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Background Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduced cardiovascular risk in type 2 diabetes patients independently of glycemic control. Although angiotensin II (Ang II) and blood-derived microparticles are major mediators of cardiovascular disease, their impact on SGLT1 and 2 expression and function in endothelial cells (ECs) and isolated arteries remains unclear. Methods ECs were isolated from porcine coronary arteries, and arterial segments from rats. The protein expression level was assessed by Western blot analysis and immunofluorescence staining, mRNA levels by RT-PCR, oxidative stress using dihydroethidium, nitric oxide using DAF-FM diacetate, senescence by senescence-associated beta-galactosidase activity, and platelet aggregation by aggregometer. Microparticles were collected from blood of patients with coronary artery disease (CAD-MPs). Results Ang II up-regulated SGLT1 and 2 protein levels in ECs, and caused a sustained extracellular glucose- and Na + -dependent pro-oxidant response that was inhibited by the NADPH oxidase inhibitor VAS-2780, the AT1R antagonist losartan, sotagliflozin (Sota, SGLT1 and SGLT2 inhibitor), and empagliflozin (Empa, SGLT2 inhibitor). Ang II increased senescence-associated beta-galactosidase activity and markers, VCAM-1, MCP-1, tissue factor, ACE, and AT1R, and down-regulated eNOS and NO formation, which were inhibited by Sota and Empa. Increased SGLT1 and SGLT2 protein levels were observed in the rat aortic arch, and Ang II- and eNOS inhibitor-treated thoracic aorta segments, and were associated with enhanced levels of oxidative stress and prevented by VAS-2780, losartan, Sota and Empa. CAD-MPs promoted increased levels of SGLT1, SGLT2 and VCAM-1, and decreased eNOS and NO formation in ECs, which were inhibited by VAS-2780, losartan, Sota and Empa. Conclusions Ang II up-regulates SGLT1 and 2 protein expression in ECs and arterial segments to promote sustained oxidative stress, senescence and dysfunction. Such a sequence contributes to CAD-MPs-induced endothelial dysfunction. Since AT1R/NADPH oxidase/SGLT1 and 2 pathways promote endothelial dysfunction, inhibition of SGLT1 and/or 2 appears as an attractive strategy to enhance the protective endothelial function.

Background Empagliflozin (empa), a selective sodium–glucose cotransporter (SGLT)2 inhibitor, reduced cardiovascular mortality and hospitalization for heart failure in patients with type 2 diabetes at high cardiovascular risk independent of glycemic control. The cardiovascular protective effect of empa was evaluated in an experimental model of metabolic syndrome, the obese ZSF1 rat, and its’ lean control. Methods Lean and obese ZSF1 rats were either non-treated or treated with empa (30 mg/kg/day) for 6 weeks. Vascular reactivity was assessed using mesenteric artery rings, systolic blood pressure by tail-cuff sphygmomanometry, heart function and structural changes by echocardiography, and protein expression levels by Western blot analysis. Results Empa treatment reduced blood glucose levels from 275 to 196 mg/dl in obese ZSF1 rats whereas normoglycemia (134 mg/dl) was present in control lean ZSF1 rats and was unaffected by empa. Obese ZSF1 rats showed increased systolic blood pressure, and blunted endothelium-dependent relaxations associated with the appearance of endothelium-dependent contractile responses (EDCFs) compared to control lean rats. These effects were prevented by the empa treatment. Obese ZSF1 rats showed increased weight of the heart and of the left ventricle volume without the presence of diastolic or systolic dysfunction, which were improved by the empa treatment. An increased expression level of senescence markers (p53, p21, p16), tissue factor, VCAM-1, SGLT1 and SGLT2 and a down-regulation of eNOS were observed in the aortic inner curvature compared to the outer one in the control lean rats, which were prevented by the empa treatment. In the obese ZSF1 rats, no such effects were observed. The empa treatment reduced the increased body weight and weight of lungs, spleen, liver and perirenal fat, hyperglycemia and the increased levels of total cholesterol and triglycerides in obese ZSF1 rats, and increased blood ketone levels and urinary glucose excretion in control lean and obese ZSF1 rats. Conclusion Empa reduced glucose levels by 28% and improved both endothelial function and cardiac remodeling in the obese ZSF1 rat. Empa also reduced the increased expression level of senescence, and atherothrombotic markers at arterial sites at risk in the control lean, but not obese, ZSF1 rat.

