Background: In the apparent indeterminate form of Chagas' disease, which lacks any overt clinical, electrocardiographic, and radiological manifestations of organ damage, lesions of the intrinsic autonomic innervation of heart are not striking features and evidences for cardiac autonomic dysfunction are elusive and conflicting. Objective: To evaluate the cardiac autonomic modulation based on Valsalva manoeuvreassociated heart interval variation in Chagas' disease subjects with apparent indeterminate form. Subjects and methods: We examined 36 outpatient volunteers aged 15 -51 years old (median: 36.5), in comparison with 52 healthy control individuals aged 17 -49 years old (median: 29) ( p < 0.001). Each subject sequentially performed in the supine position three to four manoeuvres at an intra-oral pressure of 40 mm Hg during 20 s, under continuous DII lead electrocardiographic registration, and rate-and time-dependent indices of Valsalva manoeuvre-associated R -R interval variation were obtained. The t-test or the Mann -Whitney test was employed to compare the data between the groups. Results: No correlation was found between every index and age for the control group ( p = 0.39 -0.71). The chagasic group presented similar basal to phase IV median increment (relative bradycardia) (23.7% vs. 22.7%; p = 0.63) and smaller basal to phase III median decrement of R -R interval (relative tachycardia) ( À 31.7% vs. À 35%; p = 0.02) in comparison to the control group, respectively. The median Valsalva ratio showed a tendency for reduction in chagasics (1.78 vs. 1.90; p = 0.08). Prolonged median time (14.2 vs. 10.3 s; p < 0.001) and slowed median velocity (5.1%/s vs. 8.9%/s; p < 0.001) of the phases III -IV bradycardia were also observed in chagasic group. The majority (58.3%) of the chagasics presented exclusively at least one depressed, and 8.3% presented at least one enhanced index of rateand/or time-dependent heart interval responses beyond the 25th or 75th control percentiles, and 27.8% presented at least one depressed and other enhanced index, while 5.6% showed all indices within the control interquartile range. All the indices outside the 25th or 75th control percentiles were noted in 13.9% of chagasics. Conclusion: Chagas' disease subjects without overt manifestations presented variable and subtle depression and less frequent enhancement or normality of the rate-and time-dependent tachycardia and bradycardia reflex responses related to Valsalva manoeuvre, which demonstrates distinct patterns of finely disturbed cardiac sinus parasympathetic and sympathetic modulation, probably due to inflammatory or autoimmunological damage of intrinsic innervation and/or to autoantibodies-induced derangement in neurotransmitter receptors. D

SUMMARYThe aim of this research was to evaluate the possible protective effect of pravastatin on ultrastructural alterations induced by cold stress in the myocardium of rats.Sixteen EPM-Wistar rats (Rattus norvegicus albinus) were used and distributed into four groups: 1) control; 2) pravastatin; 3) cold stress, and 4) pravastatin + cold stress. A daily oral dose of 10 mg/kg of weight of pravastatin was administered to each rat in groups 2 and 4 for 15 days. The stress induced by cold was obtained by keeping the group 3 and 4 rats in a freezer at -8°C for 4 hours. The animals were killed and the heart and fragments of the left ventricles (LV) were removed and processed prior to conducting electron microscopic analysis.The ultrastructural alterations in cardiomyocytes were quantified through the number of mitochondrial cristae pattern (cristalysis). The group subjected only to cold stress showed a significant increase in cristalysis (391.9) when compared with control group (42.0). In the cold stress and pravastatin pretreatment group, a statistically significant (96.9)*, P<0.05 cristalysis reduction was observed when compared with cold stress group. The mitochondrial cristalysis profiles of the control and pravastatin groups were 42.0 and 65.7, respectively.Cold stress induced a significant increase in the rate of mitochondrial cristalysis. In the group that received pravastatin and was exposed to cold stress, the drug protected the LV cardiomyocytes. This fact was confirmed by a reduction mitochondrial cristalysis pattern. (Jpn Heart J 2003; 44: 243-255)

There are many diseases related to ion-channel disorders, so-called "channelopathies." Hereditary short QT syndrome is a clinical-electrocardiographic entity with autosomal-dominant mode of transmission and it is the most recently described channelopathy. The syndrome may affect infants, children, or young adults with strong positive family background of sudden cardiac death. Short QT syndrome is characterized by short QT and heart-rate-corrected QTc intervals. It is frequently associated with tall-, peaked-, and narrow-based T waves that are reminiscent of the typical "desert tent" T waves of hyperkalemia. There is a high tendency for paroxysmal atrial fibrillation due to the heterogeneous abbreviation of action potential duration and refractoriness of atrial myocytes. The arrhythmia can also be induced by programmed electrical stimulation. The safest treatment suggested is an implantable cardioverter defibrillator, though the possibilities of inappropriate shocks have caused some concern, especially in teenagers. The ability of quinidine to prolong the QT interval has the potential to be an effective therapy for patients with short QT syndrome. This is particularly important in developing countries, where the implantable cardioverter-defibrillator therapy is not always available. Since these patients are at risk of sudden cardiac death from birth, and implantable cardioverter-defibrillator implantation has a lot of limitations in very young children, the utility of quinidine has to be evaluated further. Clinicians need to be aware of this deadly electrocardiographic (ECG) pattern as it portends a high risk of sudden cardiac death in otherwise healthy subjects with structurally normal hearts.

A anemia é muito prevalente em idosos; todavia, a eliptocitose hereditária, uma anemia hereditária caracterizada pela presença de eritrócitos em forma elíptica no sangue periférico; raramente causa anemia sintomática em pacientes idosos. A eliptocitose esferocítica é uma anemia hereditária com caráter autossômico dominante. A associação entre essas duas eritroenzimopatias hereditárias é rara e seu curso varia com alterações da forma eritrocitária, observando-se a presença simultânea de eliptocitose e esferocitose no sangue periférico. A hemólise pode variar de média a moderada intensidade. Relatamos o caso de uma paciente adulta idosa com eliptocitose esferocítica revelada após 26 anos, sendo realizada a esplenectomia para resolução do quadro de hemólise.