodstream is the most common pathway for dissemination of cancer cells, which gain access to the microcirculation, the present study was undertaken to search for morphologic and electrocardiographic evidence of myocardial damage associated with microcirculatory disease in rats experimentally inoculated with the Walker 256 tumor. Young albino rats inoculated intramuscularly with the Walker 256 tumor developed a cardiomyopathy characterized by diffuse small foci of myocytolytic necrosis, decreased thickness of the mean left midventricular wall associated with reduced size of the minor diameter of myocytes, and electrocardiographic abnormalities reflecting the myocardial damage, correlated with the presence of a microvascular disease, characterized by intramyocardial microvessels (less than 50 µm in diameter) partially or totally occluded because of entrapment of tumor cells and fibrin-platelet/tumor cell-cellular debris thrombi. The occlusive or subocclusive small vessel lesions preceded the development of the myocytolytic necrosis, suggesting that the microvascular disease would play an important role in the process of focal micronecrosis and consequent electrocardiographic changes. However, it must be taken into account that the tumor thromboemboli can generate related factors that could promote cell injury and cell death. In conclusion, the hematogenic dissemination of Walker 256 cells promotes the development of an experimental cardiomyopathy attributable, at least in part, to microvascular obliterative changes in the myocardium.

Ajmaline-induced electrocardiographic changes in chronic Trypanosoma cruzi-infected rats.

In the present study, the ajmaline test was applied to T. cruzi-infected rats and evaluated for the ability to reveal ECG disturbances. The test consists of intravenous injection of ajmaline (2 mg/kg body-weight) under ether anaesthesia, and continuous ECG monitoring (right precordial lead: V1 or V2, 100 mm/sec paper speed). The animals used for the test (n = 30) had been experimentally infected with the Colombia strain of T. cruzi (1,000 parasites/g body-weight, newly weaned rats) one year before the experiments. Control non-infected rats (n = 21) were similarly maintained and treated. The ECGs were analysed under baseline conditions, i.e., before ajmaline, and 15, 30, 60 and 180 seconds after completion of ajmaline injection through the dorsal vein of the penis. The following parameters were studied: heart rate, PR interval, QRS and Qat duration. Morphological changes of the QRS complex and ST-T segment were also recorded. Under baseline conditions, the two groups had comparable values for all parameters, except for the PR interval, which was significantly increased in infected rats. No changes in wave rhythm or morphology were detected under baseline conditions. The PR and QaT intervals and QRS duration were significantly longer in both groups after ajmaline injection, at all periods studied. When the two groups were compared for relative variations, consistently and significantly higher alterations (p less than 0.05) were observed in the T. cruzi-infected group, except for the QaT interval at 180 seconds. However, the severe rhythm and ventricular conduction disturbances detected in 30% of the infected rats represented clear-cut discriminative alterations.(ABSTRACT TRUNCATED AT 250 WORDS)

Portopulmonary hypertension syndrome in schistosomiasis mansoni.

Portopulmonary hypertension syndrome (PPHS) is a complication of portal hypertension where the substrate is micro-vessel lesions which are indicative of plexogenic arteriopathy. PPHS has not been linked to pulmonary schistosomiasis. We report, to the best of our knowledge for the first time, a case of PPHS associated with schistosomiasis mansoni.

Clinical course of Chagas' heart disease: a comparison with dilated cardiomyopathy.

