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1.
Glob Heart ; 16(1): 15, 2021 02 17.
Artigo em Inglês | MEDLINE | ID: mdl-33833939

RESUMO

Background: SARS-CoV-2 pandemic has modified the cardiovascular care of ambulatory patients. The aim of this survey was to study changes in lifestyle habits, treatment adherence, and mental health status in patients with cardiometabolic disease, but no clinical evidence of COVID-19. Methods: A cross-sectional survey was conducted in ambulatory patients with cardiometabolic disease using paper/digital surveys. Variables investigated included socioeconomic status, physical activity, diet, tobacco use, alcohol intake, treatment discontinuation, and psychological symptoms. Results: A total of 4,216 patients (50.9% males, mean age 60.3 ± 15.3 years old) from 13 Spanish-speaking Latin American countries were enrolled. Among the study population, 46.4% of patients did not have contact with a healthcare provider, 31.5% reported access barriers to treatments and 17% discontinued some medication. Multivariate analysis showed that non-adherence to treatment was more prevalent in the secondary prevention group: peripheral vascular disease (OR 1.55, CI 1.08-2.24; p = 0.018), heart failure (OR 1.36, CI 1.05-1.75; p = 0.017), and coronary artery disease (OR 1.29 CI 1.04-1.60; p = 0.018). No physical activity was reported by 38% of patients. Only 15% of patients met minimum recommendations of physical activity (more than 150 minutes/week) and vegetable and fruit intake. Low/very low income (45.5%) was associated with a lower level of physical activity (p < 0.0001), less fruit and vegetables intake (p < 0.0001), more tobacco use (p < 0.001) and perception of depression (p < 0.001). Low educational level was also associated with the perception of depression (OR 1.46, CI 1.26-1.70; p < 0.01). Conclusions: Patients with cardiometabolic disease but without clinical evidence of COVID-19 showed significant medication non-adherence, especially in secondary prevention patients. Deterioration in lifestyle habits and appearance of depressive symptoms during the pandemic were frequent and related to socioeconomic status.


Assuntos
COVID-19 , Doenças Cardiovasculares/terapia , Depressão/psicologia , Diabetes Mellitus/terapia , Dieta , Dislipidemias/terapia , Exercício Físico , Cooperação e Adesão ao Tratamento/estatística & dados numéricos , Adulto , Idoso , Consumo de Bebidas Alcoólicas/epidemiologia , Arritmias Cardíacas/terapia , Fatores de Risco Cardiometabólico , Fumar Cigarros/epidemiologia , Doença da Artéria Coronariana/terapia , Escolaridade , Feminino , Acessibilidade aos Serviços de Saúde , Insuficiência Cardíaca/terapia , Humanos , Hipertensão/terapia , América Latina/epidemiologia , Masculino , Saúde Mental , Pessoa de Meia-Idade , Pacientes Ambulatoriais , Doenças Vasculares Periféricas/terapia , SARS-CoV-2 , Prevenção Secundária , Classe Social , Inquéritos e Questionários
2.
JAMA Cardiol ; 3(8): 749-753, 2018 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-29898218

