Asunto(s)
Galectina 3/sangre , Antagonistas de Receptores de Mineralocorticoides/farmacología , Infarto del Miocardio/sangre , Infarto del Miocardio/mortalidad , Espironolactona/análogos & derivados , Disfunción Ventricular Izquierda/fisiopatología , Remodelación Ventricular/fisiología , Femenino , Humanos , MasculinoRESUMEN
BACKGROUND: Galectin-3 is a biomarker associated with inflammation and fibrosis that predicts adverse outcome and relates to biomarkers of extracellular matrix turnover in patients with heart failure, particularly when left ventricular (LV) systolic function is preserved. Whether galectin-3 is related to LV remodeling after acute myocardial infarction is unknown. METHODS AND RESULTS: Circulating galectin-3 and various extracellular matrix biomarkers were measured in 100 patients (age, 58.9±12.0 years; 77% men) admitted with acute myocardial infarction and LV dysfunction, at baseline (mean 46 hours) and at 24 weeks, with cardiac MRI at each time-point. LV remodeling was defined as change in LV end-systolic volume index. Relationships among galectin-3, biomarkers, and LV remodeling were analyzed across the entire cohort, then according to median baseline LV ejection fraction. Galectin-3 levels were elevated in 22 patients (22%) at baseline and increased significantly over time from 14.7±5.5 to 16.3±6.6 ng/mL (P=0.007). Baseline galectin-3 did not correlate with any LV parameters at baseline or change in any parameter over time. Galectin-3 was positively associated with remodeling in patients with supramedian baseline LV ejection fraction (ie, >49.2%; r=0.40; P=0.01) but not when LV ejection fraction was ≤49.2%. Galectin-3 correlated significantly with matrix metalloproteinase-3 and monocyte chemoattractant protein-1 at baseline, biomarkers that have been shown to relate to LV remodeling in this cohort. CONCLUSIONS: Galectin-3 correlated significantly with certain biomarkers involved in extracellular matrix turnover, although no definite relationship was identified with LV remodeling. Whether galectin-3 plays a pathological role in remodeling remains unclear but merits further study. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00132093.
Asunto(s)
Galectina 3/sangre , Antagonistas de Receptores de Mineralocorticoides/farmacología , Infarto del Miocardio/sangre , Infarto del Miocardio/mortalidad , Espironolactona/análogos & derivados , Disfunción Ventricular Izquierda/fisiopatología , Remodelación Ventricular/fisiología , Anciano , Eplerenona , Matriz Extracelular/fisiología , Femenino , Galectina 3/fisiología , Humanos , Imagen por Resonancia Magnética , Masculino , Persona de Mediana Edad , Espironolactona/farmacología , Volumen Sistólico , Remodelación Ventricular/efectos de los fármacosRESUMEN
BACKGROUND: Chronic obstructive pulmonary disease (COPD) has been identified as a risk factor for ischaemic heart disease, independent of smoking history, and inflammation is thought to play a role. OBJECTIVES: We sought to ascertain whether occult myocardial infarction (MI) was present in the COPD population, and to assess its relationship with inflammation and natriuretic peptides. METHOD: We recruited 25 patients with moderate/severe COPD and 17 control smokers without lung disease. All participants had no known cardiac disease. Contrast-enhanced cardiac magnetic resonance imaging was performed and analysed for delayed contrast enhancement (DE), indicative of previous MI. All participants had venous blood samples taken for assessment of NT-proBNP and inflammatory markers. RESULTS: DE was not found in any participant. Right ventricular ejection fraction was lower in COPD patients. Other cardiac measurements and NT-proBNP levels were similar in the 2 groups. C-reactive protein, IL-8, GM-CSF, IL-1 beta and TNF-alpha were all significantly higher in the COPD group. CONCLUSION: DE, indicating previous MI, was not found in patients with moderate/severe COPD. Occult MI does not appear to be common in this population, but a larger study would be needed to conclusively test this.
Asunto(s)
Inflamación/complicaciones , Infarto del Miocardio/etiología , Péptido Natriurético Encefálico/sangre , Fragmentos de Péptidos/sangre , Enfermedad Pulmonar Obstructiva Crónica/complicaciones , Anciano , Biomarcadores/sangre , Estudios Transversales , Femenino , Gadolinio DTPA , Humanos , Inflamación/sangre , Imagen por Resonancia Magnética , Masculino , Persona de Mediana Edad , Infarto del Miocardio/sangre , Infarto del Miocardio/diagnóstico , Enfermedad Pulmonar Obstructiva Crónica/sangre , Fumar/efectos adversosRESUMEN
As the variety and range of pharmaceutical agents available to the medical profession continues to expand, one unavoidable effect will be an increase in drug-induced disease, including cardiovascular disorders. However, given the high rates of cardiovascular disease and prevalence of recognised cardiovascular risk factors in the population, it is sometimes impossible to conclusively attribute any individual patients' ill health to one particular drug. As a result, the relationship between drugs and cardiovascular disease is often difficult to quantify. This review discusses specific forms of drug-induced cardiovascular disease such as heart failure, left ventricular systolic dysfunction, hypertension and arrhythmia. Suspected culprit drugs for all disorders are highlighted. Specific attention is given to certain drug groups with a strong association with one or more forms of cardiovascular disease: these include anthracyclines, antipsychotics, NSAIDs and cyclo-oxygenase 2 inhibitors. Additionally, advice is offered on how physicians might distinguish drug-induced cardiovascular disorders from other aetiologies.