Joseph M. Pastore

Effect of Peri-Infarct Pacing Early After Myocardial Infarction Results of the Prevention of Myocardial Enlargement and Dilatation Post Myocardial Infarction Study

Background— Left ventricular (LV) remodeling has been attributed to the segmental loss of viable myocardium due to myocardial infarction (MI), which results in redistribution of cardiac workload, with increased regional wall stress in and around the infarct zone. Because ventricular pacing has been shown to reduce regional wall stress and workload in regions near the pacing site, this trial was designed to test whether chronic pacing near the infarct attenuates LV remodeling. Methods and Results— Eighty patients with an anterior MI, peak creatine kinase >2000 mU/mL, ejection fraction ≤35%, wall motion abnormality (WMA) in >5 of 16 segments, and QRS 0.05). In a hypothesis-generating secondary analysis, there was a sustained reduction in the WMA score at 12 months in paced patients (CRT, −0.16±0.28; ICD, −0.01±0.24, 2-sample t test P =0.03). No differences were found in the therapy-related event rate, hospitalizations, or mortality (all P >0.05). Conclusions— Chronic pacing in the infarct region did not alter the primary end point of LV remodeling over 1 year. Clinical Trial Registration— URL: . Unique identifier: [NCT00605631][1]. [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT00605631&atom=%2Fcirchf%2F3%2F6%2F650.atomBackground—Left ventricular (LV) remodeling has been attributed to the segmental loss of viable myocardium due to myocardial infarction (MI), which results in redistribution of cardiac workload, with increased regional wall stress in and around the infarct zone. Because ventricular pacing has been shown to reduce regional wall stress and workload in regions near the pacing site, this trial was designed to test whether chronic pacing near the infarct attenuates LV remodeling. Methods and Results—Eighty patients with an anterior MI, peak creatine kinase >2000 mU/mL, ejection fraction ⩽35%, wall motion abnormality (WMA) in >5 of 16 segments, and QRS <120 ms, were randomized to either control (implantable cardioverter-defribillator [ICD]) or biventricular pacing with peri-infarct LV lead placement (cardiac resynchronization therapy [CRT]-D) arms between 2 and 14 days after the MI. The primary end point—change in LV end-diastolic volume (LVEDV) from baseline to 12 months—was not significantly different between the 2 groups (CRT, 10.6±27.7 mL; ICD, 11.2±31.2 mL; 2-sample t test P>0.05). In a hypothesis-generating secondary analysis, there was a sustained reduction in the WMA score at 12 months in paced patients (CRT, −0.16±0.28; ICD, −0.01±0.24, 2-sample t test P=0.03). No differences were found in the therapy-related event rate, hospitalizations, or mortality (all P>0.05). Conclusions—Chronic pacing in the infarct region did not alter the primary end point of LV remodeling over 1 year. Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT00605631.

Effect of Peri-Infarct Pacing Early After Myocardial InfarctionClinical Perspective

