Nonculprit Lesion Progression in Patients With ST Elevation Myocardial Infarction After Primary Percutaneous Coronary Intervention

Abstract

SummaryThe majority of cardiovascular events in patients with ST elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary interventions (PPCI) arise from the progression of nonculprit lesions (NCL) during the long-term follow-up period. However, the clinical and angiographic factors related to the progression of nonculprit lesions are unknown.The purpose of the study was to investigate the clinical and angiographic factors related to the progression of nonculprit lesions of patients with STEMI undergoing PPCI.A total of 492 patients with STEMI who underwent PPCI from January 2006 to December 2009 were enrolled. All patients underwent PPCI as a treatment for the culprit lesion. The clinical and angiographic follow-up was performed at 12 months. Primary endpoint: Clinically driven nonculprit lesion PCI. The levels of serum catecholamines [epinephrine (E), norepinephrine (NE)] and C-reactive protein (CRP) were assayed, and the clinical and angiographic features were also analyzed.The clinical and angiographic follow-up was performed in 492 patients, and 45 patients underwent clinically driven nonculprit lesions PCI (study group). A total of 447 patients were free of additional PCI (control group). There were significant differences in the level of catecholamines (E (621.48 ± 79.31) pg/mL versus (268.14 ± 73.26) pg/mL, P < 0.0001), NE (6212.43 ± 822.41) pg/mL versus (3218.34 ± 614.16) pg/mL, P < 0.0001), CRP (3.29 ± 1.31) mg/dL versus (2.51 ± 1.14) mg/dL, P < 0.0001, cTnI peak value (27.27 ± 4.02) ng/mL versus (16.12 ± 3.23) ng/mL, P < 0.0001), thrombotic lesion rate ((62.22% versus 23.04%), P < 0.0001), ≥ 2 vessel lesions rate (80.00% versus 46.09%), P < 0.0001), culprit lesion length ((33.2 ± 2.9 versus 28.1 ± 3.1), P = 0.013), and complex lesion rate ((57.78% versus 36.02%), P = 0.006) between the two groups. Correlation analysis between nonculprit lesion stenosis degree and serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, and complex lesion rate showed that there were signifi cant correlations between serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, complex lesion rate, and nonculprit lesion stenosis degree. The correlation coeffi cients were 0.95, 0.97, 0.83, 0.90, 0.81, 0.84, 0.95, and 0.96, respectively, and P < 0.0001, P < 0.0001, P = 0.01, P = 0.01, P = 0.01, P = 0.01, P < 0.0001, and P < 0.0001, respectively.Recurrent PCI was mainly due to nonculprit lesion progression in patients with STEMI after primary PCI. Complex nonculprit lesions may be prone to for additional PCI. Chronic infl ammation and sustained stress may be involved in the progression of nonculprit lesions in patients with STEMI. (Int Heart J 2014; 55: 48-52) Key words: Recurrent percutaneous coronary intervention, Complex nonculprit lesion, Infl ammation, Stress A lthough primary PCI can salvage dying myocardium, reduce cardiovascular events, and improve prognosis in patients w...

Effect of Ischemic Postconditioning on Cell Apoptosis and Expression of Relevant Genes in Non-Culprit Coronary Arteries

“…A clinical follow-up study of such patients after successful PPCI suggested that non-culprit lesions may progress, which may be the most important factor influencing the prognosis of patients with acute myocardial infarction after successful PPCI. 4 Few studies have examined the progression of non-culprit lesions. Hanratty et al 9 demonstrated exaggeration of nonculprit lesions during acute myocardial infarction and indicated that inflammatory and spastic mechanisms may be involved in non-culprit lesion progression.…”

“…Additionally, recent clinical studies have shown that PPCI can lead to the progression of non-culprit lesions, which might be the most significant factor influencing the prognosis after PPCI. 4 5 The molecular mechanisms of myocardial ischemia-reperfusion (IR) involve myocyte apoptosis, increased catecholamine levels, and activation of the angiotensin II/mitogen-activated protein kinase/connexin 43 (AgII/MAPK/Cx43) pathway. 6 The reason for the progression of non-culprit lesions in patients with STEMI after PPCI is not clear, but chronic inflammation and sustained stress may be involved in the progression of non-culprit lesions.…”

“…6 The reason for the progression of non-culprit lesions in patients with STEMI after PPCI is not clear, but chronic inflammation and sustained stress may be involved in the progression of non-culprit lesions. 4 Our recent experimental study showed that non-culprit lesion progression can be affected by many factors, such as increased levels of catecholamines and activation of the AgII/MAPK/Cx43 pathway. 6 In addition, Sun et al 7 found that ischemic postconditioning (IP) may inhibit the AgII/MAPK/Cx43 pathway.…”

Nicorandil Attenuates Ischemia-Reperfusion Injury Via Inhibition of Norepinephrine Release From Cardiac Sympathetic Nerve Terminals

“…[3][4][5] Previous studies 23,24) showed beneficial effects of cardiac denervation on infarct size during ischemia. Other studies, however, demonstrated that cardiac denervation had no protective effect on ischemic injury, 25) or rather had a detrimental influence.…”

“…1,2) It is generally accepted that excess levels of norepinephrine (NE) could lead to myocardial injury. [3][4][5] Prolonged myocardial ischemia releases a large amount of NE from the cardiac sympathetic nerve terminals independent of central sympathetic activation. 6) Therefore, increased levels of interstitial NE (iNE) during myocardial ischemia may be involved in the pathogenesis of I/R injury, and an intervention to reduce iNE may play a role in reducing I/R injury.…”