RESUMO

Importance: Recent studies have shown that Friedewald underestimates low-density lipoprotein cholesterol (LDL-C) at lower levels, which could result in undertreatment of high-risk patients. A novel method (Martin/Hopkins) using a patient-specific conversion factor provides more accurate LDL-C levels. However, this method has not been tested in proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor-treated patients. Objective: To investigate accuracy of 2 different methods for estimating LDL-C levels (Martin/Hopkins and Friedewald) compared with gold standard preparative ultracentrifugation (PUC) in patients with low LDL-C levels in the Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Patients With Elevated Risk (FOURIER) trial. Design, Setting, and Participants: The FOURIER trial was a randomized clinical trial of evolocumab vs placebo added to statin therapy in 27 564 patients with stable atherosclerotic cardiovascular disease. The patients' LDL-C levels were assessed at baseline, 4 weeks, 12 weeks, 24 weeks, and every 24 weeks thereafter, and measured directly by PUC when the level was less than 40 mg/dL per the Friedewald method (calculated as non-HDL-C level - triglycerides/5). In the Martin/Hopkins method, patient-specific ratios of triglycerides to very low-density lipoprotein cholesterol (VLDL-C) ratios were determined and used to estimate VLDL-C, which was subtracted from the non-HDL-C level to obtain the LDL-C level. Main Outcomes and Measures: Low-density lipoprotein cholesterol calculated by the Friedewald and Martin/Hopkins methods, with PUC as the reference method. Results: For this analysis, the mean (SD) age was 62.7 (9.0) years; 2885 of the 12 742 patients were women (22.6%). A total of 56 624 observations from 12 742 patients had Friedewald, Martin/Hopkins, and PUC LDL-C measurements. The median difference from PUC LDL-C levels for Martin/Hopkins LDL-C levels was -2 mg/dL (interquartile range [IQR], -4 to 1 mg/dL) and for Friedewald LDL-C levels was -4 mg/dL (IQR, -8 to -1 mg/dL; P < .001). Overall, 22.9% of Martin/Hopkins LDL-C values were more than 5 mg/dL different than PUC values, and 2.6% were more than 10 mg/dL different than PUC levels. These were significantly less than respective proportions with Friedewald estimation (40.1% and 13.3%; P < .001), mainly because of underestimation by the Friedewald method. The correlation with PUC LDL-C was significantly higher for Martin/Hopkins vs Friedewald (ρ, 0.918 [95% CI 0.916-0.919] vs ρ, 0.867 [0.865-0.869], P < .001). Conclusions and Relevance: In patients achieving low LDL-C with PCSK9 inhibition, the Martin/Hopkins method for LDL-C estimation more closely approximates gold standard PUC than Friedewald estimation does. The Martin/Hopkins method may prevent undertreatment because of LDL-C underestimation by the Friedewald method. Trial Registration: ClinicalTrials.gov Identifier: NCT01764633.


Assuntos
Aterosclerose/sangue , LDL-Colesterol/análise , Hiperlipidemias/sangue , Estatística como Assunto/métodos , Ultracentrifugação/métodos , Idoso , Anticorpos Monoclonais/uso terapêutico , Anticorpos Monoclonais Humanizados , Anticolesterolemiantes/uso terapêutico , Aterosclerose/tratamento farmacológico , HDL-Colesterol/análise , HDL-Colesterol/sangue , LDL-Colesterol/sangue , VLDL-Colesterol/análise , VLDL-Colesterol/sangue , Feminino , Humanos , Hiperlipidemias/tratamento farmacológico , Masculino , Pessoa de Meia-Idade , Ensaios Clínicos Controlados Aleatórios como Assunto , Medição de Risco , Triglicerídeos/análise , Triglicerídeos/sangue
3.
Int J Cardiol ; 221: 581-6, 2016 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-27420583

RESUMO

Atherosclerotic cardiovascular disease is the leading cause of death worldwide. Despite extraordinary advances in the understanding of the pathophysiology and the utilization of very effective medications such as statins, there still remains a significant residual risk. In fact, even after optimal interventional and medical therapy, the possibility of recurrent myocardial infarction remains at approximately one third for five years after acute coronary syndromes, thus emphasizing the urgent need for novel therapies to prevent the progress of atherosclerosis. In addition, over the past two decades, although atherosclerosis has been clearly identified as an inflammatory disease of the arterial wall from compelling data of animal and human studies, clinical applications related to this accumulated knowledge are scarce. This review presents a brief description of the role of inflammation in atherogenesis, and examines selected potential anti-inflammatory interventions that are being tested in on-going clinical trials which have been designed to prevent adverse cardiovascular events as well as provide a proof of concept regarding the inflammatory hypothesis of atherosclerosis.


Assuntos
Anti-Inflamatórios/uso terapêutico , Doença da Artéria Coronariana , Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico , Inflamação , Animais , Doença da Artéria Coronariana/fisiopatologia , Doença da Artéria Coronariana/prevenção & controle , Humanos , Inflamação/sangue , Inflamação/tratamento farmacológico , Mediadores da Inflamação/sangue , Conduta do Tratamento Medicamentoso/tendências
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