Plasma PCSK9 levels are elevated with acute myocardial infarction in two independent retrospective angiographic studies
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Published on: May 28, 2019
Naif A M Almontashiri1, Ragnar O Vilmundarson2, Nima Ghasemzadeh3
1Ruddy Canadian Cardiovascular Genetics Centre, University of Ottawa Heart Institute, Ottawa, Ontario, Canada; Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada; Center for Genetics and Inherited Diseases, Taibah University, Almadina, Saudi Arabia.
Insights
Elevated plasma proprotein convertase subtilisin/kexin type 9 (PCSK9) levels are associated with acute myocardial infarction (MI). This finding suggests PCSK9 may play a role in the acute phase of MI, independent of coronary atherosclerosis extent.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Genetics
Background:
- Proprotein convertase subtilisin/kexin type 9 (PCSK9) regulates low-density lipoprotein (LDL) receptor degradation.
- Genetic studies show that reduced PCSK9 function lowers LDL-cholesterol and myocardial infarction (MI) risk.
- The association of plasma PCSK9 with coronary atherosclerosis (CAD) and acute MI is not fully understood.
Purpose of the Study:
- To investigate the association between plasma PCSK9 levels and coronary atherosclerosis (CAD).
- To determine if elevated plasma PCSK9 is specifically linked to acute myocardial infarction (MI).
Main Methods:
- Plasma PCSK9 levels were measured using ELISA in two independent cohorts: the Ottawa Heart Genomics Study and the Emory Cardiology Biobank study.
- Participants included individuals with and without angiographically defined CAD, and those with and without acute MI.
- Analyses excluded individuals on lipid-lowering medications to avoid confounding factors.
Main Results:
- Plasma PCSK9 levels were not associated with the presence of CAD in the Ottawa cohort but were elevated in CAD patients in the Emory cohort.
- Significantly higher plasma PCSK9 levels were observed in patients with acute MI compared to CAD patients without MI in both cohorts.
- PCSK9 levels were similar in CAD patients with or without prior non-acute MI, suggesting elevation around the time of acute MI.
Conclusions:
- Plasma PCSK9 levels are elevated in the context of acute myocardial infarction (MI).
- The findings suggest PCSK9 may be a marker or contributor to acute MI events.
- Further research is warranted to elucidate the precise role of PCSK9 in acute MI pathogenesis.
Objective:
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a circulating protein that promotes degradation of the low density lipoprotein (LDL) receptor. Mutations that block PCSK9 secretion reduce LDL-cholesterol and the incidence of myocardial infarction (MI). However, it remains unclear whether elevated plasma PCSK9 associates with coronary atherosclerosis (CAD) or more directly with rupture of the plaque causing MI.
Methods And Results:
Plasma PCSK9 was measured by ELISA in 645 angiographically defined controls (<30% coronary stenosis) and 3,273 cases of CAD (>50% stenosis in a major coronary artery) from the Ottawa Heart Genomics Study. Because lipid lowering medications elevated plasma PCSK9, confounding association with disease, only individuals not taking a lipid lowering medication were considered (279 controls and 492 with CAD). Replication was sought in 357 controls and 465 with CAD from the Emory Cardiology Biobank study. PCSK9 levels were not associated with CAD in Ottawa, but were elevated with CAD in Emory. Plasma PCSK9 levels were elevated in 45 cases with acute MI (363.5±140.0 ng/ml) compared to 398 CAD cases without MI (302.0±91.3 ng/ml, p = 0.004) in Ottawa. This finding was replicated in the Emory study in 74 cases of acute MI (445.0±171.7 ng/ml) compared to 273 CAD cases without MI (369.9±139.1 ng/ml, p = 3.7×10(-4)). Since PCSK9 levels were similar in CAD patients with or without a prior (non-acute) MI, our finding suggests that plasma PCSK9 is elevated either immediately prior to or at the time of MI.
Conclusion:
Plasma PCSK9 levels are increased with acute MI.
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