This investigation was carried out to compare the clinical course of patients with chronic Chagas' heart disease with that of patients with dilated cardiomyopathy. A total of 125 patients (75 chagasic and 50 nonchagasic) prospectively followed up at the Cardiomyopathy clinic of Santa Casa Hospital from January 1990 to June 1993 entered the study. Patients underwent clinical history, physical examination, serological tests, resting electrocardiogram, chest X-ray and two-dimensional echocardiography. In nonchagasic patients, hypertensive cardiomyopathy was found in 17 of 50 (34%) patients, idiopathic dilated cardiomyopathy in 16 (32%), the association of hypertension and coronary artery disease in 12 (24%) and ischemic cardiomyopathy in two (4%). Twenty-one (23%) chagasic and three (6%) nonchagasic patients died during the study period (P = 0.02). Sudden cardiac death occurred in eight (38%) chagasic patients, pump failure death was detected in 10 (47%) and the mode of death could not be determined in three (14%) patients with chronic Chagas' heart disease. Thus, patients with chronic Chagas' heart disease have a clinical course worse than that of patients with nonchagasic dilated cardiomyopathy. This fact may be ascribed to the electrocardiographic and morphological peculiarities usually found in chronic Chagas' heart disease.

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.

Salmonella tricuspid endocarditis in an intravenous drug abuser with human immunodeficiency virus infection.

We describe a case of Salmonella tricuspid endocarditis in an intravenous drug abuser with human immunodeficiency virus infection. He was successfully treated with antibiotics with no clinical relapse. To our knowledge, this is the first case of this kind reported in the literature. Physicians should be on the alert for this potentially curable cardiac complication of human immunodeficiency virus infection.

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.

Congenital absence of the circumflex coronary artery associated with dilated cardiomyopathy.

We report the first autopsied case of congenital absence of the left circumflex coronary artery. The patient was a 12-year-old girl in whom the clinical diagnosis was idiopathic dilated cardiomyopathy. This type of heart disease is uncommon among children. The coexistence of the two conditions therefore suggests a possible aetiologic relationship between them. The pathological findings, however, do not support such an association. Rather, they suggest that they co-exist by chance.

Partial left ventriculectomy: preoperative risk factors for perioperative mortality.

This study aimed at determining risk factors for perioperative mortality for patients undergoing partial left ventriculectomy. Fourteen patients with end-stage congestive heart failure underwent partial ventriculectomy at our institution from February, 1995 to October, 1997. Mean age was 48+/-11 years, symptoms duration 44+/-34 months, New York Heart Association symptoms score 4+/-0, systolic blood pressure 97.69+/-20.06 mmHg, diastolic blood pressure 65.38+/-13.91 mmHg, heart rate 91+/-15 beats/min, furosemide daily dose 121.66+/-96.65 mg and captopril daily dose 68.75+/-76.76 mg. Seven (50%) patients needed inotropic support for hemodynamic stabilization. On echocardiography, left ventricular diastolic dimension was 81.71+/-11.92 mm. Left ventricular ejection fraction determined by radionuclide ventriculography or echocardiography was 16.71+/-5.13. At heart catheterization, mean right atrial pressure was 12.50+/-7.72 mmHg, mean pulmonary capillary wedge pressure 23.60+/-7.79 mmHg, and mean pulmonary artery pressure 34.10+/-12.81 mmHg. Twelve patients had idiopathic dilated cardiomyopathy and two patients had a globally dilated heart with single vessel coronary artery disease. Aneurysmectomy, mitral valve surgery or coronary artery bypass surgery were not performed in any patient. Four (28%) patients died: three in the operating theatre and one from low output syndrome 2 days after surgery. The proportion of patients operated on with cardiogenic shock was four (100%) in nonsurvivors and 0% in survivors (P=0.001). Inotropic support was necessary in three (30%) survivors and in four (100%) nonsurvivors (P=0.06). Thus, preoperative hemodynamic instability may be associated with perioperative mortality after partial left ventriculectomy.

Chronic Chagas' heart disease in children and adolescents: a clinicopathologic study.

