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Several electrocardiogram (ECG) criteria have been proposed to predict the location of the culprit occlusion in specific subsets of patients presenting with ST-segment elevation myocardial infarction (STEMI). The aim of this study was to develop, through an independent validation of currently available criteria, a comprehensive and easy-to-use ECG algorithm, and to test its diagnostic performance in real-world clinical practice.We analyzed ECG and angiographic data from 419 consecutive STEMI patients submitted to primary percutaneous coronary intervention over a one-year period, dividing the overall population into derivation (314 patients) and validation (105 patients) cohorts. In the derivation cohort, we tested60 previously published ECG criteria, using the decision-tree analysis to develop the algorithm that would best predict the infarct-related artery (IRA) and its occlusion level. We further assessed the new algorithm diagnostic performance in the validation cohort.In the derivation cohort, the algorithm correctly predicted the IRA in 88% of cases and both the IRA and its occlusion level (proximal vs mid-distal) in 71% of cases. When applied to the validation cohort, the algorithm resulted in 88% and 67% diagnostic accuracies, respectively. In a real-world comparative test, the algorithm performed significantly better than expert physicians in identifying the site of the culprit occlusion (P = .026 vs best cardiologist and P.001 vs best emergency medicine doctor).Derived from an extensive literature review, this comprehensive and easy-to-use ECG algorithm can accurately predict the IRA and its occlusion level in all-comers STEMI patients.

End-stage heart failure (ESHF) is characterized by severe cardiac dysfunction with persistent disabling symptoms and recurrent acute decompensated heart failure (ADHF), despite guideline-directed medical therapy. The aim of this study was to evaluate the efficacy and safety of intravenous diuretics administration at home through a peripherally inserted central venous catheter (PICC) in ESHF patients.Forty-one ESHF patients received PICC implantation for intravenous diuretic administration at home. The primary efficacy endpoint was the patient-level number of HF hospitalizations in the short (1-3 months), medium (six months), and long term (1 year), before and after PICC implantation. Pre- and post-PICC ADHF-free days were also evaluated as co-primary endpoint. Secondary endpoints comprised changes in clinical, laboratory and echocardiographic parameters, and device safety. A cost-effectiveness analysis was performed to estimate the economic impact of using PICC. For each time frame analyzed, a significant reduction in the number of hospitalizations due to ADHF was observed, resulting in a significant increase in ADHF-free days (71 ± 44 vs. 163 ± 136, p = 0.003). In matched patients' analysis, significant decrease in body weight (68 ± 16 kg vs. 63 ± 10 kg, p = 0.041) and mitral regurgitation grade 3/4 (55% vs. 18%, p 0.001) were also observed. Freedom from PICC-related complications was observed in 61% of patients. A significant reduction in overall ADHF-hospitalizations cost was observed.This proof-of-concept study demonstrates the effectiveness and safety of home administration of intravenous diuretic therapy via PICC in ESHF patients. This palliative cost-effective strategy can be taken in consideration for selected end-stage patients no longer responsive to conventional therapies.

Randomized controlled trials (RCTs) and observational studies provided conflicting results regarding the role of left ventricular (LV) function on outcomes after transcatheter edge-to-edge repair (TEER). The study aimed to provide a comprehensive assessment of the interplay between severe LV dysfunction and TEER outcomes. Multiple electronic databases, including PubMed, EMBASE, Scopus, Web of Science, and CENTRAL, were searched to identify studies on TEER for secondary mitral regurgitation reporting outcomes stratified for LV ejection fraction30% and ≥30%. The prespecified primary end points were the composite of all-cause death or heart failure (HF) hospitalization and New York Heart Association (NYHA) class III/IV. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by random-effects models. Multiple sensitivity analyses accounting for baseline characteristics and study design were applied. A total of 6 studies (1,957 patients) with 1 year or 2 years of follow-up were available. Severe LV dysfunction was associated with an increased risk of death or HF hospitalization (OR 1.71, 95% CI 1.14 to 2.57). Conversely, comparable rates of NYHA class III/IV (OR 1.06, 95% CI 0.82 to 1.38) or secondary end points (reinterventions, recurrence of significant secondary mitral regurgitation) were found regardless of the baseline LV function. Subgroup meta-analysis found no difference in the composite primary end point between patients with LV ejection fraction30% and ≥30% enrolled in RCTs. In conclusion, TEER seems to be associated with higher mortality or HF hospitalization rates in patients with severe LV dysfunction. However, RCTs found no differences between groups. No impact of LV function was found on the risk of NYHA class III/IV or other clinical outcomes.

