Prevalência de trombofilias congênitas em pacientes com síndrome antifosfolípide primária

Não se aplic

Pharmaceutical Care Increases Time in Therapeutic Range of Patients With Poor Quality of Anticoagulation With Warfarin

Thromboembolic events are associated with high mortality and morbidity indexes. In this context, warfarin is the most widely prescribed oral anticoagulant agent for preventing and treating these events. This medication has a narrow therapeutic range and, consequently, patients usually have difficulty in achieving and maintaining stable target therapeutics. Some studies on the literature about oral anticoagulant management showed that pharmacists could improve the efficiency of anticoagulant therapy. However, the majority of these studies included general patients retrospectively. The aim of this study was to prospectively evaluate a pharmacist’s warfarin management in patients with poor quality of anticoagulation therapy (Time in the Therapeutic Range- TTR < 50%). We included 268 patients with atrial fibrillation (AF) and without stable dose of warfarin (TTR < 50%, based on the last three values of International Normalized Ratio-INR). We followed them up for 12 weeks, INR values were evaluated and, when necessary, the dose adjustments were performed. During the first four visits, patient’s INR was measured every 7 days. Then, if INR was within the target therapeutic range (INR: 2–3), the patient was asked to return in 30 days. However, if INR was out the therapeutic target, the patient was asked to return in 7 days. Adherence evaluation was measured through questionnaires and by counting the pills taken. Comparison between basal TTR (which was calculated based on the three last INR values before prospective phase) and TTR of 4 weeks (calculated by considering the INR tests from visits 0 to 4, in the prospective phase of the study) and basal TTR and TTR of 12 weeks (calculated based on the INR tests from visits 0 to 12, in the prospective phase of the study) revealed significant statistical differences (0.144 ± 0.010 vs. 0.382 ± 0.016; and 0.144 ± 0.010 vs. 0.543 ± 0.014, p < 0.001, respectively). We also observed that the mean TTR of 1 year before (retrospective phase) was lower than TTR value after 12 weeks of pharmacist-driven treatment (prospective phase) (0.320 ± 0.015; 0.540 ± 0.015, p < 0.001). In conclusion, pharmaceutical care was able to improve TTR values in patients with AF and poor quality of anticoagulation with warfarin

Lipoprotein (a): Structure, Pathophysiology and Clinical Implications

The chemical structure of lipoprotein (a) is similar to that of LDL, from which it differs due to the presence of apolipoprotein (a) bound to apo B100 via one disulfide bridge. Lipoprotein (a) is synthesized in the liver and its plasma concentration, which can be determined by use of monoclonal antibody-based methods, ranges from < 1 mg to > 1,000 mg/dL. Lipoprotein (a) levels over 20-30 mg/dL are associated with a two-fold risk of developing coronary artery disease. Usually, black subjects have higher lipoprotein (a) levels that, differently from Caucasians and Orientals, are not related to coronary artery disease. However, the risk of black subjects must be considered. Sex and age have little influence on lipoprotein (a) levels. Lipoprotein (a) homology with plasminogen might lead to interference with the fibrinolytic cascade, accounting for an atherogenic mechanism of that lipoprotein. Nevertheless, direct deposition of lipoprotein (a) on arterial wall is also a possible mechanism, lipoprotein (a) being more prone to oxidation than LDL. Most prospective studies have confirmed lipoprotein (a) as a predisposing factor to atherosclerosis. Statin treatment does not lower lipoprotein (a) levels, differently from niacin and ezetimibe, which tend to reduce lipoprotein (a), although confirmation of ezetimibe effects is pending. The reduction in lipoprotein (a) concentrations has not been demonstrated to reduce the risk for coronary artery disease. Whenever higher lipoprotein (a) concentrations are found, and in the absence of more effective and well-tolerated drugs, a more strict and vigorous control of the other coronary artery disease risk factors should be sought

Por que os portadores de cardiomiopatia chagásica têm pior evolução que os não-chagásicos? Why do patients with chagasic cardiomyopathy have worse outcomes than those with non-chagasic cardiomyopathy?

