Acute Myocardial Infarction In Man Research Articles

Severity of contraction abnormalities after acute myocardial infarction in man: response to nitroglycerin.

Severity of contraction abnormalities after acute myocardial infarction in man: response to nitroglycerin.

Evaluation of warning arrhythmias before paroxysmal ventricular tachycardia during acute myocardial infarction in man.

In order to determine the relationship of paroxysmal ventricular tachycardia (PVT) to any antecedent (premonitory) ventricular arrhythmias during the early phases of acute myocardial infarctions, 24-hour Holter monitoring was begun on 52 male patients an average of 12.6 hours after the onset of prolonged chest pain that was documented as acute infraction. Twenty-four patients had PVT and 28 did not. We analyzed in detail the incidence of frequency of premature ventricular complexes (PVCs), prematurity and pairing during the 10 minutes immediately preceding PVT from a continuous 10-minute rhythm strip. There was no positive correlation between PVT and the number or complexity of PVCs in the 10 minutes immediately before ventricular tachycardia. These findings suggest that there is no consistent pattern or frequency of ventricular arrhythmia that could be identified as premonitory for PVT during the immediate pre-PVT period, even during the acute phase of myocardial infarction in man.

Multiple waves of enzyme release following acute myocardial infarction in man

Multiple waves of enzyme release following acute myocardial infarction in man

The variability of ST segment in the early phase of acute myocardial infarction

AbstractThe ST segment elevation was measured hourly, via a single surface unipolar lead for 48 hours after admission, in 30 patients with acute myocardial infarction (AMI), admitted, on average, 2 hours after the onset of symptoms. In 14 patients with anterior AMI, the recordings were made through the precordial lead that initially showed the maximum ST elevation. In 16 patients with inferior AMI, the aV F lead was used. Twenty‐five control patients without AMI had the ST deviation measured hourly for 24 hours; 15 of them had the recording made via the Vs, aV F being used with the others. Our data for the reliability of the method showed that the variations in ST deviations in the control group were of the same magnitude as those observed with the measuring error of the method itself.The investigation showed that the spontaneous course of the hourly measured ST elevations in the early phase of AMI was marked by pronounced variability, and that this applied to both anterior and inferior infarctions. The intra‐individual patient variation of the ST elevation was significantly greater than in the control group of patients. The inter‐individual patient variation of the ST elevation with AMI was also significant. The ST elevation was correlated to heart rate, mean arterial blood pressure, heart rate multiplied by systolic blood pressure, and respiratory rate and it could be shown partly that there was a significant dispersion of the correlation coefficients within the separate correlation groups, and partly that the correlation coefficients were variable between the groups. It was also shown that nasal oxygen therapy and cardiac pain had no bearing on ST elevation. The variability of ST elevation was thus most often inexplicable and only rarely accounted for by alterations in the clinical status.It is generally accepted that ST segment elevation in the ECG is one of the characteistic features of acute myocardial infarction (AMI), but the electrophysiological basis of changes in the ST segment in myocardial ischaemia has not been completely clarified (1).In recent years, several investigations have been carried out where ST elevation has been used as a quantitative indicator of myocardial ischaemia. With multiple leads and epicardial and precordial mapping techniques, the sum of ST elevations has been used as an estimate of the extent of ischaemic injury after coronary occlusion in animals and after AMI in man (7, 8, 9, 12, 13). However, from the theoretical and experimental bases of ST segment deviation, it has been suggested that ST segment mapping is not a reliable measure of myocardial ischaemia (4, 5). Other investigators have pointed out the limitations of this method when used for the bedside estimate of ischaemic injury (11, 15).These studies suggest that there is a considerable variability of the ST deviation after AMI. Therefore, in an attempt to elucidate this problem, we have studied the ST elevation from hour to hour in a single surface lead for the first 2 days after admission of patients with AMI and have related the ST elevation to ST deviations measured hourly in patients without AMI. In addition, the ST elevations in patients with AMI have been related to heart rate, blood pressure, respiratory rate, retrosternal pain and oxygen treatment; clinical factors that can be associated with, or can influence, myocardial ischaemia.

