Production of a critical coronary arterial stenosis in closed chest laboratory animals: Description of a new nonsurgical method based on standard cardiac catheterization techniques

A nonsurgical method for producing a critical coronary arterial stenosis in a closed chest laboratory animal would enhance our ability to study the effects of reversible myocardial ischemia on many aspects of left ventricular function and also would facilitate experiments aimed at studying the effects of various interventions on regional myocardial blood flow distal to a severe stenosis. Accordingly, a new technique was developed for the production of a critical coronary arterial lesion in a closed chest laboratory animal. Under fluoroscopic control a small plastic truncated cone (5 mm long, outside diameter 3.5 mm tapering to 3.25 mm) with a narrow, central internal lumen (diameter 0.625 mm) was passed over a guide wire into the left anterior descending coronary artery of a closed chest, heparinized pig (n = 6). Regional myocardial blood flow (microsphere technique) distal to the artificial stenosis (distal zone) and in myocardium perfused by the circumflex coronary artery was determined under the following conditions: at rest (control I), at the 10th minute of atrial pacing (190 min^?1) and 10 to 15 minutes after discontinuation of pacing (control II). At rest, transmural blood flow distal to the stenosis (1.29 ± 0.32 ml/min per g, mean ± standard deviation) was almost identical to that in the circumflex zone (1.31 ± 0.31, r = 0.93, p < 0.01). During atrial pacing transmural flow increased significantly (p < 0.01 versus control) in the circumflex zone (1.73 ± 0.27) and then returned to control value (1.34 ± 0.38) after pacing was discontinued. In contrast, transmural flow in the distal zone (1.45 ± 0.40) failed to increase significantly with pacing. In addition, during atrial pacing the endocardial to epicardial blood flow ratio distal to the stenosis decreased from 0.99 ± 0.13 (control I) to 0.68 ± 0.14 (p < 0.01), whereas it remained unchanged in the circumflex zone (1.1 ± 0.11 to 1.1 ± 0.08, difference not significant). Finally, the artificial intraluminal stenosis remained patent for the duration of the study (5.1 ± 0.05 hours) in all animals. Thus the intracoronary plastic stenosis is a promising new method for the production of a critical coronary arterial lesion in closed chest laboratory animals.