Browsing by Author "Martins, H"
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- Anemia: apenas marcador ou preditor independente de mortalidade na insuficiência cardíaca avançadaPublication . Saraiva, F; Martins, H; Costa, S; Franco, F; Gonçalves, L; Providência, LAINTRODUCTION AND OBJECTIVES: Advanced heart failure (HF) remains a major cause of mortality. Identification of new prognostic risk factors is therefore a priority. Anemia, a frequent comorbidity in HF patients and a recognized trigger of symptoms, has recently received considerable attention in this context. Several studies have demonstrated an association between anemia and increased mortality in stable chronic HF patients. However, the prognostic impact of this comorbidity on the survival of advanced HF patients remains unclear. Our aim was to assess whether anemia is not only a marker of advanced HF, but also an independent predictor of mortality. METHODS: We performed a retrospective study of 391 consecutive patients admitted to a single advanced HF care unit and divided into two groups according to the presence or absence of anemia at admission. Demographic, clinical, laboratory and therapeutic data were compared between the groups. Anemia was defined as hemoglobin at admission of <12 g/dl for women and <13 g/dl for men. Appropriate statistical tests and multivariate analysis were used to identify independent predictors of one-year and overall mortality. Median follow-up was 3.2 years. RESULTS: Group A, anemic patients (n=169, 43.2%), were older (61.7 +/- 14.7 vs. 58.0 +/- 14.5 years, p = 0.01) and included a higher number of patients with ischemic cardiomyopathy (40.7% vs. 28.6%, p = 0.01), but fewer with dilated cardiomyopathy (41.0% vs. 55.8%, p = 0.004). At admission, group A had lower systolic blood pressure (110.1 +/- 24.8 mmHg vs. 115.2 +/- 22.0 mmHg, p = 0.03) and higher mean C-reactive protein (1.90 +/- 3.6 mg/dl vs. 1.19 +/- 2.6 mg/dl, p = 0.004) and creatinine (1.50 +/- 0.9 mg/dl vs. 1.20 +/- 0.5 mg/dl, p < 0.001). Gender, prevalence of cardiovascular risk factors, previous medication and left ventricular ejection fraction were not statistically different between the groups. At discharge, fewer anemic patients received digoxin (71.1% vs. 81.8%, p = 0.03). Mortality rates at 3 months (13.6% vs. 6.7%, p = 0.05), one year (22.9% vs. 11%, p = 0.006) and during follow-up (39.8 % vs. 23.8%, p = 0.002) were significantly higher in Group A. Multivariate analysis demonstrated that anemia was an independent predictor of mortality at one year (p = 0.035) and during median follow-up: (p = 0.014). In the anemic group a linear relationship between hemoglobin levels and mortality was also detected. CONCLUSIONS: In our population, anemia was a frequent comorbidity and had an independent and negative impact on long-term mortality. Its correction could improve outcomes in advanced HF patients.
- Miocardiopatia de etiologia isquémica versus não-isquémica: haverá diferenças no prognóstico? Experiência de um centro de insuficiência cardíaca avançadaPublication . Lourenço, C; Saraiva, F; Martins, H; Baptista, R; Costa, S; Coelho, L; Vieira, H; Monteiro, P; Franco, F; Gonçalves, L; Providência, LAINTRODUCTION: Previous studies have associated heart failure (HF) of ischemic etiology with worse prognosis compared to HF from non-ischemic cardiomyopathy. HF treatment has evolved significantly in recent years. Has this evolution had an impact on this prognostic gap? OBJECTIVE: The aim of our study was to compare patients with advanced HF--nonischemic versus ischemic etiology--in terms of baseline characteristics, treatment, and in-hospital and long-term prognosis (including death, heart transplantation and hospital readmission). METHODS: We performed a retrospective study including 286 consecutive patients with systolic HF admitted to an HF unit between January 2003 and June 2006. We compared two groups according to HF etiology: Group A--ischemic cardiomyopathy (n = 109); Group B--non-ischemic cardiomyopathy (n = 177). Mean follow-up was 41 months. RESULTS: Group A were older (62.2 +/- 10.4 vs. 55.9 +/- 15.2 years, p < 0.001), with a higher proportion of males (80.7 vs. 67.8%, p = 0.017), diabetes, anemia, dyslipidemia and smokers; they required more prolonged treatment with inotropic drugs and more frequent treatment with statins, antiplatelet agents and nitrates. On admission, Group B patients presented with lower serum sodium and higher aminotransferase levels. There were no differences in the occurrence of cardiogenic shock or dysrhythmias, baseline ECG rhythm, frequency of left bundle branch block, renal function, BNP, left ventricular ejection fraction, heart rate or implantation of intracardiac devices. Group A had higher in-hospital mortality (11.0 vs. 4.0%, p = 0.020). Multivariate analysis showed that the only predictor of in-hospital mortality was serum sodium < 133 mmol/l and also showed that HF etiology was not a predictor of this endpoint; previous medication with angiotensin-converting enzyme inhibitors was a protective factor. On Kaplan-Meier analysis, it was observed that, in the long-term, there were no significant differences in either survival rates (70.0 vs. 76.8%, p = 0.258), or the combined endpoints of survival free of death or heart transplantation (55.7 vs. 54.5%, p = 0.899) and survival free of death, heart transplantation or hospital readmission (38.0 vs. 32.8%, p = 0.386). CONCLUSIONS: Although in-hospital mortality was higher in ischemic cardiomyopathy, this variable was not an independent predictor of mortality and the difference appears to fade in the long-term, in contrast to what had been reported in older studies, but in agreement with more recent data
- Síndrome Cardio-Renal: os desafios no tratamento da insuficiência cardíacaPublication . Martins, H; Pedro, N; Castellano, M; Monteiro, P; Moura, JJ; Providência, LAHeart failure is a chronic and progressive disease that is estimated to affect approximately 20 million people worldwide and is one of the major public health problems. Its prevalence is reaching epidemic levels with about 550,000 new cases diagnosed annually, partly due to increased life expectancy in developed countries. And as it is a systemic disease, it can cause dysfunction in various organs, but especially in the kidney. The renal failure is often associated with heart failure and, when present together, make the treatment more complex and the prognosis is worse. This is the cardio-renal syndrome. The definition of cardio-renal syndrome varies according to the working groups, and there isn't a consensus. The exact cause of deterioration of renal function and the mechanism behind this interaction are complex, multifactorial in nature and not fully known at present. The treatment available is the one used for the treatment of heart failure. It is necessary to maintain the normal function of filtration, secretion and reabsorption in kidney to have a real improvement of the clinical condition of the patient. Patients with higher risk of developing nephropathy and those who have diagnosed renal failure should have prescribed drugs that are handled very carefully. But as in many other clinical situations, there aren't perfect drugs available to treat cardio-renal syndrome and the existing ones may have serious side effects in medium/long term causing the deterioration of renal function and possibly an increased mortality. The treatment is truly challenging in patients with severe fluid overload that is refractory to diuretics. This article aims to present the existing definitions of cardio-renal syndrome, its epidemiology, describe the current knowledge about the pathophysiology and its relationship to therapeutic interventions, some actual strategies and future technologies in an attempt to preserve the kidney, mainly during the decompensation of chronic heart failure.