The effect of established beta-adrenoreceptor-blocking therapy on the release of cytosolic and lysosomal enzymes after acute myocardial infarction in man.

1. Serial venous blood samples were obtained from 45 patients with acute myocardial infarction. Ten of these patients were receiving beta-adreno-receptor-blocking drugs at the time of onset of chest pain and continued on these drugs during their stay in the coronary care unit. The activities of creatine kinase and its MB-isoenzyme (CK-MB) were assayed in the plasma. A lysosomal enzyme, beta-N-acetylglucosaminidase, was also assayed. 2. In the 35 untreated patients it was found that creatine kinase activity was maximal at a mean time of 21.3 +/- 1.3 h after the onset of chest pain, whereas in the patients receiving beta-adrenoreceptor-blocking drugs peak activity of the enzyme occurred at 24.4 +/- 0.7 h. 3. Peak CK-MB acitivity was also delayed from 18.1 +/- 1.6 h in the control group to 22.4 +/- 1.2 h in the treated patients. 4. The lysosomal enzyme showed a similar pattern of changes to that of CK-MB. Maximum activity in plasma occurred at 18.0 +/- 1.0 h after the onset of chest pain in the control group of patients. In the treated patients peak lysosomal enzyme activity was not found until 24.2 +/- 1.2 h. 5. These alterations in the time-course of plasma enzyme changes after acute myocardial infarction are consistent with the suggestion that beta-receptor antagonists may delay tissue damage during myocardial ischaemia.

Metabolic responses of the heart in acute myocardial infarction in man

Acute myocardial infarction evokes a characteristic neurohumoral response: Catecholamine release is increased, plasma contents of free fatty acids and glucose are elevated and glucose tolerance is diminished. To what degree the myocardium participates in this stress response was evaluated by sampling coronary sinus and arterial blood in 50 patients with acute transmural infarction. Studies were initiated an average of 8 hours after the clinical onset of infarction and were continued for up to 60 hours. A total of 173 separate metabolic studies were analyzed. Forty-one percent exhibited a pattern of predominant myocardial free fatty acid uptake (mean extraction ratio 24 percent) in the presence of elevated plasma free fatty acid and glucose contents (respective means 1,181 μmol/liter and 210 mg/100 ml). Myocardial extraction ratios for glucose, lactate and pyruvate were low (respective means 1.1, 4 and 11 percent). Twenty-one percent of the studies revealed normal myocardial metabolism and 18 percent showed enhanced carbohydrate uptake, as evidenced by increased myocardial extractions of lactate and pyruvate (respective means 42 percent) and of glucose (mean 5 percent). Plasma contents of glucose and free fatty acids were lower than in the predominant free fatty acid group (respective means 156 mg/100 ml and 743 μmol/liter). The remaining 20 percent of studies showed high plasma substrate contents and low myocardial substrate uptake suggesting metabolic breakdown. The free fatty acid metabolic pattern was observed in more than 50 percent of the studies performed at the time of or close to the occurrence of important clinical complications. Propranolol, 0.1 mg/kg intravenously, shifted myocardial substrate utilization from free fatty acids toward carbohydrates. The myocardial respiratory quotient increased from an average of 0.79 to 0.88 ( P < 0.01). The study demonstrates that the metabolic patterns of the myocardium are influenced by the systemic response to stress. Beta adrenergic blockade changed substrate utilization of the myocardium, supporting the hypothesis that adrenergic activation plays an important role in these metabolic responses.

