William Ganz

Pressures in the right side of the heart and pulmonary capillary wedge can be obtained by cardiac catheterization without the aid of fluoroscopy. A No. 5 Fr double-lumen catheter with a balloon just proximal to the tip is inserted into the right atrium under pressure monitoring. The balloon is then inflated with 0.8 ml of air. The balloon is carried by blood flow through the right side of the heart into the smaller radicles of the pulmonary artery. In this position when the balloon is inflated wedge pressure is obtained. The average time for passage of the catheter from the right atrium to the pulmonary artery was 35 seconds in the first 100 passages. The frequency of premature beats was minimal, and no other arrhythmias occurred.

A technique was developed for measurement of blood flow in the coronary sinus in man by continuous thermodilution. For single determinations, 5% dextrose at room temperature is injected at a constant rate of 35 ml/min for a period of about 20 sec. In 14 subjects with normal coronary arteries the mean coronary sinus blood flow was 122 ± 25 ml/min (range, 83 to 159 ml/min). The blood flow computed per 100 g of left ventricle was 82 ± 16 ml/min, which is in the range of values obtained by nitrous oxide and coincidence counting methods. In 35 patients with arteriographically confirmed coronary artery disease the mean flow was similar (128 ± 20 ml/min; range, 92 to 167 ml/min). A special catheter was used for simultaneous measurement of blood flow in the coronary sinus and great cardiac vein. In eight normal subjects the mean great cardiac vein flow was 68 ± 11 ml/min (range, 51 to 78 ml/min) or 65 ± 10% of the coronary sinus blood flow. The method allowed continuous measurement of flow over a period of several minutes and, for the first time, measurement of rapid changes in myocardial perfusion.

To visualize intracoronary lesions in patients with different clinical expressions of coronary disease, we performed coronary angioscopy during coronary-artery bypass surgery in 10 patients with unstable angina and 10 patients with stable coronary disease. We examined a total of 32 vessels, using flexible fiberoptic angioscopes. Twenty-two vessels had no acute intimal lesion; three had complex plaques, six had thrombi, and one had both. Coronary angiography correctly identified the absence of complex plaque and thrombus in 22 vessels, but it detected only one of four complex plaques and one of seven thrombi. On angioscopy, none of the 17 arteries in the patients with stable coronary disease had either a complex plaque or thrombus. In the "offending" arteries of the patients with unstable angina, all three patients with accelerated angina had complex plaques and all seven with angina at rest had thrombi. We conclude that angioscopy frequently reveals complex plaques or thrombi not detected by coronary angiography. Our observations suggest that anginal syndromes that are refractory to medical treatment can be caused by unstable pathologic processes in the intima. Ulceration of plaques may increase the frequency and severity of effort angina, and the subsequent development of partially occlusive thrombi may cause unstable rest angina.