State of general and renal hemodynamics in acute myocardial infarct]

The results of studying central and renal hemodynamics in 49 patients with a different course of myocardial infarction in the acute period (1st, 3rd, and 10th day) are analysed. It was established that on the 1st day the cardiac output decreases considerably in circulatory insufficiency and hardly changes in an uncomplicated course of the disease. The stroke output of the heart reduces significantly in all forms of the course of myocardial infarction. At an increase of total peripheral resistance is observed in myocardial infarction, particularly in circulatory insufficiency. A significant increase in the central hemodynamics indices is noted at the end of the acute period. On analysing the dependence of central and renal hemodynamics, the authors conclude that local mechanisms are involved in the changes in renal hemodynamics in addition to its dependence on the disorders of central hemodynamics.     

Intrahepatic hemodynamics and liver function in the acute period of myocardial infarct]

Data are presented on the state of the intrahepatic blood flow and the absorption-excretory capacity of the liver in 221 patients with acute myocardial infarction. The changes in the absorption-excretory function of the liver and of the hepatic blood circulation are described on the basis of a dynamic observation (on the 1st, 20--30th, 50--60th day of the onset of the disease) and with due regard of the extent of the myocardial infarction and the presence of complications, cardiogenic shock in particular.     

Early intervention with a beta-blocking drug after acute myocardial infarction

Several controlled studies with long-term administration of beta blockers in postinfarction patients have demonstrated a reduction in cardiac events and mortality. During acute myocardial infarction (AMI), conventional treatment is directed mainly at such complications as pump failure and arrhythmias. Another approach attempts to influence the natural evolution of impending myocardial necrosis by interrupting the process in its reversible phase. In a double-blind trial with metoprolol in suspected or definite AMI, 1,395 patients were studied, 698 of whom received metoprolol and 697 placebo. The 3-month mortality was 36% lower in the metoprolol group (p = 0.024). A reduction in severe ventricular arrhythmias (ventricular fibrillation and tachycardia) was also seen. Chest pain was reduced and there was less need of analgesic drugs in the metoprolol group. Intervention within 12 hours resulted in a limitation of infarct size, a decreased need for furosemide and a shortened hospital stay. A significant reduction in mortality was maintained after 2 years of follow-up despite the same treatment in both groups between 3 and 24 months. Early institution of metoprolol in AMI has resulted in reduced mortality and morbidity.     

Effect of digoxin on central hemodynamics in myocardial infarct]

The effect of digoxin on the cardiac index and diastolic pressure in the pulmonary artery was studied in 17 patients with acute myocardial infarction on the 1st-3rd day of the disease by the method of thermodilution. Twelve of these patients had clinical manifestations of congestive circulatory insufficiency. Digoxin was infused intravenously in a dose of 0.5 mg. Its infusion led to reduction of diastolic pressure in the pulmonary artery from 19.0 to 16.7 mm Hg and rise of cardiac index from 2.26 to 2.4 1/min/m2 (statistically untrustworhty difference). In all cases digoxin concentration in blood serum examined by the radioimmune method was therapeutical (1.64 ng/ml, on the average). The positive hemodynamic effect of digoxin infused in a dose producing its therapeutic concentration in blood is negligible.     

Influence of canrenoate potassium (aldactone pro injections) on hemodynamics and myocardial ischemia in experimental myocardial infarct]

The effects of the positive-inotropic drug Canrenoat-Kalium (CRK) on the extent and severity of myocardial ischemic injury and on hemodynamic parameters were studied in 17 dogs following coronary occlusion. Acute myocardial infarction causes depression of left-ventricular function. There eas a significant decrease in dp/dtmax, stroke volume and cardiac output; average values for mean arterial pressure were reduced, but not significantly. There was a significant increase in left-ventricular enddiastolic pressure. Heart rate was unchanged. In the healing phase of myocardial infarction a significant elevation of left-ventricular enddiastolic pressure and a significant decrease of arterial pressure persisted, but the other parameters had returned toward normal. Intravenous administration of CRK (20 mg/kg) one hour after coronary occlusion causes a significant increase in left-ventricular dp/dtmax, cardiac output and stroke volume, but no significant change in arterial pressure, heart rate and left-ventricular enddiastolic pressure. Four days after myocardial infarction administration of CRK causes also a significant incrrease in left-ventricular dp/dtmax and -n 4 out of 5 animals an increase in stroke volume. Heart rate, arterial pressure and left-ventricular enddiastolic pressure are unchanged. There is a continuous deterioration of all hemodynamic parameters in the control group 1 hour and 96 hours after experimental myocardial infarction. This spontaneous deterioration has to be taken into consideration estimating the effect of CRK in experimental conditions. 120 epicardial electrocardiographic recordings were used to assess the extent and severity of myocardial ischemic injury. The average ST-segment elevation and the number of sites with abnormal ST-segments were significantly reduced 20 min after CRK administration. The study suggests a beneficial therapeutic role for CRK treatment of left-ventricular failure in the acute and healing phase after myocardial infarction.     

