Angiology

Cardiac trauma is a leading cause of death in the United States and occurs mostly due to motor vehicle accidents. Blunt cardiac trauma and penetrating chest injuries are most common, and both can lead to aortic injuries. Timely diagnosis and early management are the key to improve mortality. Cardiac computed tomography and cardiac ultrasound are the 2 most important diagnostic modalities. Mortality related to cardiac trauma remains high despite improvement in diagnosis and management.

Recent data suggest that clopidogrel-mediated platelet inhibition is age dependent. However, so far the effect of age on adenosine diphosphate (ADP)-inducible platelet reactivity has only been investigated by test systems measuring surrogate markers of platelet aggregation. We therefore sought to study the impact of age on platelet inhibition by clopidogrel by whole-blood flow cytometry. Platelet surface P-selectin expression, activated glycoprotein (GP) IIb/IIIa, and monocyte–platelet aggregate (MPA) formation were determined by flow cytometry in 302 patients with dual antiplatelet therapy after successful angioplasty and stenting. Patient age was independently associated with ADP-inducible P-selectin expression, GPIIb/IIIa, and MPA formation (all P < .05). Moreover, platelet surface expressions of P-selectin and activated GPIIb/IIIa were significantly higher in patients ≥75 years compared with younger patients (both P ≤ .004). Likewise, MPA formation was significantly more pronounced in patients ≥75 years (P = .02). Finally, high P-selectin and high GPIIb/IIIa were significantly more frequent in patients ≥75 years compared with younger patients (both P < .001). Further, high MPA ADP occurred more frequently in patients ≥75 years compared to younger patients (P < .05). In conclusion, the antiplatelet effect of clopidogrel decreases with patient age.

Bilirubin may have important antiatherosclerotic effects. Prediabetes (PD), the intermediate stage before diabetes mellitus, is associated with increased cardiovascular morbidity and mortality. We evaluated the relationship between serum bilirubin levels and carotid intima–media thickness (cIMT), as a surrogate marker of subclinical atherosclerosis, in patients with PD. We enrolled 170 consecutive patients with PD. The patients underwent ultrasonography to evaluate cIMT. The patients were divided into groups according to cIMT values (<0.9 vs ≥0.9 mm). The patients with cIMT ≥ 0.9 mm had significantly higher diastolic blood pressure, neutrophil–lymphocyte ratio (NLR), and glycated hemoglobin values compared with patients having cIMT < 0.9 mm, whereas total and direct bilirubin values were significantly lower in this group. Multivariate regression analyses revealed NLR and total bilirubin as the independent predictors of subclinical atherosclerosis. The present study demonstrated that NLR and lower total bilirubin levels were independent predictors of subclinical atherosclerosis in patients with PD. Simple measures such as NRL and total bilirubin may provide predictive information regarding the risk of cardiovascular disease in patients with PD.

Coronary artery ectasia (CAE) is associated with coronary artery disease (CAD). The underlying pathophysiology of CAE is not fully understood. α₁-antitrypsin (A1AT) plays a role in the tissue protease system, and AAT-1 deficiency (A1ATD) has been shown to be related to CAD. We compared A1AT serum levels in patients with and without CAE to determine the association between A1AT levels and the extent of ectasia using the Markis score. We included 50 patients (38 males) with isolated CAE and 46 patients (28 males) with normal coronary arteries after coronary angiography. The levels of A1AT were measured by nephelometry. The median A1AT levels were lower in patients with isolated CAE than in the control group (1.27 ng/mL [range: 1.07-1.37 ng/mL] vs 1.43 ng/mL [range: 1.27-1.59 ng/mL]; P < .001). According to the Markis classification, the extent of CAE was not correlated with A1AT levels (P = .41). Our results demonstrate an inverse relationship between serum A1AT levels and CAE. α₁-antitrypsin is fundamental for the stability and integrity of the arterial wall. Lack of elastase inhibition in cases of A1ATD may contribute to ectasia formation by facilitating proteolysis and weakening the arterial wall.

Endocan is a soluble proteoglycan, secreted by human vascular endothelial cells. Endocan is a marker for vascular pathologies and an important mediator of angiogenesis, strongly associated with inflammation, vascular endothelial dysfunction, and atherosclerosis. The relationship between coronary artery ectasia (CAE) and endocan has not been evaluated. We aimed to investigate this association. Fifty-four patients with isolated CAE without coronary stenosis and 30 controls with normal coronary angiogram were included in this study. Endocan plasma concentrations were measured using an enzyme-linked immunosorbent assay. Patients with isolated CAE had significantly higher levels of endocan compared to the controls (18.9 ± 7.3 vs 15.6 ± 3.6 ng/mL; P = .007). There was a significant correlation between endocan levels and severity of isolated CAE according to the Markis classification (r = −.593, P < .001). Plasma endocan levels may reflect the presence and severity of isolated CAE, suggesting that endocan may be involved in pathogenesis of isolated CAE.

