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Prostaglandin E1 was administered by means of coronary venous synchronized retroperfusion and the effectiveness of the combined (prostaglandin-retroperfusion) system was examined during acute myocardial ischemia in 10 closed chest anesthetized dogs. Such treatment was administered between 30 minutes and 3 hours after occlusion of the proximal left anterior descending coronary artery. An equivalent series of 10 dogs with arterial blood retroperfusion alone and 9 untreated dogs served as control subjects. Standardized two-dimensional echocardiographic measurements of global and regional left ventricular function were performed in five short-axis cross sections. The global low left ventricular section and its profoundly ischemic anterolateral region exhibited distinctly improved systolic fractional area changes as a result of the prostaglandin E1 retroperfusion treatment between 30 minutes and 3 hours after occlusion (22.9 +/- 1.5 to 41.2 +/- 4.0% and 1.8 +/- 3.6 to 29.4 +/- 5.6%, respectively). In contrast, further deterioration in function was noted during an untreated equivalent coronary occlusion period (16.3 +/- 2.7 to 10.0 +/- 3.3% and 12.6 +/- 6.1 to 4.1 +/- 6.9%). Although arterial blood retroperfusion alone provided distinct benefits in the ischemic region of a midpapillary echo section (from 13.4 +/- 3.9 to 32.1 +/- 10.4%, p less than 0.05), no improvements were observed in profoundly jeopardized segments at the low left ventricular level (5.6 +/- 6.0 to 0.9 +/- 5.7%). Triphenyltetrazolium chloride delineation of infarction revealed significant myocardial salvage with prostaglandin E1 retroperfusion as compared with findings in untreated control dogs (3.7% +/- 1.3% of the left ventricle versus 9.3 +/- 1.9%, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

This study examined whether an occlusive thrombus within a coronary artery can be lysed by streptokinase retroperfusion into the associated regional coronary vein. Experimental coronary artery thrombosis was induced in 15 closed chest dogs by placing a small copper coil at a proximal site of the left anterior descending coronary artery. Total thrombotic obstruction of this artery was verified within 10 to 60 minutes (38.0 +/- 15.8, mean +/- standard deviation) and streptokinase was administered within 94.0 +/- 17.4 minutes from coil insertion at an average rate of 42 IU/kg per minute by one of three modes: 1) intermittent 10 minute direct coronary venous retroinfusion (five dogs); 2) continuous infusion into the pumping circuit of synchronized phased retroperfusion of the great cardiac vein with arterial blood (five dogs); and 3) for comparison, streptokinase administered intravenously (five dogs). The intracoronary thrombus was fully lysed and anterograde reperfusion established within 51.0 +/- 18.7 minutes by intermittent streptokinase retroinfusion, and in 50.0 +/- 6.1 minutes by streptokinase supplemented synchronized retroperfusion (50.5 +/- 13.2 minutes for pooled retrograde coronary venous delivery). Lysis was also induced by systemic streptokinase, but the time to lysis was significantly longer and more variable (131.6 +/- 60.6 minutes) than with retrograde administration (p less than 0.01). The retroperfusion modality appears the preferable technique because it provides early thrombolysis and, at the same time, improves cardiac function and maintains myocardial viability of the jeopardized ischemic zone pending achievement of full reflow. Thus, streptokinase retroperfusion, if promptly instituted, may be a useful complemental nonsurgical treatment of evolving acute myocardial infarction after thrombotic coronary artery occlusion.

Hypothermic synchronized retroperfusion was applied during coronary artery occlusion to determine its ability to alleviate junctional derangements of reperfusion and to reduce infarct size. The proximal left anterior descending coronary artery was occluded in 25 closed chest dogs for 3 hours and then reperfused for 7 days. Thirteen dogs with no reperfusion pretreatment served as a control group (Group A). In 12 dogs, hypothermic retroperfusion was applied from 30 minutes up to 3 hours of the occlusion period (Group B). Sequential two-dimensional echocardiographic and hemodynamic as well as metabolic measurements were performed. Compared with untreated control dogs, dogs with hypothermic synchronized retroperfusion had significantly reduced heart rate and rate-pressure product, decreased left ventricular volumes and improved ejection fraction during the occlusion period. Two-dimensional echocardiographically-derived ischemic zone systolic fractional area change and systolic wall thickening indicated significantly improved function as a result of retroperfusion. During the reperfusion period, untreated control dogs (group A) had more severe derangements in hemodynamics and wall motion than dogs treated by hypothermic retroperfusion (group B). Mortality was 30.7% in group A, 16.7% in group B and 7th day infarct size as percent of the left ventricle was 12.0 +/- 6.5 (mean +/- standard deviation) and 4.2 +/- 5.9, respectively (p less than 0.02). It is concluded that hypothermic synchronized retroperfusion applied after coronary occlusion and before reperfusion significantly improves cardiac function during occlusion, minimizes complications of reperfusion and reduces the ultimate infarct size. Because this form of circulatory assistance helps maintain cardiac function and delays the evolution of myocardial necrosis, its application may be beneficial during an evolving acute myocardial infarction before achievement of surgical or nonsurgical reperfusion.

Hypothermic synchronized retroperfusion (HSRP) was applied in closed-chest dogs after acute coronary occlusion to determine whether this intervention can significantly retard the otherwise rapidly developing irreversible ischemic injury. The left anterior descending coronary artery (LAD) was occluded for 3 hours in 22 dogs and for 6 hours in 16 dogs. Starting 30 minutes after occlusion, HSRP was applied during maintained coronary occlusion in 21 dogs. The remaining dogs served as untreated controls. Arterial blood was cooled to 20 degrees C and retroperfused in diastole into the regional coronary veins. Hemodynamics, contrast cineangiography and two-dimensional echocardiography were measured sequentially. Glycogen-depleted ischemic areas and necrotic zones were delineated in transverse slices of the left ventricle. Untreated controls dogs further deteriorated; in contrast, HSRP between 30 minutes and 3- and 6-hour LAD occlusion significantly reduced the rate-pressure product (21.3 +/- 4.0% or 26.8 +/- 8.2%) and left ventricular end-diastolic pressure (39.5 +/- 9.5% or 51.4 +/- 7.7%) and increased ejection fraction (28 +/- 17% and 33 +/- 2.0%). HSRP caused no arrhythmias and led to much less necrosis of ischemic myocardium in the treated 3- or 6-hour occlusion series (7.4 +/- 2.7% or 28.9 +/- 12.6%) than in respective untreated controls (47.1 +/- 8.9% and 72.3 +/- 5.9%). Moderately hypothermic closed-chest phased retroperfusion appears to protect reversibly injured ischemic myocardium and improve cardiac function. Such treatment may be particularly suitable in the earliest stages of evolving myocardial infarction, when maintenance of myocardial viability is essential for preservation of jeopardized myocardium while awaiting coronary bypass revascularization or nonsurgical thrombolytic reperfusion.