Quantitative analysis of infarct size, contraction band necrosis, and coagulation necrosis in human autopsied hearts with acute myocardial infarction after treatment with selective intracoronary thrombolysis.
Abstract:To assess the importance of contraction band necrosis (CBN) in patients with acute myocardial infarction (AMI) treated with selective intracoronary thrombolysis, CBN, coagulation necrosis, and infarct size (expressed as CBN + coagulation necrosis) were analyzed quantitatively in 16 autopsied hearts. Intracoronary thrombolysis was performed from 2 to 6 hr after the onset of AMI, and the time from the onset of AMI to death was 7 to 168 hr. Cineangiography revealed no evidence of good collateral circulation in an… Show more
“…5 Similar results were found in human autopsied hearts with acute MI after treatment with thrombolysis. 13 These findings from the acute phase of AMI are supported and extended by our data because biopsies were taken in the chronic healing phase 13Ϯ9 years after the index MI in 10 studied patients (28%). Likely as a result of transmural necrosis, the core infarct consisted of transmural fibrosis in nonreperfused patients, whereas the majority of early reperfused patients showed no transmural fibrosis at all with thick layers of viable myocardium even in the core infarct region.…”
Section: Reperfusion and Myocardial Scarsupporting
Background-Reperfusion therapy during acute myocardial infarction results in myocardial salvage and improved ventricular function but may also influence the arrhythmogenic substrate for ventricular tachycardia (VT). This study used electroanatomic mapping and infarct histology to assess the impact of reperfusion on the substrate and on VT characteristics late after acute myocardial infarction. Methods and Results-The study population consisted of 36 patients (32 men; age, 63Ϯ15 years) referred for treatment of VT 13Ϯ9 years after acute myocardial infarction. Fourteen patients with early reperfusion during acute myocardial infarction were compared with 22 nonreperfused patients. Spontaneous and induced VTs and the characteristics of electroanatomic voltage maps were analyzed. Twenty-seven patients were treated by radiofrequency catheter ablation. Ten patients (6 nonreperfused) were treated by ventricular restoration with intraoperative cryoablation in 9. During surgery, biopsies were obtained from the resected core of the infarct. VT cycle length of spontaneous and induced VTs was shorter in reperfused patients (reperfused, 299Ϯ52/270Ϯ58 ms; nonreperfused, 378Ϯ77/362Ϯ74 ms; Pϭ0.01). An electroanatomic patchy scar pattern was present in 71% of reperfused and 14% of nonreperfused patients (Pϭ0.004). The proportion of electroanatomic dense scar was smaller in reperfused patients (24Ϯ18% versus 45Ϯ21%; Pϭ0.02). Histological assessment in 10 patients revealed thick layers of surviving myocardium in 75% of reperfused but in none of the nonreperfused patients. Conclusions-Scar size and pattern defined by electroanatomic mapping are different between VT patients with and without reperfusion during acute myocardial infarction. Less confluent electroanatomic scars match with thick layers of surviving myocardium on histology. Early reperfusion and less confluent electroanatomic scar are associated with faster
“…5 Similar results were found in human autopsied hearts with acute MI after treatment with thrombolysis. 13 These findings from the acute phase of AMI are supported and extended by our data because biopsies were taken in the chronic healing phase 13Ϯ9 years after the index MI in 10 studied patients (28%). Likely as a result of transmural necrosis, the core infarct consisted of transmural fibrosis in nonreperfused patients, whereas the majority of early reperfused patients showed no transmural fibrosis at all with thick layers of viable myocardium even in the core infarct region.…”
Section: Reperfusion and Myocardial Scarsupporting
Background-Reperfusion therapy during acute myocardial infarction results in myocardial salvage and improved ventricular function but may also influence the arrhythmogenic substrate for ventricular tachycardia (VT). This study used electroanatomic mapping and infarct histology to assess the impact of reperfusion on the substrate and on VT characteristics late after acute myocardial infarction. Methods and Results-The study population consisted of 36 patients (32 men; age, 63Ϯ15 years) referred for treatment of VT 13Ϯ9 years after acute myocardial infarction. Fourteen patients with early reperfusion during acute myocardial infarction were compared with 22 nonreperfused patients. Spontaneous and induced VTs and the characteristics of electroanatomic