Angiology

Patients with peripheral artery disease (PAD) have an increased risk of cardiovascular (CV) and limb events, but the disease is frequently underdiagnosed and treatment options are limited. This review examines the disease burden of symptomatic PAD as well as key guideline recommendations. Publications were identified using the ProQuest portal to access the Medline, Medline In-Process, and Embase databases. Search terms for symptomatic PAD were combined with terms relevant to epidemiology, burden, treatment practice, and physiopathology. Articles in English published between January 2001 and September 2016 were screened according to the population, interventions, comparator, outcomes, and study design criteria. Relevant publications (n = 200) were identified. The reported incidence and prevalence of PAD varied depending on the definitions used and the study populations. Patients generally had a poor prognosis, with an increased risk of mortality, CV, and limb events and decreased quality of life. Guideline recommendations included ankle–brachial index measurements, exercise testing, and angiography for diagnosis and risk factor modification, antiplatelets, cilostazol, exercise therapy, or surgical interventions for treatment, depending on the patient profile. The clinical, humanistic, and economic burden of disease in patients with symptomatic PAD is substantial and needs to be reduced through improved PAD management.

Several trials have been completed in patients with heart failure (HF) treated with uric acid (UA)-lowering agents with inconsistent results. We aimed to investigate whether lowering UA would have an effect on mortality and cardiovascular (CV) events in patients with HF in a systematic review and meta-analysis. The primary outcome measures were all-cause mortality, CV mortality, CV events, and CV hospitalization in patients with HF. We included 11 studies in our final analysis. Overall, allopurinol treatment was associated with a significant increase in the risk for all-cause mortality (hazard ratio [HR]: 1.24, 95% confidence interval [CI]: 1.04-1.49, P = .02). The trial heterogeneity is high (heterogeneity χ² = 37.3, I2 = 73%, P < .001). With regard to CV mortality, allopurinol treatment was associated with a 42% increased risk of CV mortality (HR: 1.42, 95% CI: 1.11-1.81, P = .005). There was a trend toward increased CV hospitalization in the same group (HR: 1.21, 95% CI: 0.95-1.53, P = .12). Uric acid-lowering treatments increase all-cause and CV mortality but did not increase CV hospitalization significantly in this study.

The association between prior stroke/transient ischemic attack (TIA) and clinical outcomes in patients with acute coronary syndrome (ACS) has not been well explored. We evaluated the impact of prior stroke/TIA on this specific patient population. We conducted an international multicenter study including 15 401 patients with ACS from the Bleeding Complications in a Multicenter Registry of Patients Discharged With Diagnosis of Acute Coronary Syndrome registry. They were divided into 2 groups: patients with and without prior stroke/TIA. The primary end point was death at 1-year follow-up. Prior stroke/TIA was associated with higher rate of 1-year death (8.7% vs 3.4%; P < .001). It was an independent predictor of 1-year death even after adjustment for confounding variables (odds ratio, 1.705; 95% confidence interval, 1.046-2.778; P = .032). Besides, patients with prior stroke/TIA had significantly increased 1-year reinfarction (5.6% vs 3.8%, P = .015), in-hospital bleeding (8.7% vs 5.8%, P < .001), and 1-year bleeding (5.2% vs 3.0%, P < .001). No difference of antithrombotic therapies or dual antiplatelet therapy (DAPT) types on outcomes was observed in patients with prior stroke/TIA. Prior stroke/TIA was associated with higher 1-year death for patients with ACS who underwent percutaneous coronary intervention. No benefits or harms were observed with different antithrombotic therapies or DAPT types in these patients.

This study aims to explore the association between serum cotinine and severe abdominal aortic calcification (AAC) in the US adults. We examined 2840 participants with a weighted mean age of 57.4 years from the National Health and Nutrition Examination Survey 2013-2014. Serum cotinine was analyzed as the main exposure both continuously and categorically (tertiles). Abdominal aortic calcification detected with dual-energy X-ray absorptiometry was quantified using the Kauppila score system. Severe AAC was detected in 252 (8.9%) participants. The multivariable-adjusted odds ratios and 95% confidence intervals (CIs) of the middle and top cotinine categories were 1.14 (0.79-1.64) and 1.80 (1.21-2.68), respectively, P for trend = .004. Per unit increase in log-transformed serum cotinine was associated with 10% (95% CI: 6%-15%) higher odds of severe AAC when serum cotinine was analyzed as a continuous variable. The association was consistent across sex and ethnic groups. In conclusion, elevated serum cotinine level was associated with higher odds for severe AAC in a representative sample of US adults.

We evaluated the relationship between serum bilirubin levels and ankle-brachial index (ABI) to determine whether gender affected the relationship between bilirubin levels and peripheral arterial disease (PAD) in patients with hypertension. A total of 543 patients were included in our studies (78 patients with PAD and 465 without PAD). Peripheral arterial disease was defined as ABI <0.90 for either and/or both sides. Serum bilirubin levels were measured with a vanadate oxidation method by using fasting venous blood samples. Serum total bilirubin (TBiL) and direct bilirubin (DBiL) levels were higher in males compared with females (both P < .05). Total bilirubin and DBiL were significantly lower in the PAD group. After adjustment for cardiovascular risk factors, PAD was independently negatively related to TBiL and DBiL, with odds ratios (OR) 0.914 (95% confidence interval [CI]: 0.845-0.990) and 0.748 (95% CI: 0.572-0.977). In addition, there was a relationship between PAD and bilirubin levels (TBiL—OR = 0.884, 95% CI: 0.792-0.985; DBiL—OR = 0.621; 95% CI: 0.424-0.909) only in males but not in females. Future studies should further evaluate whether interventions that increase serum bilirubin levels will have a particular role in PAD prevention in males.

