Clinical and morphological characteristics associated with sudden cardiac death in patients with Chagas' disease

The medical records of 24 patients with Chagas disease who diedsuddenly, between 1982 and 1988, were examined in an attemptto determine the clinical profile of sudden death in Chagasdisease. Patient age ranged from 33 to 72 years (average: 51). Seventeen(70%) were male. Five (20%) were asymptomatic. Dyspnoea at restwas observed in 16 (66%) and palpitations in eight (33%). Onphysical examination, arrhythmias were observed in 14 (58%),ankle swelling in 13 (54%) and liver enlargement in 12 (50%)patients. Twenty-three (95%) patients had an abnormal resting electrocardiogram:ventricular premature contractions were observed in 19 patients(79%) and a left anterior fascicular block in 14 (58%). Thechest X-ray revealed cardiomegaly in 20 patients (82%), whichwas moderate in three (13%) and severe in 11 (45%). At autopsy, mean heart weight was 496 g. Dilatation of all cardiacchambers was detected in 22 (91%), and apical aneurysm in 19(79%) patients. When compared with symptomatic patients, asymptomatic patientswith Chagas disease had a higher frequency of normal physicalexamination (3/5 vs 1/19, P<0.004), normal chest X-ray (3/5vs 1/19, P<0.01), and a lower heart weight (400±43g vs 521.58±146.26 g, P<0.03). The majority of patients with Chagas disease who die suddenlyhave severe underlying myocardial disease. In some of them,however, sudden cardiac death may occur in the presence of minimal,if any, heart involvement.     

Prevention of sudden cardiac death in patients with chronic kidney disease

Cardiovascular deaths account for about 40% of all deaths of patients with chronic kidney disease (CKD), particularly those on dialysis, while sudden cardiac death (SCD) might be responsible for as many as 60% of SCD in patients undergoing dialysis. Studies have demonstrated a number of factors occurring in hemodialysis (HD) that could lead to cardiac arrhythmias. Patients with CKD undergoing HD are at high risk of ventricular arrhythmia and SCD since changes associated with renal failure and hemodialysis-related disorders overlap. Antiarrhythmic therapy is much more difficult in patients with CKD, but the general principles are similar to those in patients with normal renal function - at first, the cause of arrhythmias should be found and eliminated. Also the choice of therapy is narrowed due to the altered pharmacokinetics of many drugs resulting from renal failure, neurotoxicity of certain drugs and their complex interactions. Cardiac pacing in elderly patients is a common method of treatment. Assessment of patients’ prognosis is important when deciding whether to implant complex devices. There are reports concerning greater risk of surgical complications, which depends also on the extent of the surgical site. The decision concerning implantation of a pacing system in patients with CKD should be made on the basis of individual assessment of the patient.     

慢型克山病死亡病例中猝死病例分析

目的 了解慢型克山病猝死的有关因素，在防治工作中采取有针对性的措施，以减少或避免猝死的发生。方法 设计慢型克山病死亡(病死、猝死、意外死亡)病例有关资料的统一调查表，由专业人员查阅有关病例资料填写。工作结束后进行表格汇总、统计与分析。结果 慢型克山病无论病程长短都可能发生猝死，女性明显多于男性，发病在5年内猝死的最多，猝死的发生主要由左心室大劳损合并多源多发、单源多发性室性早搏及各种传导阻滞，再在诱发因素的作用下所引起。结论 在慢型克山病病人中，一般情况下是心胸比率越大、心功能越差，猝死的机会越大，但心功能在I级、心胸比率在0．51～0．55之间的病例猝死率也较高。     

Therapeutic efficacy of allopurinol in patients with chronic Chagas' disease

Laboratory and animal studies have demonstrated that pyrazolopyrimidines have significant activity against Trypanosoma cruzi. This clinical investigation was to ascertain the efficacy of allopurinol in the treatment of chronic Chagas' disease. Of 307 patients studied, 91 were untreated; the remaining 216 were divided into 4 treatment groups. These corresponded to 600 or 900 mg/day of allopurinol for 60 days and benznidazole or nifurtimox at conventional dosage regimens. Patients were evaluated clinically, serologically, and parasitologically. Allopurinol was found to be as efficacious as the conventional therapeutic modalities in eliminating the parasitemia and rendering patients seronegative. Adverse reactions occurred in 11% of patients who received allopurinol and in 30% of those receiving nitrofurans. Reactions with the conventional therapy were more frequent and of a more serious nature. Oral allopurinol is as effective as the nitrofurans, but has none of the side effects.     

