A L Baggish1, R N Smith2, I Palacios1, G J Vlahakes3, D M Yoerger1, M H Picard1, P A Lowry1, I-k Jang1 and M A Fifer1
1) Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA
2) Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts, USA
3) Department of Surgery, Massachusetts General Hospital, Boston, Massachusetts, USA
Background: The pathological effects and the mechanisms of action of intracoronary administration of ethanol for alcohol septal ablation (ASA) for the management of hypertrophic obstructive cardiomyopathy (HOCM) are unknown.
Methods: We examined surgical specimens and, in one case, autopsy specimens from four patients who underwent surgical septal myectomy 2 days to 14 months after unsuccessful ASA.
Results: Pathological examination early after ASA showed coagulative necrosis of both the myocardium and the septal perforator arteries. Affected arteries were distended and occluded by necrotic intraluminal debris, without platelet–fibrin thrombi. Late after unsuccessful ASA, excised septal tissue was heterogeneous, containing a region of dense scar, and adjacent tissue containing viable myocytes and interspersed scar.
Conclusions: Intracoronary administration of ethanol in patients with HOCM causes acute myocardial infarction with vascular necrosis. The coagulative necrosis of the arteries, their distension by necrotic debris and the absence of platelet–fibrin thrombi distinguish ethanol-induced infarction from that caused by atherosclerotic coronary artery disease. The direct vascular toxicity of ethanol may be an important aspect of the mechanism of successful ASA.
Abbreviations: ASA, alcohol septal ablation; CCS, Canadian Cardiovascular Society; HOCM, hypertrophic obstructive cardiomyopathy; LVOT, left ventricular outflow tract; MVR, mitral valve replacement; NYHA, New York Heart Association; SAM, systolic anterior motion
Heart 2006;92:1773-1778
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