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Maciej Antkiewicz,1 Marcin Protasiewicz,2 Wiktor Kuliczkowski,2 Tomasz Zubilewicz,3 Piotr Terlecki,3 Magdalena Kobielarz,4 Dariusz Janczak1 1Department and Clinic of Vascular, General and Transplantation Surgery, Wrocław Medical University, Wrocław, Poland; 2Department and Clinic of Cardiology, Wrocław Medical University, Wrocław, Poland; 3Department and Clinic of Vascular Surgery and Angiology, Medical University of Lublin, Lublin, Poland; 4Department of Mechanics, Materials Science and Biomedical Engineering, Wrocław University of Science and Technology, Wrocław, PolandCorrespondence: Maciej Antkiewicz, Department and Clinic of Vascular, General and Transplantation Surgery, Wrocław Medical University, Borowska 213, Wrocław, 50-556, Poland, Tel +48 71 733 2003, Fax +48 71 733 2009, Email maciej.antkiewicz@gmail.comPurpose: Numerous cases of abdominal aortic aneurysm (AAA) enlargement, and even rupture, despite endovascular aneurysm repair (EVAR), have been documented. This has been linked to increased aneurysm sac pressure (ASP). We decided to conduct further research with the aim to identify correlations between ASP during EVAR and subsequent aneurysm enlargement.Patients and Methods: This experimental prospective study included 30 patients undergoing EVAR of infrarenal AAAs. Invasive ASP measurements were done using a thin pressure wire. Aortic pressure (AP) was measured using a catheter placed over the wire. Systolic pressure index (SPI), diastolic pressure index (DPI), mean pressure index (MPI), and pulse pressure index (PPI) were calculated both for ASP and AP. The results of follow-up computed tomography angiography (CTA) at 3 months were compared with baseline CTA findings.Results: During EVAR, a significant reduction was observed for SPI (from 98% to 61%), DPI (from 100% to 87%), MPI (from 99% to 74%), and PPI (from 97% to 34%). There were no significant correlations of pressure indices with an aneurysm diameter, cross-sectional area, velocity, thrombus shape and size, number of patent lumbar arteries, length and diameter of aneurysm neck, diameter of the inferior mesenteric artery, as well as diameter and angle of common iliac arteries. On the other hand, aneurysm neck angulation was significantly inversely correlated with reduced PPI. After combining CTA findings with pressure measurements, we identified a positive correlation between PPI and aneurysm enlargement (ratio of the cross-sectional area at the widest spot at baseline and at 3 months after EVAR).Conclusion: The study showed that ASP can be successfully measured during EVAR and can facilitate the assessment of treatment efficacy. In particular, PPI can serve as a prognostic factor of aneurysm enlargement and can help identify high-risk patients who remain prior monitoring.Keywords: abdominal aortic aneurysm, aneurysm sac pressure, endovascular surgery, endoleak

Introduction Acute myocardial infarction (MI) is one of the most common causes of death in humans in highly developed countries. Among its most frequent complications affecting the patient’s prognosis are cardiac arrhythmias: ventricular tachycardia (VT) and ventricular fibrillation (VF). Material and Methods The study aimed to characterise arrhythmias in 19 pigs subjected to experimentally induced MI obtained by occlusion of the proximal left anterior descending (LAD) coronary artery using an angioplasty balloon. The anaesthetic protocol was modified to reduce mortality by including procedures stabilising haemodynamic disorders which develop during episodes of ischaemia and arrhythmia. During 30 min of experimentally induced ischaemia, the heart rhythm was recorded using a 12-lead ECG. The time, frequency, and type of arrhythmias were analysed. Results Ventricular arrhythmias were found in 94.74% of the treated pigs. The most common were ventricular premature complexes, reported in 88.89% of pigs with arrhythmia. Ventricular tachycardia was recorded in 66.67% and ventricular fibrillation in 50% of pigs with arrhythmias. Conclusion Myocardial infarction due to proximal LAD occlusion is characterised by a high incidence of ventricular arrhythmias, especially VT and VF. Because of the high survival rate, this MI porcine model may serve as a model for research on acute ischaemic ventricular arrhythmias in humans. Additionally, it reduces the total number of animals required for testing while yielding meaningful results, which is in line with the 3R principle.