Morphometric study of the spleen in chronic Chagas' disease

There is frequently an increase in spleen size in infectious systemic and chronic venous congestion. The aim of this report was to perform a comparative study of the spleen tissue of chagasic or nonchagasic autopsied patients with or without congestive heart failure. Evaluations were made of 111 cases. Connective tissue intensity, follicular density and area, and follicular arterioles wall area were determined through the morphometric study. The connective tissue was similar in all groups. The density of the lymphoid follicles was significantly less among the chagasic cases (P = 0.032). The follicular area was larger among the chagasic cases and in the chagasic group with congestive heart failure. The chagasic group without congestive heart failure presented a greater area of follicular arteriole walls. Therefore, the spleen modifications in chronic Chagas' disease could be a consequence not only of the heart failure but also of the Chagas infection itself.     

Prediction of sudden death from QTc interval prolongation in patients with chronic ischemic heart disease

Although prolongation of QTc interval has been shown to increase the risk of sudden death after recent myocardial infarction, no data exist on the relationship between sudden death and QTc duration in patients with chronic ischemic heart disease. Furthermore, it is not known whether patients with long QTc intervals (greater than or equal to 440 units) have more prevalent coronary risk factors. Thus 141 nonsurvivors (128 with coronary death and 13 with noncoronary death) representing the follow-up deaths of a cohort of 1157 medically treated patients with ischemic heart disease over a four-year period were compared to 141 consecutive long-term survivors of the same cohort. Thirty-one patients were excluded because of drug interactions, bundle-branch block or atrial fibrillation. QTc duration was calculated on the ECG immediately prior to angiography in 62 patients with sudden death, 36 with intermediate death, 13 with noncoronary death and 140 long-term survivors with chronic ischemic heart disease. In addition, in 64 nonsurvivors (58%) in whom more than one yearly follow-up ECG was available, QTc was calculated in the last ECG preceding death (mean of four months before death). These data were compared to those obtained in 140 long-term survivors at the time of last ECG (mean 48 months after enrollment). At the time of angiography, mean QTc intervals were similar in patients who later died of ischemic heart disease and in long-term survivors (423 +/- 35 vs 421 +/- 25 units). No difference in QTc duration was apparent among nonsurvivors with ischemic heart disease. All study patients were divided into normal and long QTc subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Stroke in a hospital-derived cohort of patients with chronic Chagas' disease

The aim of this study was to determine the prevalence of stroke in a hospital-derived cohort of patients with chronic Chagas' disease. Seventy-nine patients with chronic Chagas' disease were prospectively followed at the Cardiomyopathy Clinic of the Santa Casa Hospital from January 1990 to June 1993 (mean follow up = 17 +/- 12 months). Mean New York Heart Association functional class was 2.42 +/- 1.24. Fifty-six (70%) patients were on angiotensin-converting enzyme inhibitors at maximum tolerated doses, but no patient was on anticoagulation therapy. Atrial fibrillation was detected on the resting ECG in twelve (15%) patients. On echocardiography, mean left ventricular ejection fraction was 49.07 +/- 17.96% and mean left ventricular diastolic dimension 60.12 +/- 10.97 mm; mitral regurgitation was detected in 20 (29%) patients. Left ventricular thrombus was seen in three (4%) patients; all of them were in sinus rhythm and had left ventricular dysfunction on echocardiography. No thromboembolic event, however, was detected during the follow-up. One patient (1%) had a fatal stroke during the study period; she was in sinus rhythm on the resting ECG, and had mild mitral regurgitation, normal left ventricular function and no intracavitary thrombus on Doppler echocardiography. The prevalence of stroke is low in a hospital-derived cohort of patients with mild to moderate heart failure due to chronic Chagas' disease. Routine prophylactic anticoagulation, therefore, seems not to be warranted.     