Acute kidney injury (AKI) is associated with a dismal prognosis in Transcatheter Aortic Valve replacement (TAVR). Acute kidney recovery (AKR), a phenomenon reverse to AKI has recently been associated with better outcomes. Between November 2012 to May 2018, we explored consecutive patients referred to our Heart Valve Center for TAVR. AKI was defined according to the VARC-2 definition. Mirroring the VARC-2 definition of AKI, AKR was defined as a decrease in serum creatinine ([greater than or equal to]50%) or [greater than or equal to]25% improvement in GFR up to 72 hours after TAVR. AKI and AKR were respectively observed in 8.3 and 15.7% of the 574 patients included. AKI and AKR patients were associated to more advanced kidney disease at baseline. At a median follow-up of 608 days (range 355-893), AKI and AKR patients experienced an increased cardiovascular mortality compared to unchanged renal function patients (14.6% and 17.8% respectively, vs. 8.1%, CI 95%, p<0.022). Chronic kidney disease, (HR: 3.9; 95% CI 1.7-9.2; p < 0.001) was the strongest independent factor associated with AKI similarly to baseline creatinine level (HR: 1; 95% CI 1 to 1.1 p < 0.001) for AKR. 72-hours post procedural AKR (HR: 2.26; 95% CI 1.14 to 4.88; p = 0.021) was the strongest independent predictor of CV mortality. Both AKR and AKI negatively impact long term clinical outcomes of patients undergoing TAVR.

Bleeding following transcatheter aortic valve replacement (TAVR) has important prognostic implications. This study sought to evaluate the impact of baseline mean platelet volume (MPV) on bleeding events after TAVR. Patients undergoing TAVR between February 2010 and May 2019 were included. Low MPV (L-MPV) was defined as MPV ≤10 fL and high MPV (H-MPV) as MPV >10 fL. The primary endpoint was the occurrence of major/life-threatening bleeding complications (MLBCs) at one-year follow-up. Among 1,111 patients, 398 (35.8%) had L-MPV and 713 (64.2%) had H-MPV. The rate of MLBCs at 1 year was higher in L-MPV patients compared with H-MPV patients (22.9% vs. 17.7% respectively, p = 0.034). L-MPV was associated with vascular access-site complications (36.2% vs. 28.9%, p = 0.012), early (<30 days) major bleeding (15.6% vs. 9.4%, p<0.01) and red blood cell transfusion >2 units (23.9% vs. 17.5%, p = 0.01). No impact of baseline MPV on overall death, cardiovascular death and ischemic events (myocardial infarction and stroke) was evidenced. Multivariate analysis using Fine and Gray model identified preprocedural hemoglobin (sHR 0.84, 95%CI [0.75-0.93], p = 0.001), preprocedural L-MPV (sHR 1.64, 95%CI [1.16-2.32], p = 0.005) and closure time adenosine diphosphate post-TAVR (sHR 2.71, 95%CI [1.87-3.95], p<0.001) as predictors of MLBCs. Preprocedural MPV was identified as an independent predictor of MLBCs one year after TAVR, regardless of the extent of platelet inhibition and primary hemostasis disorders.

Acute kidney injury (AKI) is associated with a dismal prognosis in Transcatheter Aortic Valve replacement (TAVR). Acute kidney recovery (AKR), a phenomenon reverse to AKI has recently been associated with better outcomes. Between November 2012 to May 2018, we explored consecutive patients referred to our Heart Valve Center for TAVR. AKI was defined according to the VARC-2 definition. Mirroring the VARC-2 definition of AKI, AKR was defined as a decrease in serum creatinine (≥50%) or ≥25% improvement in GFR up to 72 hours after TAVR. AKI and AKR were respectively observed in 8.3 and 15.7% of the 574 patients included. AKI and AKR patients were associated to more advanced kidney disease at baseline. At a median follow-up of 608 days (range 355-893), AKI and AKR patients experienced an increased cardiovascular mortality compared to unchanged renal function patients (14.6% and 17.8% respectively, vs. 8.1%, CI 95%, p<0.022). Chronic kidney disease, (HR: 3.9; 95% CI 1.7-9.2; p < 0.001) was the strongest independent factor associated with AKI similarly to baseline creatinine level (HR: 1; 95% CI 1 to 1.1 p < 0.001) for AKR. 72-hours post procedural AKR (HR: 2.26; 95% CI 1.14 to 4.88; p = 0.021) was the strongest independent predictor of CV mortality. Both AKR and AKI negatively impact long term clinical outcomes of patients undergoing TAVR.

