No abstract

Objective Familial hypercholesterolemia (FH) is an important cause of premature coronary artery disease (CAD). Prognosis data are lacking in patients with FH and coronary artery disease particularly in the era of widespread statin use. We compared long-term prognosis between patients with and without FH after a coronary event. Methods In this retrospective study, 865 patients younger than 40 years of age with CAD were enrolled. FH was diagnosed based on the Dutch Lipid Clinic Network algorithm. Baseline characteristics, coronary angiographic findings and prognosis during median follow-up of 5 (3–8) years were compared between patients with or without FH. Results Definite or probable FH was detected in 37 patients (4.3%) and possible FH in 259 patients (29.9%). FH was associated with significantly higher prevalence of multi-vessel lesions ( p < 0.001) and higher Gensini score ( p = 0.008). In the subset of 706 patients for whom follow-up data were available, 127 (18.0%) suffered major adverse cardiovascular and cerebrovascular events (MACCE). FH was associated with increased risk of MACCE, independently of age, sex, smoking, body mass index, hypertension or diabetes mellitus (HR = 2.30, 95%CI = 1.09 to 4.84, p = 0.028). Conclusions FH is an independent risk factor for MACCE in young patients after a coronary event during long-term follow-up. It is necessary to optimize lipid treatment of patients with FH after a coronary event.

Abstract.To investigate the effects of cellular membrane connexin 43 (Cx43) and the potential details in ischemic postconditioning (IPOC)-induced cardioprotection, ischemia/reperfusion (IR) models were generated in 8-week-old male Sprague-Dawley rats by ligating the left coronary artery anterior descending branch. The serum levels of myocardial creatases, nitric oxide (NO) and malondialdehyde (MDA) levels, infarct size, arrhythmia events, expression and distribution of Cx43, ultrastructure and apoptosis in the myocardium in different treatments with IR, IR + IPOC, IR + diazoxide or IR + IPOC + 5-hydroxydecanoate acid (5-HD) were investigated. Consequently, IPOC decreased infarct size (10.9 vs. 43.3%, P<0.01) and the levels of myocardial creatases, NO and MDA, and improved the expression (16.8 vs. 25.2% and 6.4 vs. 32.8%, after 1-and 3-h reperfusion, respectively; P<0.01) and distribution of Cx43, ultrastructure and apoptosis (19.2 vs. 42.9%, P<0.01) significantly. Diazoxide partly simulated the effects, and 5-HD attenuated but not completely abolished the effects of IPOC. In addition, the phosphorylated Cx43 (p-Cx43) level in the IR + IPOC group was lower than that in the IR + diazoxide group after 1-h reperfusion (26.1 vs. 29.4%, P>0.05); however, it was reversed after 3-h reperfusion and the p-Cx43 level in the IR + IPOC group was significantly higher than that in the IR + diazoxide group (32.8 vs. 18.7%, P<0.01). In conclusion, cell membrane Cx43 is also involved in the process of IPOC-induced cardioprotection and the improvement of membrane Cx43 is more dependent on mitochondrial K ATP in the earlier phase of IPOC compared to the late phase of IPOC.