Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review introduces recent progress in molecular genetics of cardiovascular diseases. Many genes and their mutations causing familial cardiovascular diseases have been discovered, including familial hypertrophic cardiomyopathy which is caused by mutated cardiac beta myosin heavy chain, light chains, troponin T, troponin I, or alpha-tropomyosin, and long QT syndrome by KvLQT1, HERG, minK or cardiac voltage-dependent Na channel mutation. The mutations in causative genes can affect clinical courses of diseases; amino acid substitutions of cardiac beta myosin heavy chain with charge changes seem to cause poorer prognosis of hypertrophic cardiomyopathy. Besides monogenic diseases, there are many cardiovascular diseases affected with genetic polymorphisms, such as hypertension, ischemic heart disease and atherosclerosis. Specific amino acid mutations or polymorphisms in the promoter region of the genes are known to become a risk factor of these diseases. Polymorphisms of genes encoding apolipoprotein E, angiotensin converting enzyme, angiotensinogen and endothelial NO synthase (ecNOS) have been well characterized as an important risk factor of cardiovascular diseases. We recently found a novel gene which seems to affect human aging phenotype and vascular endothelial function. It is important as a future study to clarify the regulatory mechanisms of the klotho gene in the cardiovascular system and the clinical significance of klotho gene polymorphisms.
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PMID:[Molecular genetics of cardiovascular diseases]. 956 64

Delayed rectifier K+ current (IK) is the major outward current responsible for ventricular repolarization. Two components of IK (IKr and IKs) have been identified in many mammalian species including humans. IKr plays a pivotal role in normal ventricular repolarization. A prolongation of action potential duration (APD) under a variety of conditions would favor the activation of IKs so that to prevent excessive repolarization delay causing early afterdepolarization. The pore-forming a subunits of IKr and IKs are composed of HERG (KCNH2) and KvLQT1 (KCNQ1), respectively. KvLQT1 is associated with a function-altering beta subunit, minK to form IKs. HERG may be associated with mink (KCNE1) and/or minK-related protein (MiRP1) to form IKr, but the issue remains to be established. IKs is enhanced, whereas IKr is usually attenuated by beta-adrenergic stimulation via cyclic adenosine 3',5'-monophosphate (cAMP)/protein kinase A-dependent pathways. There exist regional differences in the density of IKr and IKs transmurally (endo-epicardial) and along the apico-basal axis, contributing to the spatial heterogeneity of ventricular repolarization. A decrease of IKr or IKs by mutations in either HERG, KvLQT1, or KCNE family results in inherited long QT syndrome (LQTS) with high risk for Torsades de pointes (TdP)-type polymorphic ventricular tachycardia and ventricular fibrillation. As to the pharmacological treatment and prevention of ventricular tachyarrhythmias, selectively block of IKs is expected to be more beneficial than selectively block of IKr in terms of homogeneous prolongation of refractoriness at high heart rates especially in diseased hearts including myocardial ischemia.
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PMID:Two components of delayed rectifier K+ current in heart: molecular basis, functional diversity, and contribution to repolarization. 1476 99

Bromocriptine-induced coronary spasm (BICS) causing myocardial infarction has been reported. Association between BICS and Takotsubo syndrome (TS) has not been described. We report on a 37-year-old woman presenting with a clinical picture of acute coronary syndrome 1 day after initiation of treatment with bromocriptine for ablactation 3 weeks after a full-term spontaneous vaginal delivery. Coronary angiography showed diffuse narrowing of a large diagonal branch. Left ventriculography showed widespread hypokinesia extending beyond the diagonal branch supply region. There was a slight elevation of myocardial infarction biomarkers that was disproportional to the degree of left ventricular dysfunction. Follow-up coronary angiography, intravascular ultrasound and left ventriculography showed normal coronary arteries including the diagonal branch and complete normalization of the left ventricular function. Cardiac magnetic resonance examination showed no signs of late myocardial gadolinium enhancement. The clinical picture and course of the disease was consistent with TS. Consequently, we describe for the first time a case of TS triggered by myocardial ischemia caused by BICS. Furthermore, our case and sufficient supporting data from the literature demonstrate that acute coronary syndrome is an important and frequent but up till now missed trigger factor for TS.
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PMID:Bromocriptine-induced coronary spasm caused acute coronary syndrome, which triggered its own clinical twin--Takotsubo syndrome. 2175