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It is known that patients with heart failure (HF) have an increased risk of developing central sleep apnoea (CSA), with Cheyne-Stokes respiration. The development of servo-ventilation aimed to treat CSA and improve the quality of life (QoL) of these patients. A large randomized clinical study, SERVE-HF, was conducted in order to test this theory in patients with HF and reduced ejection fraction (HFrEF). The results from this trial seemed to indicate that, in these patients, there was no beneficial effect of the assisted ventilation in CSA treatment. More surprisingly, an increased rate of all-cause or cardiovascular mortality was observed. This has led to dramatic changes in clinical practice, with decreased frequency of servo-ventilation prescription across Europe, including Portugal, due to changes in the guidelines. However, SERVE-HF was conducted only in severe systolic HF patients with CSA, and caution must be taken when extrapolating these results to HF patients with preserved ejection fraction or CSA patients without HF. The study also showed poor adherence, methodological and statistical gaps, including study design, patient selection, data collection and analysis, treatment adherence, and group crossovers, which have not been discussed in the trial as potential confounding factors and raise several concerns. Moreover, the adaptive servo-ventilation (ASV) device used in SERVE-HF was unable to lower the minimum support pressure below 3 mm H20, and this has been suggested as one of the probable contributing reasons to the excess mortality observed in this study. This limitation has since been solved, and this ASV device is no longer used. This paper describes the results of a Portuguese Task Force on the treatment of central sleep apnoea in patients with chronic HF.

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BACKGROUND: In breast cancer treated with breast-conserving radiotherapy, the influence of the boost dose on cosmetic outcome after long-term follow-up is unknown. PATIENTS AND METHODS: We included 348 patients participating in the EORTC 'boost versus no boost' mega trial with a minimum follow-up of 6 years. Digitalised pictures were analysed using specific software, enabling quantification of seven relative asymmetry features associated with different aspects of fibrosis. RESULTS: After 3 years, we noted a statistically significantly poorer outcome for the boost patients for six features compared with those of the no boost patients. Up to 9 years of follow-up, results continued to worsen in the same magnitude for the both patient groups. We noted the following determinants for poorer outcome: (i) boost treatment, (ii) larger excision volumes, (iii) younger age, (iv) tumours located in the central lower quadrants of the breast and (v) a boost dose administered with photons. CONCLUSIONS: A boost dose worsens the change in breast appearance in the first 3 years. Moreover, the development of fibrosis associated with whole-breast irradiation, as estimated with the relative asymmetry features, is an ongoing process until (at least) 9 years after irradiation.

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No other form of therapy, whether medical or surgical, has an impact comparable to heart transplantation on quality of life and survival of the patients with severe heart failure. In the EC and in the USA about 10 patients per million people are transplanted each year. Since Portugal has a population of 10 million, 100 patients should be transplanted each year. However only 8 patients were in fact transplanted in Portugal in 1998, 2 of them at Hospital S. João. We transplanted less than 10% of the predicted needs. We have the second lowest rate of heart transplantation per million people of the 23 European countries with registries of this activity. This is due to structural and organizational deficiencies which, at least in the case of Hospital S. João have a triple nature: the lack of a professional team devoted to severe heart failure treatment and heart transplantation; the lack of infrastructures, namely a heart failure ward and a heart failure outpatient clinic; and thirdly an inappropriate distribution of the tasks associated with heart transplantation and patient follow-up. A prediction of the resources needed for a successful heart transplantation program at Hospital S. João is presented. This was based on what is known regarding the natural history, morbidity and mortality of severe heart failure, on our own experience in this field, and finally on the experience of a large Spanish heart transplantation centre. The recommendations of the British Transplantation Society and those of the Department of Cardiothoracic Surgery of Stanford were also taken into account.

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The use of angiotensin converting enzyme inhibitors (ACEIs), as well as of acetyl salicylic acid (ASA) in patients with hypertension, myocardial infarction or heart failure is recommended by the guidelines issued by several respected cardiological societies. However, some authors have argued that ASA may decrease the effectiveness of ACEIs by decreasing the release of prostagandins. Although such negative interaction is still not conclusively demonstrated, the merits of the use of this association should be judged in each individual patient with heart failure. It seems prudent to use low doses of ASA (< or = 250 mg/day) in these patients. ADP antagonists may constitute an alternative to ASA since they do not block prostaglandin synthesis.

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While the prognosis of patients with heart failure is related to the progression of left ventricular dysfunction and to the activation of several regulatory systems--neurohormones, cytokines and others--the symptoms relate to hemodynamic and skeletal muscle disturbances. This is why the relief of symptoms by pharmacological intervention is not always accompanied by an improvement in prognosis. Hemodynamic improvement is no longer the main issue of therapy. The antagonism of the neurohormonal and other regulatory systems, as a means to influence prognosis, stands as the main challenge for the future. Until now only ACE inhibitors, beta-blockers, spironolactone, the combination of nitrates and hydralazine, and heart transplantation have achieved this goal.

