Central aortic pulse pressure, thrombogenicity and cardiovascular risk

High central aortic pulse pressure (CPP) and thrombin-induced platelet–fibrin clot strength (TIP–FCS) have been associated with ischemic outcomes in patients with coronary artery disease in separate studies. But, the ischemic risk associated with these factors has never been analyzed in a single study and their interrelation is unknown. The primary aim of the study was to establish cut points for CPP and TIP–FCS measured at the time of catheterization associated with long term major adverse cardiovascular events. We enrolled 334 consecutive patients undergoing cardiac catheterization and assessed thrombogenicity by thrombelastography. Patients were followed up to 3 years. The primary endpoint was a composite of cardiovascular death, myocardial infarction, and ischemic stroke and the secondary endpoint was occurrence of the primary endpoint or recurrent ischemic events requiring hospitalization. Patients with primary and secondary endpoint occurrence had higher CPP (83 ± 20 vs. 60 ± 18 mmHg, p < 0.0001; 70 ± 21 vs. 59 ± 18 mmHg, p < 0.0001, respectively) and TIP–FCS (68.5 ± 5.8 vs. 65.5 ± 5.0 mm, p = 0.008; 67.4 ± 5.9 vs. 65.2 ± 4.8 mm, p = 0.001, respectively). CPP >60 mmHg and TIP–FCS >69 mm were both independent predictors of primary endpoint occurrence (p = 0.0001 and p = 0.02, respectively). ROC analysis for CPP and TIP–FCS showed a C-statistic of 0.81 (p < 0.0001) and 0.68 (p = 0.007) for the primary endpoint, respectively. Patients with CPP >60 mmHg had higher TIP–FCS (66.8 ± 5.1 vs. 64.8 ± 5.0 mm, p < 0.001) and primary and secondary endpoint occurrence (13 vs. 1.1%, p < 0.0001 and 31.8 vs. 14.4%, p = 0.0002, respectively). CPP >60 mmHg + TIP–FCS > 69 mm was associated with a markedly increased risk of primary endpoint occurrence [HR (95% CI) 5.4(2.3–12.5), p = 0.0001]. High CPP and thrombogenicity are interrelated; each are independently associated with increased cardiovascular risk; and simultaneous presence markedly enhances risk. The mechanistic link between CPP and thrombogenicity deserves further study.