Clinical study
Quantitative coronary arteriography: Coronary anatomy of patients with unstable angina pectoris reexamined 1 year after optimal medical therapy

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Abstract

The effect of optimal medical therapy on coronary arterial anatomy was evaluated in 25 patients with unstable angina pectoris. Coronary arterial diameter and the extent of stenosis were exactly quantified in two successive coronary angiograms performed in each patient at approximately a 1 year interval (range 4 to 31 months, average 12.4 months). The measuring device was a vernier caliper with an accuracy of 0.05 mm. After 1 year of medical treatment 69 stenoses of the three major coronary branches showed no significant change: The average degree of area obstruction of 27 stenoses of the right coronary artery was 79 and 84 percent in the initial and second studies, respectively; that of 26 stenoses of the left anterior descending artery 78 and 77 percent, respectively, and that of 16 stenoses of the left circumflex artery 73 and 83 percent, respectively. In 11 patients, 14 stenoses showed a distinct progression of more than 20 percent area obstruction. All six stenoses showing more than 90 percent obstruction in the first angiogram progressed to complete obstruction within 1 year. In five other patients area obstruction in five stenoses regressed by more than 20 percent. The anatomy of vessel segments distal to obstructions remained unchanged within 1 year. It is concluded from these quantitative measurements that the distribution and severity of coronary lesions are similar in patients with stable and unstable angina pectoris. Coronary anatomy showed no significant change after 1 year of medical treatment. The rate of progression was substantially lower than previously reported in patients with stable angina pectoris.

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    This research was supported by the Specialized Center of Research for Ischemic Heart Disease, Contract 5P50HL 17667-04, the Cardiovascular Research and Training Center, Program Project Grant HL310 (Division of Heart and Vascular Disease, National Heart and Lung Institute), the Clinical Research Unit Grant M01-RR0003213 (General Clinical Research Centers Program, Division of Research Resources National Institutes of Health), and by a grant (Ra 275) of the Deutsche Forschungsgemeinschaft, Bonn, Federal Republic of Germany.

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