Rupture of a submitral ventricular aneurysm into the left atrium diagnosed by transesophageal echocardiography.

Submitral ventricular aneurysm is a thoroughly studied pathology but is not well known due to its rarity. Clinically, it is manifested by symptoms and signs of heart failure, mitral regurgitation and/or ventricular arrhythmias, and may be associated with thromboembolic phenomena and myocardial ischemia due to compression of the coronary arteries by the aneurysm. A rare complication of this type of aneurysm is rupture into the left atrium. Transthoracic echocardiography plays an important role in the definitive diagnosis of this pathology, although the role of transesophageal echocardiography in the evaluation of these patients is less known. We report a case of a submitral ventricular aneurysm complicated by rupture into the left atrium, which was diagnosed by transesophageal echocardiography.     

Transesophageal echocardiography-guided cardioversion of atrial fibrillation. Selection of a low-risk group for immediate cardioversion.

INTRODUCTION: In patients (pts) with atrial fibrillation (AF) of more than 48 hours' duration, electrical cardioversion (ECV) should only be performed after 3 weeks of effective anticoagulation. Transesophageal echocardiography (TEE) allows earlier ECV; however, despite exclusion of thrombi in the atrium and left atrial appendage (LAA), cases of thromboembolism related to ECV have been documented in AF. To define a low-risk group for cardioversion without previous anticoagulation, pts were selected for immediate ECV if no thrombi or dynamic spontaneous echo contrast (auto-contrast) were found after TEE and if LAA velocity was more than 0.25 m/sec. METHODS AND RESULTS: We performed TEE in 31 consecutive pts referred for ECV for AF of more than 48 hours' duration and without previous anticoagulation. After TEE the pts eligible for immediate ECV began anticoagulation with low molecular weight heparin (enoxaparin), subcutaneously in therapeutic doses, together with warfarin immediately before cardioversion. Enoxaparin was continued until an INR of over 2 was reached. Based on the TEE findings, the pts were divided in 2 groups: immediate ECV, group A, 20 pts with a mean age of 62 +/- 13 years, 6 female; and conventional therapy with warfarin before ECV, group B, 11 pts, mean age of 67 +/- 10 years (p < 0.05), 2 female. None of the pts in either group had mitral stenosis or previous episodes of thromboembolism. The mean transverse diameter of the left atrium in the 31 pts was 47 +/- 4.5 mm, without statistically significant differences between the 2 groups. Of the 11 pts in group B, 3 had a thrombus in the LAA, 6 dynamic spontaneous echo contrast and the remainder LAA velocities of less than 0.25 m/sec. ECV was achieved in all the pts, with no complications. Oral anticoagulation was maintained for at least a month. At one month, sinus rhythm was maintained in 75% of group A and 45% of group B (p < 0.01). CONCLUSION: In pts with AF of more than 48 hours' duration and no previous history of thromboembolism, the use of our exclusion criteria during TEE enabled stratification of a low-risk population for immediate ECV, which was accomplished effectively and safely in 2/3 of the pts. This strategy is associated with early symptomatic improvement, and may contribute to maintenance of sinus rhythm after one month, which was significantly better than in the pts who had prolonged therapy with warfarin before ECV, despite the differences found in age and left ventricular function.     

Pulmonary embolism.

Pulmonary embolism (PE) is an important health problem and often a major clinical challenge, not only because of the low specificity of its clinical manifestations but also because of the increasing number of medical circumstances that are risk factors for this illness and the importance of early identification, since prompt and appropriate treatment can decrease mortality from this disease by about 25%. In recent years research on PE has been extensive, directed mainly at trying to determine and characterize its risk factors, establish new clinical probability algorithms, develop new diagnostic methods and put existing ones into perspective, seek new therapeutic approaches (pharmacological and non-pharmacological), and above all establish protocols that can guide the clinician from the stage of clinical suspicion to measures to prevent recurrence. It was the authors' aim to review the most significant literature on this subject, in order to produce a text that reflects the state of the art concerning PE and that can be used as a guide in the clinical approach to this pathology.     

Short stature, abdominal obesity, insulin resistance and alterations in lipid profile in very low-income women living in Maceió, north-eastern Brazil.