Cardiovascular disease (CVD) is associated with intestinal barrier dysfunction and increased intestinal permeability. Increased intestinal permeability to gut microbial metabolites may accelerate the progression of CVD. Plasma citrulline levels are a marker of functional enterocyte mass, and reduced citrulline levels indicate intestinal epithelial damage. Citrulline was reported as a useful prognostic marker in critically ill patients. However, data are lacking on the association of citrulline with long-term mortality in patients with CVD and with the levels of trimethylamine N-oxide (TMAO), a microbiota-derived metabolite which has been implicated in the pathogenesis of CVD.To assess the effect of citrulline levels, a marker of intestinal barrier disruption, on long-term mortality in patients with CVD. Moreover, the relationship between the concentrations of 2 biomarkers - citrulline and TMAO - was assessed.Serum citrulline levels were retrospectively assessed in 1036 consecutive patients with CVD (median age: 62 years; 61% men) hospitalized between 2013 and 2015. Associations of citrulline levels with 5-year mortality rates as well as anthropometric and biochemical parameters were evaluated for the entire study group and in subgroups of patients with acute coronary syndrome (ACS), chronic coronary syndrome, chronic heart failure (chronic HF), and atrial fibrillation (AF). Correlations between serum citrulline and TMAO levels were assessed.The median citrulline level in the study population was 22.5 μM (interquartile range (IQR): 17.8-27.9). Citrulline levels were not associated with 5-year mortality in patients with CVD (hazard ratio (HR) = 0.99; 95% confidence interval (95% CI): 0.97-1.00; p = 0.49). Median citrulline levels differed significantly between deceased patients and survivors at 5 years in patients with ACS (p = 0.025). There were no significant correlations between citrulline and TMAO levels (Kendall's tau = 0.027).Decreasing citrulline levels do not predict long-term mortality of hospitalized patients with CVD. Moreover, they are not associated with the serum levels of TMAO in these patients.

Although traditional cardiovascular risk factors are well established and understood, mortality and morbidity in patients with cardiovascular disease (CVD) remains high. Exploring new pathophysiological pathways enables a better understanding of CVD at both the molecular and clinical levels. Gut microbiota as a potential modulator of CVD are the subject of extensive research. In recent years, trimethylamine N-oxide (TMAO), a biologically active molecule generated by the gut microbiota, has been widely tested in studies on various populations of patients. The ultimate TMAO levels depend on individual features and gut microbiota composition. Most of the research on TMAO has focused on atherosclerotic CVD and heart failure (HF). Studies conducted so far support the use of TMAO as a prognostic marker in CVD. Several studies describe diverse interventions aimed at reducing the concentration of TMAO and its harmful effects. This article summarizes the findings from research, discusses the major insights into TMAO metabolism and related pathophysiological processes, as well as indicates the directions for future research.

Introduction: Trimethylamine N-oxide (TMAO) is an organic compound with a well-established involvement in the pathogenesis of cardiovascular disease (CVD). However, data on the links between TMAO levels and cardiovascular mortality in Polish patients are lacking. Objectives: We aimed to assess the relationship between serum TMAO levels and 5-year mortality in Polish patients with CVD. Patients and Methods: We retrospectively assessed serum TMAO levels in 1,036 consecutive patients (median age, 62 years; men, 61%) hospitalized between 2013 and 2015. Correlations between TMAO levels and 5-year mortality as well as anthropometric and biochemical parameters were assessed for the whole population and the subgroups of patients with acute coronary syndrome, stable coronary syndrome (SCS), chronic heart failure (HF), and atrial fibrillation (AF). Results: In the univariate analysis, increased TMAO levels predicted 5-year mortality without clinically significant power (hazard ratio [HR], 1.01; 95% CI: 1.006–1.018; p < 0.0001). However, even this weak effect was lost in the multivariate analysis after adjustment for age, sex, comorbidities, and laboratory parameters. In the whole study group, TMAO levels in the fourth quartile of concentration (>6.01 µM) predicted 5-year mortality only in the univariate analysis (HR: 1.55; 95% CI: 1.34–1.79; p < 0.0001). In subgroup univariate analysis, TMAO levels predicted 5-year mortality in patients with SCS, chronic HF, and AF. Conclusions: Despite the promising results of previous studies, our study shows that the level of TMAO has at most moderate value in predicting all-cause mortality. TMAO levels depend on other clinical variables, which limits the use of TMAO as an independent predictor of mortality in these patients.