Previous studies have shown that circulating chromogranin A (CgA) increases in patients with chronic systolic heart failure (HF). Aim of the present study is to evaluate the potential role of circulating vasostatin-1 (VS-1), a cardioregulatory fragment of CgA, as prognostic marker in patients with chronic HF.The plasma levels of CgA and VS-1 were determined in 80 patients with chronic systolic HF. Patients were followed-up to evaluate the occurrence of cardiovascular (CV) events.CgA and VS-1 plasma levels were significantly higher in patients with CV events at follow-up. VS-1, but not CgA, was associated to NT-proBNP. No significant association of CgA and VS-1 with left ventricular ejection fraction (LVEF) was observed. CgA, NT-proBNP and age, but not VS-1, were independent predictors of CV events.In patients with chronic systolic HF those who experienced CV events had higher levels of VS-1 and CgA. Given its established effect on cardiac cells, the association of VS-1 levels with NT-proBNP levels but not with LVEF, suggests that this fragment might provide complementary information to NT-proBNP and CgA in HF patients.

BACKGROUND Limited real-world data are available regarding the comparison about safety and efficacy of DOACs prescription in very elderly patients (≥85 years) with non-valvular atrial fibrillation (NVAF). Concern about the risk of bleeding with anticoagulation in very older patients still represents an important challenge for clinicians. OBJECTIVE To evaluate the different prevalence of major bleeding and thromboembolic events between very elderly NVAF patients (≥85 years) compared to those non very elderly (

Background Anthracyclines effectiveness is burdened by numerous side effects, among which cardiotoxicity (CTX) is the one carrying the highest impact on survival. Prevention of CTX is known to be far more effective than its treatment. Nonetheless, present patients stratification does not predict different post-treatment outcomes. The inter-individual variability in the response to treatment likely resides at the molecular level. In this context, mitochondrial ferritin (FtMt) has been studied in preclinical models of doxorubicin-induced cardiotoxicity. Both in cell lines and animal models, overexpression of this protein has been found to be protective against the cytotoxic oxidative damage deriving from anthracycline use. Aim of the study The primary aim of the study was to evaluate – for the first time in humans and in mouse myocardial cells lines – the expression of FtMt and its relationship with the potential development of cardiotoxicity in patients undergoing chemotherapy with anthracyclines. Methods Twenty-nine patients referred to our Oncology Outpatient Clinic to start treatment with anthracyclines – for either lymphoma or breast cancer – were enrolled before treatment initiation. All patients were above 18 years of age and free from any cardiovascular pathology at baseline. Troponin T (TnT), Brain Natriuretic Peptide (NT-proBNP), FtMt and creatinine were evaluated at baseline, before any chemotherapy cycle, at the end of the protocol, at 6 and 12 months from the first cycle. TnT and NT-proBNP were quantified through ECLIA and the expression of FtMt through qRT-PCR performed on peripheral white blood cells. Left ventricular function was evaluated through standard echocardiography at baseline, at the end of chemotherapy, at 6 and 12 months. Furthermore, variations in FtMt expression in response to doxorubicin treatment were studied on mouse primary cardiomyocytes. Results Direct evaluation of FtMt expression in mouse myocardial cells showed higher levels of FtMt in cardiomyocytes exposed to doxorubicin (p=0.0239). In the clinical model FtMt expression was found to be decreased after treatment initiation, with a trend that in the descriptive analysis appeared to be opposite to the one registered for TnT. For any unit of FtMt at baseline, single TnT values after treatment and at one year were found to be decreased of 1,89 ng/L and of 1,57 ng/L, respectively. TnT was the only cardiac parameter showing significant variation following anthracycline administration, with an average increase of 10 ng/L (p Conclusions Our results confirm that exposure to anthracyclines influences FtMt expression. The study performed on mouse primary cardiomyocytes demonstrate for the first time the ability of cardiac myocytes to increase FtMt expression in response to doxorubicin. In the clinical model any additional unit of FtMt at baseline was associated with a reduction in TnT values at the end of the treatment and at 1 year, potentially indicating a protective role of this protein in this context. The lack of frank cardiotoxicity in this group impeded the evaluation of the prognostic meaning of this event. In the future drugs able to upregulate the expression of this protein should be investigated as potential strategy to prevent anthracycline-induced cardiotoxicity.

