Myocardial infarction patients referred to the primary care physician after 1­year treatment according to a guideline-based protocol have a good prognosis.

INTRODUCTION: Identifying ST-elevation myocardial infarction (STEMI) patients who can be referred back to the general practitioner (GP) can improve patient-tailored care. However, the long-term prognosis of patients who are returned to the care of their GP is unknown. Therefore, the aim of this study was to assess the long-term prognosis of patients referred back to the GP after treatment in accordance with a 1-year institutional guideline-based protocol. METHODS: All consecutive patients treated between February 2004 up to May 2013 who completed the 1­year institutional MISSION! Myocardial Infarction (MI) follow-up and who were referred to the GP were evaluated. After 1 year of protocolised monitoring, asymptomatic patients with a left ventricular ejection fraction >45% on echocardiography were referred to the GP. Long-term prognosis was assessed with Kaplan-Meier curves and Cox proportional hazards analysis was used to identify independent predictors for 5­year all-cause mortality and major adverse cardiovascular events (MACE). RESULTS: In total, 922 STEMI patients were included in this study. Mean age was 61.6 ± 11.7 years and 74.4% were male. Median follow-up duration after the 1­year MISSION! MI follow-up was 4.55 years (interquartile range [IQR] 2.28-5.00). The event-free survival was 93.2%. After multivariable analysis, age, not using an angiotensin-converting enzyme (ACE) inhibitor/angiotensin-II (AT2) antagonist and impaired left ventricular function remained statistically significant predictors for 5­year all-cause mortality. Kaplan-Meier curves revealed that 80.3% remained event-free for MACE after 5 years. Multivariable predictors for MACE were current smoking and a mitral regurgitation grade ≥2. CONCLUSION: STEMI patients who are referred back to their GP have an excellent prognosis after being treated according to the 1­year institutional MISSION! MI protocol.

Pathophysiology and treatment of atherosclerosis : Current view and future perspective on lipoprotein modification treatment.

Recent years have brought a significant amount of new results in the field of atherosclerosis. A better understanding of the role of different lipoprotein particles in the formation of atherosclerotic plaques is now possible. Recent cardiovascular clinical trials have also shed more light upon the efficacy and safety of novel compounds targeting the main pathways of atherosclerosis and its cardiovascular complications.In this review, we first provide a background consisting of the current understanding of the pathophysiology and treatment of atherosclerotic disease, followed by our future perspectives on several novel classes of drugs that target atherosclerosis. The focus of this update is on the pathophysiology and medical interventions of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG) and lipoprotein(a) (Lp(a)).

Determinants of calcification growth in atherosclerotic carotid arteries; a serial multi-detector CT angiography study.

BACKGROUND: Little is known about the natural course of atherosclerotic plaque in the carotid artery bifurcation. This study investigated the growth pattern of calcifications in atherosclerotic carotid arteries and its determinants using serial multi-detector CT angiography (MDCTA). METHODS: From a cohort of consecutive patients with TIA or ischemic stroke and a baseline MCDTA scan of the carotid arteries, subjects were invited for a follow-up scan after 4-6 years. Calcification volumes were scored semi-automatically on baseline and follow-up scans. Progression of calcification and its determinants were analyzed in two ways: 1. as incidence of newly detectable calcification in patients free of calcification at baseline, using logistic regression analysis; 2. as annual change in calcification volume in all patients, using linear regression analysis. RESULTS: Two-hundred-twenty-two patients (aged 61.0 ± 9.6 years, follow-up time 4.7 ± 0.8 years) were included. Calcification volumes increased significantly (median 2.9 mm³ at baseline versus 9.4 mm³ at follow-up, p < 0.001). Newly detectable calcification during follow-up was found in 27 out of 67 patients without baseline calcification (40.3%) and was independently associated with age (OR 4.6 per 10 years increase in age, p < 0.001) and hypertension (OR 8.2, p = 0.008). Annual calcification growth was independently associated with age, calcification load, glucose, hypertension, and smoking. Baseline calcification load was the most important risk factor for calcification growth in multivariable analysis. CONCLUSION: Several modifiable cardiovascular risk factors are associated with carotid calcification growth, however, time and baseline calcification load remain the most important determinants of calcification development.