Open thoracoabdominal repair is the gold standard in the TAAA treatment. However, there are endovascular techniques, that sometimes may be an alternative, such as branched endovascular aneurysm repair (BEVAR) or implantation of the multilayer flow modulator (MFM). In this study, we aimed to assess differences in the aneurysm sac pressure (ASP) between patients undergoing BEVAR and MFM implantation. The study included 22 patients with TAAA (14 patients underwent BEVAR, while eight MFM implantation). The pressure sensor wire was placed inside the aneurysm. A measurement of ASP and aortic pressure (AP) was performed during the procedure. The systolic pressure index (SPI), diastolic pressure index (DPI), and pulse pressure index (PPI) were calculated as a quotient of the ASP and AP values. After the procedure, SPI and PPI were lower in the BEVAR group than in the MFM group. During a procedure, a drop in SPI and PPI was noted in patients undergoing BEVAR, while no changes were revealed in the MFM group. This indicates that BEVAR, but not MFM, is associated with a reduction in systolic and pulse pressure in the aneurysm sac in patients with TAAA.

The assessment of functional severity of moderate coronary stenoses is challenging. Coronary angiography remains the standard technique for diagnosis, although, due to its limitations, it is frequently insufficient to detect relevant myocardial ischemia. Fractional flow reserve (FFR) is defined as the ratio between the mean hyperemic coronary artery pressure distal to the lesion and mean pressure in the aorta. The FFR measurement is currently supported by guidelines to evaluate the hemodynamic significance of lesions. Proper identification of patients that have the potential to benefit from revascularization is crucial. Based on already published literature, we focus on the long-term follow-up of patients with FFR-driven treatment. We also provide a review of specific clinical cases such as borderline FFR values, comorbidities or lesions in anatomical risk locations, in which interpretation can be challenging during the physiological assessment. The aim of this paper is to provide an overview of the evidence of FFR implementation in daily clinical practice and determine issues that raise doubts.

Acute coronary syndrome is a factor for poor prognosis and recurrent cardiovascular events. Adequate antiplatelet therapy is crucial in patients with the acute coronary syndrome for risk reduction. Such treatment is well described in four documents issued by the European Society of Cardiology, which precisely illustrate the use of antiplatelets in the settings of ST-elevated and non-ST elevated myocardial infarction. Despite its unquestioned role in the treatment of acute coronary syndrome, recent real-world-data from Polish registries reveal poor adherence to the guidelines-recommended antiplatelet treatment in Poland. Thus, we present here a comprehensive review of the use of antiplatelets in the settings of the acute coronary syndrome. Each phase of the treatment, i.e. pre-hospital, in-hospital and post-hospital, is discussed separately for a better understanding of the decision-making process at each step. We also present unpublished data from Polish registries (e.g. PL-ACS 2019, National Registry of Procedures of Invasive Cardiology, RECEPTOmetrPEX panel) regarding adherence to the guidelines-recommended treatment in Poland, thus highlighting the points of care which should be immediately improved. It has to be stressed here that careful assessment of ischaemic and bleeding risk has to be performed in each patient with acute coronary syndrome individually and repeated at successive phases of the treatment. Only such an approach allows for appropriate antiplatelet therapy tailoring.

