Atherosclerosis 153 (2000) 259
Letter to the Editors
www.elsevier.com/locate/atherosclerosis
Why is atherosclerosis non-existent in human intramy-ocardial coronary arteries?
To the Editor
In explaining the’neglected’ phenomenon of absence of atherosclerosis in human intramyocardial (or intra-mural) coronary arteries, Scher advanced the theory of’protective’ action of myocardial contraction on the transfer phase of the development of atherosclerosis [1]. He also cited as supporting evidence that atherosclero-sis is rare beneath myocardial bridges in superficial coronary arteries [2] where myocardial contraction plays a significant role but common in venous bypass grafts [3] which are superficially located and therefore not subject to the effects of myocardial contraction.If contraction of the myocardium is the sole or principal mechanism in preventing atherosclerosis in human in-tramyocardial coronary arteries, then a paradox exists in hypertrophic cardiomyopathy. In the latter condition where strong myocardial contraction is the sine qua non, atherosclerosis of intramyocardial coronary arter-ies is common, existing in more than 80% of the patients studied at necropsy [4 – 6], although the epicar-dial coronary arteries are typically free of obstructive atherosclerotic disease [7]. Although abnormal intramy-ocardial coronary arteries which was found in three of the eight infants with hypertrophic cardiomyopathy [5] could represent a congenital component of the underly-ing cardiomyopathic process [5,8], this findunderly-ing still poses a strong challenge to the theory that myocardial contraction per se is’protective’ against atherosclero-sis.Perhaps it is the altered flow pattern that results from myocardial contraction rather than myocardial contraction per se that is mainly responsible for absence of atherosclerosis in human intramyocardial coronary arteries. In the case of myocardial bridges, flow under the bridges is laminar and therefore less intimal thick-ening is produced there, whereas the intimal thickthick-ening
proximal to the bridging is striking due to greater force from arterial blood flow at the boundary area [2]. This also explains why coronary arteriosclerotic plaque for-mation is enhanced just proximal to branching points with relative sparing of the flow dividing regions [9].
References
[1] Scher AM. Absence of atherosclerosis in human intramyocardial coronary arteries: a neglected phenomenon. Atherosclerosis 2000;149:1 – 3.
[2] Ishii T, Hosoda Y, Osaka T, Imai T, Shimada H, Takami A, et al. The significance of myocardial bridge upon atherosclerosis in the left anterior descendng coronary artery. J Path 1986;148:279 – 91. [3] Davies MG, Hagen PO. Pathophysiology of vein graft failure: a
review. Eur J Vasc Endovasc Surg 1995;9:7 – 18.
[4] Tanaka M, Fujiwara H, Onodera T, Wu D-J, Matsuda M, Hamashima Y, et al. Quantitative analysis of narrowings of intramyocardial small arteries in normal hearts, hypertensive hearts, and hearts with hypertrophic cardiomyopathy. Circulation 1987;75:1130 – 9.
[5] Maron BJ, Wolfson JK, Epstein SE, Roberts WC. Intramural (‘small vessel’) coronary artery disease in hypertrophic cardiomy-opathy. J Am Coll Cardiol 1986;8:545 – 57.
[6] Maron BJ, Bonow RO, Cannon RO III, Leon MB, Epstein SE. Hypertrophic cardiomyopathy. Interrelations of clinical manifes-tations, pathophysiology, and therapy. New Engl. J. Med. 1987;316:780 – 789, 844 – 852.
[7] Louie EK, Edwards LC, III. Hypertrophic cardiomyopathy. Prog Cardiovasc Dis 1994;36:275 – 308.
[8] Braunwad E. Heart disease. A textbook of cardiovascular medicine, 5th edn. Philadelphia, PA: Saunders, 1997:1416. [9] Julian DG, Camm AJ, Fox KM, Hall RJC, Poole-Wilson PA.
Diseases of the heart, 2nd edn. Philadelphia, PA: Saunders, 1996:946.
Tsung O. Cheng
Department of Medicine The George Washington Uni6ersity Medical Center
2150 Pennsyl6ania A6enue
N.W., Washington, D.C.20037 USA
.
