Non surgical coronary artery recanalization in acute transmural myocardial infarction.

Abstract

SUMMARY In 41 consecutive patients with an acute transmural myocardial infarction (AMI) admitted within 3 hours after the onset of symptoms, we tried to recanalize the occluded coronary artery by an intracoronary infusion of streptokinase (SK) (2000 units/min). SK infusion was preceded by (1) an intracoronary injection of 0.5 mg nitroglycerin to rule out coronary artery spasm, (2) an attempt to recanalize the vessel mechanically with a flexible guidewire, and (3) an intracoronary injection of plasminogen (500 units) to increase the efficacy of the subsequent SK infusion. Coronary angiography revealed a total coronary artery occlusion in 39 patients and a subtotal occlusion in two patients. In 30 patients (73%), the occluded coronary artery was successfully recanalized within 1 hour (mean 29 ± 15 minutes), resulting in prompt contrast filling of the previously occluded vessel. An arteriosclerotic stenosis always remained at the site of the occlusion. Nitroglycerin opened the occluded coronary artery in one patient, contrast injection in seven patients and guidewire perforation in four of the 15 patients, in whom it was attempted. In 18 patients the occluded coronary artery was recanalized by intracoronary SK infusion alone. After the initial opening of the occluded coronary artery, subsequent SK infusion markedly reduced the degree of stenosis and visible thrombi disappeared. Clinically, recanalization was associated with significant relief of ischemic chest pain.None of the successfully recanalized patients died, including three patients with cardiogenic shock. ST-segment elevation was present on the ECG with no changes in the QRS complexes.Informed consent for recanalization was obtained from the patient and his relatives; in patients in cardiogenic shock, consent was obtained only from the patient's relatives. ProtocolRecanalization was performed on a 24-hour basis. In preparation for the procedure, patients with cardiogenic shock were intubated and artificially ventilated. The patients were heparinized with 10,000 units as a i.v. bolus. To avoid significant bradycardia during coronary angiography, in most patients a pacing catheter was placed in the apex of the right ventricle. In patients with left-heart failure, a Swan-Ganz catheter was advanced to the pulmonary artery. The coronary artery judged to be occluded, based on the distribution of ST-segment elevation on the ECG, was catheterized by a second investigator using a #8F Judkins catheter. In most cases, the "infarct-vessel" was easy to recognize and was either totally or subtotally occluded. The acute nature of a total occlusion was often characterized by a poor washout of the contrast medium (meglumine and sodium diatrizoate) from the area proximal to the occlusion. A

Antiarrhythmic Efficacy of Dipyridamole in Treatment of Reperfusion Arrhythmias

“…Even among clinical studies, varied incidence of reperfusion arrhythmias has been demonstrated. 2,[27][28][29][30][31] These results suggest that mechanisms responsible for AIVR and VT in clinical cases might be somewhat different from those observed in experimental models. In the present study, we clinically demonstrated for the first time that AIVR and VT that occur after reperfusion are probably cAMP-mediated arrhythmias and are therefore likely to be triggered arrhythmias.…”

A Novel Modified Tissue-Type Plasminogen Activator (t-PA), E6010, Gradually Increases Coronary Blood Flow after Thrombolysis Compared with Native t-PA, Urokinase and Balloon Catheter Occlusion-Reperfusion

“…Fur thermore, there have been many previous experimental reports of serious arrhythmias induced by the rapid re lease of coronary occlusion (18)(19)(20). In clinical studies, Goldberg et al (21) reported that reperfusion arrhyth mias occurred in 82010 of patients during restoration of anterograde coronary flow, and Mathey et al (22) reported that 5 of 41 patients showed ventricular fibrilla tion during thrombolytic reperfusion. In reperfusion ar rhythmias, there may be increased heterogeneity of electri cal activity in necrotic versus viable cells, leading to the instability of the cell membrane balance (20); the etiology of reperfusion arrhythmias appears to be different from that of arrhythmias produced during coronary occlusion (18).…”

Prospective randomized trial of intravenous and intracoronary streptokinase in acute myocardial infarction.

“…Patients who met all the following criteria were included in this study: (1) age 70 years or less, (2) clinical presentation suggestive of evolving acute myocardial infarction, (3) electrocardiogram showing ST segment elevation of ¢ 1.5 mm in two or more leads or marked T wave changes alone in an otherwise classic clinical presentation, (4) no contraindication to thrombolytic therapy or anticoagulation, (5) emergency catheterization and thrombolytic therapy available within 12 hr of onset of pain (as an exception, patients with evolving acute infarction and recurrent severe pain 12 to 24 hr after infarction were eligible, and (6) consent given for emergency coronary and left ventriculography and reperfusion intervention.…”