Turk Kardiyoloji Dernegi Arsivi-Archives of the Turkish Society of Cardiology最新文献

Objective: MicroRNAs have been explored as potential biomarkers for many pathological processes including coronary artery disease. In this study, we aimed to compare the circulating levels of selected atherosclerosis-associated miRNAs in patients with a history of early-onset coronary artery disease with that of age- and sex-matched healthy controls and older patients with late-onset coronary artery disease.

Methods: Study population consisted of 30 patients with early onset coronary artery disease, 31 age- and sex-matched healthy controls, and 30 patients with late-onset coronary artery disease. Plasma levels of 13 microRNAs (endothelial cell-related miR-126, -92a/b; vascular smooth muscle cell-related miR-145; inflammation-related miR-16, -21, -125b, -146a/b, -147b, -150, -155; lipometabolism-related miR-27b, -122, -370) were evaluated by using real-time polymerase chain reaction.

Results: In patients with early onset coronary artery disease, plasma expressions of the lipometabolism-related miR-27b, miR-122; inflammation-related miR-125b, miR-146a/b, miR-147b, miR-150, miR-155; and VSMC-related miR-145 were significantly downregulated and endothelial cell-related miR-126 was significantly upregulated compared to age- and sexmatched healthy controls. Circulating microRNA profile of patients with early onset coronary artery disease was also different from that of older patients with late-onset coronary artery disease. Plasma levels of miR-21, miR-27b, miR-122, miR-125b, miR-146b, miR-147b, and miR-155 were lower and plasma levels of miR-16 and miR-92a were higher in patients with early onset coronary artery disease compared to older patients with late-onset coronary artery disease.

Conclusion: MicroRNAs are promising biomarkers for early onset coronary artery disease.

Heart failure (HF) has been classified as reduced ejection fraction (HFrEF), mildly reduced ejection fraction (HFmrEF) and preserved ejection fraction (HFpEF) by the recent HF guidelines. In addition, HF with improved ejection fraction has been defined as a subgroup of HFrEF. In HFrEF, diagnostic workup and evidence-based pharmacological and device-based therapies have been well established. However, HFpEF, which comprises almost half of the HF population, represents significant uncertainties regarding its pathophysiology, clinical phenotypes, diagnosis and treatment. Diagnostic criteria of HFpEF have been changed a few times over the years and still remained a matter of debate. New paradigms including a prominent role of co-morbidities, inflammation, endothelial dysfunction have been proposed in its pathophysiology. As a complex, multifactorial syndrome HFpEF consists of many overlapping clinical and hemodynamic phenotypes. In contrast to HFrEF, clinical outcomes of HFpEF have not improved over the last decades due to lack of proven effective therapies. Although HFrEF and HFpEF have different clinical spectrums and proposed pathophysiological mechanisms, there is no clear defining syndrome postulated for HFmrEF. Clinical characteristics and risk factors of HFmrEF overlap with HFrEF and HFpEF. HFmrEF is also referred as a transitional zone for dynamic temporal changes in EF. So, HFpEF and HFmrEF, both namely HF with non-reduced ejection fraction (HF-NEF), have some challenges in the management of HF. The purpose of this paper is to provide a comprehensive review including epidemiology, pathophysiology, clinical presentation and phenotypes of HF-NEF and to guide clinicians for the diagnosis and therapeutic approaches based on the available data in the literature.