Background. Platelet reactivity and response to antiplatelet drugs, acetylsalicylic acid (ASA) and clopidogrel, in patients with thrombocytopenia and thrombocythemia can have a potentially important effect on the outcome. The effectiveness and safety of antiplatelet drugs in such patients has not been well examined. Measuring the effect of ASA and clopidogrel on platelets could help guide the therapy. Nevertheless, platelet response to antiplatelet drugs is not routinely measured in platelet count disorders and relevant evidence is scarce. Aims. The study aimed to measure platelet reactivity and response to ASA and clopidogrel in patients with platelet count disorders. Materials and Methods. This was a cross-sectional study of consecutive patients hospitalized in cardiology and hematology departments in the years 2018–2019. The study included patients with thrombocytopenia (PLT 450 G/L) on ASA or dual antiplatelet therapy (DAPT; ASA plus clopidogrel). Controls included patients on antiplatelet drugs with normal platelet count. Platelet reactivity was measured in whole blood (Multiplate aggregometer, Roche, Switzerland) using arachidonic acid (AA), adenosine-5′-diphosphate (ADP), and thrombin receptor agonist peptide-6 (TRAP) as agonists. Platelet aggregation was expressed in arbitrary units (AU). AA-induced aggregation was used as a measure of response to ASA with a cut-off above 30 AU showing high on-treatment platelet reactivity to ASA (HTPR-A). ADP-induced aggregation measured response to clopidogrel with a cut-off above 48 AU for high on-treatment platelet reactivity to clopidogrel (HTPR-C). TRAP-induced aggregation measured baseline platelet reactivity not affected by oral antiplatelet drugs. Results. The study included 174 patients. There were 64 patients with thrombocytopenia, 30 patients with chronic thrombocythemia, and 80 controls. All patients were on 75 mg of ASA and 32% of them additionally on 75 mg of clopidogrel due to a history of recent coronary artery angioplasty. AA- and ADP-induced aggregation was comparable between thrombocytopenic patients and controls (median (IQR) 19 (7–28) vs. 23 (15–38) for AA AU and 32 (16–44) vs. 50 (32–71) for ADP AU, respectively), while it was significantly higher in thrombocythemic patients (median (IQR) 80 (79–118) for AA AU and 124 (89–139) for ADP AU). TRAP-induced aggregation showed significantly lowest aggregation in thrombocytopenic (median (IQR) 41 (34–60) for TRAP AU) and highest in thrombocythemic patients (median (IQR) 137 (120–180) for TRAP AU). HTPR-A was frequent in thrombocythemic patients in comparison with thrombocytopenic patients and controls (60% vs. 4% vs. 15%, respectively; p < 0.0002 ). HTPR-C was highly common in thrombocythemic patients and least common in thrombocytopenic ones in comparison with controls (80% vs. 8% vs. 40%, respectively; p < 0.001 ). Conclusion. Chronic thrombocytopenia does not significantly affect platelet reactivity and response to ASA and clopidogrel in comparison with controls. Thrombocytosis significantly increases platelet reactivity and attenuates response to both ASA and clopidogrel.

Bleeding remains a complication during dual antiplatelet therapy (DAPT) for acute coronary syndrome (ACS). Some data suggest a link between bleeding and worsened vascular outcomes. However, this association is unclear, due to omitting of minor bleedings when applying conservative scales. In contrast, the Platelet Inhibition and Outcomes (PLATO) trial classification used broad realistic capturing of all bleedings.Access was gained to the Food and Drug Administration-issued adjudication data set on which post hoc analyses of bleeding, myocardial infarction (MI), stroke, and death were conducted. Bleeding was defined as minimal, minor, major, and life-threatening or fatal (LTOF) as per the original PLATO scale.Among 18,624 enrollees, 10,705 adjudicated events occurred across 7171 patients. There were 618 minimal, 1412 minor, 1216 major, and 536 LTOF bleedings for the total of 3782 events reported in 3387 patients. There were 938 deaths, 2751 MIs and 359 strokes. The overall bleeding was 20.3%, exhibited in 19.2% patients. Total bleeds were associated with less deaths (odds ratio [OR]: 0.55, 95% confidence interval [CI]: 0.47-0.63) and MI (OR: 0.47, 95% CI: 0.41-0.54; P.001 for both). There were no differences in deaths (OR: 1.11, 95% CI: 0.93-1.34; P = .24), but less MIs (OR: 0.72. 95% CI: 0.59-0.86; P.001), and more strokes (OR: 2.17, 95% CI: 1.64-2.88; P.001) after LTOF. Major, minor, and minimal bleeds were associated with less deaths and MI but not strokes.These large uniformly adjudicated data reveal that within 12 months of dual antiplatelet therapy, 1 out of 5 patients experiences bleeding. Overall, bleeding was associated with diminished incidence of death and MI but not strokes.