Background Chronic heart valve regurgitation induces left ventricular (LV) volume overload, leading to the development of hypertrophy and progressive dilatation of the ventricle to maintain physiological cardiac output. In order to prevent potential irreversible LV structural changes, the identification of the best timing for treatment is pivotal. Objective To assess the presence and extent of fibrosis in myocardial tissue in asymptomatic patients with valvular heart disease (VHD) and preserved LV dimensions and function undergoing cardiac surgery. Methods Thirty-nine patients were enrolled. Sixteen patients were affected by aortic or mitral regurgitation: they were all asymptomatic, undergoing valve surgery according to VHD European Society of Cardiology guidelines. Twentythree patients with end-stage nonischemic dilated cardiomyopathy (DCM) and severe LV dysfunction undergoing cardiac surgery for implantation of a durable left ventricular assist device (LVAD) served as controls. During surgery, VHD patients underwent three myocardial biopsies at the level of the septum, the lateral wall and LV apex, while in LVAD patients the coring of the apex of the LV was used. For both groups, the tissue samples were analyzed on one section corresponding to the apical area. All slides were stained with hematoxylin and eosin and Masson's trichrome staining and further digitalized. The degree of fibrosis was then calculated as a percentage of the total area. Results Of 39 patients, 23 met the inclusion criteria: 12 had mitral or aortic insufficiency with a preserved ejection fraction and 11 had idiopathic dilated cardiomyopathy. Quantitative analysis of apical sections revealed a myocardial fibrosis amount of 10±6% in VHD patients, while in LVAD patients the mean apical myocardial fibrosis rate was 38±9%. In VHD patients, fibrosis was also present in the lateral wall (9±4%) and in the septum (9±6%). Conclusion Our case series study highlights the presence of tissue remodeling with fibrosis in asymptomatic patients with VHD and preserved LV function. According to our results, myocardial fibrosis is present at an early stage of the disease, well before developing detectable LV dysfunction and symptoms. Since the relationship between the progressive magnitude of myocardial fibrosis and potential prognostic implications are not yet defined, further studies on this topic are warranted.

Background Intracranial hemorrhage (ICH) represents the most serious complication of oral anticoagulant therapy (OAT) in patients with atrial fibrillation (AF), and AF patients with previous ICH are a challenge for clinicians. Left atrial appendage (LAA) occlusion has emerged as an alternative option for AF patients not suitable for OAT. Currently, few data are available on long term outcomes after LAA occlusion in this population. We evaluated the safety and efficacy of LAA occlusion in a cohort of patients with AF and previous ICH. Methods This is a multicenter, observational, retrospective study involving 5 LAA occlusion centers in Italy. It includes all consecutive patients (n = 120) with previous ICH who underwent LAA occlusion for nonvalvular AF and high thromboembolic risk. Procedural outcomes, post-procedural therapies and 12-months follow-up data were analyzed. Results The device was successfully implanted in 100% of cases, with a 6% of major peri-procedural complications. 59% had a prior ICH during OAT. The sample had a high risk of stroke (5.18%/year) and bleeding (6.62%/year). 30% were discharged on single and 54.2% on dual antiplatelet therapy. The expected annual risk for thromboembolism was 5.1%. Excluding periprocedural ischemic complications, the stroke annual rate was 1.8%. The expected annual risk of bleeding was 6.7%. The observed annual bleeding rate was 5.45%. Conclusions Percutaneous LAA occlusion is an effective option for AF patients and previous intracranial hemorrhage. After LAA occlusion, a single antiplatelet therapy strategy could be considered for patients with the highest risk of recurrent bleeding.

BACKGROUND Elderly constitute a high-risk subset of patients but are under-represented in clinical revascularization trials. Our aim was to investigate clinical outcomes and prognosis predictors after percutaneous coronary intervention (PCI) in this population. METHODS Unrestricted consecutive patients with ≥75 years who underwent PCI from 2012 to 2015 were enrolled. The primary ischemic endpoint was the composite of 1-year myocardial infarction, definite/probable stent thrombosis and target vessel revascularization. The primary bleeding endpoint was defined according to the Bleeding Academic Research Consortium (BARC) classification as BARC ≥ 2. RESULTS We enrolled 708 patients (mean age 80 ± 4): 14% were very elderly patients (≥85 years), 27% of patients were diabetic, 23% had chronic kidney disease (CKD), 17% atrial fibrillation and 37% presented acute coronary syndrome. The primary ischemic endpoint was reported in 67 patients (12%): 29 had myocardial infarction (5%), 25 had definite/probable stent thrombosis (4.4%) and 44 had target vessel revascularization (8%). BARC ≥ 2 bleeding was reported in 43 patients (8%). No differences were found in terms of both ischemic and bleeding events between patients with

