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Joint Effect of Carotid Plaque and C-Reactive Protein on First-Ever Ischemic Stroke and Myocardial Infarction?
Agnethe Eltoft1,2, Kjell Arne Arntzen3,2, Tom Wilsgaard4
1Department of Clinical Medicine, UiT The Arctic University of Norway, Tromsø, Norway agnethe.eltoft@unn.no.
Insights
Elevated C-reactive protein (CRP) and carotid plaque significantly increase the risk of ischemic stroke and myocardial infarction. Combining these markers improves cardiovascular disease risk prediction beyond traditional factors.
Area of Science:
- Cardiovascular Medicine
- Inflammation Biology
- Epidemiology
Background:
- Atherosclerosis and C-reactive protein (CRP) are known cardiovascular risk factors.
- Their combined effect on ischemic stroke (IS) and myocardial infarction (MI) risk is not well understood.
- Subclinical atherosclerosis, indicated by carotid plaque, and systemic inflammation (CRP) may interact to influence cardiovascular events.
Purpose of the Study:
- To investigate the synergistic effect of atherosclerosis and CRP on IS and MI risk.
- To determine if CRP mediates the risk associated with prevalent carotid plaque.
- To assess the added value of CRP and carotid plaque in predicting cardiovascular events beyond traditional risk factors.
Main Methods:
- Longitudinal study of 10,109 participants from the Tromsø Study (1994-2008).
- Measurement of C-reactive protein (CRP) levels and carotid total plaque area (TPA).
- Cox proportional hazard models used to calculate hazard ratios (HRs) for incident IS and MI, with time-varying covariates.
Main Results:
- High CRP (>3 mg/L) was associated with increased IS (HR 1.84) and MI (HR 1.46) risk.
- Carotid plaque (TPA above median) was linked to higher IS (HR 1.65) and MI (HR 1.64) risk.
- The highest incidence of IS and MI occurred in individuals with both high CRP and significant plaque; combined assessment improved risk prediction.
Conclusions:
- The co-occurrence of subclinical atherosclerosis and elevated CRP significantly elevates the risk of IS and MI.
- Assessing both atherosclerosis and inflammatory biomarkers enhances cardiovascular disease risk stratification.
- This combined approach offers improved prediction of major adverse cardiovascular events.
Background:
The joint effect of atherosclerosis and CRP (C-reactive protein) on risk of ischemic stroke (IS) and myocardial infarction (MI) has been sparsely studied. The aim of this study was to explore whether CRP mediates the risk of events in subjects with prevalent carotid plaque, examine synergism, and test whether CRP and carotid plaque add to risk prediction beyond traditional risk factors.
Methods And Results:
CRP and carotid total plaque area (TPA) were measured in 10 109 participants in the Tromsø Study from 1994 to 2008. Incident IS (n=671) and MI (n=1079) were registered until December 31, 2013. We calculated hazard ratios (HRs) of MI and IS according to categories of CRP (<1, 1-3, and >3 mg/L) and plaque status (no plaque and TPA below and above median) in Cox proportional hazard models with time-varying covariates. Multivariable-adjusted CRP >3 versus <1 mg/L was associated with risk of IS (HR, 1.84; 95% confidence interval, 1.49-2.26) and MI (HR, 1.46; 95% confidence interval, 1.23-1.73). TPA above median versus no plaque was associated with risk for IS (HR, 1.65; 95% confidence interval, 1.36-2.01) and MI (HR, 1.64; 95% confidence interval, 1.41-1.92). In participants with plaque, adjustment for CRP minimally attenuated the risk estimates. The highest incidence rates for MI and IS were seen in the group with both CRP >3 mg/L and TPA is above the median. TPA and CRP combined added to risk prediction beyond traditional risk factors.
Conclusions:
The simultaneous presence of subclinical atherosclerosis and elevated CRP was associated with increased risk of IS and MI. The combined assessment of subclinical atherosclerosis and inflammatory biomarkers may improve cardiovascular disease risk stratification.
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