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Acute myocardial infarction (MI) and its sequelae are leading causes of morbidity and mortality worldwide. Nitroglycerin (glyceryl trinitrate [GTN]) remains a first-line treatment for angina pectoris and acute MI. Nitroglycerin achieves its benefit by giving rise to nitric oxide (NO), which causes vasodilation and increases blood flow to the myocardium. However, continuous delivery of GTN results in tolerance, limiting the use of this drug. Nitroglycerin tolerance is caused, at least in part, by inactivation of aldehyde dehydrogenase 2 (ALDH2), an enzyme that converts GTN to the vasodilator, NO. We recently found that in a MI model in animals, in addition to GTN's effect on the vasculature, sustained treatment negatively affected cardiomyocyte viability following ischemia, thus resulting in increased infarct size. Coadministration of Alda-1, an activator of ALDH2, with GTN improves metabolism of reactive aldehyde adducts and prevents the GTN-induced increase in cardiac dysfunction following MI. In this review, we describe the molecular mechanisms associated with the benefits and risks of GTN administration in MI.
Department of Chemical and Systems Biology, Stanford University School of Medicine.
This article was published in the following journal.
Name: Circulation journal : official journal of the Japanese Circulation Society
To identify patients with type 2 myocardial infarction (MI) and patients with non-ischaemic myocardial injury (NIMI) and to compare their prognosis with those of patients with type 1 MI.
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The purpose of this study is to quantify the risk of hypotension due to field treatment with nitroglycerin in patients with ST-elevation myocardial infarction, particularly right ventricul...
Prospective cohort evaluating patients in the State of Santa Catarina (Brazil) with the diagnosis of the first acute myocardial infarction from July 2016 until December 2020.
The study is an open, single center, observational study at the Cardiology Dept at Uppsala University Hospital. The number of patients included will be 410. The objectives are to: Evaluat...
This is a multicenter retrospective observational study with STEMI (ST Elevation Myocardial Infarction) patients who have been treated in the northern Galician Hospitals. The study tries t...
Recent clinical studies have shown that systemic therapeutic hypothermia improving the outcomes in patients with ST segment elevated myocardial infarction (STEMI) received primary percutan...
MYOCARDIAL INFARCTION in which the anterior wall of the heart is involved. Anterior wall myocardial infarction is often caused by occlusion of the left anterior descending coronary artery. It can be categorized as anteroseptal or anterolateral wall myocardial infarction.
A myocardial infarction that does not produce elevations in the ST segments of the ELECTROCARDIOGRAM. ST segment elevation of the ECG is often used in determining the treatment protocol (see also ST Elevation Myocardial Infarction).
A clinical syndrome defined by MYOCARDIAL ISCHEMIA symptoms; persistent elevation in the ST segments of the ELECTROCARDIOGRAM; and release of BIOMARKERS of myocardial NECROSIS (e.g., elevated TROPONIN levels). ST segment elevation in the ECG is often used in determining the treatment protocol (see also NON-ST ELEVATION MYOCARDIAL INFARCTION).
MYOCARDIAL INFARCTION in which the inferior wall of the heart is involved. It is often caused by occlusion of the right coronary artery.
A phenylethylamine derivative that acts as a calcium antagonist showing hemodynamic effects in patients with acute myocardial infarction.
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