SUMMARY Streptokinase was infused into the ischemia-related coronary artery at a rate of 1000-2000 U/min for 15-95 minutes in 29 patients with acute myocardial infarction(AMI group) and in five patients with unstable angina pectoris (UAP group). Reopening of the completely obstructed vessel or increase of diameter at the site of subtotal lesions occurred in 22 AMI patients within 15-90 minutes of streptokinase infusion. In four of these patients, antegrade flow to the distal segments of the infarct vessel was seen after intracoronary nitroglycerin or sublingual nifedipine administration, which preceded streptoklinase infusion, and in two patients, streptokinase infusion was combined with recanalization by means of a guide wire. Chest pain was alleviated after reperfusion; ejection fraction was 50.5 ± 12% before and 54.6 ± 9% immediately after successful intracoronary lysis (p < 0.05). Repeat angiography, performed 25 ± 11 days after the acute intervention in 19 AMI patients, revealed reocclusion of the infarct vessel in one patient. Aortocoronary bypass surgery was performed electively in six AMI patients at varying intervals after successful lysis. Upon intraoperative inspection, the bulk of myocardium perfused by the recanalized vessel was found to be viable.Intracoronary streptokinase infusion did not result in opening the complete obstruction or improvement of lumen at the site of subtotal lesions in seven AMI patients and in all UAP patients. The total dose of 128,000 ± 36,000 U of streptokinase resulted in only minor decrease of fibrinogen, from 451 ± 93 mg% to 430 ± 91 mg%. Bleeding from the arterial puncture site in two patients, the only complications that could be attributed to the procedure, was due to heparinization.Intracoronary streptokinase application appears to be a safe and efficient method of achieving reperfusion and alleviating ischemia in the majority of patients with acute myocardial infarction. The method was not beneficial in treating unstable angina pectoris, and its potential for salvage of myocardium is yet to be assessed.IN A PREVIOUS STUDY, coronary angiography performed in 18 medically treated infarct patients during the acute and chronic stage revealed spontaneous recanalization of the infarct vessel in 40% of the cases.' In another study, acutely occluded coronary arteries could be recanalized mechanically by use of guide wires and catheters in 10 patients.2 Repeat angiography in the chronic stage of myocardial infarction showed increases in diameter of the recanalization canal in six of these patients. Most 307Materials and Methods Study GroupThe study group consisted of 34 patients in whom acute coronary angiography was performed between June 22, 1979 and March 30, 1980. The final diagnosis of AMI (patients 1-29) and UAP (patients 30-34) was based on serial CPK4 and CK-MB5 values. These enzymes were normal in the UAP patients, but were increased to pathologic levels (peak CPK 879 ± 816 U/1) in the AMI patients. All patients were admitted to the hospital because they had ches...

Summary: In five patients with acute myocardial infarction. the effects of both intracoronary nitroglycerin (NTG) and subsequent intracoronary streptokinase application were evaluated. In addition. transluminal recanalization was performed in one of these patients. Injection of NTG into the infarct-related coronary artery resulted in improved distal filling of the subtotally occluded left circumflex artery in one patient, and in transient patency of the completely occluded right coronary artery in a second patient. In a third patient patency of the totally occluded left anterior descending artery (LAD) was achieved by transluminal recanalization with a guide wire. In a fourth patient with occlusion of the LAD. there was no response to intracoronary NTG and mechanical recanalization was not attempted. Subsequent intracoronary infusion of streptokinase (1.000-2.000 U /min for 15-60 min) resulted in a further and long-term reduction of narrowing at the site of acute occlusion in patients I-III and in opening of the completely occluded LAD in patient IV. Improvement of lumen was paralleled by alleviation of symptoms. In a fifth patient. in whom the LAD was subtotally occluded. the degree of coronary obstruction could not be changed by intracoronary application of NTG or by lysis. In this patient. symptoms and ECG changes improved with reduction of pathologically elevated blood pressure values. The findings suggest that myocardial infarction had been caused by thrombotic occlusion in four patients. and that spasm of the infarct vessel could have been an additional factor in two of these patients. In the fifth patient. an increase of afterload in the presence of a subtotal lesion might have caused the critical imbalance between oxygen supply and demand. resulting in cell death.

Paraoxonase is an HDL-associated enzyme implicated in the pathogenesis of atherosclerosis by protecting lipoproteins against peroxidation. Its biallelic gene polymorphism at codon 192 (glutamine/arginine) has been associated with coronary artery disease (CAD). To further evaluate the role of this paraoxonase gene polymorphism for CAD in type 2 diabetes, we determined the paraoxonase genotype in 288 type 2 diabetic patients (170 with and 118 without angiographically documented CAD). The paraoxonase 192 Gln/Arg genotype was assessed using polymerase chain reaction followed by AlwI digestion. The frequency of the Gln allele was 0.656 in the CAD patients and 0.746 in the controls (chi2 = 5.36, P = 0.02). Compared with the Gln/Gln genotypes, the age-adjusted odds ratio for CAD was 1.78 (95% CI 1.08-2.96, P = 0.02) in subjects carrying at least one Arg allele. In the multivariate analysis, this association was even stronger after correction for the possible confounders age, sex, smoking history, and hypertension. Among current and former smokers, the odds ratio (OR) for having CAD among patients with at least one Arg allele was 3.58 (1.45-9.53, P < 0.01). The paraoxonase Arg allele was not associated with the history of myocardial infarction (OR 1.20 [0.73-1.99, NS]), but was with the extent of CAD (OR for three-vessel disease 1.92 [1.15-3.27, P = 0.01]). Our data indicate that the 192 Arg allele of the human paraoxonase gene is a risk factor for CAD but not myocardial infarction in type 2 diabetic patients, a risk factor further modified by cigarette smoking. This risk could possibly be explained by a reduced ability of the paraoxonase Arg isoform to protect lipoproteins against peroxidation.