Mechanical circulatory support (MCS) methods are used in patients with both acute and chronic heart failure, who have exhausted other options for pharmacological or surgical treatments. The purpose of their use is to support, partially or completely, the failed ventricles and ensure adequate organ perfusion, which allows patients to restore full cardiovascular capacity, prolonging their life and effectively improving its quality. The three most popular devices include an intra-aortic balloon pump (IABP), percutaneous assist devices (including Impella, TandemHeart), and venoarterial extracorporeal membrane oxygenation (VA-ECMO). A multidisciplinary approach with the special participation of the Heart Team is required to determine the proper MCS strategy, the choice of the supporting method, and the time of its use. The studies published so far do not allow us to determine which MCS method is the safest and the most effective. Thus, the site experience and accessibility of the method seem to matter most today. MCS finds particular application in patients with acute coronary syndromes complicated by refractory cardiogenic shock, as well as in patients with acute heart failure of the high potential for reversibility. It can also serve as a backup for percutaneous coronary interventions of high risk (complex and high-risk indicated percutaneous coronary intervention [PCI], complex and high-risk indicated PCI [CHIP]). The use of appropriate supportive drugs, precise hemodynamic and echocardiographic monitoring, as well as optimal non-invasive or mechanical ventilation, are extremely important in the management of a patient with MCS. The most serious complications of MCS include bleeding, thromboembolic events, as well as infections, and hemolysis.

Background Platelets are key players in hemostasis. These blood cells contain different types of granules. Recently, there has been a growing interest in the role of inorganic polyphosphate (polyP) structures stored in dense granules of platelets and secreted during platelet activation. Objectives To measure platelet polyP levels in patients with thrombocytopenia and thrombocythemia, and to examine the relationship of this indicator with platelet aggregation. Material and methods The study included 36 patients with hematological disorders (26 with primary chronic thrombocytopenia and 10 with essential thrombocythemia (ET)) and 40 healthy subjects. Platelet reactivity was measured using whole blood impedance aggregometry. The polyP levels were isolated from lysed platelets, which were obtained from citrated platelet-rich plasma. The procedure included inactivating endogenous phosphatases, removing phosphate units derived from DNA and proteins, and finally hydrolyzing them into monophosphate units. A colorimetric assay using malachite green and ammonium molybdate was performed in order to quantify polyP levels. Results The polyP concentrations were significantly higher in the patients with thrombocytopenia than in the patients with thrombocythemia or the controls. The polyP level was not correlated with the level of aggregation. Conclusions The higher polyP levels observed in the patients with low platelet counts may indicate the existence of a compensatory mechanism that prevents excessive bleeding in such patients. Our study provides evidence of an essential role of polyP in platelet function and the coagulation process.

Introduction: Platelets play a fundamental role in the pathogenesis of acute coronary syndrome (ACS). The platelet count (PC) at hospital admission is easy to obtain, but whether thrombocytopenia or/and thrombocytosis impact long-term mortality (LTM) after ACS is unclear. Objective: To evaluate the effect of PC at hospital admission on LTM in patients with ACS. Methods: This retrospective cohort study included patients with the ICD-10 codes for unstable angina (I.20) and acute myocardial infarction (I.21, I.22). Thrombocytopenia was defined as a blood PC 450 G/L. Additional platelet indices which were tested included plateletcrit (PCT), the mean platelet volume (MPV), the platelet distribution width (PDW), and the platelet larger cell ratio (P-LCR). Data on all-cause death were obtained from the National Health Fund database. Results: The study included 3,162 patients with a median follow-up of 27.2 months (interquartile range 12.5–46.8 months; max 68.7 months). Patients with thrombocytopenia and thrombocytosis yielded a higher maximal analyzed 5-year mortality rate in comparison with normal PC patients (45.8 and 47.7 vs. 24.2%, respectively; p < 0.00001) which was mainly driven by higher deaths at 1–2 years after ACS. The 5-year LTM was also significantly higher in patients with abnormal PCT and MPV levels in comparison with patients with PCT and MPV within the normal range. Other platelet indices (PDW, P-LCR) were not associated with a worse outcome. The Cox proportional hazards model revealed that thrombocytopenia at admission was independently associated with higher LTM after ACS (RR 1.83; 95% CI 1.1–3.0; p = 0.01). Conclusions: Both thrombocytopenia and thrombocytosis at hospital admission in post-ACS patients are associated with a significant almost two times higher 5-year mortality rate.