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Foram analisados histologicamente 64 ovários de ovelhas lanadas adultas, procedentes do Centro de Pesquisa dos Campos Sul Brasileiros-Embrapa, Bagé-RS. Constatou-se, em 55 dos 64 ovários (85,9 por cento), a presença da rete ovarii, localizada no tecido periovariano, no hilo, na medular ou na cortical. A semelhança do observado em outros mamíferos, a rete ovarii na ovelha é morfologicamente dividida em três porçöes: rete intra-ovárica, rete conectante e rete extra-ovárica. Em cinco ovários (7,8 por cento) foi possível verificar uma continuidade entre a rete extra-ovárica e a tuba uterina sugerindo uma conexäo tubo-retial, de maneira similar à descrita para bovinos e para a corça. Quanto à patologia da rete, observaram-se a formaçäo de cistos envolvendo a rete conectante e/ou extra-ovárica em sete casos (10,9 por cento) e um caso de hiperplasia da rete extra-ovárica (1,6 por cento)

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We evaluated left ventricular function by echocardiography in a prospective study that included 98 consecutive human immunodeficiency virus (HIV)-infected patients and 40 HIV-seronegative normal controls. When compared with controls, HIV patients showed increased isovolumic relaxation time (101+/-18 ms versus 71+/-10 ms; p<0.0001) and left ventricular diastolic diameters (51+/-6 mm versus 47+/-3 mm; p<0.0005), and decreased fractional shortening (31+/-6% versus 37+/-2%; p<0.0001). Diastolic dysfunction was the most frequent finding (63% of the patients). We found depressed ejection fraction in 31 (32%) patients. Only 8 (8%) patients had symptomatic congestive heart failure. Left ventricular dysfunction was not attributable to intravenous drug abuse or to therapy. It was less severe in earlier stages of the infection (fractional shortening: acquired immunodeficiency syndrome=30%+/-6%, asymptomatic HIV-seropositives 34%+/-5%; p<0.005) and in HIV-2-infected patients. Patients with opportunistic infections (all aetiologies mixed) had more frequent congestive heart failure than those without infections (16% of the patients with versus 4% of the patients without infections; p<0.05). The fact that even asymptomatic HIV-seropositives had signs of left ventricular dysfunction (fractional shortening: asymptomatic HIV-seropositives=34%+/-5%; controls=37%+/-2%; p<0.05) favours the hypothesis of the HIV being one of the causes of these abnormalities.

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We evaluated the effect of chronic Pneumocystis carinii pneumonia (PCP) prophylaxis, with a once a month dose of 300 mg of inhalatory pentamidine isethionate, on QT interval duration. We included 22 human immunodeficiency virus (HIV)-infected patients: 11 were on this medication and 11 were not. The two groups were matched for age, sex and HIV infection stage. No patient had any clinical condition or was under any medication known to affect the duration of the QT interval. The heart rate-corrected QT (QTc) was obtained by averaging the observations of three independent observers. QTc duration was similar in both groups. The time separating pentamidine administration and the performance of the ECG did not influence the results, neither did the duration of inhalatory pentamidine therapy. Our results suggest that inhalatory pentamidine does not prolong the QT interval duration and so, as opposed to what has been reported concerning intravenous pentamidine therapy, does not seem to induce an increased risk of torsades de pointes.

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Human immunodeficiency virus-infected (HIV) patients frequently present left ventricular dysfunction. Its etiology is not elucidated but zidovudine has been postulated as a possible cause factor. This study is an attempt to clarify this issue by evaluating the effect of zidovudine therapy on left ventricular function in these patients. We prospectively studied by echocardiographic examination 11 consecutive HIV-infected patients who were assigned for zidovudine therapy. We excluded patients that had a history or a physical examination suggestive of ischemic, rheumatic, congenital, or hypertensive heart disease. Patients with diabetes mellitus, excessive ethanol intake and patients on potentially cardiodepressant drugs were also excluded. Echocardiographic examination was performed immediately before the initiation of zidovudine therapy and 1 and 3 months later. Left ventricular diameters, mass and fractional shortening showed no significant difference from baseline, at 1 or 3 months after the initiation of zidovudine therapy. Our results suggest that zidovudine therapy has no effect on left ventricular diameters, mass or fractional shortening during a short term.