voltage maps were analyzed. Twenty-seven patients were treated by radiofrequency catheter ablation. Ten patients (6 nonreperfused) were treated by ventricular restoration with intraoperative cryoablation in 9. During surgery, biopsies were obtained from the resected core of the infarct. VT cycle length of spontaneous and induced VTs was shorter in reperfused patients (reperfused, 299Ϯ52/270Ϯ58 ms; nonreperfused, 378Ϯ77/362Ϯ74 ms; Pϭ0.01). An electroanatomic patchy scar pattern was present in 71% of reperfused and 14% of nonreperfused patients (Pϭ0.004). The proportion of electroanatomic dense scar was smaller in reperfused patients (24Ϯ18% versus 45Ϯ21%; Pϭ0.02). Histological assessment in 10 patients revealed thick layers of surviving myocardium in 75% of reperfused but in none of the nonreperfused patients. Conclusions-Scar size and pattern defined by electroanatomic mapping are different between VT patients with and without reperfusion during acute myocardial infarction. Less confluent electroanatomic scars match with thick layers of surviving myocardium on histology. Early reperfusion and less confluent electroanatomic scar are associated with faster
“…3 Histological studies in patients and animal models of acute MI have shown that the duration of coronary artery occlusion is proportionally correlated to the size and transmural extent of myocardial scar. 4,5,26 Scar size and geometry are important determinants for the reentrant circuit geometry and may contribute to occurrence and CL of VT. 9,27 We recently demonstrated that reperfused patients referred for ablation of recurrent VT late after MI appeared to have smaller and less confluent electroanatomic scars with thick layers of surviving myocardium found at histology. Interestingly, the CL of spontaneous and induced VTs was shorter in reperfused than in nonreperfused patients, probably because of the observed differences in scar geometry after reperfusion therapy.…”
Section: Effect Of Early Reperfusion and Inducible Vtclmentioning
Background-This study aimed to evaluate the impact of early reperfusion during acute myocardial infarction (MI) on ventricular tachycardia (VT) inducibility, inducible VT cycle length (CL), and occurrence of spontaneous VT late after MI. Methods and Results-Five hundred six patients (440 men; age, 63Ϯ11 years) with prior MI who underwent electrophysiology study before implantation of an implantable cardioverter-defibrillator for primary or secondary prevention were assessed. Patients were classified according to the reperfusion strategy (reperfusion: thrombolysis, nϭ44, or percutaneous coronary intervention, nϭ65, versus no reperfusion, nϭ397) during acute MI. Monomorphic sustained VT was inducible in 351 (69%) patients. Inducibility in reperfused and nonreperfused patients was similar in primary prevention patients (56% versus 58%) but significantly higher for nonreperfused patients in secondary prevention patients (56% versus 79%, Pϭ0.001). Induced VTCL was shorter (247Ϯ40 versus 287Ϯ63, PϽ0.001) and very fast VT (CL Յ250 ms) was more often induced in reperfused patients (71% versus 47%, Pϭ0.001). In primary prevention patients, nonreperfusion was associated with a doubled risk for first spontaneous VT during follow-up. Conclusions-There are important differences in VT inducibility, induced VTCL, and occurrence of spontaneous VT in the chronic infarct healing phase between patients with and those without successful reperfusion during acute MI. These findings suggest differences in the chronic arrhythmogenic substrate.
“…The section (3 μm thick) was stained with phosphotungstic acid hematoxylin (PTAH). CBN was identified from the appearance of a deep blue color, multiple granulations, and hypercontraction bands, as described by Matsuda et al 9 The whole area of the section was divided into 25-27 regions and photographed with a microscope (Eclipse E400, Nikon, Tokyo, Japan) at ×40 magnification. CBN-positive cells were marked using digital image editing software Photoshop ® 6.0 (Adobe Systems, San Jose, CA, USA).…”
Section: Measurement Of the Cbn Areamentioning
confidence: 99%
“…CBN is thought to spread during the first minutes of reperfusion and to contribute to development of infarct in the later phase. 5,9,10 Temporary inhibition of contraction at the onset of reperfusion results in infarct limitation. 36 Consistent with those observations, infusion of CBX for only 1 min before onset of reperfusion not only prevented CBN in the early phase, but also delayed infarct development in the late phase of reperfusion.…”
Section: Involvement Of Gjic In Spread Of Cbn and Infarct Developmentmentioning
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