Evolution and Prediction of Infarct Size after Acute Myocardial Infarction in Man

Evolution and Prediction of Infarct Size after Acute Myocardial Infarction in Man

Electrophysiologic effects of acute myocardial infarction in man

Six patients undergoing surgery for ischemic heart disease were studied by means of epicardial electrodes affixed to the left ventricle. One patient who underwent triple coronary arterial bypass and plication of a left ventricular aneurysm had evidence of an acute myocardlal infarction 1 day after operation. A surface electrocardiogram and a bipolar electrogram from the left ventricle were recorded before and after development of the infarction. The bipolar electrogram showed a marked toss of voltage and delay of conduction that were not present in the patients who underwent surgery but did not sustain an acute myocardlal Infarction. Thus, any acute myocardial infarction in conscious persons appears to be associated with areas of delayed epicardial action and diminution of local voltage. This observation suggests that the electrophystotogic mechanisms of infarction in man are similar to those of infarction in the dog.

Effect of dopamine on hemodynamics and myocardial metabolism in shock following acute myocardial infarction in man

Eight patients in shock associated with acute myocardial infarctions were treated with dopamine. We titrated the dopamine dose to increase mean arterial pressure to 65-70 mm Hg and urine output to greater than 40 ml/hr. Increase of heart rate to 120-125 beats/min and occurrence of potentially dangerous arrhythmias were limiting end-points. Dopamine administration averaged 17.2 microgram/kg/min. Heart rate increased from 95 to 118 beats/min (P less than 0.001), and mean arterial pressure rose from 60 to 65 mm Hg (P less than 0.05). Dopamine increased myocardial contractility as indicated by increase in cardiac index and systolic ejection rate, with only moderate decrease in systemic vascular resistance. Pulmonary wedge pressure and right atrial pressure decreased from 23 to 18 mm Hg (P less than 0.05) and from 10 to 8 mm Hg (P less than 0.001) respectively. Improvement in hemodynamic status by dopamine was associated with deterioration of myocardial metabolism. Myocardial oxygen extraction ratios and arter...

Effect of dopamine on hemodynamics and myocardial metabolism in shock following acute myocardial infarction in man.

Eight patients in shock associated with acute myocardial infarctions were treated with dopamine. We titrated the dopamine dose to increase mean arterial pressure to 65-70 mm Hg and urine output to greater than 40 ml/hr. Increase of heart rate to 120-125 beats/min and occurrence of potentially dangerous arrhythmias were limiting end-points. Dopamine administration averaged 17.2 microgram/kg/min. Heart rate increased from 95 to 118 beats/min (P less than 0.001), and mean arterial pressure rose from 60 to 65 mm Hg (P less than 0.05). Dopamine increased myocardial contractility as indicated by increase in cardiac index and systolic ejection rate, with only moderate decrease in systemic vascular resistance. Pulmonary wedge pressure and right atrial pressure decreased from 23 to 18 mm Hg (P less than 0.05) and from 10 to 8 mm Hg (P less than 0.001) respectively. Improvement in hemodynamic status by dopamine was associated with deterioration of myocardial metabolism. Myocardial oxygen extraction ratios and arterial-coronary sinus oxygen differences increased from 73 to 76% (P less than 0.05) and from 13.02 to 14.19 ml/100 ml (P less than 0.02) respectively. Myocardial lactate production increased from -8 to -15% (P = 0.05). We conclude that dopamine improved cardiac performance at the expense of myocardial oxygenation and that dopamine is potentially harmful to acutely ischemic myocardium.

Serum myoglobin in myocardial infarction: the “ staccato phenomenon.” Is acute myocardial infarction in man an intermittent event? : Kagen L, Scheidt S, Butt A: Am J Med 62: 86–92, 1977

Serum myoglobin in myocardial infarction: the “ staccato phenomenon.” Is acute myocardial infarction in man an intermittent event? : Kagen L, Scheidt S, Butt A: Am J Med 62: 86–92, 1977

Evaluation of Radiopharmaceuticals for the Detection of Acute Myocardial Infarction in Man

The accuracy of the scintigraphic diagnosis of acute myocardial infarction with 99mTc-pyrophosphate, 99mTc-tetracycline and 99mTc-glucoheptonate was assessed in 63 patients, 43 of whom had clinical evidence of acute myocardial infarction. In 15, studies with both 99mTc-tetracycline and 99mTc-pyrophosphate were performed. Accuracy was greatest with 99mTc-pyrophosphate (17/17 true positives, 8/10 true negatives) contrasted with 99mTc-tetracycline (12/25 true positives, 6/11 true negatives) and 99mTc-glucoheptonate (3/13 true positives, 2/2 true negatives). 99mTc-pyrophosphate was the most sensitive tracer for the detection of acute myocardial infarction. The diagnostic accuracy with 99mTc-glucoheptonate was poor.

