Timing and magnitude of serum creatine kinase-MB after transcatheter cardiac tissue fulguration in man

This study examined the impact of transcatheter fulguration on creatine kinase-MB release in 21 patients (age range 17-71 years). Arrhythmia diagnoses were ventricular tachycardia 9, atrial fibrillation with a rapid ventricular response 7, atrioventricular nodal reentry 2, and reciprocating tachycardia utilizing a posteroseptal accessory pathway 3. Seven patients had apparently normal hearts while 8 had ischemic heart disease and 6 cardiomyopathy. Timing of initial elevated creatine kinase-MB activity (mean 1.34 ± 0.69 SD hours) and peak creatine kinase-MB activity (mean 3.73 ± 0.89 SD hours) was relatively uniform in all patients. Time to peak creatine kinase-MB activity was unrelated to either underlying cardiac disease (normal: 3.9 ± 1.0 hours; ischemic heart disease: 3.5 ± 0.9 hours; cardiomyopathy: 3.8 ± 0.9 hours), or fulguration site (His bundle (n = 9): 4.2 ± 0.9 hours, proximal coronary sinus (n = 3): 3.3 ± 0.3 hours, ventricle (n = 9): 3.4 ± 0.8 hours). The magnitude of peak serum creatine kinase-MB activity was independent of myocardial diagnosis or fulguration site, but was linearly related to total energy delivered (r = 0.5, P < 0.022). The latter correlation was particularly strong within cardiac diagnosis subgroups (normal: r = 0.92, P < 0.002; ischemic heart disease: 0.73, P < 0.04; non-ischemic cardiomyopathy: r = 0.57, P = NS). Thus, serum creatine kinase-MB activity following transcatheter fulguration is linearly related to the magnitude of delivered energy, and is similar to that observed after transient coronary artery occlusion and reperfusion.