Within the physiological range of flow, calculated aortic valve area was less dependent on hemodynamic conditions than were valvular resistance and stroke work loss, which varied as a function of flow. Thus, for the assessment of the severity of aortic stenosis, the Gorlin valve area is superior over valvular resistance and stroke work loss, which must be indexed for flow to adequately quantify the hemodynamic severity of the obstruction.

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We randomly assigned patients with a clinical diagnosis of acute myocardial infarction to one of four treatment groups: intracoronary streptokinase, intracoronary nitroglycerin, intracoronary streptokinase and intracoronary nitroglycerin, or conventional therapy without initial angiography. Of 124 patients 122 sustained acute myocardial infarction. Initial angiography revealed total occlusion of the coronary artery responsible for infarction in 67 per cent (61 of 91). Acute recanalization occurred in 74 per cent (32 of 43) of patients receiving streptokinase but in only 6 per cent (1 of 18) of patients treated with nitroglycerin alone (P less than 0.01). At angiography of all four groups on Day 10 to 14 the vessel responsible for acute myocardial infarction was patent in 77 per cent (71 of 92) of patients; there was no difference among groups, indicating gradual, endogenous thrombolysis in patients not treated with streptokinase. Patients with subtotal obstruction initially had significant improvement in left ventricular function, significantly lower peak creatine kinase levels, and a trend toward lower mortality than patients with total occlusion initially. Mortality at six months in patients receiving streptokinase (21 per cent, 13 of 62) did not differ significantly from that in patients not treated with streptokinase (10 per cent, 6 of 61). Additional studies will be necessary to assess treatment effects in the angiographic subsets identified by this trial.

In previous experimental and pediatric studies, the ratio of pulmonary to systemic flow (Qp/Qs) was accurately estimated by Doppler echocardiography in various cardiac shunt lesions. The purpose of this study was to assess the accuracy of pulsed Doppler echocardiography in determining the magnitude of shunt flow in adult patients with an ostium secundum type atrial septal defect. In 32 patients with high quality echocardiograms and excellent Doppler signals, blood flow was measured in the right and left ventricular outflow tract by Doppler echocardiography. In 16 patients without heart disease, the correlation (r) between systemic (Qs) and pulmonary (Qp) blood flow was 0.96 (SEE = 0.417 liter/min, y = 1.05x - 0.21) and the mean Qp/Qs ratio was 1.01 +/- 0.09. In 16 patients with an atrial septal defect, the Qp/Qs ration measured by oximetry ranged from 1.34 to 4.61 and by pulsed Doppler echocardiography from 1.31 to 4.46 (p = NS). In these 16 patients, the correlation between the Qp/Qs ratio determined by oximetry and pulsed Doppler echocardiography was significant (r = 0.82, SEE = 0.54). In the total group of 32 patients, the correlation was stronger (r = 0.93, SEE = 0.37). Systematic differences between the invasive and noninvasive shunt calculations did not occur. Thus, in adult patients with an atrial septal defect of the secundum type and high quality echocardiograms, the magnitude of left to right shunt can be accurately assessed by pulsed Doppler echocardiography. In the absence of pulmonary hypertension, pulsed Doppler echocardiography provides precise information for the decision to undertake conservative or operative treatment.

In 7 patients, the recently occluded infarct‐related vessel was recanalized by transluminal catheter techniques during acute myocardial infarction (Group A). 4 patients had single‐vessel disease, 2 patients two‐vessels disease and one, involvement of three vessels. Control angiography was performed in 6 patients, 8 days to 7 months later. Changes of coronary artery anatomy and left ventricular function were compared with a group of 9 conventionally treated patients, who were found to have occlusion of the infarct‐related vessel in the acute stage (Group B). Five Group B patients had one‐vessel disease, 3 patients two‐vessel disease and 1 patient, involvement of all three vessels. In the chronic stage, all transluminally recanalized vessels were found to be patent in Group A. There was spontaneous recanalization of the infarct vessel in 4 of 9 Group B patients. In Group A, the length of the akinetic segment (AKS) decreased significantly (p < 0.05) from 145.4±48.5 mm to 73.2 ± 73.4 mm (mean ± SD). Volume parameters did not change significantly. In Group B, length of the AKS did not change significantly, EDVI increased significantly from 81.1 ±19.8 to 106.8±40.6 ml/m2 (p < 0.05); ESVI increased significantly from 41.7 ± 13.7 ml/m2 to 66.8 ± 37.9 ml/m2 (p < 0.01). In the acute stage, length of the AKS and volume parameters did not differ significantly between the two groups. In the chronic stage, AKS was significantly shorter (A: 73.2 ± 63.4 mm; 144.9 ± 59 mm (p < 0.0025)) and EF was significantly higher (A: 54.6 ±11.6%; B: 40.9 ±14.5% (p < 0.05)) in Group A. Peak CPK was lower in Group A (A: 1009 ± 827 U/l; B: 1324 ± 655 U/l), but this difference did not achieve statistical significance. Results of this pilot study suggest that transluminal recanalization in the early phases of acute myocardial infarction might result in limitation of myocardial injury. However, further research will be needed to improve the technique and to test its results.