Plasma propranolol concentration in patients with angina and acute myocardial infarction.

1. Plasma levels of propranolol were measured fluorometrically in patients with angina pectoris and in patients admitted to the Coronary Care Unit with acute myocardial infarction. 2. In thirty patients with stable angina pectoris, plasma propranolol levels varied almost linearly with doses between 10 and 120 mg during 6-hourly chronic oral administration. Plasma levels greater than 100 ng/ml produced 70-80% reduction in the tachycardia induced by strenous exercise on a treadmill. 3. In nineteen patients with acute myocardial infarction given oral propranolol, 20 mg 6-hourly, peak as well as trough plasma levels of the drug increased progressively but remained below 100 ng/ml in all except two patients during the first 24 h after their admission to the Coronary Care Unit. 4. The data suggest that the use of low and fixed doses of propranolol may not produce adequate plasma levels or significant beta-adrenoceptor blockade in the early stages of acute myocardial infarction in man.

Experimental myocardial ischemia. III. Protective effect of glucose on myocardial function

Glucose has been long known as an important substrate for muscle cells and a number of laboratories have demonstrated that carbohydrate metabolism can contribute significantly to energy production both in aerobic and anerobic heart muscle. It has been suggested that these findings may have additional application in localized myocardial ischemic and infarction. Accordingly, experiments were performed to determine the effect of glucose on the mechanical and electrical activity of the heart. Left ventricular pressure (LVP), left ventricular dp dt ( LVdp dt , left ventricular end diastolic pressure (LVEDP), and the incidence of ventricular premature beats (VPB) and ventricular fibrillation (VF) were determined before and after ligation of the anterior descending coronary artery in three different canine heart experimental models. Thirty minutes after ligation of the left anterior descending coronary artery, the mean left ventricular pressure and mean left ventricular dp dt in the control group had decreased by 85 ± 6% and 74 ± 5% respectively. Under similar conditions glucose treatment produces an increase in left ventricular pressure and left ventricular dp dt of 111 ± 5% and 123 ± 8% respectively. The simultaneously measured mean left ventricular end diastolic pressure was 7.2 ± 0.9 ml for the control group and 3.7 ± 1 for the glucose treated group. Eighty-three percent of the control dogs developed ventricular ectopic activity. Fifty-eight percent of the control hearts developed ventricular fibrillation. In contrast, only 10% of the glucose treated hearts demonstrated ventricular ectopic activity and only 10% developed ventricular fibrillation. Glucose, as a bolus, consistently improved myocardial contractility and prevented ventricular fibrillation even after serum osmolality and serum glucose levels had returned to normal. These results demonstrate that glucose has a protective effect on the electrical and mechanical function of the canine heart during acute segmental myocardial ischemia. These findings may have application in the treatment of acute myocardial infarction in man.

The effect of intravenous digoxin on the occurrence of ventricular tachyarrhythmias in acute myocardial infarction in man