In patients with severe or critical Coronavirus disease 2019 (COVID-19) manifestations, a thromboinflammatory syndrome, with diffuse microvascular thrombosis, is increasingly evident as the final step of pro-inflammatory cytokines storm. Actually, no proven effective therapies for novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection exist. Preliminary observations on anticoagulant therapy appear to be associated with better outcomes in moderate and severe COVID-19 patients with signs of coagulopathy and in those requiring mechanical ventilation. The pathophysiology underlying the prothrombotic state elicited by SARS-CoV-2 outlines possible protective mechanisms of antithrombotic therapy (in primis anticoagulants) for this viral illness. The indications for antiplatelet/anticoagulant use (prevention, prophylaxis, therapy) are guided by the clinical context and the COVID-19 severity. We provide a practical approach on antithrombotic therapy management for COVID-19 patients from a multidisciplinary point of view., Highlights • An endothelial thromboinflammatory syndrome is involved in severe COVID-19 manifestations. • A pathophysiological rationale (anti-inflammatory and direct antiviral effects) motivates the use of antithrombotic therapy • Anticoagulant therapy is associated with better outcomes in case of coagulopathy and mechanical ventilation. • A potential role for antithrombotic therapy in COVID-19 prevention and treatment needs further investigation.

BACKGROUND Coronary artery disease (CAD) is one of the leading causes of death among people living with HIV (PLWH). We evaluated ECG stress testing (EST) for detecting CAD in PLWH with multiple cardiovascular risk factors. METHODS CORDIS was a cross-sectional study conducted in PLWH. Inclusion criteria were men at least 50 years or postmenopausal women, HIV-1 RNA less than 50 copies/ml and at least one of the following cardiovascular risk factor: familial history of CAD, smoking, hypertension, hypercholesterolemia or diabetes. Patients with a previous diagnosis of CAD or with cardiac symptoms were excluded. EST was performed concomitantly with bilateral carotid color-Doppler ultrasonography (CDU) and evaluated by a cardiologist. Results were described by median (interquartile range) or frequency (%). Logistic regression was applied to evaluate predictive factors of inducible myocardial ischemia (IMI). RESULTS EST and CDU were performed in 309 individuals; IMI prevalence was 7.4% [95% confidence interval (CI): 5.0-11.0%]. Among patients with a normal CDU, no cases of IMI were observed. In people with abnormal CDU, IMI prevalence increased accordingly with the atherosclerotic cardiovascular disease (ASCVD) risk score: 10.2%, 16.9%, 19.7%, 27.8% and 30.4% among individuals with ASCVD score 7.5% or less, more than 7.5%, more than 10%, more than 15% and more than 20%, respectively (P for trend: 0.02). At multivariate analysis, ASCVD risk score was associated with EST suggestive of IMI (adjusted odds ratio for 1% increase = 1.08; 95% CI: 1.02-1.13, P = 0.005) and with confirmed IMI (adjusted odds ratio for 1% increase = 1.11; 95% CI: 1.04-1.19, P = 0.003). CONCLUSION Prevalence of IMI was 7.4% in the CORDIS study. We suggest EST as first-line screening for CAD in PLWH without cardiac symptoms, with an abnormal CDU and a high ASCVD risk score.

Myocardial fibrosis is a remarkably dynamic process mediated by different molecular pathways that represent potential targets of novel therapeutic interventions. Transforming Growth Factor-beta (TGF-β), connective Tissue Growth Factor (cTGF) and Galectin-3 (Gal-3) represent the most promising targets on which research has been currently focusing.This review initially discusses those drugs used in clinical practice for their anti-fibrotic properties and later examines emerging pathway-specific agents in preclinical and clinical development [phase I and II-concluded or ongoing trials]. We performed a PubMed, Embase and Google Scholar research including original articles, systematic reviews, ongoing and completed trials using combinations of keywords such as 'myocardial fibrosis', 'reverse remodeling', 'RAAs', 'therapy'.A variety of preclinical evidences suggest that new drugs and molecules are potentially useful to target cardiac fibrosis and improve left ventricular function, reduce infarct size and scars, delay incident heart failure and cardiac dysfunction in animal models. However, there are very few clinical trials investigating the effect of such drugs in this setting, as well as a lack of new engineered molecules for specific targets.

