Pathological effects of alcohol septal ablation for hypertrophic obstructive cardiomyopathy
A L Baggish1, R N Smith, I Palacios
1Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.
Insights
Ethanol septal ablation for hypertrophic obstructive cardiomyopathy causes acute myocardial infarction and vascular necrosis. This ethanol-induced infarction differs from atherosclerotic disease, suggesting direct vascular toxicity is key to the procedure’s success.
Area of Science:
- Cardiovascular Pathology
- Interventional Cardiology
Background:
- The mechanism of alcohol septal ablation (ASA) for hypertrophic obstructive cardiomyopathy (HOCM) is not fully understood.
- Pathological effects of intracoronary ethanol administration require elucidation.
Observation:
- Surgical and autopsy specimens from four patients post-ASA were examined.
- Tissue analysis occurred 2 days to 14 months after unsuccessful ASA.
Findings:
- Early post-ASA, coagulative necrosis of myocardium and septal arteries was observed.
- Affected arteries showed distension and occlusion by necrotic debris, lacking thrombi.
- Late specimens revealed heterogeneous scarring with viable myocytes.
Implications:
- Intracoronary ethanol induces acute myocardial infarction with vascular necrosis in HOCM.
- Ethanol-induced infarction is distinct from atherosclerotic infarction due to coagulative necrosis and lack of thrombi.
- Direct vascular toxicity of ethanol is a likely mechanism for successful ASA.
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.
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