Acute Myocardial Infarction Injury Research Articles

Identification of the optimal electrocardiographic leads for detecting acute epicardial injury in acute myocardial infarction

Current coronary care electrocardiographic (ECG) monitoring techniques are aimed at detection of cardiac arrhythmias rather than myocardial ischemia. However, in patients with acute myocardial infarction (AMI) who undergo reperfusion therapy, monitoring ST-segment deviation could provide an early noninvasive indicator of coronary artery reocclusion. In this study, the admission 12-lead ECGs of patients with initial AMI were used to propose optimal lead locations for ST-segment monitoring. The study population was selected from consecutive Duke University Medical Center admissions during 1965 to 1981 who met the following inclusion criteria: chest pain for no more than 8 hours, initial AMI documented by ECG and 3 of 4 enzyme criteria, greater than or equal to 0.1 mV (1 mV = 10 mm) of ST elevation in at least 1 of the standard 12 leads (not aVR) on admission ECG, and no ECG evidence of conduction disturbances, ventricular hypertrophy or tachycardia. ST-segment deviation was quantified; AMI location was assigned based on the lead with maximal deviation. Of the 80 patients who had an inferior AMI, lead III was both the most frequent location for ST elevation (94%) and the most common site with maximal ST deviation. Lead V2 had the highest incidence of ST-segment depression (60%). In the 68 patients who had an anterior AMI, lead V2 had the highest frequency of ST elevation (99%). Leads V2 and V3 were the most common sites of maximal elevation. Thus, for monitoring ST deviation, leads III and V2 may be superior to leads II and V1, which are commonly used in arrhythmia monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)

Estimation of acute myocardial infarct size in man by serum CK-MB measurements.

This study was performed to determine the relationship between myocardial infarct size estimated by serum CK-MB methods and the extent of irreversible injury in acute myocardial infarction. In 321 consecutive patients, infarct size was estimated by different mathematical models, and in 22 patients who died in hospital, the extent of myocardial necrosis was determined by autopsy. We also investigated the depletion of CK-MB in infarcted tissue, the recovery of CK-MB in the plasma volume, and the estimation of CK-MB from plasma. Myocardial CK-MB depletion was relatively greater in the larger infarcts, whereas the recovery of enzyme in plasma was independent of the infarct size. Correction of serum CK-MB for changes in plasma volume improved the estimate significantly (p less than 0.05). The correlation between the measured infarct size (g) and the estimated infarct size (units per liter and gram-equivalents) was highly significant (r = 0.85--0.89, SEE = 23--27%, p less than 0.001). Thus, a semiquantitative expression of the extent of myocardial necrosis can be determined in vivo.

Effect of Sublingually Administered Isosorbide Dinitrate on Ischemic Injury in Patients with Acute Myocardial Infarction

To evaluate reversible myocardial ischemic areas in acute myocardial infarction (AMI), we have developed the following methods : (1) 2mCi of thallium-201 was injected intravenously and myocardial per fusion images were obtained ; (2) immediately thereafter, 5 mg of isosorbide dinitrate (ISD) was administered sublingually ; and (3) 10 minutes after the administration, another bolus of 2 mCi of thallium-201 was given and myocardial per fusion imaging was repeated (double scan method). Ten patients with AMI (within 24 hours after onset) were studied by the double scan method. Myocardial per fusion defect areas were reduced from 29±3% of the entire left ventricle to 19±4% by ISD administration, indicating that there were reversibly ischemic areas in AMI which could be transiently reduced by ISD. For clinical implication, 80 patients with AMI were divided into 2 groups at random : Group I-40 patients treated with conventional methods, and Group II-40 patients treated with continuos ISD administration (every 3 hours for 3 days). There was no significant difference in prognostic indices at the time of admission. Final MI sizes estimated by thallium-201 2 months after onset (percent of per fusion defects to the total left ventricle) were significantly smaller in Group II (19.8±3.1%) than in Group I (32.1±3.7%) (p<0.02). Mortality was 25% in Group I and 10% in Group II. This preliminary report indicates that nitrates have possibly beneficial action in decreasing ischemic injury of acute myocardial infarction.

Effect of paired ventricular pacing upon myocardial infarction size

Although paired ventricular pacing may improve cardiodynamics following acute myocardial infarction, its effect on myocardial infarct size is not known. In 22 dogs, acute myocardial infarction was produced by selective coronary artery ligation. High fidelity left ventricular pressure, dp dt max , acceleration of aortic flow ( dQ dt ), coronary flow and epicardial mapping were recorded before and at 15-min intervals following acute myocardial infarction for a total of 90 min. Coronary sinus CPK was measured before coronary occlusion and then every 30 min for a period of 150 min. In Group A ( n = 10) animals had an acute myocardial infarction only, while in Group B ( n = 12), paired ventricular pacing was initiated 30 min postinfarction and continued throughout the study. Two dogs from Group A and six from Group B developed ventricular fibrillation and were excluded from the study. In Group A dp dt p , dQ dt and heart rate did not change, while in Group B dp dt p increased from 20.0 ± 1.5 to 30.2 ± 1.5 ( P < 0.05) and dQ dt increased from 19.0 ± 1.7 to 27.1 ± 2.5 ( P < 0.05). Coronary flow, arterial and coronary sinus blood gases were similar in both groups. CPK increased more in Group B than in Group A ( P < 0.05). ΣST was unchanged in Group a between 30 and 90 min post-infarction while in Group B ΣST increased at the same period from 36.0 ± 2.8 to 62.5 ± 8.6 ( P < 0.05). These data indicate that paired ventricular pacing increased ischemic injury in acute myocardial infarction, due to increased oxygen consumption resulting from the positive inotropic effect exceeding the influence of a decreased heart rate.

Electrocardiographic localization of injury in acute myocardial infarction: Relation to left ventricular function and cardiac pump failure

Electrocardiographic localization of injury in acute myocardial infarction: Relation to left ventricular function and cardiac pump failure