Amyloidosis is a group of progressive and devastating disorders resulting from extracellular deposition of misfolded proteins into tissues. When deposition of fibrils occurs in cardiac tissues, this systemic disease can lead to a very poor prognosis. Systemic amyloidosis can be acquired [light chain (AL) amyloidosis; AA amyloidosis], or hereditary [transthyretin (ATTR) amyloidosis]. Cardiac disease in amyloidosis is usually secondary to a systemic disease. The diagnosis of cardiac involvement is often delayed and yields an adverse prognosis.in this review, the authors report current literature on advances in pharmacotherapy for cardiac amyloidosis, mainly focused on AL and ATTR amyloidosis treatment.Most pharmacological trials in amyloidosis patients, both AL and TTR, are directed to study the effects of drugs on polyneuropathy. However, since cardiac involvement carries a prominent negative survival impact in amyloidosis patients, future research should be more focused on amyloidosis cardiomyopathy as primary endpoint. Additionally, in AL amyloidosis therapies are mainly derived from experience on multiple myeloma treatment. In this specific setting, possible future research could particularly focus on immunotherapeutic agents able to optimize the standard chemotherapy results and, thus, allowing a larger population of patients to be treated by bone marrow stem cell transplantation.

Initially developed as glucose-lowering drugs, sodium-glucose co-transporter type 2 inhibitors (SGLT2i) have demonstrated to be effective agents for the risk reduction of cardiovascular (CV) events in patients with type 2 diabetes mellitus (T2DM). Subsequently, data has emerged showing a significant CV benefit in patients treated with SGLT2i regardless of diabetes status. Renal protection has been initially evaluated in CV randomized trials only as secondary endpoints; nonetheless, the positive results gained have rapidly led to the evaluation of nephroprotection as primary outcome in the CREDENCE trial. Different renal and vascular mechanisms can account for the CV and renal benefits enlightened in recent literature. As clinical guidelines rapidly evolve and the role of SGLT2i appears to become pivotal for CV, T2DM, and kidney disease management, in this review, we analyze the renal effects of SGLT2, the benefits derived from its inhibition, and how this may result in the multiple CV and renal benefits evidenced in recent clinical trials.

Background Limited real-world data are available regarding the outcome of patients treated with inappropriate dose of nonvitamin-K antagonist oral anticoagulants (NOACs). Objective To assess the prevalence and factors associated with inappropriate dose prescription of NOACs and to evaluate adverse events that come from this inappropriate prescription. Methods Single-center multidisciplinary registry including nonvalvular atrial fibrillation patients treated with NOACs. Based on guidelines criteria for dose reduction, two subcohorts were defined as treated with appropriate or inappropriate NOACs dose. Primary efficacy endpoint was 2-year rate of thromboembolic events. Primary safety endpoint was 2-year rate of major bleeding. Event-free survival curves among groups were compared using Cox-Mantel test. Results A total of 760 nonvalvular atrial fibrillation patients were included; 32% patients were treated with dabigatran, 34% with apixaban, 24% with rivaroxaban and 10% with edoxaban. An inappropriate dose was prescribed in 96 patients (12.6%), and in most cases (68%) it was too low. Rivaroxaban (15%) and apixaban (18.5%) were the most frequently prescribed with an inappropriate dose. Patients treated with an inappropriate dose were elderly people, with low-creatinine clearance value, who had experienced previous bleeding and with a high CHADS2 VASc score. In 2 years, a trend for higher numbers of thromboembolic events (5.2 vs. 3.3%, P = 0.348) and less major bleeding (2.1 vs. 4.2%, P = 0.316) has been observed in patients with inappropriate NOACs prescriptions. Conclusion Nearly 13% of patients were treated with an inappropriate dose of NOACs, in this single-center study. A trend for higher numbers of thromboembolic events was observed in these patients. The results should be considered as hypothesis generating.

Transcatheter mitral valve intervention using the MitraClip system has evolved as a new tool for the treatment of secondary mitral regurgitation (SMR) in patients with heart failure and reduced lef...

Objectives The aim of the present analysis is to evaluate the clinical impact of chronic total occlusions (CTOs) recanalization in patients with left ventricular (LV) systolic dysfunction. Background According to contemporary knowledge, patient selection for percutaneous CTO revascularization is not yet standardized. In particular, data on outcomes in patients with LV systolic dysfunction undergoing percutaneous coronary intervention (PCI) for CTO are scarce. Methods From a total of 2,421 consecutive patients with at least one CTO, 436 patients with ejection fraction (EF) ≤45%, who were referred for coronary angiography between January 1998 and September 2014, were selected. Patients with successful recanalization of the target CTO were assigned to CTO-revascularized group and those with failed or not attempted recanalization to the CTO-not revascularized (CTO-NR) group. Study endpoints were all-cause death, cardiac death, and occurrence of myocardial infarction on follow-up. Results Out of 436 CTO patients with reduced EF, 228 (52.3%) were successfully recanalized and 208 patients (47.7%) were not, either due to CTO-PCI failure (n = 106, 24.3%) or because CTO-PCI was not attempted (n = 102, 23.4%). At long-term follow-up, CTO-NR patients had significantly higher rate of overall (p = .021) and cardiac mortality (p = .035) compared to those successfully revascularized. Conclusion In patients with systolic LV dysfunction (EF ≤ 45%), CTO revascularization was associated with significant lower rate of total and cardiac mortality compared to those with nonrevascularized CTO.

