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1. 冠動脈の心筋架橋 myocardial bridging of the coronary arteries
2. ST上昇型心筋梗塞後の有害転帰の危険因子 risk factors for adverse outcomes after st elevation myocardial infarction
3. 無症候性心筋虚血：予後および治療 silent myocardial ischemia prognosis and therapy
4. 心筋梗塞または不安定狭心症の予後における心電図 electrocardiogram in the prognosis of myocardial infarction or unstable angina
5. ST上昇型心筋梗塞の急性期マネージメントの概要 overview of the acute management of st elevation myocardial infarction

Mitochondrial aldehyde dehydrogenase obliterates endoplasmic reticulum stress-induced cardiac contractile dysfunction via correction of autophagy.

Zhang B, Zhang Y, La Cour KH, Richmond KL, Wang XM, Ren J.SourceDepartment of Geriatrics, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, PR China.
Biochimica et biophysica acta.Biochim Biophys Acta.2013 Apr;1832(4):574-84. doi: 10.1016/j.bbadis.2013.01.013. Epub 2013 Jan 23.
ER stress triggers myocardial contractile dysfunction while effective therapeutic regimen is still lacking. Mitochondrial aldehyde dehydrogenase (ALDH2), an essential mitochondrial enzyme governing mitochondrial and cardiac function, displays distinct beneficial effect on the heart. This study was d
PMID 23354068

The independent relationship of epicardial adipose tissue with carotid intima-media thickness and endothelial functions: the association of pulse wave velocity with the active facilitated arterial conduction concept.

Kocaman SA, Durakoğlugil ME, Cetin M, Erdoğan T, Ergül E, Canga A.SourceaDepartment of Cardiology, Rize Education and Research Hospital bDepartment of Cardiology, Faculty of Medicine, Rize University, Rize, Turkey.
Blood pressure monitoring.Blood Press Monit.2013 Apr;18(2):85-93. doi: 10.1097/MBP.0b013e32835ebbb5.
BACKGROUND: Hypertension, identifiable by elevated blood pressure (BP), is a heterogeneous multifactorial disorder. Epicardial adipose tissue (EAT), a special fat depot that is related to visceral fat rather than total adiposity, shares the same microcirculation with myocardial tissue and coronary v
PMID 23388404

Elevated rates of force development and MgATP binding in F764L and S532P myosin mutations causing dilated cardiomyopathy.

Palmer BM, Schmitt JP, Seidman CE, Seidman JG, Wang Y, Bell SP, Lewinter MM, Maughan DW.SourceDepartment of Molecular Physiology and Biophysics, University of Vermont, Burlington, VT 05405, USA. Electronic address: bmpalmer@uvm.edu.
Journal of molecular and cellular cardiology.J Mol Cell Cardiol.2013 Apr;57:23-31. doi: 10.1016/j.yjmcc.2012.12.022. Epub 2013 Jan 8.
Dilated cardiomyopathy (DCM) is a disease characterized by dilation of the ventricular chambers and reduced contractile function. We examined the contractile performance of chemically-skinned ventricular strips from two heterozygous murine models of DCM-causing missense mutations of myosin, F764L/+
PMID 23313350