Patients with acute myocardial infarction were allocated to two groups according to a double blind-system of radomization. The patients (n = 18) in one of the groups received digoxin intravenously as an injection of 0.01 mg. per kilogram of body weight during 10 minutes. The patients in the other group (n = 15) received saline and served as controls. A continuous ECG record was obtained from each patient during 1 hour preceding the administration of digoxin or saline and was continued for 3 hours following the injection. No antiarrhythmic treatment was given during the time of the study. Based on the continuous ECG, calculations were made of the relative incidence of patients with different types of ventricular tachyarrhythmias during the period of observation as well as the percentage of arrhythmia-containing 1 minute intervals observed during this period. There was no statistical difference between the incidence of ventricular tachyarrhythmias in the two groups in the 1 hour period preceding drug injection. The administration of digoxin and saline did not change the incidence of ventricular tachyarrhythmias and there was also no statistically significant difference between the two groups as regards the incidence of patients showing different types of ventricular tachyarrhythmias during the 3 hour period following drug administration, Considering the 1-minute intervals, those without any ventricular premature contractions were less in the digoxin group (92 per cent) than in the saline group (88 per cent; p less than 0.001). Serum levels of digoxin at the end of the observation period were well above what is considered the minimum therapeutic level and in three patients the level approached or reached the toxic range. In these three patients there was still no increased incidence of ventricular tachyarrhythmias. It is concluded that patients with acute myocardial infarction complicated by incipient left ventricular failure do not show an increased sensitivity to an ordinary dose of digoxin as measured by the occurrence of ventricular tachyarrhythmia.

The relation of sinus rate to the frequency of paroxysmal ventricular tachycardia during acute myocardial infarction in man

Continuous tape recordings of cardiac rhythm were made in 51 male patients with acute myocardial infarction within 24 hours of their infarction. These tracings were analyzed for the incidence of paroxysmal ventricular tachycardia (PVT) and the sinus rate immediately preceding each episode of PVT. In 26 patients, 112 episodes of PVT at a rate greater than 100 beats/min were documented. Although 67 per cent of the episodes of PVT were preceded by sinus rates between 60 and 100 beats/min, 15 per cent occurred at sinus rates below 60 beats/min and 18 per cent occurred at sinus rates above 100 beats/min. The data remained essentially unchanged regardless of whether ventricular tachycardia was defined at rates in excess of 100, 120 or 140 beats/min. The results of this study show that during the early phases of acute myocardial infarction in man, PVT was most common during sinus rates generally thought to be within the normal range (60 to 100 beats/min). A lower, but close to equal incidence of PVT was observed during sinus bradycardia and sinus tachycardia.

Formation of coronary arterial thrombi in relation to onset of necrosis in acute myocardial infarction in man: A clinical and autoradiographic study

The presence of radioactivity in coronary arterial thrombi was studied at necropsy by autoradiography in 12 patients with acute myocardial infarction. Seven patients had been given 125I-and five patients 131I-labeled fibrinogen. With a short interval (less than 10 hours) between onset of symptoms and injection of fibrinogen the entire thrombus was radioactive in four of five patients, whereas with longer time intervals only parts or none of the thrombus contained detectable radioactivity. The findings give further evidence that thrombus formation in acute myocardial infarction probably is a slow process and that the major part of the thrombus may form after the onset of necrosis.

The relation of sinus rate to the frequency of paroxysmal ventricular tachycardia during acute myocardial infarction in man : de Soyza N, Bissett JK, Kane JJ, Murphy ML: Am J Med 60: 642–644, 1976

The relation of sinus rate to the frequency of paroxysmal ventricular tachycardia during acute myocardial infarction in man : de Soyza N, Bissett JK, Kane JJ, Murphy ML: Am J Med 60: 642–644, 1976

Propranolol in acute myocardial infarction in man. Effects of hemodynamics and myocardial oxygenation.

Propranolol in acute myocardial infarction in man. Effects of hemodynamics and myocardial oxygenation.

Changes in coagulation factors following acute myocardial infarction in man.

The whole blood clotting time, plasma fibrinogen and individual coagulation factors II, V, VII, VIII, IX, X, XI, and XII were serially measured in 14 patients over a 10-day period following acute myocardial infarction. A further six patients with similar symptoms but without evidence of myocardial infarction were also studied. The whole blood clotting time was significantly shorter within the first 24 h after infarction than on subsequent days. There were significant increases in the levels of fibrinogen and of factors VIII, IX, and XI and a significant decrease in factor XII in the patients who had sustained a myocardial infarction. The patients without myocardial infarction had no significant change in any of the coagulation factors measured.