Angiology

The Mediterranean Diet (MedDiet) has been reported to be protective against the occurrence of several diseases. Increasing evidence suggests that the MedDiet could counter diseases associated with chronic inflammation, including metabolic syndrome, atherosclerosis, cancer, diabetes, obesity, pulmonary diseases, and cognition disorders. Adoption of a MedDiet was associated with beneficial effects on the secretion of anti-inflammatory cytokines, antioxidant cellular and circulating biomarkers as well as with regulation of gene polymorphisms involved in the atherosclerotic process. The MedDiet has been considered for the prevention of cardiovascular and other chronic degenerative diseases focusing on the impact of a holistic dietary approach rather than on single nutrients. Epidemiological dietary scores measuring adherence to a MedDiet have been developed. This narrative review considers the results of up-to-date clinical studies (with a focus on the last 5 years) that evaluated the effectiveness of the MedDiet in reducing the prevalence of chronic and degenerative diseases.

We evaluated the impact of clopidogrel 150 mg/d in patients with chronic kidney disease (CKD) having clopidogrel resistance (CR) after percutaneous coronary intervention (PCI); 1076 consecutive patients with coronary artery disease (CAD) having CKD were enrolled. Maximal platelet aggregation (MPA) was assessed before, 24 hours, and 30 days after a 300-mg loading dose of clopidogrel prior to PCI. After PCI, 370 patients with CR were randomized to receive clopidogrel 75 mg/d (n = 184) or 150 mg/d (n = 186) for 30 days. Stent thrombosis (ST), major adverse cardiac events (MACEs), and bleeding were analyzed after 1 month. Patients in the 150 mg group had significant lower rates of ST and MACE. There was no significant difference in major or minor bleeding. Patients in the 150 mg group had lower MPA and greater inhibition of platelet aggregation. One-month administration of 150 mg/d of clopidogrel decreases the rate of ST and MACE without increasing bleeding in patients with CKD having CR after PCI.

Using data from 2007 to 2011 of the Korea National Health and Nutrition Examination Survey, we evaluated the influence of coronary heart disease (CHD) on health-related quality of life (HRQoL) as measured by the EQ-5D in comparison with the general population and the predictors of HRQoL in CHD. Compared with the general population, HRQoL was impaired in the EQ-5D dimensions of mobility, usual activities, pain/discomfort, and anxiety/depression. The impairment of HRQoL was much greater in the older age group and in females. In subjects with CHD, the predictors for a low EQ-5D index were old age, female sex, low education, stroke, and noncardiovascular comorbidities, and the predictors for a low EQ Visual Analogue Scale were low income and noncardiovascular comorbidities. For the improvement in HRQoL, preventing stroke and noncardiovascular comorbidities is important, especially among female and older Asian patients with CHD.

Contrast-induced nephropathy (CIN) is a common complication in patients with impaired kidney function undergoing coronary angiography/angioplasty. We evaluated whether elevated homocysteine (known to be associated with free radical generation and oxidative stress) increases the risk of CIN. Patients (n = 876) with creatinine clearance <60 mL/min undergoing coronary angiography or percutaneous coronary intervention (PCI) were divided into tertiles of homocysteine levels. Contrast-induced nephropathy was defined as ≥0.5 mg/dL or ≥25% creatinine increase 24 to 48 hours post-PCI. A significant relationship was observed between homocysteine levels and the risk of CIN (P = .033), confirmed after correction for baseline confounding factors, adjusted odds ratio, OR (95% confidence interval, [CI]) = 1.68 (1.09-2.59), P = .019. This association was also significant applying the new definition of contrast-induced acute kidney injury (11.9% in group 1, 10.4% in group 2, and 22.8% in group 3; P < .001), adjusted OR (95% CI) = 1.96 (1.3-2.95), P = .001. Future studies are needed to confirm our findings and to define the role of homocysteine in CIN.

Reactive oxygen species have been implicated in the pathogenesis of contrast-induced nephropathy (CIN). We investigated the relationship between CIN with paraoxonase 1 (PON-1) activity and oxidative stress markers (total antioxidant status [TAS], total oxidant status [TOS], and oxidative stress index [OSI]) in patients with anterior ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention; 289 consecutive patients with STEMI were prospectively included. The patients were divided into 2 groups: CIN (n = 69) and non-CIN (n = 220). Activity of PON-1 and TAS levels were significantly lower and OSI and TOS levels were significantly higher in patients with CIN compared to the non-CIN group (P < .05, for all). On multivariate logistic regression analysis, PON-1 activity and OSI as well as the amount of contrast medium and diabetes were independent predictors for CIN in patients with anterior STEMI. Activity of PON-1 and oxidative stress may play a role in the pathogenesis of CIN.

This was a retrospective study that assessed achievement of lipid-lowering treatment targets in the setting of a University Hospital Lipid Clinic. Low-density lipoprotein cholesterol (LDL-C) goal attainment according to National Cholesterol Education Program-Adult Treatment Panel III (NCEP ATP III) and European Society of Cardiology/European Atherosclerosis Society (ESC/EAS) guidelines was recorded in 1000 consecutive adult patients followed for ≥3 years (mean 8 years). The LDL-C targets according to the NCEP ATP III were attained by 66% and 86% of patients with “very high” (n = 477) and “high” (n = 408) cardiovascular risk, respectively. Fewer patients were within LDL-C goals according to the ESC/EAS guidelines: 25% and 42%. Overall, 92% of the patients were on statins: 67% were on statin monotherapy, while 33% were on combinations with ezetimibe (25%), ω-3 fatty acids (5%), fibrates (4%), or colesevelam (2%). Even in a specialist lipid clinic, a large proportion of patients are not at goal according to the recent ESC/EAS guidelines.

