(1) Background: Prescribing apixaban for stroke prevention has significantly increased in patients with non-valvular atrial fibrillation (NVAF). The ABCB1 genotype can influence apixaban absorption and bioavailability. The aim of the present study was to assess the factors that influence apixaban’s plasma level and to establish if a certain relationship has clinical relevance. (2) Methods: Fifty-three NVAF patients were treated with 5 mg apixaban twice/day (70.0 years, range: 65–77, 60.4% men). Trough and peak plasma concentrations of apixaban were determined by liquid chromatography-tandem mass-spectrometry (LC-MS/MS), and ABCB1 genotyping was performed. (3) Results: Apixaban plasma concentrations varied considerably. They were higher in women than in men (311.2 ng/dL vs. 252.2 ng/dL; p = 0.05) and were lower in patients with heart failure (149.4 ng/dL vs. 304.5 ng/dL; p < 0.01). Creatinine clearance was inversely correlated with the apixaban plasma level (Spearman correlation: r = −0.365; p = 0.007 for trough concentrations). No statistically significant differences between the genotypic groups of ABCB1 rs1045642 and ABCB1 rs4148738 were found in the trough or peak apixaban plasma concentrations. (4) Conclusions: Pharmacokinetic parameters are influenced by several clinical factors of which renal function is the major determinant. Plasma concentrations measured in women had higher values than those measured in men, and heart failure was associated with decreased plasma levels of apixaban.

The aim of this study was to investigate the relationship between coronary wedge pressure (CWP), measured as a marker of pre-procedural microvascular obstruction, and left ventricular remodelling in high-risk ST-segment elevation myocardial infarction (STEMI) patients. Pre-revascularization CWP was measured in 25 patients with high-risk anterior STEMI. Left ventricular volumes and ejection fraction were echocardiographically measured at discharge and at follow-up. A 20% increase in left ventricular volumes was used to define remodelling. Patients with CWP ≤ 38 mmHg were characterized by late ventricular remodelling. Patients with CWP > 38 mmHg developed a progressive remodelling process which was associated with a significant 60 months increase in left ventricular volumes (P = 0.01 for end-systolic volume and 0.03 for end-diastolic volume) and a significant decrease in left ventricular ejection fraction (P = 0.05). A significant increase in both left ventricular end-systolic (P = 0.009) and end-diastolic volume (P = 0.02) from baseline to 60 months follow-up was recorded in patients with extracted thrombus length ≥2 mm. Pre-revascularization elevated CWP was associated with increased left ventricular volumes and decreased ejection fraction at long-term follow-up. CWP was a predictor of severe left ventricular enlargement, besides extracted thrombus quantity.Infarct size, microvascular obstruction (MVO) and most probably inflammation are important determinants of left ventricular remodelling after acute ST-segment elevation myocardial infarction (STEMI). Left ventricular remodelling is an important factor in the development of heart failure and a predictor of mortality [1][2][3] . Detection and treatment of MVO during acute STEMI is of the utmost importance since it frequently occurs even after timely culprit artery revascularization [1][2][3] . None of the prophylactic and therapeutic approaches available are effective for MVO treatment 3,4 . Recently, it has also been observed that intracoronary pressure measurement is significantly influenced by the presence and severity of MVO in STEMI. Moreover, it can predict the final extent of global and regional irreversible myocardial injury and left ventricular function at long term follow-up 5 . On the other hand, patients with high collateralization, defined as visible collaterals on the coronary angiogram or as Rentrop scores 1-3, had a 36% reduced all-cause mortality risk compared with patients with Rentrop score 0 6 . Pressure measurements can also define collateral flow. There are some controversies regarding collateral flow and pressure measurements in coronary arteries affected by MVO in acute myocardial infarction 7,8 .

Objectives: In this prospective, randomized trial in patients with acute myocardial infarction (AMI) admitted for primary percutaneous coronary intervention (PPCI), loaded with 600 mg clopidogrel, we hypothesized that eptifibatide administered downstream of the coronary occlusion leads to a lower degree of microvascular obstruction compared with no additional eptifibatide. Methods: Fifty patients with AMI, loaded with 600 mg of clopidogrel at the first hospital contact, with occlusion of the left anterior descending artery (LAD), were randomized to an eptifibatide group (EG) or a control group (CG). In both groups, stenting was performed after thrombus aspiration. Microvascular reperfusion was assessed by angiography, electrocardiography, and transthoracic Doppler ultrasonography of the LAD. Results: TIMI myocardial perfusion grade 2–3 was not different between the EG (72%) and the CG (84%) (p = 0.31). ST segment resolution >70% was similarly detected in both groups (32 vs. 40%; p = 0.56). The mean diastolic deceleration time did not differ significantly between the CG (856.36 ± 397.88 ms) and the EG (935.72 ± 252.22 ms) (p = 0.41). Multivariate logistic regression revealed no significant influence of the treatment with eptifibatide on ST segment resolution (OR 0.47; 95% CI 0.11–2.10, p = 0.32), TIMI myocardial perfusion (OR 0.52; 95% CI 0.10–2.59, p = 0.42), and diastolic deceleration time (OR 0.21; 95% CI 0.03–1.51, p = 0.12). Conclusions: In AMI patients loaded with 600 mg of clopidogrel undergoing PPCI, intracoronary administration of eptifibatide does not clearly improve microvascular obstruction.

Among tested parameters, GLS and NT-proBNP were the most reliable predictors of MACEs in patients with severe AS, while Galectin-3 performed more poorly.

To analyse the predictive ability and incremental value of left ventricular longitudinal axis strain (LAS) and late gadolinium enhancement (LGE) using standard cardiovascular magnetic resonance (CMR) imaging for the diagnosis and prognosis of severe aortic stenosis (AS) in patients with an indication for aortic valve replacement. We conducted a prospective study on 52 patients with severe AS and 52 volunteers. The evaluation protocol included standard biochemistry tests, novel biomarkers of myocardial fibrosis, 12-lead electrocardiograms and 24-hour Holter, the 6-minute walk test and extensive echocardiographic and CMR imaging studies. Outcomes were defined as the composite of major cardiovascular events (MACEs). Among AS patients, most (n = 17, 77.2%) of those who exhibited LGE at CMR imaging had MACEs during follow-up. Kaplan–Meier curves for event-free survival showed a significantly higher rate of MACEs in patients with LGE (p < 0.01) and decreased LAS (p < 0.001). In Cox regression analysis, only reduced LAS (hazard ratio 1.33, 95% CI (1.01 to 1.74), p < 0.01) and the presence of LGE (hazard ratio 11.3, 95% CI (1.82 to 70.0), p < 0.01) were independent predictors for MACEs. The predictive value increased if both LGE and reduced LAS were added to left ventricular ejection fraction (LVEF). None of the biomarkers of increased collagen turnover exhibited any predictive value for MACEs. LAS by CMR is an independent predictor of outcomes in patients with AS and provides incremental value beyond the assessment of LVEF and the presence of LGE.