FUNDAMENTO: A insuficiência cardíaca é uma doença de alta prevalência, com prognóstico dependente de diferentes fatores preditores. OBJETIVO: A doença de Chagas é um preditor de mau prognóstico em pacientes com insuficiência cardíaca (IC) crônica. O objetivo deste estudo é analisar se ela também prediz pior evolução para pacientes agudamente descompensados. MÉTODOS: Estudamos 417 pacientes hospitalizados por IC descompensada. A idade média foi de 51,8 anos, sendo 291 (69,8%) homens. Os pacientes foram divididos em dois grupos: 133 (31,9%) chagásicos (CH) e 284 com outras etiologias. Num subgrupo de 63 pacientes (15,1% com doença de Chagas), dosaram-se citocinas e noradrenalina. RESULTADOS: Na internação, 24,6% necessitaram de inotrópicos, e em um ano a mortalidade foi de 54,7%. Os CH apresentaram maior mortalidade (69,2% vs. 47,9%, p < 0,001). Na comparação de dados, os CH eram mais jovens (47,6 vs. 53,8 anos, p < 0,001) e apresentavam, em média, PA sistólica (96,7 vs. 111,2 mmHg, p < 0,001), fração de ejeção (32,7 vs. 36,4%, p < 0,001), Na sérico (134,6 vs. 136,0, p = 0,026) mais baixos e TNF-alfa mais elevado (33,3 vs. 14,8, p = 0,001). A presença de hipotensão necessitando de inotrópicos, o diâmetro diastólico do ventrículo esquerdo (VE), os dados de função renal, os níveis de interleucina-6 e os de noradrenalina não diferiram nos dois grupos. CONCLUSÃO: Os pacientes chagásicos hospitalizados com IC descompensada tiveram pior prognóstico quando comparados com aqueles de outras etiologias. Esse fato pode dever-se ao maior comprometimento cardíaco (fração de ejeção mais baixa), maior instabilidade hemodinâmica (pressão sistólica e freqüência cardíaca mais baixas) e maior ativação do sistema renina angiotensina (sódio mais baixo) e das citocinas (TNF-alfa).<br>BACKGROUND: Heart failure is a highly prevalent disease, the prognosis of which depends on different predictive factors. OBJECTIVE: Chagas disease is a predictor of poor prognosis in patients with chronic heart failure (HF). The purpose of this study is to investigate whether this condition also predicts poor outcome in acutely decompensated patients. METHODS: Four hundred and seventeen patients admitted for decompensated heart failure were studied. Mean age was 51.8 years, and 291 (69.8%) were male. They were divided into two groups: 133 (31.9%) patients with Chagas heart disease (CH) and 284 patients with heart failure of other etiologies. Cytokine and norepinephrine plasma levels were measured in a subgroup of 63 patients (15.1% with Chagas disease). RESULTS: At admission, 24.6% of the patients needed inotropic support, and one-year mortality was 54.7%. Mortality rates were higher in the CH group (69.2% vs. 47.9%, p < 0.001). When data were compared, patients with Chagas disease were younger (47.6 vs. 53.8 years, p < 0.001) and, on average, showed lower systolic blood pressure (96.7 vs. 111.2 mmHg, p < 0,001), ejection fraction (32.7 vs. 36.4%, p < 0.001), and serum Na (134.6 vs. 136.0, p = 0.026), in addition to higher TNF-&#945; levels (33.3 vs. 14.8, p = 0.001). The presence of hypotension requiring inotropic support, left ventricular (LV) diastolic diameter, renal function findings, and interleukin-6 and norepinephrine plasma levels did not differ between both groups. CONCLUSION: Chagas disease patients admitted with decompensated heart failure had worse prognoses than patients with heart failure of other etiologies. This may be owing to a greater degree of cardiac impairment (lower ejection fraction) and hemodynamic instability (lower systolic blood pressure and heart rate), increased activation of the renin-angiotensin system (lower sodium), and increased cytokine levels (TNF-&#945;)

Evaluation of a pharmacogenetic-based warfarin dosing algorithm in patients with low time in therapeutic range – study protocol for a randomized controlled trial

Abstract Background Time in therapeutic range (TTR) is a measurement of quality of warfarin therapy and lower TTR values (<50%) are associated with greater risk of thromboembolic and bleeding events. Recently, we developed a pharmacogenetic-based warfarin dosing algorithm specifically calibrated for a Brazilian patient sample. The aims of this study are: to evaluate the impact of a genetic-based algorithm, compared to traditional anticoagulation, in the time to achieve the therapeutic target and in TTR percentage; and to assess the cost-effectiveness of genotype-guided warfarin dosing in a specific cohort of patients with low TTR (<50%) from a tertiary cardiovascular hospital. Methods/design This study is a randomized controlled trial in patients (n = 300) with atrial fibrillation with TTR < 50%, based on the last three INR values. At the first consultation, patients will be randomized into two groups: TA group (traditional anticoagulation) and PA group (pharmacogenetic anticoagulation). For the first group, the physician will adjust the dose according to current INR value and, for the second group, a pharmacogenetic algorithm will be used. At the second, third, fourth and fifth consultations (with an interval of 7 days each) INR will be measured and, if necessary, the dose will be adjusted based on guidelines. Afterwards, patients who are INR stable will begin measuring their INR in 30 day intervals; if the patient’s INR is not stable, the patient will return in 7 days for a new measurement of the INR. Outcomes measures will include the time to achieve the therapeutic target and the percentage of TTR at 4 and 12 weeks. In addition, as a secondary end-point, pharmacoeconomic analysis will be carried out. Ethical approval was granted by the Ethics Committee for Medical Research on Human Beings of the Clinical Hospital of the University of São Paulo Medical School. Discussion This randomized study will include patients with low TTR and it will evaluate whether a population-specific genetic algorithm might be more effective than traditional anticoagulation for a selected group of poorly anticoagulated patients. Trial registration ClinicalTrials.gov, NCT02592980 . Registered on 29 October 2015