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Several authors have reported a low mortality and salvage of ischemic myocardium in patients undergoing coronary revascularization after recent myocardial infarction. In this study, 20 surviving pigs with a coronary circulation similar to that of man were divided into two groups of 10 animals each. In the first group, the left anterior descending coronary artery (LAD) was ligated just beyond the first diagonal branch. Five animals were put to death at 24 hours and the remaining five animals, at 7 days. In the other group of 10 animals, the LAD was occluded just beyond the first diagonal branch and reperfused 3 hours after occlusion. Five of these animals were put to death at 24 hours and the remaining five animals, at 7 days. The left atrial pressure (LAP), heart rate, mean arterial pressure (MAP), and cardiac output were continuously monitored. Myocardial infarct size was determined planimetrically after the myocardium was sliced and stained with nitroblue tetrazolium. In five animals subjected to ligation for 24 hours, myocardial infarct size was 20.3 +/- 0.53 standard error mean (SEM) grams infarct per 100 gm left ventricular and septal mass (gm/100 gm LVS). In five animals subjected to occlusion, reperfusion in 3 hours, and death at 24 hours, the infarct size was 22.9 +/- 1.7 SEM gm/100 gm LVS. At 1 week in the ligated animals the infarction decreased to 15.5 +/- 1.7 SEM gm/100 gm LVS. In the reperfused animals at 1 week the infarction size was 14.5 +/- 1.7 SEM gm/100gm LVS. There was no significant difference in these values (Student's t test). Light and electron micrographs demonstrated hemorrhagic necrosis in every instance with reperfusion. Cardiac output, LAP, and MAP remained unchanged after reperfusion. These data suggest that in human beings without well-developed inherent collaterals sustaining myocardial infarction with coronary occlusion, that reperfusion as early as 3 hours after infarction would not be beneficial.

A 26-year-old black woman presented with a febrile illness and subsequently sustained an inferior myocardial infarction with chest pain. CPK-MB elevation and ECG changes. Left ventriculography revealed inferior wall hypokinesis, and coronary angiography demonstrated multiple aneurysms of the coronary arteries. Findings on visceral angiography of multiple organs was normal. Various etiologies were considered; however, her clinical course was felt to be most consistent with periarteritis nodosa and steroid therapy was instituted.

Although intra-aortic balloon pumping (IABP) is reported to reduce myocardial infarct size in dogs, this phenomenon may be due to pre-existing collaterals in this species. Pigs more closely approximate human coronary anatomy, having poor inherent collateralization. This study evaluates hemodynamic changes and quantitates myocardial infarct size 24 hours after coronary occlusion in swine, with and without IABP. Eighteen pigs underwent ligation of the left anterior descending coronary artery distal to the first diagonal branch: Nine were treated with IABP beginning 45 minutes after coronary occlusion and nine served as control subjects. Three in each group died prior to completion of the study. In both groups myocardial infarction resulted in a significant (p less than 0.05) decrease of cardiac output (28.5%) and mean aortic pressure (p less than 0.05) improvement of mean aortic pressure (4 to 7%) during the switch on period. After 24 hours, mean aortic pressure in IABP-treated animals (105 +/- 20 mm Hg) was significantly (p less than 0.01) higher than in control pigs (73 +/- 12 mm Hg). Myocardial infarct size as detected by staining with nitroblue tetrazolium was 22.7 +/- 4.9 gm infarct/100 gm left ventricular and septal mass in control pigs and 19.4 +/- 5.9 gm infarct/100 gm left ventricular and septal mass in treated animals (p less than 0.3). In conclusion, IABP, despite significantly improving circulatory parameters, does not significantly reduce the size of an acute myocardial infarction after coronary ligation in swine.

This study compared intraaortic balloon pumping (IABP) and transapical left ventricular (LV) bypass for their effectiveness in reducing infarct size in swine. In 28 pigs (25.4 +/- 4.7 kg) the left anterior descending coronary artery was ligated distal to the first diagonal branch. Nine animals served as controls. Nine animals were treated with IABP and the remaining 10, with transapical bypass. Ten animals-3 control, 3 IABP, and 4 transapical bypass--died prior to completion of the study, thereby resulting in 6 animals in each group. Both assist devices were begun 45 minutes after coronary ligation, this being as rapid as mechanical intervention could be accomplished in the patient after infarction. With transapical LV bypass, 70 to 100% bypass was accomplished and the LV systolic pressure remained in the range between mean aortic pressure and 30 mm Hg less than that. All animals were killed after 24 hours. The hearts were excised and stained with nitroblue tetrazolium, and infarct size was quantitated in grams of infarct per 100 gm of LV and septal mass. After 24 hours the mean aortic pressure was 73 +/- 12 mm Hg in controls, 105 +/- 20 mm Hg in animals with IABP (p less than 0.01), and 91 +/- 13 mm Hg in those with transapical LV bypass (p less than 0.05). The infarct size was 22.7 +/- 4.9 gm per 100 gm of LV and septal mass in control animals. With IABP, the infarct size was nonsignificantly changed to 19.4 +/-5.9 gm per 100 gm (p greater than 0.3). With transapical LV bypass, the infarct size was significantly reduced to 15.9 +/- 3.5 gm per 100 gm (p less than 0.025). This represented a 30% reduction of infarct size from controls. These results demonstrate that despite hemodynamic improvement with IABP, transapical LV bypass is necessary to markedly decrease myocardial work and significantly reduce infarct size.