COAPT-trial entry criteria are useful to identify patients with better outcomes after transcatheter edge-to-edge repair (TEER). However, up to one-half of real-world patients with secondary mitral regurgitation (SMR) undergoing TEER do not meet these highly selective criteria and no study has formally investigated them. The aim of this study was to evaluate the predictors of good outcome after TEER in COAPT-ineligible patients.All consecutive patients with SMR and heart failure (HF) treated with MitraClip at 3 European centres were retrospectively screened. The presence of at least 1 COAPT exclusion criterion was used to define a COAPT-ineligible profile, allowing the inclusion in the study population. Freedom from all-cause death or HF hospitalisation was evaluated at 2-year follow-up (primary end point).A total of 305 patients (47%) had a COAPT-ineligible profile. An overall 58% rate of all-cause death or HF hospitalisation was detected at 2 years. Patients with a single COAPT exclusion criterion experienced fewer adverse events than those with multiple criteria (55% vs 69%). At multivariable Cox regression analysis, New York Heart Association functional class II, younger age (75 years), lower serum creatinine (2 mg/dL), lower left ventricular end-diastolic volume (240 mL), and the absence of hemodynamic instability, atrial fibrillation, and chronic obstructive pulmonary disease were independently associated with good outcome.In this real-world series of patients with SMR undergoing TEER, a COAPT-ineligible profile was common. The presence of only 1 COAPT exclusion criterion or the absence of hemodynamic instability were associated with the most favourable outcomes.

Up to half of real-world patients with secondary mitral regurgitation who underwent transcatheter edge-to-edge repair (TEER) do not meet the highly selective COAPT (Cardiovascular Outcomes Assessment of the MitraClip Percutaneous Therapy for Heart Failure Patients with Functional Mitral Regurgitation) criteria. No randomized trials or standardized and validated tools exist to evaluate the risk: benefit ratio of TEER in this specific population. We sought to derive and externally validate a clinical risk score to predict the risk of death or heart failure (HF) hospitalization for COAPT-ineligible patients who underwent TEER (CITE score). The study population consisted of patients with secondary mitral regurgitation having at least 1 exclusion criterion of the COAPT trial. The derivation cohort included 489 patients from the GIOTTO (GIse registry of Transcatheter treatment of Mitral Valve regurgitaTiOn) registry. Cox proportional hazards regression was used to identify predictors of 2-year death/HF hospitalization and develop a numerical risk score. The predictive performance was assessed in the derivation cohort and validated in 268 patients from the MiZüBr (Milan-Zürich-Brescia) registry. The CITE score (hemodynamic instability, left ventricular impairment, New York Heart Association class III/IV, peripheral artery disease, atrial fibrillation, brain natriuretic peptide, and hemoglobin) showed a c-index for 2-year death or HF hospitalization of 0.70 (95% confidence interval [CI] 0.67 to 0.73) in the derivation cohort, and 0.68 (95% CI 0.64 to 0.73) in the validation cohort. A cutoff of12 points was selected to identify patients at lower risk of adverse outcomes, hazard ratio of 0.35 (95% CI 0.26 to 0.46). In conclusion, the CITE score is a simple 7-item tool for the prediction of death or HF hospitalization at 2 years after TEER in COAPT-ineligible patients. The score may support clinical decision-making by identifying those patients who, even if excluded from clinical trials, can still benefit from TEER.