OBJECTIVE: To test the hypothesis that short stature is associated with abdominal obesity, insulin resistance and lipid profile changes. METHODS: Anthropometric data were collected from 237 women (18-60 years old), residents of a shantytown in Maceió. Biochemical profiles of 60 individuals drawn from this population were determined. RESULTS: Total and low-density lipoprotein (LDL) cholesterol levels and insulin resistance rose with increasing waist : hip circumference ratio, particularly in women. Short, overweight individuals exhibited larger biochemical alterations than overweight individuals of average stature. CONCLUSION: Short stature, when associated with overweight, is a risk factor for increased insulin resistance and alterations in lipid profile.     

Cyclophosphamide affects the dynamics of granuloma formation in experimental visceral leishmaniasis

We observed histopathological and ultrastructural hepatic changes following the intracardiac inoculation ofLeishmania donovani amastigotes into inbred LHC hamsters (group I). Since granuloma formation is known to be T-cell-dependent, we also examined infected hamsters under cyclophosphamide immunosuppressive treatment (group ICy) and evaluated the production of interleukin-2 (IL-2) by their cells. Group I showed more intense hepatocyte and endothelial cell clasmatosis as well as hepatocyte degeneration and necrosis, deposits of connective tissue fibers, granulomas with multinucleated giant cells (MGCs) of foreign-body and Langhans' types and reduced production of IL-2 by spleen cells. In contrast, group ICy hamsters exhibited larger eosinophil and lymphocyte populations within sinusoids and peri-sinusoidal areas but showed no MGCs in granulomas. A striking decline in IL-2 production was noted. These results suggest that cyclophosphamide induces a delay in the natural evolution ofL. donovani-induced granulomatous hepatic inflammation.     

Optionen der postpartalen Therapie bei pränatal diagnostizierten Herzfehlern

Zusammenfassung Viele Herzerkrankungen k?nnen heute im Rahmen von Schwangerschaftsvorsorgeuntersuchungen frühzeitig diagnostiziert werden. So ist in vielen F?llen, besonders bei Herzrhythmusst?rungen, eine kurative pr?natale Therapie m?glich. Bei strukturellen Herzfehlern ist eine Therapie jedoch, abgesehen von der Behandlung einer m?glichen Herzinsuffizienz oder begleitender Herzrhythmusst?rungen, h?ufig erst nach der Geburt m?glich. Ist der Herzfehler bereits pr?natal erkannt, so kann das herzkranke Neugeborene ohne Zeitverz?gerung in einer kinderkardiologischen Klinik weiter betreut werden. Neben medikament?sen Behandlungsm?glichkeiten ist in vielen F?llen eine frühzeitige interventionelle und/oder chirurgische Therapie für die Prognose des herzkranken Neugeborenen besonders wichtig. Im folgenden werden aktuelle Behandlungsmethoden für angeborene Herzfehler anhand einiger typischer Beispiele mit besonderer Berücksichtigung von herzkranken Neugeborenen und S?uglingen aufgezeichnet.     

Carvedilol protects ischemic cardiac mitochondria by preventing oxidative stress.

Ischemia negatively affects mitochondrial function by inducing the mitochondrial permeability transition (MPT). The MPT is triggered by oxidative stress, which occurs in mitochondria during ischemia as a result of diminished antioxidant defenses and increased reactive oxygen species production. It causes mitochondrial dysfunction and can ultimately lead to cell death. Therefore, drugs able to minimize mitochondrial damage induced by ischemia may prove to be clinically effective. We analyzed the effect of carvedilol, a beta-blocker with antioxidant properties, on mitochondrial dysfunction. Carvedilol decreased levels of TBARS (thiobarbituric acid reactive substances), an indicator of oxidative stress, which is consistent with its antioxidant properties. Regarding cell death by apoptosis, although ischemia did increase caspase-8-like activity, there were no changes in caspase-3-like activity, which is activated downstream of caspase-8; this may indicate that the apoptotic cascade is not activated by 60 minutes of ischemia. We conclude that carvedilol protects ischemic mitochondria by preventing oxidative mitochondrial damage, and, by so doing, it may also inhibit the formation of the MPT pore.