C-reactive protein (CRP) and high-sensitivity CRP (hsCRP), along with a series of hematological indices, platelet to lymphocyte ratio (PLR), neutrophil to lymphocyte ratio (NLR), mean platelet volume (MPV), platelet distribution width (PDW), and red blood cell distribution width (RDW), are regarded to be related to the incidence of no-reflow or slow flow. Clinical studies were retrieved from the electronic databases of PubMed, EMBASE, Google Scholar, Clinical Trials, and science direct from their inception to August 24, 2019. A total of 21 studies involving 7403 patients were included in the meta-analysis. Pooled analysis results revealed patients with higher hsCRP (odds ratio [OR] = 1.03, 95% confidence interval [CI], 1.01-1.05, P = .006), hsCRP (OR = 1.04, 95% CI: 1.0-1.08, P = .012), NLR (OR = 1.23, 95% CI: 1.11-1.37, P < .0001), PLR (OR = 1.13, 95% CI: 1.07-1.20, P < .0001), and MPV (OR = 2.13, 95% CI: 1.57-2.90, P < .0001) all exhibited significantly higher no-reflow incidence, but there was no significant association between no-reflow risk and RDW or PDW. Patients with higher CRP/hsCRP also performed higher rate of slow flow (OR = 1.06, 95% CI: 1.01-1.11, P = .018). Preangiographic CRP/hsCRP could independently predict no-reflow and slow flow. Moreover, some hematological indices are associated with no-flow.

Several laboratory parameters have been used to assess inflammatory process and determine cardiovascular risk. The C-reactive protein to albumin ratio (CAR) is a novel marker of inflammation and its clinical importance has not been clearly elucidated in coronary artery disease (CAD). We compared the diagnostic value of CAR with other inflammatory parameters in detecting significant CAD. Patients (n = 421) with stable angina pectoris who underwent coronary angiography for the suspected CAD were included. Neutrophil to lymphocyte ratio (NLR), monocyte to lymphocyte ratio (MLR), platelet to lymphocyte ratio, uric acid, monocyte to high-density cholesterol (HDL-C) ratio, mean platelet volume to lymphocyte ratio (MPVLR), and platelet to mean corpuscular volume (MCV) ratio were measured. Patients with significant CAD had a significantly higher NLR (P = .043), MLR (P = .004), uric acid (P < .001), monocyte to HDL-C ratio (P = .004), and CAR (P < .001) compared to patients without significant CAD. However, MPVLR and platelet to MCV ratio weren’t different between 2 groups. The area under the curve (AUC) of CAR was the highest AUC among all inflammatory parameters for predicting significant CAD. Multivariate analysis showed that age (odds ratio [OR]: 1.046, 95% confidence interval [CI], 1.020-1.072, P < .001) and CAR (OR: 1.175, 95% CI, 1.126-1.226, P < .001) were the only independent predictors of significant CAD. In conclusion, CAR had the strongest diagnostic value in detecting significant CAD among the inflammatory parameters evaluated in this study.

Contrast-induced nephropathy (CIN) accounts for about 10% of all hospital-acquired acute kidney injury. We aimed to assess the role of the combination of 2 inflammatory biomarkers, the C-reactive protein (CRP)/albumin ratio (CAR), in the development of CIN after percutaneous coronary intervention (PCI) in patients with non-ST-elevation myocardial infarction (NSTEMI). Patients with NSTEMI (n = 205) treated by PCI were classified according to the development of CIN. Both groups were compared according to clinical, laboratory, and demographic characteristics, including inflammatory biomarkers and specifically, CAR. Contrast-induced nephropathy was observed in 10.2% of patients. More advanced age, the presence of diabetes and dyslipidemia, left ventricular ejection fraction, and CAR correlated with the development of CIN. Analysis also showed a significant association between CAR and the development of CIN (CAR in CIN (+): 8.54 ± 8.48, range: 0.7-32, median: 7.13 vs CAR in CIN (−): 2.36 ± 3.01, range: 0.1-24, median: 1.33, P < .001). Multivariate logistic regression analysis showed the impact of CAR on the development of CIN (odds ratio: 1.244, 95% confidence interval: 1.102; 1.392, P < .01). We conclude that CAR, as a combination of 2 inflammatory biomarkers, is a more accurate predictor of CIN development compared with the single-marker assessment of albumin and CRP in the context of NSTEMI.

Chronic obstructive pulmonary disease (COPD) is a risk factor for non-ST-segment elevation–acute coronary syndromes (NSTE-ACS). Whether early invasive strategy (EIS) or ischemia-guided strategy (IGS) confers better outcomes in NSTE-ACS with COPD is largely unknown. Nationwide Inpatient Sample database of the United States was queried from 2010 to 2015 to identify NSTE-ACS with and without COPD. Early invasive strategy was defined as coronary angiogram with or without revascularization on admission day 0 or 1, whereas IGS included patients who did not receive EIS. Standardized morbidity ratio weight was used to calculate the adjusted odds ratio. A total of 228 175 NSTE-ACS admissions with COPD were identified of which 34.0% received EIS. In-hospital mortality was lower with EIS in patients with COPD (3.1% vs 5.5%, adjusted odds ratio 0.57, 95% confidence interval 0.50-0.63) compared to IGS, but the magnitude of mortality reduction observed in EIS in patients with COPD was less compared to non-COPD patients (P _interaction = .02). Length of stay was shorter (4.2 vs 4.7 days, P < .0001) but the cost was higher (US$23 804 vs US$18 533, P < .0001) in EIS in COPD. Early invasive strategy resulted in lower in-hospital mortality and marginally shorter length of stay but higher hospitalization cost in NSTE-ACS with COPD.