Reversibility of tachycardia-induced cardiomyopathy after cure of incessant supraventricular tachycardia.

Seven of 17 patients with incessant supraventricular tachycardia caused by an accessory pathway with a long retrograde conduction time were seen with symptoms or echocardiographic signs of a tachycardia-induced cardiomyopathy. Three patients were in New York Heart Association functional class II with dyspnea and four were in class III. Eight patients (six with tachycardia-induced cardiomyopathy) underwent surgery because of failure of medical treatment (including one patient in functional class I) and one underwent direct current catheter ablation of the atrioventricular (AV) node. In six patients echocardiograms recorded before and after the procedure were available. Before surgery or direct current ablation the mean left ventricular ejection fraction was 36.3 +/- 8.7%, the left ventricular end-diastolic diameter 55.7 +/- 7.6 mm and the left ventricular end-systolic diameter 44.3 +/- 7.8 mm. A mean of 21.6 +/- 6.8 months after the procedure the mean left ventricular ejection fraction increased to 58.6 +/- 8.0%, the left ventricular end-diastolic diameter decreased to 49.0 +/- 3.6 mm and the left ventricular end-systolic diameter decreased to 32.2 +/- 2.7 mm; all six patients were in functional class I. These results confirm that control of incessant tachycardia leads to a regression of symptoms and signs of cardiomyopathy and progressive normalization of the dimensions of the heart. Because of these findings, surgery should be considered early in patients with an accessory AV pathway and incessant tachycardia. The presence of a tachycardia-induced cardiomyopathy should therefore be an indication for surgery rather than a contraindication.

[Efficacy of sotalol in idiopathic ventricular arrhythmia originating in the right ventricular outflow tract]. / Eficácia do sotalol nas arritmias ventriculares idiopáticas com origem em trato de saída de ventrículo direito.

PURPOSE: To evaluate the effects of sotalol in patients (pts) with idiopathic ventricular arrhythmias (VT) from right ventricular outflow tract. METHODS: Eighteen pts with VT were enrolled (five with monomorphic repetitive ventricular tachycardia - MRVT). Pts were submitted to a double-blind crossover randomized study (placebo vs. 320 mg/po/d/sotalol; four weeks each), after a wash-out control period. Holter recording were recorded in control and placebo and drug periods. Eligible pts have > 50/h isolated ventricular premature beats (VPB) in control, with or without paired VPB or nonsustained VT (NSVT- > 3 beats, > 100bpm). Drug efficacy criteria was: > 75% reduction in isolated VPB and > 90% of paired VPB or NSVT. The effects of the drug on uncorrected QT interval was evaluated and also on circadian rhythm of VT through the hourly pNN50/VPB ratios. Values are given as mean +/- SD. Three recordings were compared by using paired Student's "t" test. Statistical significance was assumed for p < 0.05. RESULTS: Differences between control and placebo were NS. Drug was effective in 61% of pts, reducing the 3 types of ET (VPB: placebo = 23.508 +/- 34.537; drug: 975 +/- 1357; paired placebo = 443 +/- 587; drug = 9 +/- 20). The drug was evaluated in 4 pts with MRVT, reducing all ectopic events, with efficacy of 60% over VPB and paired and 80% over NSVT (VPB: placebo = 52.639 +/- 42.207; drug: 1631 +/- 2062; paired: placebo = 796 +/- 754; drug: 20 +/- 30; NSVT: placebo = 4287 +/- 6343; drug: 9 +/- 11). Mean QT interval was 0.40 +/- 0.01s in control and 0.50 +/- 0.04s in the drug period, with no correlation between duration and efficacy. Sotalol modified the circadian rhythm of VPB in the non-responders group, mainly during the morning. CONCLUSION: Sotalol was effective in control of VT, mainly the MRVT. Its effect on VPB circadian rhythm may independently contribute to the overall efficacy profile and myocardial protective effect of this drug.

Helminths from an introduced species (Tupinambis merianae), and two endemic species (Trachylepis atlantica and Amphisbaena ridley) from Fernando de Noronha Archipelago, Brazil.

