Role of vasodilators in the changing phases of acute myocardial infarction. 1982

H J Swan, and P K Shah, and S Rubin

Application of vasodilators in evolving myocardial infarction has not yet received wide acceptance. Heretofore, clinical trials of a variety of vasodilator agents have been conducted without regard to the phase of the disease with its changing pathologic features and altering cardiac function. A classification of these phases based on the underlying myocardial disease--ischemia, necrosis, compensation, and healing--may allow a more rational interpretation of the available information. At present, vasodilators are not recommended during the ischemic phase, although some evidence suggests that preload modification by use of nitroglycerin may be beneficial in certain instances. Vasodilator drugs productive of arterial impedance reduction are probably of the greatest value late in the necrotic phase and in the compensation and healing phases. It is in these circumstances that heart failure becomes clinically manifest and maximal short-term efficacy of this intervention can be achieved. Impedance reduction, using agents such as sodium nitroprusside, will cause a prompt improvement manifested by a reduction in left ventricular filling pressure and in pulmonary congesting pressure and an increase in cardiac output. A significant improvement in short-term survival, at least, should be expected by judicious use of vasodilators.

UI MeSH Term Description Entries
D007511 Ischemia A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION. Ischemias
D009203 Myocardial Infarction NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION). Cardiovascular Stroke,Heart Attack,Myocardial Infarct,Cardiovascular Strokes,Heart Attacks,Infarct, Myocardial,Infarction, Myocardial,Infarctions, Myocardial,Infarcts, Myocardial,Myocardial Infarctions,Myocardial Infarcts,Stroke, Cardiovascular,Strokes, Cardiovascular
D009336 Necrosis The death of cells in an organ or tissue due to disease, injury or failure of the blood supply.
D009599 Nitroprusside A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins. Nitroferricyanide,Sodium Nitroprusside,Cyanonitrosylferrate,Ketostix,Naniprus,Nipride,Nipruton,Nitriate,Nitropress,Nitroprussiat Fides,Nitroprusside, Disodium Salt,Nitroprusside, Disodium Salt, Dihydrate,Disodium Salt Nitroprusside,Nitroprusside, Sodium
D002302 Cardiac Output The volume of BLOOD passing through the HEART per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with STROKE VOLUME (volume per beat). Cardiac Outputs,Output, Cardiac,Outputs, Cardiac
D005996 Nitroglycerin A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives. Glyceryl Trinitrate,Anginine,Dynamite,Gilustenon,Nitrangin,Nitro-Bid,Nitro-Dur,Nitrocard,Nitroderm,Nitroderm TTS,Nitroglyn,Nitrol,Nitrolan,Nitrong,Nitrospan,Nitrostat,Perlinganit,Susadrin,Sustac,Sustak,Sustonit,Transderm Nitro,Tridil,Trinitrin,Trinitrolong,Nitro Bid,Nitro Dur,NitroBid,NitroDur,Trinitrate, Glyceryl
D006322 Heart Aneurysm A localized bulging or dilatation in the muscle wall of a heart (MYOCARDIUM), usually in the LEFT VENTRICLE. Blood-filled aneurysms are dangerous because they may burst. Fibrous aneurysms interfere with the heart function through the loss of contractility. True aneurysm is bound by the vessel wall or cardiac wall. False aneurysms are HEMATOMA caused by myocardial rupture. Cardiac Aneurysm,Aneurysm, Cardiac,Aneurysm, Heart,Aneurysms, Cardiac,Aneurysms, Heart,Cardiac Aneurysms,Heart Aneurysms
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000787 Angina Pectoris The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION. Angor Pectoris,Stenocardia,Stenocardias
D013318 Stroke Volume The amount of BLOOD pumped out of the HEART per beat, not to be confused with cardiac output (volume/time). It is calculated as the difference between the end-diastolic volume and the end-systolic volume. Ventricular Ejection Fraction,Ventricular End-Diastolic Volume,Ventricular End-Systolic Volume,Ejection Fraction, Ventricular,Ejection Fractions, Ventricular,End-Diastolic Volume, Ventricular,End-Diastolic Volumes, Ventricular,End-Systolic Volume, Ventricular,End-Systolic Volumes, Ventricular,Fraction, Ventricular Ejection,Fractions, Ventricular Ejection,Stroke Volumes,Ventricular Ejection Fractions,Ventricular End Diastolic Volume,Ventricular End Systolic Volume,Ventricular End-Diastolic Volumes,Ventricular End-Systolic Volumes,Volume, Stroke,Volume, Ventricular End-Diastolic,Volume, Ventricular End-Systolic,Volumes, Stroke,Volumes, Ventricular End-Diastolic,Volumes, Ventricular End-Systolic

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