Cell-mediated immune response in megacolon from patients with chronic Chagas' disease

PURPOSE: The mechanisms that control chronic infection in vivo and the immunologic mechanisms involved in the pathogenesis of chagasic megacolon are not completely characterized. Although autoimmunity may play a role in the pathogenesis of Chagas' disease, recent studies, both in mice and in humans, suggest a positive association of tissue parasitism, inflammation, and severity of lesions. The aim of this study was to evaluate the role of inflammatory cells and the subclasses of lymphocytes involved in neuropathic lesions in the colon of patients who underwent resection for advanced megacolon. METHODS: Specimens from 23 patients were selected based on histopathologic analysis. Paraffin-embedded tissue blocks were sectioned and evaluated by immunohistochemistry for cluster of differentiation 3, cluster of differentiation 8, cluster of differentiation 20, and natural killer cell antibodies by an avidin-biotin peroxidase method. RESULTS: Almost all myenteric plexuses were damaged, characterized by degenerative changes, necrosis of ganglion cells, and inflammatory response. Mild lymphocytic infiltration around degenerated and normal ganglion cells was observed in all cases. Collagen fibers and mononuclear cells surrounded some ganglion cells. Most of the inflammatory cells were lymphocytes, identified as cluster of differentiation 3-positive cells. Cluster of differentiation 8-positive lymphocytes were associated with degenerated ganglion cells. Natural killer cell antibodies were detected in a lower proportion of cells and were distributed between muscle layers or in proximity to the myenteric plexus. All these findings were also observed in the submucosal plexus. Cluster of differentiation 20-positive lymphocytes were not present in muscle layers or in the vicinity of either plexus. CONCLUSION: Pathogenesis of the megacolon is based on a continuous process of ganglion cell damage with participation of T lymphocytes expressing cluster of differentiation 8 and natural killer cell membrane antigens. B lymphocytes do not take part in the chronic inflammatory reaction.     

Persistent infections in chronic Chagas' disease patients treated with anti-Trypanosoma cruzi nitroderivatives

We used a molecular method and demonstrated that treatment of the chronic human Trypanosoma cruzi infections with nitroderivatives did not lead to parasitological cure. Seventeen treated and 17 untreated chronic Chagas' disease patients, with at least two out of three positive serologic assays for the infection, and 17 control subjects formed the study groups. PCR assays with nested sets of T. cruzi DNA primers monitored the efficacy of treatment. The amplification products were hybridized to their complementary internal sequences. Untreated and treated Chagas' disease patients yielded PCR amplification products with T. cruzi nuclear DNA primers. Competitive PCR was conducted to determine the quantity of parasites in the blood and revealed < 1 to 75 T. cruzi/ml in untreated (means 25.83+/-26.32) and < 1 to 36 T. cruzi/ml in treated (means 6.45+/-9.28) Chagas' disease patients. The difference between the means was not statistically significant. These findings reveal a need for precise definition of the role of treatment of chronic Chagas' disease patients with nitrofuran and nitroimidazole compounds.     

Brugada syndrome--an under-recognized electrical disease in patients with sudden cardiac death

In 1992, Brugada and Brugada described 8 patients with a history of aborted sudden death and a distinct ECG pattern of right bundle-branch block with ST segment elevation in leads V1-V3 and normal QT interval in the absence of any structural heart disease. It is called Brugada syndrome now and is believed to be responsible for 4-12% of all sudden deaths and around 20% of deaths in patients with structurally normal hearts. Although this syndrome is observed worldwide and the exact prevalence is unknown, it is more common in the Southeast Asian countries. Repeated syncope, ventricular fibrillation, and sudden cardiac death have been reported in patients with Brugada syndrome. The clinical presentation of Brugada syndrome is distinguished by a male predominance and the appearance of arrhythmic events at an average age of 40 years. The Brugada syndrome is inherited in an autosomal dominant manner with incomplete penetrance and an incidence ranging between 5 and 66 per 10,000. The surface ECG manifestations of the syndrome can transiently disappear, but can be unmasked by potent sodium channel blockers in some cases. Mutations of the cardiac sodium channel SCN5A have been detectable in <20% of patients with Brugada syndrome. Recent genetic studies have confirmed the genetic heterogeneity of the disorder. Antiarrhythmic drugs appear to be of little use in prolonging survival and in preventing recurrences of ventricular arrhythmias. To date, implantable cardioverter defibrillator remains the best therapy to prevent sudden death in these patients.