Elevated Lipoprotein(a) Lp(a) levels are associated with coronary atherosclerosis as detected by cardiac computed tomography angiography (CCTA). However, quantitative data including coronary plaque vo Show more
Elevated Lipoprotein(a) Lp(a) levels are associated with coronary atherosclerosis as detected by cardiac computed tomography angiography (CCTA). However, quantitative data including coronary plaque volumes and characteristics are scarce. The current study evaluated the sex-specific correlations between (Lp(a)) levels and the extent and composition of coronary stenosis and plaques. 1,946 patients undergoing CCTA (third-generation dual-source scanner) for suspected coronary artery disease were included whose Lp(a) levels were available. Lp(a) values ≥ 125 nmol/L were classified as high. High Lp(a) levels were observed in 336 patients, who had greater maximum degree of stenosis (49.5 ± 26.4% vs. 43.5 ± 27.6%, P = 0.002), mainly as a result of the pronounced difference in males (53.8 ± 26.0% vs. 46.2 ± 26.8%, P = 0.001). A strong correlation between higher Lp(a) values and high-risk plaque features was noted in the overall cohort (odds ratio [OR]: 1.645; 95% confidence interval [CI]: 1.011 to 2.593; P = 0.037), independent of age and LDL-cholesterol values. In males, high Lp(a) levels were associated with greater total plaque volumes (118.1 [IQR 18.3-284.4] vs. 83.2 [IQR 11.8-226.3] mm Our study identifies novel sex-specific correlations between Lp(a) levels and coronary plaque characteristics. High Lp(a) levels in men seems to be associated with increased fibrotic plaque volumes and may contribute to greater total plaque burden and high-risk plaque features. Show less
Diagnosis of myocardial infarction (MI) is based on ST-segment elevation on electrocardiographic evaluation and/or elevated plasma cardiac troponin (cTn) levels. However, troponins lack the sensitivit Show more
Diagnosis of myocardial infarction (MI) is based on ST-segment elevation on electrocardiographic evaluation and/or elevated plasma cardiac troponin (cTn) levels. However, troponins lack the sensitivity required to detect the onset of MI at its earliest stages. Therefore, to confirm its viability as an ultra-early biomarker of MI, this study investigates the release kinetics of cardiac myosin binding protein-C (cMyBP-C) in a porcine model of MI and in two human cohorts. Release kinetics of cMyBP-C were determined in a porcine model of MI (n = 6, pigs, either sex) by measuring plasma cMyBP-C level serially from 30 min to 14 days after coronary occlusion, with use of a custom-made immunoassay. cMyBP-C plasma levels were increased from baseline (76 ± 68 ng/l) at 3 h (767 ± 211 ng/l) and peaked at 6 h (2,418 ± 780 ng/l) after coronary ligation. Plasma cTnI, cTnT, and myosin light chain-3 levels were all increased 6 h after ligation. In a cohort of patients (n = 12) with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy, cMyBP-C was significantly increased from baseline (49 ± 23 ng/l) in a time-dependent manner, peaking at 4 h (560 ± 273 ng/l). In a cohort of patients with non-ST segment elevation MI (n = 176) from the SYNERGY trial, cMyBP-C serum levels were significantly higher (7,615 ± 4,514 ng/l) than those in a control cohort (416 ± 104 ng/l; n = 153). cMyBP-C is released in the blood rapidly after cardiac damage and therefore has the potential to positively mark the onset of MI. Show less