Chronic heart valve regurgitation induces left ventricular (LV) volume overload, leading to the development of hypertrophy and progressive dilatation of the ventricle to maintain physiological cardiac output. In order to prevent potential irreversible LV structural changes, the identification of the best timing for treatment is pivotal.To assess the presence and extent of fibrosis in myocardial tissue in asymptomatic patients with valvular heart disease (VHD) and preserved LV dimensions and function undergoing cardiac surgery.Thirty-nine patients were enrolled. Sixteen patients were affected by aortic or mitral regurgitation: they were all asymptomatic, undergoing valve surgery according to VHD European Society of Cardiology guidelines. Twenty-three patients with end-stage nonischemic dilated cardiomyopathy (DCM) and severe LV dysfunction undergoing cardiac surgery for implantation of a durable left ventricular assist device (LVAD) served as controls. During surgery, VHD patients underwent three myocardial biopsies at the level of the septum, the lateral wall and LV apex, while in LVAD patients the coring of the apex of the LV was used. For both groups, the tissue samples were analyzed on one section corresponding to the apical area. All slides were stained with hematoxylin and eosin and Masson's trichrome staining and further digitalized. The degree of fibrosis was then calculated as a percentage of the total area.Of 39 patients, 23 met the inclusion criteria: 12 had mitral or aortic insufficiency with a preserved ejection fraction and 11 had idiopathic dilated cardiomyopathy. Quantitative analysis of apical sections revealed a myocardial fibrosis amount of 10 ± 6% in VHD patients, while in LVAD patients the mean apical myocardial fibrosis rate was 38 ± 9%. In VHD patients, fibrosis was also present in the lateral wall (9 ± 4%) and in the septum (9 ± 6%).Our case series study highlights the presence of tissue remodeling with fibrosis in asymptomatic patients with VHD and preserved LV function. According to our results, myocardial fibrosis is present at an early stage of the disease, well before developing detectable LV dysfunction and symptoms. Since the relationship between the progressive magnitude of myocardial fibrosis and potential prognostic implications are not yet defined, further studies on this topic are warranted.

Background Acute chest pain with mild troponin rise and inconclusive diagnosis after clinical evaluation represents a diagnostic challenge. Triple-rule-out (TRO) CT may exclude coronary artery disease (CAD), as well as acute aortic syndrome and pulmonary embolism, but cannot help identify other causes of myocardial injury. Purpose To investigate the diagnostic value of a comprehensive CT protocol including both an angiographic and a late contrast enhancement (LCE) scan in participants with troponin-positive acute chest pain. Materials and Methods In this prospective study, consecutive patients with troponin-positive acute chest pain or anginal equivalent and inconclusive diagnosis after clinical evaluation (symptoms, markers, electrocardiography, and echocardiography) who underwent TRO CT between June 2018 and September 2020 were enrolled. TRO CT was performed to evaluate the presence of obstructive CAD (stenosis ≥50%), acute aortic syndrome, and pulmonary embolism. If the findings on the TRO CT scan were negative, an LCE CT scan was acquired after 10 minutes to assess the presence and pattern of scar and quantify the myocardial extracellular volume fraction. CT-based diagnoses were compared with diagnoses obtained with reference standard methods, including invasive coronary angiography, cardiac MRI, and endomyocardial biopsy. Results Eighty-four patients (median age, 69 years [interquartile range, 50-77 years]; 45 men) were enrolled. TRO CT helped identify obstructive CAD in 35 participants (42%), acute aortic syndrome in one (1.2%), and pulmonary embolism in six (7.1%). LCE CT scans were acquired in the remaining 42 participants. The following diagnoses were reached with use of LCE CT: myocarditis (22 of 42 participants [52%]), takotsubo cardiomyopathy (four of 42 [10%]), amyloidosis (three of 42 [7.1%]), myocardial infarction with nonobstructed coronary arteries (three of 42 [7.1%]), dilated cardiomyopathy (two of 42 [4.8%]), and negative or inconclusive findings (eight of 42 [19%]). The addition of LCE CT improved the diagnostic rate of TRO CT from 42 of 84 participants (50% [95% CI: 38.9, 61.1]) to 76 of 84 (90% [95% CI: 82.1, 95.8]) (P < .001). Conclusion A CT protocol including triple-rule-out and late contrast enhancement CT scans improved diagnostic rate in participants presenting with acute chest pain syndrome. © RSNA, 2021 Online supplemental material is available for this article. See also the editorial by Nagpal and Bluemke in this issue.

Chronic kidney disease (CKD) is strongly related to outcomes in cardiovascular diseases. Limited data are available regarding the independent prognostic role of CKD after transcatheter mitral valve repair with MitraClip. We sought to evaluate the real impact of CKD in a large series of patients with heart failure (HF) and secondary mitral regurgitation (SMR) who underwent MitraClip treatment. The study included 565 patients with severe SMR from a multicenter international registry. Patients were stratified into 3 groups according to estimated glomerular filtration rate (eGFR) assessment before MitraClip implantation: normal eGFR (≥60ml/min/1.73m2) (n=196), mild-to-moderate CKD (30 to 59ml/min/1.73m2) (n=267), and severe CKD (