The present study reports the occurrence of helminths in the introduced species Tupinambis merianae (tegu lizard), and in two endemic species Trachylepis atlantica (small lizard) and Amphisbaena ridleyi (two-head-snake lizard ), from Fernando de Noronha Archipelago, State of Pernambuco, Brazil. Nine species of helminths were found, mainly in the digestive tract and accessory organs, with the following prevalence (P) and mean infection intensity (MII). Tupinambis merianae: Diaphanocephalus galeatus (P = 96%, MII = 20.5), Spinicauda spinicauda (P = 100%, MII = 197.8), and Oochoristica sp.l (P = 20%, MII = 4.4). Trachylepis atlantica: Moaciria alvarengai (P = 20%, MII = 1.4), S. spinicauda (P = 92%, MII = 22.1), Mesocoelium monas (P = 4%, MII = 3.0), Platynosomum sp. (P = 8%, MII = 7.0), and Oochoristica sp.2 (P = 16%, MII = 1.25). Amphisbaena ridleyi: Aplectana albae (P = 96%, MII = 143.4), Thelandros alvarengai (P = 4%, MII = 1.0), Me. monas (P = 44%, MII = 2.8), Platynosomum sp. (P = 36%; MII = 13.8), and Oochoristica sp.2 (P = 48%; MII = 2.17). More than 80% of T. merianae were infected with 2, or more, helminth species. In Tr. atlantica, single-species infections were present in 50% of the specimens, but co-occurrence of 2 parasites was also high (41.7%). In A. ridleyi, multiple infections were more common, with up to 5 parasite species present. The helminth fauna observed allowed us to conclude that helminths can be carried together with their host when they colonize new geographic localities and that these introduced helminths can, in turn, colonize endemic, or native, hosts.

Cardiac receptors affect regional flow during acute infarction in conscious rats.

This study was conducted to determine if cardiac receptors have a role in the control of the regional circulations during small acute myocardial infarction in the conscious rat. Cardiocirculatory dynamics and cardiac output distribution (microspheres) were measured in conscious rats 24 and 48 h after surgery for left main coronary artery ligation or the sham procedure. Data from animals without treatment were compared to data from animals treated to induce chemical cardiac denervation (85% phenol applied to the supraventricular surface of the heart and the root of the great vessels). The results suggest that neurogenic vasopressor stimuli originating from the heart contribute to changes in peripheral resistance secondary to small, acute, experimentally induced myocardial infarction in the conscious rat.

Effects of acute myocardial infarction on the circulation of the conscious rat.

This study was conducted to determine if experimental left coronary artery ligation resulting in a small myocardial infarction (MI, 15% of the left ventricle) affects the peripheral circulation in conscious rat during the first 48 h of recovery. At 24 or 48 h post-MI or sham surgery, animals were instrumented and evaluated using the radioactive microsphere technique. There were no overt central hemodynamic changes 24 h post-MI but at 48 h, left ventricular end diastolic pressure was significantly increased compared to the parallel control (MI: 5.9 +/- 0.6, sham 2.0 +/- 0.5 mm Hg, P less than 0.005). At 24 h post-MI, renal vascular resistance was increased and similar but non-significant changes occurred in the gut. At 48 h post-MI, vascular resistance in the skeletal muscle, spleen, gut and cutaneous circulations were significantly reduced compared to sham-operated rats. Similar changes at 24 h were seen in a separate group of conscious rats with MI which had previously undergone cardiac denervation suggesting that cardiac afferent activity was not directly responsible for the peripheral response to MI at 24 h. Denervation did eliminate the 48 h peripheral vasodilator response. In denervated animals, circulating renin levels were similar in MI and sham-operated rats and were unchanged between 24 and 48 h. Thus, small MI in conscious rat induces a sequela of effects on the peripheral circulation over 48 h. These changes are associated with cardiac afferent nerve activity but appear to be unrelated to plasma renin levels.

Taquicardias ventriculares idiopáticas

A taquicardia ventricular, geralmente, é consequência de anormalidades cardíacas. Aquelas cuja etiopatogenia näo pode ser definida pelos métodos diagnósticos atuais, Säo classificadas como idiopáticas. Gallavardin foi o primeiro, em 1922, a descrever a presença de taquicardias ventriculares, em pacientes jovens, sem cardiopatia aparente. Dentre as taquicardias ventriculares, este de de taquiarritmia tem incidência maior do que a esperada, podendo chegar a 10 por cento. O pequeno registro de ocorrênas deve-se a pouco frequente sintomatologia e ao insuficiente conhecimento médico deste distúrbio do ritmo cardíaco. O advento de métodos complementares de diagnóstico mais sofisticados permitiu melhor compreensäo destas arritmias, de seus mecanismos de produçäo, dos locais de origem e de seus fatores desencadeantes.