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Published on: January 28, 2020
Baseline systemic inflammatory status and no-reflow phenomenon after percutaneous coronary angioplasty for acute
Giampaolo Niccoli1, Gaetano A Lanza, Cristina Spaziani
1Institute of Cardiology, Catholic University of the Sacred Heart, Rome, Italy. gniccoli73@hotmail.it
Insights
This study found no link between C-reactive protein (CRP) levels and the no-reflow phenomenon in acute myocardial infarction (AMI) patients undergoing percutaneous coronary intervention (PCI). Elevated CRP did not correlate with poorer angiographic or ECG outcomes after PCI in AMI.
Area of Science:
- Cardiology
- Biomedical Science
- Inflammation Research
Background:
- Systemic inflammation is implicated in cardiovascular diseases.
- The role of inflammation, specifically C-reactive protein (CRP), in the no-reflow phenomenon after percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) remains unclear.
Purpose of the Study:
- To investigate the association between baseline high-sensitivity C-reactive protein (hs-CRP) levels and the occurrence of the no-reflow phenomenon in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary or rescue PCI.
Main Methods:
- The study included 60 patients with STEMI treated within 6 hours of symptom onset.
- No-reflow was assessed using angiographic parameters (TIMI flow, corrected TIMI frame count, myocardial blush grade) and ECG criteria (ST-segment resolution).
- Patients were stratified into high (CRP > 5 mg/L) and low (CRP < 5 mg/L) baseline hs-CRP groups.
Main Results:
- No significant differences in the prevalence of angiographically defined no-reflow (TIMI flow < 3, myocardial blush grade < 3) were observed between high and low CRP groups.
- Coronary TIMI frame count and myocardial blush grade were similar in both groups.
- ECG-based assessment of ST-segment resolution also showed no significant difference between patients with high and low CRP levels.
Conclusions:
- This study did not find a significant association between admission hs-CRP levels and the incidence of coronary no-reflow.
- Neither angiographic nor ECG parameters indicated a link between CRP levels and no-reflow in STEMI patients treated with successful PCI.
Background:
Systemic inflammation is involved in several pathological cardiovascular processes. However, whether it plays a role in the no-reflow phenomenon occurring in patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI) is unknown.
Methods:
We studies 60 consecutive patients (59.5+/-12 years, 82% males) with a first ST-segment elevation AMI, treated by primary or rescue PCI within 6 h of symptom onset. Angiographic indexes of no-reflow, evaluated at the end of the procedure, included coronary TIMI flow grading, corrected TIMI frame count (c-TFC) and myocardial blush grade (MBG). ECG indexes of no-reflow included the lack of ST segment resolution (defined as a reduction <50% of the measured ST-segment elevation at 90 min, compared to the admission ECG), as analyzed both in the single lead with the maximal ST elevation and in all leads showing ST elevation on admission. Patients were divided into two groups according to baseline high-sensitivity C-reactive protein (CRP) serum levels measured on admission: high CRP group (CRP>5 mg/L) and low CRP group (CRP<5 mg/L).
Results:
A similar prevalence of final TIMI flow<3 and MBG<3 was observed in patients with high and low CRP serum levels (30% vs. 12%, p=0.1, and 50% vs. 53%, p=1.0, respectively), and c-TFC was also similar in the two groups (26+/-4.5 vs. 24+/-6, p=0.5). Accordingly, the prevalence of lack of ST-segment resolution in the two groups was similar, both by the single-lead method (25% vs. 25%, p=1.0) and the multiple-lead method (29% vs. 19%, p=0.4).
Conclusion:
In this study we failed to demonstrate any significant association between CRP serum levels on admission and coronary no-reflow, as assessed by both angiographic and ECG parameters in AMI patients treated by successful primary or rescue PCI within 6 h of chest pain onset.
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