Hemodynamic and Metabolic Responses to Vasodilator Therapy in Acute Myocardial Infarction

Hemodynamic effects of vasodilator therapy (phentolamine or nitroprusside) were studied in 38 patients with acute myocardial infarction (AMI). Cardiac metabolism was studied in 19 of the 38 patients. According to the initial level of left ventricular filling pressure (LVFP) and left ventricular stroke work index (SWI), patients were divided into three groups: Group I-nine patients with LVFP 15 mm Hg or less; Group II-14 patients with LVFP > 15 mm Hg and SWI >20 g-m/m2; Group III-15 patients with LVFP > 15 mm Hg and SWI < 20 g-m/ m2. In Group I most patients were clinically uncomplicated. In Group IL most patients had clinical left ventricular failure including one patient who had clinical features of cardiogenic shock. Group III patients all had severe left ventricular failure, with eight patients in clinical shock.In all groups LVFP, pulmonary artery pressure, right atrial pressure, and systemic and pulmonary vascular resistance decreased significantly with vasodilator therapy with only a slight to moderate decrease in arterial pressure. In Group I patients SVI decreased (-7%) together with an increase in heart rate. Significant improvement in left ventricular performance, however, was observed in Groups II and III as indicated by increased stroke volume index (SVI) and cardiac index (CI) and decreased LVFP. The increase in SVI and CI was of similar magnitude in both Group LI (SVI +18%, CI +24%) and Group III (SVI +28%, CI +29%) patients, a change suggesting that vasodilation thereby may be applicable and beneficial even in the presence of severe depression of cardiac performance.Improved left ventricular performance in group II and III patients was accompanied by a slight decrease in coronary blood flow, myocardial oxygen consumption, and transmyocardial oxygen extraction. There was no change in myocardial lactate metabolism in any group. In vitro studies in isolated cat papillary muscle preparations showed no direct positive inotropic effect of either phentolamine or nitroprusside. Thus, significant improvement in left ventricular performance occurs during vasodilator therapy in patients with AMI and elevated LVFP, even in the presence of severe depression of cardiac performance. Furthermore, this improvement is not accompanied by increased metabolic cost. Vasodilator therapy, therefore, may have an important role in the treatment of pump failure complicating myocardial infarction.

[1]  W. Parmley,et al.  Beneficial Effects of Vasodilator Agents in Severe Mitral Regurgitation Due to Dysfunction of Subvalvar Apparatus , 1973, Circulation.

[2]  J. Forrester,et al.  Renal and extrarenal hemodynamic effects of furosemide in congestive heart failure after acute myocardial infarction. , 1973, The New England journal of medicine.

[3]  B. Pitt,et al.  Use of Phentolamine in Acute Myocardial Infarction Associated with Hypertension and Left Ventricular Failure , 1973, Circulation.

[4]  G. Dagenais,et al.  Effects of intravenously administered digoxin on mild left ventricular failure in acute myocardial infarction in man. , 1972, The American journal of cardiology.

[5]  G. Diamond,et al.  Hemodynamic Spectrum of Myocardial Infarction and Cardiogenic Shock: A Conceptual Model , 1972, Circulation.

[6]  J. Cohn,et al.  IMPROVED LEFT VENTRICULAR FUNCTION DURING NITROPRUSSIDE INFUSION IN ACUTE MYOCARDIAL INFARCTION , 1972 .

[7]  H. Swan,et al.  Measurement of blood flow by thermodilution. , 1972, The American journal of cardiology.

[8]  G. Diamond,et al.  Effect of Coronary Artery Disease and Acute Myocardial Infarction on Left Ventricular Compliance in Man , 1972, Circulation.

[9]  R. Russell,et al.  Left Ventricular Function in Acute Myocardial Infarction and its Clinical Significance , 1972, Circulation.

[10]  G. Diamond,et al.  Thermodilution cardiac output determination with a single flow-directed catheter. , 1972, American heart journal.

[11]  H. Swan,et al.  A new technique for measurement of cardiac output by thermodilution in man. , 1972, The American journal of cardiology.

[12]  W. Hood.  Pathophysiology of ischemic heart disease. , 1971, Progress in cardiovascular diseases.

[13]  J. Enrico,et al.  Phentolamine for vasodilator treatment of severe heart-failure. , 1971, Lancet.

[14]  S. Taylor,et al.  Phentolamine for vasodilator treatment of severe heart-failure. , 1971, Lancet.

[15]  H. Swan,et al.  Measurement of Coronary Sinus Blood Flow by Continuous Thermodilution in Man , 1971, Circulation.

[16]  J. Cohn,et al.  Left ventricular function in acute myocardial infarction. , 1971, The Journal of clinical investigation.

[17]  J. Covell,et al.  Factors Influencing Infarct Size Following Experimental Coronary Artery Occlusions , 1971, Circulation.

[18]  R. Russell,et al.  Effects of increasing left ventricular filling pressure in patients with acute myocardial infarction , 1970 .

[19]  R. Russell,et al.  Effects of increasing left ventricular filling. Pressure in patients with acute myocardial infarction. , 1970, The Journal of clinical investigation.

[20]  M. Zahir,et al.  Phentolamine and cardiovascular performance. , 1969, British heart journal.

[21]  M H Weil,et al.  Rapid enzymatic measurement of blood lactate and pyruvate. Use and significance of metaphosphoric acid as a common precipitant. , 1967, Clinical chemistry.