Key result
Platelets from patients with acute myocardial infarction expressed PKCε at a significantly higher frequency (87.5%) compared to both stable coronary artery disease (33.3%) and healthy subjects (12.5%).
Why the study?
Does platelet PKCε expression differ in patients with acute myocardial infarction compared to stable CAD and healthy subjects?
Case-Control (n=72)
No
Does platelet PKCε expression differ in patients with acute myocardial infarction compared to stable CAD and healthy subjects?
Absolute Event Rate: 87.5% vs 12.5%
p-value: p=0.0001
Platelets from patients with acute myocardial infarction ectopically express PKCε, which increases their hyper-responsiveness and adhesion, suggesting a pathophysiological role in the acute event.
May mark acute platelet activation in AMI; leaves open causality and biomarker utility pending prospective studies.
OBJECTIVE: Platelets play crucial roles in the pathophysiology of thrombosis and myocardial infarction. Protein kinase C ε (PKCε) is virtually absent in human platelets and its expression is precisely regulated during human megakaryocytic differentiation. On the basis of what is known on the role of platelet PKCε in other species, we hypothesized that platelets from myocardial infarction patients might ectopically express PKCε with a pathophysiological role in the disease. METHODS AND RESULTS: We therefore studied platelet PKCε expression from 24 patients with myocardial infarction, 24 patients with stable coronary artery disease and 24 healthy subjects. Indeed, platelets from myocardial infarction patients expressed PKCε with a significant frequency as compared to both stable coronary artery disease and healthy subjects. PKCε returned negative during patient follow-up. The forced expression of PKCε in normal donor platelets significantly increased their response to adenosine diphosphate-induced activation and adhesion to subendothelial collagen. CONCLUSIONS: Our data suggest that platelet generations produced before the acute event retain PKCε-mRNA that is not down-regulated during terminal megakaryocyte differentiation. Results are discussed in the perspective of peri-infarctual megakaryocytopoiesis as a critical component of myocardial infarction pathophysiology.
No takes yet. Share an insight, caveat, or question.
Carubbi et al. (2012) conducted a case-control in Acute Myocardial Infarction (n=72). Acute Myocardial Infarction vs. Stable coronary artery disease and healthy subjects was evaluated on Platelet PKCε mRNA expression frequency (p=0.0001). Platelets from patients with acute myocardial infarction expressed PKCε at a significantly higher frequency (87.5%) compared to both stable coronary artery disease (33.3%) and healthy subjects (12.5%).
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: