risk factors in primary, secondary, and tertiary prevention of CVD. Smoking cessation in tertiary prevention is the most important single lifestyle intervention and its effect is stronger than lipid profile modification. 6 The devastating effect of tobacco smoke is related to a mixture of more than 7000 chemicals contributing to endothelial dysfunction, inflammation, dyslipidemia, vascular and hemodynamic function, and a prothrombotic state. Cigarette smoking influences all phases of atherosclerosis from endothelial dysfunction to the occurrence of acute coronary syndrome (ACS). Smoking induced activation of inflammation is characterized by increased plasma levels of fibrinogen, C-reactive protein, and interleukin 6. 6,7 In patients with ACS, smoking is associated with higher levels of inflammation markers and infarct zone hemorrhage. 8 Higher levels of homocysteine, tissue factor, and decreased activity of tissue plasminogen activator factor and matrix metalloproteinases were observed among Introduction Cardiovascular diseases (CVDs) account for 31% of all deaths, that is, 17.9 million deaths per year. Tobacco use is among the greatest risk factors for CVD and accounts for 1 in 4 deaths due to CVDs. 1,2 In addition, the 10-year risk of death is doubled in smokers compared with nonsmokers, 3 and smoking is the most important cause of premature death. 4 Apart from the cardiovascular system, smoking affects other systems including respiratory, digestive, endocrine, and genitourinary systems. Interventions to increase smoking cessation are among the most cost-effective lifestyle modifications. The aim of this review was to discuss the risk of smoking and the potential increase of thrombotic risk related to smoking cessation. Smoking as a classic risk factor for cardiovascular diseases The prevalence of cigarette smoking in general population is decreasing 5 but smoking remains one of the most important modifiable

Background Cigarette smoking is associated with enhanced clopidogrel effect and platelet inhibition. However, the effect of smoking cessation on clopidogrel pharmacokinetics (PK) and pharmacodynamics (PD) is unknown. We aimed to determine the effect of smoking cessation, confirmed by cotinine measurement, on clopidogrel PK and PD after percutaneous coronary intervention (PCI). Methods and Results Following successful PCI, patients treated with 75 mg/day clopidogrel who reported smoking ≥10 cigarettes/day with NicAlert urine cotinine level 6 were enrolled. Clopidogrel and its metabolite concentrations, VerifyNow P2Y12 reaction units (PRUs), and NicAlert levels were measured in the study group before and at 30 days after smoking cessation and in a control group. CYP1A2 and CYP2C19 genotypes were determined. At 30-day visit (n = 87), 45 patients continued smoking, whereas 42 patients stopped smoking. Baseline PRUs were similar between groups. At 30 days, the smoking cessation group had higher PRUs (150.5 ± 68.6 vs. 118.4 ± 65.9, p = 0.03), greater absolute PRU change (27.7 ± 39.8 vs. −12.9 ± 55.4, p = 0.0002), greater change of PRUs adjusted for baseline platelet reactivity (38.6 ± 10.0, p < 0.01), greater risk of high platelet reactivity (HPR) (odds ratio: 10.14 [1.52–67.5], p = 0.017), and a trend towards decreased H3 clopidogrel metabolite levels (−3.41 ng/mL [−11.00 to 0.54 ng/mL], p = 0.072). CYP2C19 LoF carriers who stopped smoking had the highest PRUs, whereas those with the wild type who continued smoking had the lowest PRUs (p < 0.008). Conclusion Smoking cessation in clopidogrel-treated patients after PCI is associated with increased platelet reactivity and greater risk of HPR. Alternative P2Y12 inhibitors may be considered in selected patients who stop smoking after PCI.

(1) Background: We aimed to assess the impact of the selection of a larger radial or ulnar artery on the efficacy of access and vascular complications, based on preprocedural ultrasonographic examination. (2) Methods: This prospective, randomized trial included patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI). Patients were randomized into either a larger ulnar artery (UA) or radial artery (RA) group or smaller UA/RA group. The primary endpoint was successful CAG/PCI without crossover to another artery. The secondary endpoints were incidences of radial or ulnar artery occlusion (RAO/UAO) at the 24 h and 30 day follow-up. (3) Results: Between 2017 and 2018, 200 patients (107 men, mean age 68 ± 8 years) were enrolled. The success of CAG/PCI via the access site was 98% and 83% (p < 0.001) in the larger UA/RA group and smaller UA/RA group, respectively. The independent factor for CAG/PCI success was the larger artery (OR 9.8, 95%CI 2.11–45.5; p < 0.005). The larger UA/RA was superior, with RAO/UAO at 24 h: OR 0.07, 95%CI 0.09–0.61; p < 0.016; and RAO/UAO at 30 days: OR 0.25, 95%CI 0.05–0.12; p < 0.001. (4) Conclusions: Larger artery access was shown to be more efficient and safer than recessive forearm artery access.

Introduction Transradial access (TRA) for coronary angiography (CAG) and percutaneous coronary intervention (PCI) is superior to transfemoral access (TFA). Transulnar access (TUA) is an alternative to TRA. Aim To compare the efficacy and safety of TRA vs. TUA in patients scheduled for CAG or PCI. Material and methods This was a prospective, single-center, randomized study conducted between 2013 and 2016. Two hundred patients referred for the first elective CAG were included in the study. Eligible patients were then randomly assigned to the TRA or TUA group. Before and after the invasive procedure, all patients underwent ultrasonographic measurements of the right upper limb arteries. Results The primary endpoint was efficacy, defined as a successful CAG without a crossover of vascular access. The secondary endpoint was safety, assessed as the number of vascular complications. Successful coronary angiography via the access site was 95% vs. 75% in the TRA vs. TUA groups, respectively ( p < 0.001). It depended on the anatomy of UA and the operator experience. No differences were observed in early and late follow-up complications. Conclusions TRA was superior to TUA with regard to efficacy. TUA occurred a safe approach for CAG and PCI and could be used as an alternative method of forearm access.

