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Heart Fail Rev ; 2019 Aug 08.
Artigo em Inglês | MEDLINE | ID: mdl-31396762


Meta-analysis on immunohistological (IHC) concepts for the detection of inflammatory cardiomyopathy (InfCM) in endomyocardial biopsies (EMB). We included 61 publications, with 10,491 patients (mean age 47.1 years; men 66%) who underwent EMB and IHC evaluation. The 460 control patients were devoid of IHC proof of InfCM. The mean IHC detection rate of InfCM was 50.8% (95% CI 47.7-53.8%; range 18.4-91.7%). A publication bias was excluded (Funnel Plot p = 0.4264). This IHC detection rate was significantly (p < 0.0001) higher compared to the histological detection of myocarditis according to the Dallas criteria (mean 8.04%; 95% CI 5.08-12.5%; subset of 3274 patients in 30 publications). However, 13 different diagnostic IHC criteria were described in the publications, with various thresholds of diverse phenotypes of quantified infiltrates, and endothelial expression of diverse cell adhesion molecules (CAM), quantified either visually or by digital image analysis (DIA). The comparison of IHC with cardiac magnetic resonance (CMR) data available in a subset of 13 publications with 1185 patients revealed a sensitivity for CMR of 69% (95% CI 58-79%), a specificity of 73% (95% CI 59-84%), and a ROC-AUC of 0.77 (95% CI 0.73-0.81). This meta-analysis encompassing 10,491 patients confirms a mean detection rate of InfCM in 50.8% of EMB, being significantly more sensitive compared to the histological Dallas criteria. IHC cannot be fully substituted by CMR. However, standardization of the diverse IHC markers and protocols seems pertinent, especially considering the published adverse prognostic impact of IHC-confirmed InfCM and its published suitability for the selection of candidates responding favorably to immunosuppression.

Curr Cardiol Rep ; 21(8): 69, 2019 Jun 21.
Artigo em Inglês | MEDLINE | ID: mdl-31227914


PURPOSE OF REVIEW: Low-density lipoprotein cholesterol (LDL-C) is one major cause of cardiovascular disease (CVD). In this review, we discuss current developments in the understanding of LDL-C as lifelong risk factor, treatment targets, and emerging approaches to reduce cardiovascular risk by lowering LDL-C. RECENT FINDINGS: Recent evidence underscores the importance of LDL-C lowering in CVD prevention by mechanisms that increase the hepatic clearance of apolipoprotein B-containing lipoproteins from the plasma. Mendelian randomization studies provided evidence on both safety and efficacy of lower LDL-C in the long term. For young individuals, metrics other than 10-year CVD risk are required. Despite this evidence, LDL-C treatment target attainment is poor. Novel approaches are therefore needed. These include individualized strategies and new LDL-C-lowering pharmaceuticals. Early, long-term treatment with LDL-C-lowering therapies has the potential to markedly reduce CVD incidence and progression. Future research should aim to identify patient characteristics that enable physicians to tailor therapy to each individual patient.