Peripheral artery disease (PAD) is associated with exercise impairment and greater thrombotic risk. We investigated whether clot formation and platelet aggregation assessed by thromboelastography and light-transmission aggregometry correlate with the severity of symptomatic PAD assessed by ambulatory function measures. We studied 40 symptomatic patients with PAD in whom severity of disease was assessed using ankle–brachial index, peak walking time (PWT), claudication onset time, peak oxygen uptake, daily ambulatory activity, and walking impairment questionnaire (WIQ) scores. Clot strength correlated negatively with peak oxygen uptake, PWT, WIQ distance, and stair-climbing scores. Time to clot formation did not correlate with exercise parameters. Platelet aggregation was negatively correlated with WIQ distance score and was positively correlated with PWT and peak oxygen uptake. In conclusion, clot strength and platelet aggregation correlated with objective and self-perceived ambulatory measures. Patients with PAD having more severe walking impairment may be likely to form stronger clots.

We evaluated the prevalence and severity of occult coronary artery disease (CAD) and cerebrovascular disease (CeVD) in patients with abdominal aortic aneurysm (AAA). We studied 100 consecutive patients with no history of CAD, normal electrocardiogram, normal systolic function, and no angina or dyspnea. All patients underwent carotid Doppler study and invasive coronary angiography. Significant CAD was observed in 61% of patients. In all, 51% of patients with significant CAD showed either left main (n = 7), 3-vessel (n = 17), or proximal left anterior descending (n = 7) CAD, corresponding to 31% of the total cohort. Cerebrovascular disease was detected in 53% of patients, and in 38% of them was significant (peak systolic flow velocity ≥125 <230 cm/s). In 36% of patients with CeVD either left main (n = 5), 3-vessel (n = 11), or proximal left anterior descending (n = 3) CAD was observed. Severe asymptomatic CAD is prevalent in AAA, and 31% of patients fulfill indications for coronary revascularization.

We evaluated whether altered reporting of ischemic symptoms occurs in diabetic patients with peripheral arterial disease (PAD) and stable claudication. Patients (n = 152) with claudication were enrolled (120 males; mean age: 71.0 ± 8.6 years): 74 with diabetes (DM-PAD) and 78 without (DM_free-PAD). The degree of muscle oxygenation at symptom onset and maximal speed (Smax) during an incremental treadmill test was recorded at the gastrocnemius by near-infrared spectroscopy (NIRS) and quantified by area under the curve of oxygenated hemoglobin (AUC-Hbo₂) and area under the curve of differential hemoglobin (AUC-dHb). The DM-PAD and DM_free-PAD showed similar exercise capacities inversely correlated with the degree of muscle oxygenation but significantly lower values of AUC-Hbo₂ and AUC-dHb for DM-PAD at symptom onset and Smax (−356 vs −122 and −1200 vs −359, P < .0001). During a NIRS-assisted test, the report of claudication in the presence of diabetes was delayed, occurring at a lower degree of oxygenation than in patients with PAD only, with potential implications for testing, functional staging, and balance disorders.

Platelets contribute to the pathogenesis of atherosclerosis. Platelet activation has been linked with increased mean platelet volume (MPV) and platelet distribution width (PDW). We investigated the association between PDW, MPW, and the degree of carotid artery stenosis (CS). Patients (n = 229) were divided into 3 groups according to the North American Symptomatic Carotid Endarterectomy Trial criteria. Demographic and clinical features were collected retrospectively. Correlation analysis showed a positive association between PDW and the degree of CS. However, there was no significant correlation between CS and MPV. Moreover, we observed that PDW and low-density lipoprotein cholesterol were independent predictors of the degree of CS. This study showed that PDW, not MPV, is related to the degree of CS. Platelet distribution width could be a useful biomarker for CS. Whether targeting PDW will be of clinical benefit remains to be established.

The aim of this study was to follow the thrombus progression and regression in superficial veins of lower limbs in patients with superficial vein thrombosis (SVT) treated with low-molecular-weight heparin. Patients (n = 68) with a first symptomatic SVT of the lower limbs received 2 different dosages of dalteparin. The primary outcome was a change in the diameter and length of thrombus in the affected veins. The regression of thrombus was not significantly different between the groups (P = .19). The reduction in the length of thrombus as well as thrombus diameter was significantly greater in females. At the end of the observation period, the length of thrombus in the distal part was more reduced than in the proximal segments. It seems that the dosage of anticoagulant drug does not have a significant impact on thrombus resolution.

Several publications have pointed out the importance of coagulation and fibrinolysis in the occurrence of chronic urticaria (CU), but only a few indicated the direct role of platelets. We assessed platelet aggregation and evaluated parameters of coagulation and fibrinolysis in patients with CU. Patients (n = 34) diagnosed as having CU and 36 healthy controls were enrolled. Platelet aggregation was assayed using an impedance aggregometer and adenosine diphosphate, arachidonic acid, thrombin receptor-activating peptide (TRAP), and ristocetin as agonists. In patients with CU, significantly decreased platelet aggregation to some agonists (ristocetin and TRAP) was observed. The D-dimer levels were elevated, mean platelet volume was decreased, but no alteration was observed in other coagulation assays. Elevated D-dimer levels indicated that coagulation and fibrinolysis are activated in the patients with CU. Evaluation of platelet function may contribute to identify the role of these cells in the pathogenesis of CU.