Background— Left ventricular (LV) remodeling has been attributed to the segmental loss of viable myocardium due to myocardial infarction (MI), which results in redistribution of cardiac workload, with increased regional wall stress in and around the infarct zone. Because ventricular pacing has been shown to reduce regional wall stress and workload in regions near the pacing site, this trial was designed to test whether chronic pacing near the infarct attenuates LV remodeling. Methods and Results— Eighty patients with an anterior MI, peak creatine kinase >2000 mU/mL, ejection fraction ≤35%, wall motion abnormality (WMA) in >5 of 16 segments, and QRS 0.05). In a hypothesis-generating secondary analysis, there was a sustained reduction in the WMA score at 12 months in paced patients (CRT, −0.16±0.28; ICD, −0.01±0.24, 2-sample t test P =0.03). No differences were found in the therapy-related event rate, hospitalizations, or mortality (all P >0.05). Conclusions— Chronic pacing in the infarct region did not alter the primary end point of LV remodeling over 1 year. Clinical Trial Registration— URL: . Unique identifier: [NCT00605631][1]. [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT00605631&atom=%2Fcirchf%2F3%2F6%2F650.atomBackground—Left ventricular (LV) remodeling has been attributed to the segmental loss of viable myocardium due to myocardial infarction (MI), which results in redistribution of cardiac workload, with increased regional wall stress in and around the infarct zone. Because ventricular pacing has been shown to reduce regional wall stress and workload in regions near the pacing site, this trial was designed to test whether chronic pacing near the infarct attenuates LV remodeling. Methods and Results—Eighty patients with an anterior MI, peak creatine kinase >2000 mU/mL, ejection fraction ⩽35%, wall motion abnormality (WMA) in >5 of 16 segments, and QRS <120 ms, were randomized to either control (implantable cardioverter-defribillator [ICD]) or biventricular pacing with peri-infarct LV lead placement (cardiac resynchronization therapy [CRT]-D) arms between 2 and 14 days after the MI. The primary end point—change in LV end-diastolic volume (LVEDV) from baseline to 12 months—was not significantly different between the 2 groups (CRT, 10.6±27.7 mL; ICD, 11.2±31.2 mL; 2-sample t test P>0.05). In a hypothesis-generating secondary analysis, there was a sustained reduction in the WMA score at 12 months in paced patients (CRT, −0.16±0.28; ICD, −0.01±0.24, 2-sample t test P=0.03). No differences were found in the therapy-related event rate, hospitalizations, or mortality (all P>0.05). Conclusions—Chronic pacing in the infarct region did not alter the primary end point of LV remodeling over 1 year. Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT00605631.

Effect of Peri-Infarct Pacing Early After Myocardial InfarctionClinical Perspective: Results of the Prevention of Myocardial Enlargement and Dilatation Post Myocardial Infarction Study

Background— Left ventricular (LV) remodeling has been attributed to the segmental loss of viable myocardium due to myocardial infarction (MI), which results in redistribution of cardiac workload, with increased regional wall stress in and around the infarct zone. Because ventricular pacing has been shown to reduce regional wall stress and workload in regions near the pacing site, this trial was designed to test whether chronic pacing near the infarct attenuates LV remodeling. Methods and Results— Eighty patients with an anterior MI, peak creatine kinase >2000 mU/mL, ejection fraction ≤35%, wall motion abnormality (WMA) in >5 of 16 segments, and QRS 0.05). In a hypothesis-generating secondary analysis, there was a sustained reduction in the WMA score at 12 months in paced patients (CRT, −0.16±0.28; ICD, −0.01±0.24, 2-sample t test P =0.03). No differences were found in the therapy-related event rate, hospitalizations, or mortality (all P >0.05). Conclusions— Chronic pacing in the infarct region did not alter the primary end point of LV remodeling over 1 year. Clinical Trial Registration— URL: . Unique identifier: [NCT00605631][1]. [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT00605631&atom=%2Fcirchf%2F3%2F6%2F650.atomBackground—Left ventricular (LV) remodeling has been attributed to the segmental loss of viable myocardium due to myocardial infarction (MI), which results in redistribution of cardiac workload, with increased regional wall stress in and around the infarct zone. Because ventricular pacing has been shown to reduce regional wall stress and workload in regions near the pacing site, this trial was designed to test whether chronic pacing near the infarct attenuates LV remodeling. Methods and Results—Eighty patients with an anterior MI, peak creatine kinase >2000 mU/mL, ejection fraction ⩽35%, wall motion abnormality (WMA) in >5 of 16 segments, and QRS <120 ms, were randomized to either control (implantable cardioverter-defribillator [ICD]) or biventricular pacing with peri-infarct LV lead placement (cardiac resynchronization therapy [CRT]-D) arms between 2 and 14 days after the MI. The primary end point—change in LV end-diastolic volume (LVEDV) from baseline to 12 months—was not significantly different between the 2 groups (CRT, 10.6±27.7 mL; ICD, 11.2±31.2 mL; 2-sample t test P>0.05). In a hypothesis-generating secondary analysis, there was a sustained reduction in the WMA score at 12 months in paced patients (CRT, −0.16±0.28; ICD, −0.01±0.24, 2-sample t test P=0.03). No differences were found in the therapy-related event rate, hospitalizations, or mortality (all P>0.05). Conclusions—Chronic pacing in the infarct region did not alter the primary end point of LV remodeling over 1 year. Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT00605631.