Comparative effects of ajmaline and lidocaine on hemodynamics in myocardial infarct

Haemodynamic changes after single intravenous injection of antiarhythmic doses of ajmaline (50 mg) and lidocain (100 mg) were measured comparatively in 10 patients with acute myocardial infarction, stable cardiac rhythm and without manifest left heart failure. The effects of ajmaline were characterized by a significant decrease of systolic arterial pressure (9%), of left ventricular stroke work index (15%) as well as by an increase of the mean pressure of the pulmonary artery (7%) in the early phase after application. No significant changes in cardiac index, stroke volume index, systemic vascular resistance, right and left ventricular filling pressures and heart rate occurred. The effects of lidocain on the cardiac circulation were comparatively small. The intravenous administration of lidocain did not result in significant changes of the cardiac index or left and right ventricular filling pressures. Diastolic arterial pressure increased significantly (5%), while the heart rate decreased (5%).     

Hemodynamic effects of enalapril in patients with non-complicated acute myocardial infarct]

To evaluate the hemodynamic effects of the first oral administration of enalapril maleate, a long-acting ACE-inhibitor, in the early phase of an acute uncomplicated myocardial infarction, we studied 15 patients, in Killip class I or II, within 72 hours from the onset of symptoms. Hemodynamic measurements were obtained by a triple lumen 7 F Swan-Ganz catheter, inserted into the pulmonary artery, under control conditions and 2, 4, 6, 8 and 12 hours after 10 mg (15 patients) and 20 mg (11 patients) of the drug. Ten milligrams of enalapril reduced systolic and mean arterial blood pressure (from 118 +/- 17 to 111 +/- 18 mmHg, p < .05, and from 92 +/- 12 to 83 +/- 12 mmHg, p < .01, respectively), with a maximum effect after 4 hours from administration. Heart rate and vascular resistances showed an insignificant trend toward reduction, and no changes were observed in left ventricular systolic work index, right and left ventricular filling pressures or cardiac index. Hemodynamic changes induced by 20 mg of the drug, in a smaller group of patients, had a similar trend, which did not reach a statistical significance. In conclusion, in patients with acute uncomplicated myocardial infarction, a single oral dose of enalapril maleate is safe and well tolerated, does not induce severe hypotension, and produces potentially beneficial changes in hemodynamics.     

Late ventricular potentials in acute and rehabilitative periods of myocardial infarct

The study was undertaken to examine 121 individuals: 48 apparently healthy subjects, 43 patients with angina pectoris and 42 patients with acute myocardial infarction (MI). Late ventricular potentials (LVP) were recorded in 6.2% of healthy subjects, 25.6% of patients with angina and 40.5% of those with MI in the first 24 hours, 28.5% on day 3, and 45.2% on day 14 of the onset of infarction. They were not recorded in 35.7% of MI patients. On days 3-4 of MI, the presence of LVP depended on the severity of diastolic left ventricular dysfunction; on day 14, LVP occur more frequently with circular than with anterior MI; in days 3 and 14, LVP were recorded much more frequently with Q wave; the total R-wave amplitude in leads V2-V4 is of definite importance for LVP in anterior MI, whereas that in 35 leads is of definite significance in posterior MI.     

Hemodynamic variants of acute myocardial infarct]

In 165 patients with myocardial infarction admitted to the clinic within the first 24 hours of the disease the size of the zone of the lesion and its dynamics were appraised in the immediate 4-5 days. Cartographic ECG analysis and study of the vectorcardiogram in dynamics and analysis of the creatine phosphokinase activity curves make it possible to appraise the dynamics of the necrotic zone in the first days of myocardial infarction. It was found that in most patients with macrofocal myocardial infarction the zone of the necrosis increases both in length and in depth in the first days of the disease.     

Disorders of hemodynamics and pulmonary gas exchange in the acute period of myocardial infarct

In 40 patients with massive myocardial infarction, the central hemodynamics was examined by probing the right-sided chambers of the heart and the pulmonary artery. The cardiac output was measured by thermodilution. The gas exchange (respiratory minute volume, capnography, gas analysis of arterial and mixed venous blood) was explored. Arterial hypoxemia was found to be associated with increased intrapulmonary blood shunting in patients with acute myocardial infarction complicated by congestive heart failure. Deterioration of arterial hypoxemia was promoted by a combination of increased overall pulmonary shunting and decreased residual venous oxygenation. Abnormalities in the ventilation-perfusion relations are of great importance.     

Accelerated idioventricular rhythm in acute myocardial infarct]

A continuous (for 24 hours) ECG recording on a magnetic tape with its subsequent decodification on a special analyser was performed in 31 patients with acute myocardial infarction during the 1st day of the onset of the disease in order to reveal an accelerated idioventricular rhythm and ventricular tachycardia. An accelerated idioventricular rhythm was found to occur within the 1st and early during the 2nd day of the disease in 29% of the patients. The importance of some factors, that of the sinus rhythm rate in particular, was studied with reference to the development of an accelerated idioventricular rhythm. The causes of its development are discussed, as well as those of its disappearance, interrelationship with ventricular tachycardia, and the prognostic importance of the accelerated idioventricular rhythm recorded throughout a 3-month observation and its place in the differential diagnosis in acute myocardial infarction.