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Circulation, Vol 59, 913-919, Copyright © 1979 by American Heart Association

ARTICLES

The pathophysiology and diverse etiology of septal perforator compression

JB Kostis, AE Moreyra, N Natarajan, M Hosler, PT Kuo and HL Conn Jr

Compression of the septal perforator branches of the left anterior descending artery (systolic obliteration and diastolic reopacification during arteriography) has been proposed as a marker of idiopathic hypertrophic subaortic stenosis (IHSS). Among 568 unselected coronary arteriograms this angiographic finding was pronounced in 11 of 17 patients with IHSS; in 12 of 44 with aortic stenosis (AS); in five of 46 patients with severe (95%) proximal stenosis of the left anterior descending coronary artery; in three of 18 with myocardial bridge; in three of 12 with hypertrophic cardiomyopathy; in one of 62 with normal right and left heart catheterization; and in none of the 369 patients with other cardiac diseases. Mild septal perforator compression (SPC) was observed in six other patients with IHSS, one patient with hypertrophic cardiomyopathy, 19 patients with AS, eight patients with severe stenosis of the LAD and one patient with myocardial bridge. SPC was more pronounced in patients with high systolic pressure gradients (Spearmann Rank r = 0.64, p = 0.003 and Pearson r = 0.31, p = 0.159 for IHSS; Spearmann Rank r = 0.47, p = 0.001; Pearson r = 0.51, p = 0.001 for AS) and increased septal thickness (Spearmann Rank r = 0.45, p = 0.05, Pearson r = 0.61, p = 0.011 for IHSS; Spearmann r = 0.44, p = 0.013, Pearson r = 0.42, p = 0.018 for AS). SPC is not specific for IHSS. It may result from a decrease of the intraluminal pressure in the septal perforators resulting from obstruction at the left ventricular, aortic valvular or coronary arterial level and from increased septal thickness which may lead to higher extraluminal pressure.