The problem with limited venous access may occur in patients receiving long-term hemodialysis treatment with no possibility of arteriovenous access or in patients with cardiac implantable electronic device–related infection leading to the removal of cardiac implantable electronic device. We present a case report where both situations occur simultaneously. Using recent development in cardiac pacing—leadless cardiac pacemaker—we manage to overcome the vascular access problem. The described case emphasizes the necessity of multispecialty collaboration and gains of new pacing technology in patients who need placement of vascular access for hemodialysis and cardiac implantable electronic device where vascular access is scarce.

Purpose: To analyze the long-term outcomes of a hybrid treatment method combining rotational atherectomy with drug-coated balloon (DCB) angioplasty in patients with total in-stent occlusion in the iliac and/or infrainguinal arteries. Materials and Methods: Between April 2014 and June 2017, 74 consecutive patients (mean age 66.7±9.7 years; 49 men) with total occlusion of a previously implanted stent underwent endovascular recanalization using the Rotarex system and DCB angioplasty. Half (37, 50%) of the patients had critical limb ischemia (CLI), and 30 (41%) of the procedures were performed in emergency. Mean lesion length was 22±15 cm. Results: Overall procedure success was achieved in 73 (98.6%) patients. Six (8.1%) CLI patients developed distal embolism that responded to thrombolysis. Three (4.1%) dissections did not require treatment, while 1 (1.4%) perforation necessitated stent-graft implantation. In all, 33 (44.6%) patients had an additional stent implanted, mainly due to a suboptimal outcome (n=28) or complications (n=5 including the stent-graft). The restenosis rate assessed by duplex ultrasound at 12 months was 20.5% (15/73); 4 (5.5%) patients underwent target lesion revascularization. Recurrent restenosis was more frequent in patients with Rutherford category 5 ischemia (p=0.005), in emergency procedures (p=0.021), after extensive procedures involving 3 independent vessel segments (p=0.016), and if a complication arose during the procedure (p

Aims Currently available data indicate that reduction of ticagrelor maintenance dose (MD) 1-3 years after acute myocardial infarction (AMI) not only provides sufficient platelet inhibition but also can improve ticagrelor's safety profile. The aim of this study was to compare the antiplatelet effect of reduced and standard ticagrelor MD in stable patients beginning 1 month after AMI. Methods and results In a single-centre, randomized, open-label, active-controlled trial, on Day 30 following AMI, 52 patients (26 in each study arm) were assigned in a 1:1 ratio to receive either reduced (60 mg b.i.d) or standard (90 mg b.i.d) ticagrelor MD for the following 2 weeks. On Day 45 after AMI the antiplatelet effect of ticagrelor was evaluated with the VASP assay and Multiplate, and there were no significant differences in platelet inhibition between patients on reduced vs. standard MD [VASP: 10.4 (5.6-22.2) vs. 14.1 (9.4-22.1) platelet reactivity index; P = 0.30; Multiplate: 30.0 (24.0-39.0) vs. 26.5 (22.0-35.0) U; P = 0.26]. Likewise, no differences were found regarding the prevalence of on-ticagrelor high platelet reactivity between patients on ticagrelor 60 mg b.i.d vs. 90 mg b.i.d (VASP: 4% vs. 8%; P = 0.67; Multiplate: 15% vs. 8%; P = 0.54). Administration of reduced MD resulted in proportionally lower plasma concentrations of ticagrelor and its active metabolite on Day 45 after AMI. Conclusion These results suggest that lowering ticagrelor MD 1 month after AMI confers an adequate antiplatelet effect that is comparable to the standard dose. The tested strategy warrants further research to assess its clinical efficacy and safety. Clinicaltrials.gov identifier NCT03251859.