(1) Background: The exact mechanism underlying hand strength reduction (HSR) after coronary angiography with transradial access (TRA) or transulnar access (TUA) remains unknown. (2) Methods: This study aimed to assess the impact of using a larger or smaller forearm artery access on the incidence of HSR at 30-day follow-up. This was a prospective randomized trial including patients referred for elective coronary angiography or percutaneous coronary intervention. Based on the pre-procedural ultrasound examination, the larger artery was identified. Patients were randomized to larger radial artery (RA) or ulnar artery (UA) or a group with smaller RA/UA. The primary endpoint was the incidence of HSR, while the secondary endpoint was the incidence of subjective HSR, paresthesia, and any hand pain. (3) Results: We enrolled 200 patients (107 men and 93 women; mean age 68 ± 8 years) between 2017 and 2018. Due to crossover between TRA and TUA, there were 57% (n = 115) patients in larger RA/UA and 43% (n = 85) patients in smaller RA/UA. HSR occurred in 29% (n = 33) patients in larger RA/UA and 47% (n = 40) patients in smaller RA/UA (p = 0.008). Subjective HSR was observed in 10% (n = 12) patients in larger RA/UA and 21% (n = 18) patients in smaller RA/UA (p = 0.03). Finally, paresthesia was noted in 7% (n = 8) patients in larger RA/UA and 22% (n = 15) in smaller RA/UA (p = 002). Independent factors of HSR were larger RA/UA (OR 0.45; 95% CI, 0.24–0.82; p < 0.01) and the use of TRA (OR 1.87; 95% CI, 1.01–34; p < 0.05). (4) Conclusions: The use of a larger artery as vascular access was associated with a lower incidence of HSR at 30-day follow-up.

Hemostatic devices used in the transradial approach (TRA) and transulnar approach (TUA) are limited. This study compared the efficacy and safety of hemostasis using the QuikClot Radial hemostatic pad (QC) vs. standard mechanical compression (SC) after coronary angiography (CAG). This prospective single-center randomized trial included CAG patients. The primary and secondary endpoints were efficacy (successful hemostasis) and safety (total artery occlusion [TAO], pseudoaneurysm, hematoma), respectively. A visual analog scale (VAS) evaluated patient pain during compression. In 2013-2017, 200 patients were randomized 2 × 2 into the: (1) TRA and TUA groups and (2) QC and SC groups. Successful hemostasis was achieved in 92 (92%) patients in the QC group and 100 (100%) patients in the SC group (p < 0.006). The TRA SC subgroup showed significantly better results than the TRA QC subgroup (100% vs. 90.0%; p < 0.03). Similar results were obtained in the TUA QC and TUA SC subgroups (95% vs. 100%; p = 0.5). The secondary endpoint was achieved in the QC and SC groups (8% vs. 9%; p = 0.8). Patients reported significantly less pain during QC application than during SC (VAS: 2.6 ± 2.6 vs. 3.4 ± 2.9; p < 0.03). In patients undergoing CAG with TRA or TUA, QC was associated with lower efficacy, less discomfort, and similar safety compared to SC.

This article is available in open access under Creative Common Attribution-Non-Commercial-No Derivatives 4.0 International (CC BY-NC-ND 4.0) license, allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially.Is cytisine contraindicated in smoking patients with coronary artery disease after percutaneous coronary intervention?

Background/Introduction: Cigarette smoking is a potent modifiable risk factor for coronary artery disease (CAD). However, little is known about alterations to prothrombotic state and platelet reactivity early after smoking cessation following percutaneous coronary interventions (PCI). Purpose: We investigated alterations to platelet reactivity, coagulation and markers of platelet, endothelial, inflammatory and coagulation activation in clopidogrel-treated patients with CAD after PCI before and after smoking cessation. Methods: Smoking patients aged 18 years or older at least 30 days after PCI were recruited and encouraged to quit the habit. At baseline and at 30 days, we measured platelet reactivity with VerifyNow system, thrombomodulin, P-selectin, platelet factor 4 (CXCL4/PF4), citrullinated histone H3 (H3cit) and cotinine level. Results: Among 117 patients, 84 patients (72%) at a median age of 60.5 years (40 [interquartile range 30–47] pack-years) completed a 30-day follow-up. At day 30, 30 (35.7%) patients stopped smoking with cotinine level < 50 ng/ml. Baseline characteristics were similar in both groups. In smoking quitters a change in platelet reactivity was larger (Δ platelet reactivity units (PRU) 19 [2, 43] vs. -6 [-32, 37], p = 0.018), along with a change in P-selectin concentration (-11.82 [-23.62, 1.34] vs. 7.19 [-14.24, 17.19] ng/ml, p = 0.005). Positive correlations was noticed between cotinine and both P-selectin ( r = 0.23, p = 0.045) and CXCL4 (r = 0.27, p = 0.02). Conclusion: After smoking cessation in CAD patients following PCI an increase in platelet reactivity and a decrease in P-selectin levels were observed. The risk of thrombotic complications post PCI might be paradoxically enhanced among patients who stopped smoking.