Pathological effects of alcohol septal ablation for hypertrophic obstructive cardiomyopathy.

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.

Effect of electrode position and gel-application technique on predicted transcardiac current during transthoracic defibrillation.

STUDY OBJECTIVE: In transthoracic defibrillation, the American Heart Association (AHA) recommends wide separation of electrodes and avoidance of gel smearing between electrodes. Few data support this recommendation. Our objective was to determine the importance of electrode placement and gel-application technique on transcardiac defibrillation current and the effect of changes caused by postexercise vasodilation and sweating. METHODS: Our subjects were 10 normal adults, 5 men and 5 women, who ranged in age from 22 to 48 years. We determined interelectrode impedance (Z) using a validated test-pulse method that does not require shock delivery. Electrode placement/gel-application techniques were varied among four types: (1) AHA-recommended technique (apex-to-anterior electrode placement, no smearing of gel between electrodes); (2) parasternal-to-anterior placement, electrodes within 2 cm of each other, no smearing of gel between electrodes; (3) parasternal-to-anterior placement, electrodes within 2 cm of each other with smearing of gel between electrodes (worst-case scenario); and (4) apex-to-anterior placement, smearing of gel between electrodes. To assess the effect of cutaneous vasodilation and sweating on interelectrode impedance, we repeated these measurements after the subjects performed 12 to 18 minutes of treadmill exercise. The ratio of predicted transcardiac current of the AHA technique to that of the nonstandard technique was estimated with this formula: square root of Z, non-standard technique divided by square root of Z, AHA technique. RESULTS: Resting interelectrode impedance declined 38% from 58 +/- 10.3 omega (AHA-recommended technique) to 36 +/- 7.6 omega (electrode paddles adjacent, gel smeared between) (P < .01). Predicted transcardiac current ratio was reduced to .78 +/- .09 (P < .01), a 22% reduction. We noted no change in the results after exercise. CONCLUSION: Adjacent placement of electrodes and smearing of gel between electrodes creates a low-impedance pathway along the chest wall, which shunts current away from the heart. Thus improper application of electrodes and gel substantially degrades transcardiac current and may result in failed defibrillation. Sweating and vasodilation did not cause a similar problem.