br Materials and methods br Results br
Materials and methods
Discussion Our results demonstrated that patients who underwent ICD implantation and received 15J-DT exhibited evidence of myocardial damage as indicated by increased serum c-TNT and H-FABP levels. On the other hand, ≤10J-DT (9J or 10J) was associated with an acceptable successful DT rate and no significant elevation in either marker. We used the specific myocardial injury markers c-TNT and H-FABP. Some reports clearly show the clinical usefulness of c-TNT among patients with myocardial infarctions [15,16] and cardiac contusions . In addition, H-FABP elevation is associated with minimal damage to cardiomyocytes and reflects superficial myocardial injury. Basic and clinical research in rats, as well as human autopsy analyses have revealed that H-FABP leakage occurs despite the absence of myocyte necrosis . H-FABP is a low-molecular-weight protein that is normally confined to the cytoplasm and released into the circulation through the porous membranes of damaged myocardial Apoptosis Compound Library [19,20]. There are some reports regarding the relationship between internal shocks and myocardial injury. Hurst et al. reported that mean defibrillation energy during DT was significantly higher in patients with cardiac troponin I (c-TNI) elevation (20.0±3.8J) than in those without marker elevation (14.6±3.4J). Multivariate analysis revealed that a mean defibrillation energy ≥18J was a strong risk factor for a rise in c-TNI . Boriani et al. confirmed asymptomatic, minor myocardial injuries in patients with persistent atrial fibrillation who underwent atrial cardioversion. In these subjects, two catheters were placed in the right atrium and the coronary sinus, respectively, to administer internal shocks. The level of c-TNI was elevated in 15 of 35 (43%) patients, and the total delivered energy ranged from 28.7±10.4 to 35.3±32.6J . In accordance with earlier reports, we found that both c-TNT and H-FABP levels were elevated in patients undergoing 15J-DT. If myocardial damage only affected the limited focal myocardium, it might not be a serious problem. However, endocardial shock affects the entire heart. Schirmer et al. showed that in 13 fox hounds, the use of endocardial lead systems with low-energy countershocks caused severe myocardial alterations such as swollen mitochondria, disruption of mitochondrial crests, and the loss of integrity of the inner and outer mitochondrial membranes . Takano et al. assessed 17 patients with ICD implantation and found a significant correlation between shock strength and the change in cardiac index; lower energy shocks did not affect cardiac hemodynamics . Although the precise relationship between increased myocardial damage marker levels and altered hemodynamic status is unclear, high-energy DT may induce focal myocardial damage and affect cardiac hemodynamics. Several studies concluded that neither ICD shock frequency nor mortality was different between patients who underwent DT and those who did not [10,12]. Conversely, patients who did not undergo intraoperative DT had significantly higher overall mortality rates than those who did [9,11]. In addition to this controversy, we need to consider the possibility of device malfunction. A single successful DT for VF was just as useful as repeat DTs [23,24]. Recently, sub-analysis of the Shockless IMPLant Evaluation (SIMPLE) trial demonstrated that elevated troponin levels after ICD implantation were associated with a high mortality rate (adjusted hazard ratio 1.43, p=0.001) and a high risk of arrhythmic death (adjusted hazard ratio 1.80, p=0.002). Abnormal troponin level elevation was frequently observed in patients who underwent DT (>17J) compared with those without DT (42.1% vs 37.5%, p=0.04) . From this viewpoint, a single minimally invasive DT may be acceptable. Although the success rate for DT was not significantly different between ≤10J-DT and ≥15J-DT, the former tended to have a lower success rate. Minimally invasive DT is a promising strategy; however, unsuccessful attempts are followed by the administration of additional higher energy DTs. Therefore, ≤10J-DT should be avoided in patients who may have a high risk for an unsuccessful DT. Unfortunately, we could not identify specific risk factors associated with an unsuccessful DT in the present investigation. Earlier studies reported that atrial fibrillation, left ventricular systolic dysfunction, left ventricular hypertrophy, and amiodarone usage were predictive of a high defibrillation threshold [26,27].