Novel markers of plaque rupture in patients with chest pain
Chest pain presentations to the accident and emergency department account for approximately 20% of admissions. Determining those patients at high risk of plaque rupture the squeal of which is ischemia and myocardial necrosis continues to be clinically challenging. Current clinical pathways identify those who have undergone plaque rupture utilizing cardiac troponins and electrocardiogram changes but this confirms plaque rupture after myocardial injury.
We previously identified a number of proteins in an Apolipoprotien B mouse model that were present at significantly higher or lower levels in the serum prior to plaque rupture and thus were predictive of a higher risk of plaque rupture in mice. None of these proteins had been identified in plaque rupture previously.
My MD thesis evaluated the clinical utility of these markers in an unselected cohort of 203 patients presenting with chest pain to either the accident and emergency department or cardiac catheterization suite at St James’s Hospital, Dublin. We found that Galectin 3 was significantly elevated in patients with cardiac chest pain i.e. stable angina and acute coronary syndrome (ACS). In ACS patients Galectin 3 was significantly elevated prior to plaque rupture and correlated with the duration of symptoms. IL-15Rα was significantly elevated in patients presenting both with stable angina and ACS.IL-15Rα was also elevated prior to plaque rupture and thrombosis in patients with unstable angina. This correlated strongly with the duration of symptoms suggesting its utility as a marker of unstable plaque. IL-15Rα also correlated significantly with Gal-3 in patients with ACS, specifically in those with unstable angina with unstable plaque. TGFIIβR was significantly elevated in patients with stable angina and decreased in those with unstable symptoms but did not correlate with the duration of chest pain symptoms. The other markers DTK and HF7 were not significantly elevated and found not to be predictive of unstable plaque.