Obstructive sleep apnea (OSA) is associated with dyslipidemia and increased cardiovascular risk. We assessed the effects of apolipoprotein E (APOE) genotype on low-density lipoprotein (LDL) and high-density lipoprotein (HDL) particle size and lipid subclasses (separated by gradient gel electrophoresis) in patients with OSA. Stable patients (n = 181) prospectively recruited underwent full polysomnography. Both LDL particle size and LDL I proportion were reduced from ∊3∊3 homozygotes to ∊2 carriers and to ∊4 carriers (analysis of variance: P = .024; P = .040, respectively); carriers of the ∊4 allele of the APOE genotype had significantly lower LDL particle size and LDL I proportion compared to ∊3∊3 homozygotes (P < .05 for both comparisons). Insulin resistance increased from patients with no OSA to those with mild–moderate and to those with severe OSA (P < .001). In multivariate analysis, LDL size was independently predicted by APOE genotype, male gender, and the presence of metabolic syndrome (MetS; P = .001, P = .020, P = .027, respectively). The HDL particle size was not affected by APOE genotype. Our data demonstrate that both the ∊4 APOE genotype and MetS are independently related to smaller LDL size in patients with OSA.

Some emerging risk factors such as oxidative stress biomarkers and microRNAs (miRs) may add additional value to the established risk factors for peripheral artery disease (PAD). We enrolled 27 patients with PAD and 27 age-matched controls. We examined the levels of a series of miRs (miR-130a, miR-27b, and miR-210) in serum samples. The level of well-established oxidative stress biomarkers, such as lipid hydroperoxides, isoprostanes, hemeoxygenase-1 (HO-1) and reduced glutathione, was also measured in plasma and their relationship with the miRs was determined. Levels of miR-130a, miR-27b, and miR-210 were significantly increased in patients with PAD when compared to the controls. The level of miR-130 was positively correlated with body mass index, whereas miR-210 was inversely associated with pain-free walking distance (PfWD). None of the evaluated miRs was associated with lowered PfWD of patients with PAD (stage IIa > 250 m, IIb < 250 m) or oxidative stress parameters. In conclusion, our findings suggest the need for more research to assess if miRs can serve as useful markers for the early diagnosis and monitoring of PAD.

Copeptin is a sensitive and more stable surrogate marker for arginine vasopressin. In this study, we evaluated copeptin levels in carotid endarterectomy (CEA) patients, perioperatively, to determine whether copeptin levels can be related to carotid artery cross clamping (CC) time and to postoperative neurological outcomes. Copeptin, interleukin 6, C-reactive protein, cortisol, and brain natriuretic peptide were measured preoperatively (T1) and 3 hours postoperatively (T3) as well as intraoperatively (T2). We recruited 77 patients. Values of copeptin rose gradually over the observed times: T1 = 7.9 (6.4-9.6), T2 = 12.6 (9.3-16.8), and T3 = 72.3 (49.1-111.2) pmol/L. There was a significant difference for repeated measurement (P = .000, P = .000, and P = .000). Duration of carotid artery CC during CEA does not affect postoperative copeptin level (CC ≤ 13 minutes: 106.8 ± 93.6 pmol/L, CC > 13 minutes: 96.7 ± 89.1 pmol/L; P = .634). Preoperative copeptin level was significantly higher in patients with ulcerated plaque morphology. Activation of the stress axis in patients undergoing CEA results in copeptin elevation. Duration of CC during CEA does not affect postoperative copeptin levels.

Impaired fasting glucose (IFG) and impaired glucose intolerance (IGT) are predictors of cardiovascular disease (CVD). We tested the hypothesis that epicardial fat thickness (EFT) and carotid intima–media thickness (cIMT), as markers of early atherosclerosis, are increased in patients with prediabetes. We prospectively enrolled 246 patients (162 with prediabetes and 84 controls). Prediabetes was defined according to American Diabetes Association criteria, and patients were divided into 3 groups: group 1—IFG, group 2—IGT, and group 3—IFG + IGT. Both cIMT and EFT were significantly greater in patients with prediabetes compared with controls (0.81 ± 0.20 mm vs 0.68 ± 0.16 mm, P < .001 and 7.0 ± 2.0 mm vs 5.6 ± 1.6 mm, P < .001, respectively). This difference was mainly attributed to patients with IGT. Age, waist circumference, and 2-hour glucose independently predicted cIMT, while 2-hour glucose was the only independent predictor of EFT in multivariate analysis among other relevant parameters for cIMT and EFT. The cIMT and EFT (measured noninvasively) could be useful indicators of CVD risk in these patients. In order to prove this hypothesis, long-term prospective studies with greater patient numbers are required.