BACKGROUND An endoleak is a typical complication of endovascular aneurysm repair (EVAR). It is characterized by persistent blood flow between a stent graft and the aneurysm sac. Usually, it can be visualized during primary EVAR, but in many cases, this remains impossible. Therefore, other methods of endoleak assessment are urgently needed. The measurement of aneurysm sac pressure (ASP) seems to be a promising direction of research in this area. OBJECTIVES We aimed to evaluate the safety and efficacy of a new method for invasive pressure measurement inside the abdominal aortic aneurysm (AAA) during EVAR. We also assessed a correlation between pressure values and early angiographic occurrence of an endoleak after the procedure. MATERIAL AND METHODS A total of 20 patients with AAA were included in this experimental prospective study. During EVAR, systolic, diastolic and mean pressure values were recorded both for ASP and aortic pressure (AP) before procedure, after stent graft opening and after final stent graft ballooning. RESULTS The measurements were successfully obtained in all participants without any complications. There were no significant differences between all ASP and AP before procedure. After the procedure, blood pressure significantly decreased in the aneurysm sac but not in the aorta. Systolic ASP was significantly lower than systolic AP both after stent graft opening (80.4 ±20.9 mm Hg compared to 110.7 ±21.6 mm Hg, p < 0.01) and after its balloon post-dilatation (65.6 ±26.1 mm Hg compared to 107.4 ±22.1 mm Hg, p < 0.001). Diastolic ASP decreased significantly in comparison to diastolic AP only after stent graft ballooning (48.0 ±14.6 mm Hg compared to 56.4 ±13.6 mm Hg, p < 0.05). CONCLUSIONS Our study confirmed that the novel method for the measurement of ASP during EVAR, using a thin pressure wire, is feasible and safe.

Background: Data regarding the use of percutaneous coronary intervention with drug-eluting balloons (DEB) versus thin-strut drug-eluting stents (thin-DES) for treating DES in-stent restenosis in everyday clinical practice is scarce. Our goal was to evaluate the efficacy and safety profile of DEB versus thin-DES in DES in-stent restenosis. Methods: Consecutive patients with DES in-stent restenosis who underwent percutaneous coronary intervention between 2008 and 2019 entered the multicenter DEB-DRAGON Registry with a follow-up of 3 years. Patients who received DEB at the index procedure (n=557, 49.9%) were compared with those who received thin-DES (n=560, 50.1%). Results: Analysis of the unmatched cohort revealed lower rates of target lesion revascularization (9.1% versus 13.6%; hazard ratio [HR], 0.58 [95% CI, 0.41–0.83], P =0.003), target vessel revascularization (11.8% versus 16.7%; HR, 0.62 [95% CI, 0.45–0.84], P =0.003) and device-oriented composite end point, defined as a composite of cardiac death, target lesion revascularization, and target vessel myocardial infarction (12.7% versus 16.0%; HR, 0.69 [95% CI, 0.50–0.94], P =0.018) in the thin-DES group compared with the DEB group. The incidence of cardiac death, target vessel-myocardial infarction, and myocardial infarction were similar in both groups. However, after propensity score matching, there were no significant differences in target lesion revascularization (11.2% versus 11.2%; HR, 0.91 [95% CI, 0.55–1.51], P =0.707), target vessel revascularization (13.4% versus 14.2%; HR, 0.86 [95% CI, 0.55–1.36], P =0.523), and device-oriented composite end point (14.2% versus 14.2%; HR, 0.91 [95% CI, 0.58–1.42], P =0.667) between the thin-DES and DEB group, respectively. Conclusions: This analysis of a real-life registry revealed similar long-term outcomes of thin-DES and DEB in DES in-stent restenosis regarding target lesion revascularization, myocardial infarction, cardiac death, and device-oriented composite end point. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04415216.