Background CHA 2 DS 2 -VASc score-related differences have been reported in atrial fibrotic remodeling and prognosis of atrial fibrillation (AF) patients after ablation. There are currently no data on the efficacy of low voltage zone (LVZ)-guided ablation in persistent AF patients according to CHA 2 DS 2 -VASc score. We assessed in a cohort of persistent AF patients the extent of LVZ, the regional distribution of LA voltage and the outcome of LA voltage-guided substrate ablation in addition to PVI according to CHA 2 DS 2 -VASc score. Methods 138 consecutive persistent AF patients undergoing a first voltage-guided catheter ablation were enrolled. 58 patients with CHAD 2 DS 2 -VASc score ≥ 3 and 80 patients with CHAD 2 DS 2 -VASc score ≤ 2 were included. LA voltage maps were obtained using 3D-electroanatomical mapping system in sinus rhythm. LVZ was defined as < 0.5 mV. Results In the high CHAD 2 DS 2 -VASc score group, LA voltage was lower (1.5 [1.1–2.5] vs. 2.3 [1.5–2.8] mV, p  = 0.02) and LVZs were more frequently identified (40% vs. 18%), p  < 0.01). Female with CHA 2 DS 2 -VASc score ≥ 3 ( p  = 0.031), LA indexed volume ( p  = 0.009) and P-wave duration ≥ 150 ms ( p  = 0.001) were predictors of LVZ. After a 36-month follow-up, atrial arrhythmia-free survival was similar between the two groups (logrank test, P  = 0.676). Conclusions AF patients with CHAD 2 DS 2 -VASc score ≥ 3 display more LA substrate remodeling with lower voltage and more LVZs compared with those with CHAD 2 DS 2 -VASc score ≤ 2. Despite this atrial remodeling, they had similar and favorable 36 months results after one single procedure. Unlike male with CHAD 2 DS 2 -VASc score ≥ 3, female with CHAD 2 DS 2 -VASc score ≥ 3 was predictor of LVZ occurrence.

To reduce the iodine load required for CT Transcatheter Aortic Valve Replacement (TAVR) planning on a 320-row scanner by acquiring the two CT TAVR steps (ECG-gated aortic root CTA and non-gated aorto-ilio-femoral CTA) within a single contrast media bolus injection. 50 consecutive patients (82.6±6.9 years; 56% female) were prospectively enrolled and underwent a TAVR planning using a 320-row CT, with ECG-gated aortic root CTA immediately followed by a non-gated aorto-iliac acquisition, all within a single bolus of 40-70mL of Iohexol 350mgI/mL. The Iodine load, image quality, SNR, CNR and radiation dose were compared using a Mann-Whitney test to that of 24 consecutive patients (84.3±4.8 years, 58% female) previously imaged on a 64-row scanner with a conventional two-step protocol. Iodine load was reduced by 44%. All examinations were of diagnostic quality, with improvement of the aortic root CTA image quality (4.9±0.3 versus 4.6±0.5, p<0.01) and a non-significant decrease of the aorto-iliac CTA image quality (4.7±0.6 versus 4.9±0.3, p = 0.07). SNR and CNR were significantly improved in the aortic root CTA (14.0±5.3 and 10.4±4.5 versus 10.3±4.2 and 6.8±3.3, p<0.01 for both) and non-significantly higher in the aorto-iliac CTA (16.5±8.0 and 14.1±7.9 versus 14.7±5.5 and 12.5±5.0, p = 0.42 and p = 0.66). Total radiation dose was reduced by 32%. 320-row CT scanner enables a 44% reduction of iodine load in TAVR planning, while maintaining excellent aorto-ilio-femoral arterial enhancement and lowering radiation dose.

To date, no randomized study has investigated the value of optical coherence tomography (OCT) in optimizing the results of coronary angioplasty for non–ST-segment elevation acute coronary syndromes. DOCTORS is a randomized, prospective, multicenter, open-label clinical trial to evaluate the utility of OCT to optimize results of angioplasty of a lesion responsible for non–ST-elevation acute coronary syndromes. Patients (n = 250) will be randomized to undergo OCT-guided angioplasty (use of OCT to optimize procedural result, including change to strategy with the possibility of additional interventions) or angioplasty under fluoroscopy alone. The primary end point is the functional result of the angioplasty procedure as assessed by fractional flow reserve (FFR) measured at the end of the procedure. Secondary end points include safety of OCT in the context of angioplasty for ACS, percentage of patients in whom OCT reveals suboptimal result of stenting, percentage of patients in whom a change in procedural strategy is decided based on OCT data, correlation between quantitative measures by OCT and FFR, determination of a threshold for quantitative OCT measure that best predicts FFR ≥0.90, and identification of OCT variables that predict postprocedure FFR. Adverse cardiac events (death, recurrent myocardial infarction, stent thrombosis, and repeat target lesion revascularization) at 6 months will be recorded. The DOCTORS randomized trial (ClinicalTrials.gov NCT01743274) is designed to investigate whether use of OCT yields useful additional information beyond that obtained by angiography alone and, if so, whether this information changes physician strategy and impacts on the functional result of angioplasty as assessed by FFR.