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The purpose of the present study was to noninvasively evaluate left (LV) systolic and diastolic function in patients with atrial septal defect (ASD) using the phonomechanocardiogram. We studied 40 patients with atrial septal defect, 16 males and 24 females, ages ranging from 6 to 56 years (mean 21.1 years), consecutively observed before surgery in our institution, during a four year period. We measured the systolic time intervals (Q-A2c, Q-S1, ICT, PEP, LVETc, PEP/LVET), the Apex Cardiographic (ACG) diastolic parameters A2-Oc and A/H and the hemodynamic variables Qp/Qs, Pulmonary Vascular Resistance (PVR) and Left Ventricular End Diastolic Pressure (LVEDP). We compared the data with 74 normal individuals using the Student t-test and linear regression analysis. We found significant Q-S1 lengthening (81.2 +/- 16.4 ms, p < 0.001); PEP, ICT and A2-Oc were significantly reduced (101.2 +/- 21.7 ms, p < 0.001, 20.0 +/- 5.3 ms, p < 0.05 and 117.1 +/- 26.3 ms, p < 0.001, respectively) and A/H was significantly increased (17.4 +/- 12.1%, p < 0.005). Except for the case of Q-S1, where there was a weak positive linear correlation with Qp/Qs (r = 0.37), we found no correlation between the other parameters and Qp/Qs or PVR. Sixty-seven percent of the patients had Q-S1 prolongation and a Q-S1 > 76.2 ms identified left-right shunts > 2 with a positive predictive value of 82%; 62% of the patients had a reduced A2-Oc and a A2-Oc < 110 ms identified shunts > 2 with a positive predictive value of 90%.(ABSTRACT TRUNCATED AT 250 WORDS)

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PURPOSE: To evaluate the cardiac involvement in Human Immunodeficiency Virus (HIV) infection. DESIGN: Prospective and normal individuals group controlled study. SETTING: The departments of cardiology and infectious diseases of an university hospital. PATIENTS: 137 consecutive HIV infected patients at all stages of the infection and 40 normal noninfected controls. MEASUREMENTS AND MAIN RESULTS: Clinical and echocardiographic evaluation was performed. Cardiac symptoms were observed in 10 (7.3%) patients, manifested as congestive heart failure. The global HIV infected population had increased left ventricular (LV) dimensions and wall thickness and decreased LV fractional shortening and ejection fraction when compared with the control population. Seven (5.1%) patients had dilated cardiomyopathy, 9 (6.5%) had global LV hypokinesis with or without LV dilatation and 17 (12.4%) had segmental LV wall motion abnormalities. Right ventricular dilatation was present in 23 (16.8%). Mitral or tricuspid regurgitation of a moderate or severe degree was found in 3 (2.2%) patients. No valvular vegetations were found. Fifty nine (43.1%) patients presented a pericardial effusion. An echocardiogram with at least one abnormality was observed in 104 (75.9%) and a severely abnormal echocardiogram in 34 (24.8%). The presence of cardiac symptoms and of abnormal and severely abnormal echocardiograms was more frequent in patients with the acquired immunodeficiency syndrome than in asymptomatic HIV infected patients. When comparing HIV-1 with HIV-2 populations the first showed increased LV systolic and diastolic diameters and LV mass index. There was no statistically significant difference between all risk behavior groups regarding the frequency of cardiac symptoms or the echocardiographic abnormalities found. HIV infected patients with CD4+ lymphocytes counts < or = 100/mm3 had more frequent abnormal and severely abnormal echocardiograms than those with CD4+ lymphocytes counts > 100/mm3. CONCLUSIONS: Although cardiac symptoms were rare in our population, subclinical cardiac involvement detected by echocardiography was frequent and could involve any cardiac layer. It was not influenced by the patients' risk behavior. The left ventricular trophic response observed in HIV-2 infection seemed less intense than that in HIV-1 infection. Cardiac involvement was more frequent in the more advanced stages of the infection and in patients with lower CD4+ lymphocyte counts.

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Mutagenesis induced by several genotoxic agents has been reported to be inhibited by cobaltous chloride. In order to study the effects of this metal in some SOS functions we evaluated mutagenesis, lysogenic induction and phage reactivation in Escherichia coli cells treated with CoCl2. We detected that cobaltous chloride, when present in the plating medium, was able to block mutagenesis and lysogenic induction promoted by UV irradiation. We also found that CoCl2 blocked protein synthesis, so we propose that this effect can be responsible for the antimutagenic and antilysogenic effects of this metal. On the other hand, if the cells were treated for a short period of time with CoCl2, in the absence of Mg, we observed that cobaltous chloride per se was able to promote lysogenic induction as well as to enhance the phage reactivation induced by UV irradiation. We conclude that depending on experimental conditions, cobaltous chloride may act either as an inhibitor or as an inducer of the SOS functions.

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