332 Correlation between wall thickening and quantitative perfusion changes during dobutamine echocardiography and MIBI-SPECT early after myocardial infarction

Myocardial infarction (MI) is the leading cause of morbidity and mortality in the world. The infarcted heart displays typical cell death cascades characterized by a loss of cells and fibrotic scarring in the myocardium. Cardiac hypertrophy and fibrosis largely contribute to ventricular wall thickening and stiffening, altogether defining an adverse cardiac remodeling that ultimately leads to impaired cardiac function and subsequent heart failure. Finding a strategy to promote therapeutic, instead of detrimental, cardiac remodeling may pose as a potent MI treatment. Accumulating evidence shows that microRNAs (miRNAs) may play an essential role in cardiovascular diseases. In particular, microRNA-133a (miR-133a) is one of the most abundant miRNAs in the heart. Multiple studies have demonstrated that miR-133a participates in the early pathology of MI, as well as in subsequent cardiac remodeling. In this review, we summarize recent research progress highlighting the regulatory effects of miR-133a in ischemic myocardial diseases, such as inhibiting angiogenesis, apoptosis, fibrosis, hypertrophy, and inflammation, while promoting therapeutic cardiac remodeling. The goal is to elicit a critical discussion on the translational direction of miRNA-mediated treatments towards a safe and effective MI therapy.

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Syphilitic Coronary Artery Ostial Stenosis Resulting in Acute Myocardial Infarction Treated by Percutaneous Coronary Intervention

Case Reports in Medicine ◽

10.1155/2010/830583 ◽

2010 ◽

Vol 2010 ◽

pp. 1-4 ◽

Cited By ~ 5

Author(s):

Marcelo A. Nakazone ◽

Maurício N. Machado ◽

Raphael B. Barbosa ◽

Márcio A. Santos ◽

Lilia N. Maia

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Percutaneous Coronary Intervention ◽

Coronary Artery ◽

Case Reports ◽

Coronary Intervention ◽

Wall Thickening ◽

Percutaneous Coronary ◽

St Elevation ◽

Ostial Lesion

Cardiovascular abnormalities are well-known manifestations of tertiary syphilis infections which although not frequent, are still causes of morbidity and mortality. A less common manifestation of syphilitic aortitis is coronary artery ostial narrowing related to aortic wall thickening. We report a case of a 46-year-old male admitted due to acute anterior ST elevation myocardial infarction submitted to primary percutaneous coronary intervention successfully. Coronary angiography showed a suboccluded ostial lesion of left main coronary artery. VDRL was titrated to 1/512. The patient was discharged with treatment including benzathine penicillin. Previous case reports of acute myocardial infarction in association with syphilitic coronary artery ostial stenosis have been reported, but the fact that the patient was treated by percutaneous coronary intervention is unique in this case.

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Late preconditioning enhances recovery of myocardial function after infarction in conscious rabbits

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.279.5.h2372 ◽

2000 ◽

Vol 279 (5) ◽

pp. H2372-H2381 ◽

Cited By ~ 6

Author(s):

Hitoshi Takano ◽

Xian-Liang Tang ◽

Eitaro Kodani ◽

Roberto Bolli

Keyword(s):

Myocardial Infarction ◽

Infarct Size ◽

Left Ventricular ◽

Nitric Oxide Donor ◽

Lv Function ◽

Wall Thickening ◽

Triphenyltetrazolium Chloride ◽

Independent Evidence ◽

Late Preconditioning ◽

Conscious Rabbits

It is unknown whether late preconditioning (PC) enhances the recovery of left ventricular (LV) function after a myocardial infarction. Thus 25 conscious rabbits were subjected to a 30-min coronary occlusion followed by 28 days of reperfusion after PC 24 h earlier with either ischemia or nitric oxide donor administration [ S-nitroso- N-acetylpenicillamine (SNAP)]. The recovery of wall thickening (WTh) after reperfusion was significantly improved in the ischemic PC and SNAP PC groups compared with controls, both at rest and during dobutamine stress. Interestingly, neither ischemia- nor SNAP-induced late PC attenuated myocardial stunning from day 1 through day 14. Infarct size was smaller in the ischemic PC and SNAP PC groups compared with controls. In all groups, WTh at 28 days was positively and linearly related to the percentage of viable tissue in the region underlying the ultrasonic crystal ( r = 0.90), indicating that the improvement in LV function after both ischemia-induced and NO donor-induced late PC can be fully explained by the reduction in infarct size; a separate effect of late PC on LV remodeling or LV contractility need not be invoked. In conclusion, in conscious rabbits late PC, induced either by ischemia or pharmacologically, not only limits infarct size but also enhances the recovery of LV function after myocardial infarction. This finding has important clinical implications and provides triphenyltetrazolium chloride-independent evidence that late PC limits myocellular death after sustained ischemia.

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