Transcatheter aortic valve implantation (TAVI) has become an alternative to surgical aortic valve replacement for patients with symptomatic severe aortic stenosis in elderly and comorbid population. Significant improvement in heart function has been observed in patients undergoing TAVI, but numerous patients are readmitted to hospital for heart failure (HF). Moreover, repeat HF hospitalization is strongly associated with an adverse prognosis and increases the financial burden of health care. Although studies have identified pre‐existing and post‐procedural factors that contribute to HF hospitalization after TAVI, there is a paucity of data regarding optimal post‐procedural pharmacological treatments. This review aims to provide an overview of the current understanding of mechanisms, determinants, and potential treatments of HF following TAVI. We first review the pathophysiology of left ventricular (LV) remodelling, coronary microcirculation disorder, and endothelial dysfunction in patients with aortic stenosis and then examine the impact of TAVI on these conditions. We then present evidence of various factors and complications that may interplay with LV remodelling and contribute to HF events after TAVI. Next, we describe the triggers and predictors of early and late HF rehospitalizations following TAVI. Lastly, we discuss the potential of conventional pharmacological treatments, including renin–angiotensin blockers, beta‐blockers, and diuretics in TAVI patients. The paper explores the potential of newer drugs, including sodium–glucose co‐transporter 2 inhibitors, anti‐inflammatory drugs, and ion supplementation. Comprehensive knowledge in this field may aid in recognizing successful existing therapies, developing effective new treatments, and establishing dedicated patient care strategies during follow‐up after TAVI.

Aims There is a growing body of literature on long‐term outcomes post‐transcatheter aortic valve replacement (TAVR), but to our knowledge, few research have focused on patients with advanced cardiac dysfunction. This challenging category of patients was excluded from the Partner 3 clinical trial. There are no data to guide the choice of valve type in patients with severely depressed ejection fraction. This study evaluates the safety, efficacy, and outcomes of TAVR in patients with severe aortic stenosis and left ventricular ejection fraction (LVEF) ≤ 35%. It compares post‐TAVR survival outcomes with self‐expanding (SEV) versus balloon‐expandable (BEV) valves in the context of cardiac dysfunction. Methods and results A retrospective cohort was conducted on 977 patients who underwent TAVR at Toulouse University Hospital between January 2016 and December 2020. The study population included two groups: LVEF ≤ 35% (N = 157) and LVEF ≥ 50% (N = 820). The group of LVEF ≤ 35% was divided into two subgroups according to the type of implanted device: self‐expanding (N = 66) versus balloon‐expandable (N = 91). The living status of each of study's participants was observed in December 2022. Patients with low ejection fraction were younger (82 vs. 84.6 years) and commonly males (71.3% vs. 45.6%). Procedural success was almost 98% in both study groups (97.5% vs. 97.9%). The prevalence of all in‐hospital post‐TAVR complications [acute kidney injury (3.8% vs. 2.2%), major bleeding events (2.5% vs. 3.2%), stroke (1.3% vs. 1.6%), pacemaker implantation (10.2% vs. 10.7%), major vascular complication (4.5% vs. 4.5%), new onset atrial fibrillation (3.2% vs. 3.4%), and in‐hospital death (3.2% vs. 2.8%)] were similar between groups (LVEF ≤ 35% vs. LVEF ≥ 50%). No difference in long‐term survival has been revealed over 3.4 years (P = 0.268). In patients with LVEF ≤ 35%, except for post‐TAVR mean aortic gradient (7.8 ± 4.2 vs. 10.2 ± 3.6), baseline and procedural characteristics were comparable between SEV versus BEV subgroups. An early improvement in LVEF (from 29.2 ± 5.5 to 37.4 ± 10.8) was observed. In patients with LVEF ≤ 35%, the all‐cause mortality rate was significantly higher in BEV than that in SEV subgroups, respectively (40.7% vs. 22.7%, P = 0.018). Kaplan–Meier curve showed better survival outcomes after SEV implantation (P = 0.032). A Cox regression identified BEV as independent predictor of mortality [HR = 3.276, 95% CI (1.520–7.060), P = 0.002]. Conclusions In the setting of low LVEF, TAVR remains a safe and effective procedure not associated with an increased risk of complications and mortality. SEV implantation may likely result in superior survival outcomes in patients with advanced cardiac dysfunction.