Early treatment of patients with acute coronary syndromes (ACS) is crucial to reduce morbidity and mortality. The purpose of this study was to examine delay in seeking care for ACS symptoms in a Lebanese sample and identify predictors of delay. Medical record reviews and interviews using the Response to Symptoms Questionnaire were conducted with 204 ACS patients in coronary care within 72 hours of admission. Median time from symptom onset to hospital arrival was 4.5 hours. Higher education, presence of dyspnea, intermittent symptoms, and waiting for symptoms to go away predicted longer delays, whereas intensity of symptoms and active response (going to the hospital) predicted shorter delays. The findings suggest lack of knowledge of ACS symptoms and the need for public education in this regard.
The locus identified in this study for familial dilated cardiomyopathy, 1q32, is rich in candidate genes, such as MEF-2, renin, and helix loop helix DNA binding protein MYF-4. Identification of the genetic defect could provide insight into the molecular basis for the cardiac dilatory response in both familial and acquired disorders.
The manifestation of coronary artery disease (CAD) follows a well-choreographed series of events that includes damage of arterial endothelial cells and deposition of lipids in the sub-endothelial layers. Genome-wide association studies (GWAS) of multiple populations with distinctive genetic and lifestyle backgrounds are a crucial step in understanding global CAD pathophysiology. In this study, we report a GWAS on the genetic basis of arterial stenosis as measured by cardiac catheterization in a Lebanese population. The locus of the phosphatase and actin regulator 1 gene (PHACTR1) showed association with coronary stenosis in a discovery experiment with genome wide data in 1,949 individuals (rs9349379, OR = 1.37, p = 1.57×10−5). The association was replicated in an additional 2,547 individuals (OR = 1.31, p = 8.85×10−6), leading to genome-wide significant association in a combined analysis (OR = 1.34, p = 8.02×10−10). Results from this GWAS support a central role of PHACTR1 in CAD susceptibility irrespective of lifestyle and ethnic divergences. This association provides a plausible component for understanding molecular mechanisms involved in the formation of stenosis in cardiac vessels and a potential drug target against CAD.
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