Impact of high-sensitivity c-reactive protein on predicting long-term mortality of acute myocardial infarction

Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a promising target for lowering plasma low-density lipoprotein cholesterol and preventing cardiovascular (CV) disease. Whether plasma PCSK9 measured during the acute phase predicts recurrent CV events in patients with acute myocardial infarction (AMI) remains unresolved. Methods and Results: Plasma PCSK9 levels were measured in 1,646 patients with AMI from the China PEACE-Prospective AMI Study at the acute phase. Additionally, 248 patients were resampled and measured at 1 month post-AMI. Associations of acute-phase PCSK9 tertiles with clinical characteristics and recurrent CV events within 1 year were assessed. Female gender (OR 1.94, 95% CI 1.24–3.03), premature coronary heart disease (CHD; OR 2.12, 95% CI 1.37–3.26), higher high-sensitivity C-reactive protein (OR 1.67, 95% CI 1.44–1.95), and higher triglycerides (OR 1.46, 95% CI 1.03–2.09) were associated with higher baseline PCSK9. Plasma PCSK9 levels in the highest tertile (versus lowest) did not have an increased risk of 1-year recurrent CV events in the AMI cohort (HR 0.78, 95% CI 0.52–1.16) or any subgroup. There was also no association between percentage changes in PCSK9 over the first month and 1-year recurrent events, although there was a trend of differences between patients in the upper versus lower tertiles. Conclusion: Plasma PCSK9 levels measured during the acute phase were associated with high-sensitivity C-reactive protein, triglycerides, premature CHD, and gender in patients with AMI but did not predict recurrent CV events within 1 year. Dynamic changes in PCSK9 suggested a trend yet no significance value in predicting recurrent CV events.

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Abstract 3532: Lipoprotein-Associated Phospholipase A 2 and High Sensitivity C-Reactive Protein Levels and the Prediction of Cardiovascular Risk Among Coronary Artery Disease Patients With Differing Clinical Presentations

Circulation ◽

10.1161/circ.116.suppl_16.ii_799-c ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Heidi T May ◽

Jeffrey L Anderson ◽

Benjamin D Horne ◽

Robert R Pearson ◽

Robert L Wolfert ◽

...

Keyword(s):

Myocardial Infarction ◽

Coronary Artery Disease ◽

Acute Myocardial Infarction ◽

Coronary Artery ◽

High Sensitivity ◽

Phospholipase A ◽

Specific Marker ◽

C Reactive Protein ◽

Reactive Protein ◽

Artery Disease

Background : Inflammation plays a role in the development and progression of coronary artery disease (CAD), with circulating markers of vascular inflammation being used in risk assessment including high sensitivity C-reactive protein (hsCRP) and lipoprotein-associated phospholipase A 2 (LpPLA 2 ). While hsCRP responds to the systemic inflammatory stimulus of acute myocardial infarction (AMI), LpPLA 2 has been proposed to be more vascular-specific and to vary minimally based upon clinical presentation. To test this hypothesis, we evaluated both biomarkers among CAD patients presenting with stable angina (SA), unstable angina (USA) or acute myocardial infarction (AMI). Methods : LpPLA 2 (PLAC TM test, diaDexus, Inc.) and hsCRP were measured from samples donated by consenting patients (N=1,010) enrolled in the registry of the Intermountain Heart Collaborative Study that underwent angiographic evaluation for CAD. Patients were categorized by presentation status (SA=637; USA=205; and AMI=168), stratified according to median levels of LpPLA 2 (350.2 ng/mL) and hsCRP above and below 3 mgl/L and followed for 7.5 ± 2.4 years for CAD death. Results : Age averaged 64 ± 12 years and 70% were male. While median hsCRP (mg/L) levels differed significantly by presentation [2.86, 2.80, and 13.7 for SA, USA, and AMI, respectively (p<0.0001)], median LpPLA 2 (ng/mL) levels [350.2, 353.1, and 348.1 for SA, USA, and AMI, respectively (p=0.67)], did not. LpPLA 2 was not only a better predictor of CAD death among the entire cohort (LpPLA 2 : adjusted Hazard Ratio [HR]= 1.47, p=0.04; hsCRP: adjusted HR=0.95, p=0.81), it was a better predictor among patients presenting with AMI (LpPLA 2 : adjusted HR3 1.80, p=0.30; hsCRP adjusted HR=0.76, p=0.63). Conclusions : Among CAD patients, LpPLA 2 varies minimally among differing presentations compared to hsCRP and is a better a predictor of CAD death among those presenting with AMI. This information supports the hypothesis that LpPLA 2 is a vascular specific marker of inflammation and independent of transient systemic inflammatory effects.

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Concomitant Impact of High-Sensitivity C-Reactive Protein and Renal Dysfunction in Patients with Acute Myocardial Infarction

Yonsei Medical Journal ◽

10.3349/ymj.2014.55.1.132 ◽

2014 ◽

Vol 55 (1) ◽

pp. 132 ◽

Cited By ~ 4

Author(s):

Yong Un Kang ◽

Min Jee Kim ◽

Joon Seok Choi ◽

Chang Seong Kim ◽

Eun Hui Bae ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Renal Dysfunction ◽

High Sensitivity ◽

C Reactive Protein ◽

Reactive Protein

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High-Sensitivity C-Reactive Protein and Acute Kidney Injury in Patients with Acute Myocardial Infarction: A Prospective Observational Study

Journal of Clinical Medicine ◽

10.3390/jcm8122192 ◽

2019 ◽

Vol 8 (12) ◽

pp. 2192 ◽

Cited By ~ 2

Author(s):

Nicola Cosentino ◽

Stefano Genovese ◽

Jeness Campodonico ◽

Alice Bonomi ◽

Claudia Lucci ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Acute Kidney Injury ◽

Kidney Injury ◽

High Sensitivity ◽

Future Research ◽

Hospital Death ◽

C Reactive Protein ◽

Reactive Protein ◽

Hs Crp

Background. Accumulating evidence suggests that inflammation plays a key role in acute kidney injury (AKI) pathogenesis. We explored the relationship between high-sensitivity C-reactive protein (hs-CRP) and AKI in acute myocardial infarction (AMI). Methods. We prospectively included 2,063 AMI patients in whom hs-CRP was measured at admission. AKI incidence and a clinical composite of in-hospital death, cardiogenic shock, and acute pulmonary edema were the study endpoints. Results. Two-hundred-thirty-four (11%) patients developed AKI. hs-CRP levels were higher in AKI patients (45 ± 87 vs. 16 ± 41 mg/L; p < 0.0001). The incidence and severity of AKI, as well as the rate of the composite endpoint, increased in parallel with hs-CRP quartiles (p for trend <0.0001 for all comparisons). A significant correlation was found between hs-CRP and the maximal increase of serum creatinine (R = 0.23; p < 0.0001). The AUC of hs-CRP for AKI prediction was 0.69 (p < 0.001). At reclassification analysis, addition of hs-CRP allowed to properly reclassify 14% of patients when added to creatinine and 8% of patients when added to a clinical model. Conclusions. In AMI, admission hs-CRP is closely associated with AKI development and severity, and with in-hospital outcomes. Future research should focus on whether prophylactic renal strategies in patients with high hs-CRP might prevent AKI and improve outcome.

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