Effects Of Acute Myocardial Infarction Research Articles

Editorial: Bed rest after myocardial infarction.

Editorial Notes1 September 1973Bed Rest After Myocardial InfarctionRICHARD S. CRAMPTON, M.D.RICHARD S. CRAMPTON, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-79-3-449 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptDespite the apparent benefits of prehospital treatment and early mobilization, many physicians who are ignorant of the biological, psychological, and economic effects of acute myocardial infarction, leave prehospital treatment to chance, prolong bed rest unnecessarily, and unduly put off ambulation, discharge, and return to gainful work for their patients. The facts are that ending bed rest early does not increase complication or death rates (1-4), that 60% of patients who receive prehospital resuscitation return to active life (5), and that community mortality is reduced 15% by the community-wide coronary care system (6). In England, Ireland, The Netherlands, Russia, Scotland, and...

Right and left heart pressures in acute myocardial infarction.

In dogs the effects of acute myocardial infarction (AMI) on right and left heart pressure relationships were studied. Right atrial pressure was a poor predictor of left heart pressures. Pulmonary artery end-diastolic, left atrial, and left ventricular end-diastolic pressures tended to equalize in normals (except with tachycardia) and after AMI. In a previously scarred left ventricle, however, after superimposed AMI and marked elevations in left ventricular end-diastolic pressure, prominent atrial impact waves resulted in this being appreciably higher than the other two pressure measurements.

Hemodynamic Effects of Acute Myocardial Infarction

Hemodynamic Effects of Acute Myocardial Infarction

Effects of acute myocardial infarction and of noradrenaline infusion on fatty acid composition of serum lipids

Changes in the fatty acid composition of serum free fatty acids (FFA), triglycerides, cholesterol esters and phospholipids have been studied during the first 3 days after acute myocardial infarction and after noradrenaline infusion.When compared with healthy subjects or patients with a long history of ischaemic heart disease, the only significant change in patients after acute myocardial infarction was elevated oleic acid in the FFA fraction. The composition of triglyceride, cholesteryl and phospholipid fatty acids was not consistently altered.Immediately after a 15-min infusion of noradrenaline, serum FFA were raised and the percentage of free oleic acid and linoleic acids were increased; there was a significant decrease in the percentages of stearic and palmitic acid. Hyperlipidaemic patients did not show any increase in free linoleic acid in response to noradrenaline.In the healthy subjects there were increases in the percentages of triglyceride oleate and of cholesteryl and phospholipid arachidonate. The total phospholipid concentrations and the percentage of phospholipid palmitate decreased. In general, less significant changes were seen in hyperlipidaemic patients given noradrenaline. Changes in composition and concentration during the time of fatty acid mobilisation by noradrenaline suggest an interrelationship between the mechanism of fatty acid mobilisation and metabolism of serum phospholipids. Thus, the increased fatty acid mobilisation which follows myocardial infarction is associated with fewer changes in the composition, particularly of esterified fatty acids, than immediately after noradrenaline infusion.

Hemodynamic effects of acute myocardial infarction in man

Hemodynamic effects of acute myocardial infarction in man

Effect of Acute Myocardial Infarction on Electrical Recovery and Transmural Temperature Gradient in Left Ventricular Wall of Dogs

Accelerated recovery, as manifested by shortening of the effective refractory period after coronary artery ligation, occurred at either the epicardial or endocardial surface or both in 11 of 13 animals tested with a mean shortening of 15.7 per cent at the epicardial and 13 per cent at the endocardial levels. These changes are attributed to severe anoxia and are believed to be limited to the ischemic area, since studies in the periphery of an infarcted zone show no significant changes in the first 3 hours. In one instance a minor acceleration of recovery was found after 3 hours at the endocardium. All studies showed a final period of delayed recovery. It is felt that this probably reflects a prolonged duration of the membrane action potential during the later stages of myocardial infarction. This is supported by both experimental and human electrocardiographic data which show prolongation of the Q-T interval in association with deeply inverted T waves following the period of acute injury. Transmural temperature studies after coronary artery ligation showed a prompt fall in 2 studies out of 7 and no acute change in the others. Irrigating the pericardial sac with warm Ringer's solution reversed the pre-existing transmural temperature gradient, caused the T waves in epicardial leads to change from negative to positive, and reduced the duration of the effective refractory period at both the endocardial and epicardial surfaces, especially the latter. During the time that the T waves were upright, recovery was completed earlier at the epicardial than at the endocardial surface.