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Published on: May 28, 2019
Nonculprit lesion progression in patients with ST elevation myocardial infarction after primary percutaneous coronary
Jian Wang1, Jing-hua Liu, Xiao-ling Zhu
1Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Vessel Diseases.
Insights
Cardiovascular events after ST-elevation myocardial infarction (STEMI) primary percutaneous coronary intervention (PPCI) often stem from nonculprit lesion progression. Elevated catecholamines, CRP, and complex lesions correlate with this progression, indicating chronic inflammation and stress are key factors.
Area of Science:
- Cardiology
- Interventional Cardiology
- Biomarkers in Cardiovascular Disease
Background:
- Cardiovascular events in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary interventions (PPCI) frequently result from nonculprit lesion progression during long-term follow-up.
- The clinical and angiographic determinants of nonculprit lesion progression remain largely unknown, necessitating further investigation.
Purpose of the Study:
- To identify and analyze the clinical and angiographic factors associated with the progression of nonculprit lesions in patients with STEMI who have undergone PPCI.
Main Methods:
- A cohort of 492 STEMI patients treated with PPCI between January 2006 and December 2009 were analyzed.
- Clinical and angiographic follow-up was conducted at 12 months, with the primary endpoint being clinically driven nonculprit lesion PCI.
- Serum levels of catecholamines (epinephrine, norepinephrine), C-reactive protein (CRP), and cardiac troponin I (cTnI) were measured, alongside assessment of lesion characteristics.
Main Results:
- Forty-five patients required clinically driven nonculprit lesion PCI, compared to 447 who did not.
- Significant differences were observed in catecholamine levels (epinephrine, norepinephrine), CRP, peak cTnI, thrombotic lesion rate, multi-vessel disease, culprit lesion length, and complex lesion rates between groups.
- Correlation analysis revealed significant associations between nonculprit lesion stenosis degree and serum E, NE, CRP, peak cTnI, thrombotic lesions, multi-vessel disease, culprit lesion length, and complex lesions.
Conclusions:
- Nonculprit lesion progression is a primary driver of recurrent PCI in STEMI patients post-PPCI.
- Complex nonculprit lesions are more susceptible to requiring additional PCI.
- Chronic inflammation and sustained physiological stress are implicated in the progression of nonculprit lesions in STEMI patients.
Abstract:
The 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 significant 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 coefficients 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 inflammation and sustained stress may be involved in the progression of nonculprit lesions in patients with STEMI.
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