A retrospective study of the medical records filed at the University Hospital from 1965 to 1983 and of 18456 autopsies carried out in the Department of Pathology of this Institution from 1953 to 1983, referring to patients aged less than 18 years was performed in an attempt to fully characterize chronic Chagas' heart disease in children and adolescents. Only 19 of these patients fulfilled the criteria for inclusion in the present study (12 cases with only clinical information and 7 cases with clinical and pathological information). We noted that the clinical manifestations of chronic Chagas' heart disease are congestive heart failure, thromboembolism and sudden death. Radiologic, electrocardiographic and anatomo-pathological findings demonstrated serious myocardial involvement. This set of alterations is also detected in adults with chronic Chagas' heart disease. Among adolescents, however, the disease exhibits relevant peculiarities such as rapid evolution to death within a short period of time (128 days), diagnostic difficulty related to the presence of significant mitral regurgitation (61% erroneous initial diagnosis), and low frequency of right bundle branch block (11% of cases). These findings suggest that among children and adolescents, chronic Chagas' heart disease may be of a peculiar type and therefore may be useful to clarify the pathogenetic mechanism of the disease.

Clinical profile of patients with Chagas' disease before and during sustained ventricular tachycardia.

Sustained ventricular tachycardia was diagnosed in 15 patients undergoing ordinary activity with Chagas' disease seen at our Institute from 1978 to 1989. Palpitations were observed in 11 (66%) of the patients, dyspnea in 7 (46%), atypical chest pain in 5 (33%) and syncope in 2 (13%). Cardiac arrhythmia was detected in 4 (26%) on physical examination. The resting electrocardiogram showed premature ventricular contractions in 13 (86%) patients, ST-T changes in 12 (80%), left axis deviation in 9 (60%) and right bundle branch block in 4 (26%). Chest X-rays showed mild cardiomegaly in 8 (53%) and moderate cardiomegaly in 3 (20%) patients. Mild left ventricular dysfunction was detected echocardiographically in 1 (10%), moderate in 3 (30%) and severe in 1 (10%) of the 10 patients studied. During sustained ventricular tachycardia, dyspnea was found in 7 of 15 (46%) patients, palpitations in 6 (40%), atypical chest pain in 6 (40%), syncope in 1 (6%), systemic arterial hypotension in 3 (20%) and cardiogenic shock in 2 (13%). The electrocardiographic findings were as follows: mean heart rate was 201 bpm; mean QRS lengthening was 0.16 sec; right bundle branch block plus right axis deviation was seen in 5 of 15 (33%) patients; right bundle branch block plus left axis deviation in 4 (26%); and a positive concordance of all precordial leads in 5 (33%) patients. Based on these findings, we conclude that the majority of patients with Chagas' disease who develop sustained ventricular tachycardia do not have severe myocardial disease, show an uncommon electrocardiographic pattern of this arrhythmia, and most importantly, have a benign clinical course.

Clinical characteristics of acute myocardial infarction in patients with Chagas' disease.

From 1981 to 1988, 404 patients at our institution were found to have acute myocardial infarction. Of them, 18 (4%) had a positive fixation test for Chagas' disease. Patient age ranged from 41 to 80 years (median = 59). Eleven patients were males. Eighteen nonchagasic patients were matched by 2 year age intervals and sex with each chagasic patient. Before acute myocardial infarction, there were no differences between chagasic and nonchagasic patients with regard to the proportion of stable angina, unstable angina and coronary risk factors. Atypical chest pain occurred in 8 of 15 (53%) chagasic patients for whom this information was found in the medical records and in 1 of 18 (5%) nonchagasic patients (p = 0.003); dyspnea and palpitations occurred in 6 of 15 (40%) chagasic and 1 of 17 (5%) nonchagasic patients (p = 0.025). There were no differences between chagasic and nonchagasic patients with respect to both clinical characteristics and cardiac complications of acute myocardial infarction. Nonetheless, 4 of 11 (36%) chagasic patients for whom this information was listed in the medical records but none of 16 nonchagasic patients had normal coronary arteries (p = 0.019). Thus, chagasic patients who develop acute myocardial infarction have some peculiarities both in the clinical profile before the acute event and in the anatomy of the coronary arteries.

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.

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.