Coronary-cameral fistulae drained into left ventricle causing acute coronary syndrome?

Coronary-cameral fistulae are rare and predominantly congenital communication between the coronary arterial circulation and the chambers or great vessels of the heart, accounted for less than 0.4% of all congenital heart abnormalities. We presented a case of 47 year-old female with troponin positive acute coronary syndrome admitted to our coronary care unit in whom we diagnosed coronary-cameral fistulae which could cause myocardial ischaemia.     

等位基因特异性引物延伸法在婴儿型和幼儿型神经元蜡样质脂褐质沉积病产前诊断中的应用

Theinfantile (INCL ,NCL1,OMIM :2 5 6 730 )andlate infantile (LINCL ,NCL2 ,OMIM :2 0 4 5 0 0 )neuronalceroid lipofuscinosis (NCLs)areamongthemostcommonchildhoodlysosomallipid proteindisor ders.Theyarecharacterizedbyrapidlyincreasingseverityofseizures ;dete…     

Role of chronic ryanodine receptor phosphorylation in heart failure and β-adrenergic receptor blockade in mice

Increased sarcoplasmic reticulum (SR) Ca2+ leak via the cardiac ryanodine receptor/calcium release channel (RyR2) is thought to play a role in heart failure (HF) progression. Inhibition of this leak is an emerging therapeutic strategy. To explore the role of chronic PKA phosphorylation of RyR2 in HF pathogenesis and treatment, we generated a knockin mouse with aspartic acid replacing serine 2808 (mice are referred to herein as RyR2-S2808D+/+ mice). This mutation mimics constitutive PKA hyperphosphorylation of RyR2, which causes depletion of the stabilizing subunit FKBP12.6 (also known as calstabin2), resulting in leaky RyR2. RyR2-S2808D+/+ mice developed age-dependent cardiomyopathy, elevated RyR2 oxidation and nitrosylation, reduced SR Ca2+ store content, and increased diastolic SR Ca2+ leak. After myocardial infarction, RyR2-S2808D+/+ mice exhibited increased mortality compared with WT littermates. Treatment with S107, a 1,4-benzothiazepine derivative that stabilizes RyR2-calstabin2 interactions, inhibited the RyR2-mediated diastolic SR Ca2+ leak and reduced HF progression in WT and RyR2-S2808D+/+ mice. In contrast, β-adrenergic receptor blockers improved cardiac function in WT but not in RyR2-S2808D+/+ mice.Thus, chronic PKA hyperphosphorylation of RyR2 results in a diastolic leak that causes cardiac dysfunction. Reversing PKA hyperphosphorylation of RyR2 is an important mechanism underlying the therapeutic action of β-blocker therapy in HF.     

Why does aspirin decrease the risk of venous thromboembolism? On old and novel antithrombotic effects of acetyl salicylic acid

It is well established that aspirin, an irreversible inhibitor of platelet cyclooxygenase activity, is effective in secondary prevention of arterial thromboembolic events. The pooled results of the recent randomized, multicenter WARFASA and ASPIRE aspirin trials showed a 32% reduction in the rate of recurrence of venous thromboembolism (VTE) in patients receiving aspirin following VTE. These clinical data support evidence that platelets contribute to the initiation and progression of venous thrombosis and aspirin inhibits thrombin formation and thrombin‐mediated coagulant reactions. In addition to the known acetylation of serine 529 residue in platelet cyclooxygenase‐1, the postulated mechanisms of aspirin‐induced antithrombotic actions also involve the acetylation of other proteins in blood coagulation, including fibrinogen, resulting in more efficient fibrinolysis. This review summarizes current knowledge on the aspirin‐induced antithrombotic effects that potentially explain clinical studies showing reduced rates of VTE events in aspirin‐treated subjects.