Aims Although heart failure (HF) is one of the most common conditions affecting the heart, little attention has been placed on the role of arteries in contributing to the progression of this disease. We sought to determine the haemodynamic change of arteries in HF patients subdivided according to left ventricular ejection fraction. The major goal was to establish the active compensatory role of arteries in HF. Methods and results Using sphygmography, we systematically studied a cohort of 228 HF patients and 52 healthy controls. We focused on the common carotid as the main elastic artery and the posterior tibial as the main muscular artery (Figure 1). Moreover, we categorized the three HF groups, HFrEF, HFmrEF, HFpEF, into two subgroups (A and B) according to the presence or absence of HF signs at baseline. We discovered that all the parameters of measured arterial kinetics, i.e. work, power, acceleration, and speed, were significantly increased (P Conclusions We provide the first documentation of an active compensatory role of arteries during HF. Mechanistically, we explain these findings by a dual activity of large arteries accomplished via an active propulsive work and a concurrent haemodynamic suction. These underestimated arterial functions partially compensate for the heart dysfunction in HF, underlining a key interplay between the heart and the vessels. We propose a new paradigm that we define as ‘heart and vessels failure’ that explicitly focuses on both heart and vessels’ interaction during the progression of HF.

Background Patients with non-valvular atrial fibrillation (nvAF) who experienced a cardioembolic (CE) event despite adequate oral anticoagulation (OAC) are at high risk of recurrence, and further prevention strategies are deemed necessary. The present study aimed to evaluate the safety and efficacy of off-label use of left atrial appendage closure (LAAC) in this subset of patients. Methods and results Seventy-five consecutive patients with nvAF who experienced a CE event despite adequate OAC therapy were retrospectively enrolled from two Italian centers. Patients were divided according to the treatment strategy following the index event: DOAC group (49 patients who continued OAC therapy with DOACs) and LAAC group (26 patients who underwent LAAC procedure). 1:1 propensity-score matching between the two groups was performed. LAAC group was made up of two subgroups according to the post-procedural pharmacological regimen: (a) dual antiplatelet therapy (DAPT) for 3 months followed by indefinite single antiplatelet therapy (LAAC+SAPT) or (b) aspirin plus DOAC for 3 months followed by indefinite DOAC therapy (LAAC+DOAC). The primary endpoint was a composite of CE event, major bleeding, or procedurerelated major complication. During a median follow-up of 3.4 years (IQR 2.0-5.3), LAAC was a predictor of primary endpoint-free survival (HR 0.28, 95%CI 0.08-0.97; p=0.044); within LAAC group, no procedure-related major complication occurred. Moreover, a trend toward a lower rate of both CE events and major bleedings was observed in LAAC group, particularly in the subgroup LAAC+DOAC. Conclusions LAAC is a reasonable therapeutic option in nvAF patients who suffered a CE event despite adequate OAC therapy.

Background Although heart failure (HF) is one of the most common conditions affecting the heart, little attention has been placed on the role of arteries in contributing to the progression of this disease. Purpose We sought to determine the hemodynamic change of arteries in HF patients subdivided according to left ventricular ejection fraction. The major goal was to establish the active compensatory role of arteries in HF Methods Using sphygmography, we systematically studied a cohort of 228 HF patients and 52 healthy controls. We focused on the common carotid as the main elastic artery and the posterior tibial as the main muscular artery (Figure 1). Moreover, we categorized the three HF groups, HFrEF, HFmrEF, HFpEF, into two subgroups (A and B) according to the presence or absence of HF signs at baseline. Results We discovered that all the parameters of measured arterial kinetics, i.e., work, power, acceleration, and speed, were significantly increased (p Conclusions We provide the first documentation of an active compensatory role of arteries during HF. Mechanistically, we explain these findings by a dual activity of large arteries accomplished via an active propulsive work and a concurrent hemodynamic suction. These underestimated arterial functions partially compensate for the heart dysfunction in HF, underlining a key interplay between the heart and the vessels. We propose a new paradigm that we define as “heart and vessels failure” that explicitly focuses on both heart and vessels' interaction during the progression of HF. Funding Acknowledgement Type of funding sources: None. Figure 1. Sphygmograms of CCA and PTAFigure 2. Patients disposition & Results

What is the optimal antithrombotic therapy in patients with atrial fibrillation (AF) undergoing percutaneous coronary intervention (PCI) remains one of the most doubtful and demanding topics in cardiology. As of today, there are no trial powered to prove the efficacy of double versus triple antithrombotic therapy in terms of ischemic coronary events prevention after PCI. Until further evidence on this topic becomes available, we recommend a personalized strategy, with a careful individual assessment of the patient ischemic and bleeding risk.

Background The ULISSE registry evaluated the real-world performance of the Ultimaster® biodegradable polymer sirolimus-eluting stent (BP-SES) in a multicenter-independent cohort of patients undergoing percutaneous coronary intervention, including a large proportion of diabetes mellitus (DM) patients. Methods In this subgroup analysis, 1,660 consecutive patients, 2,422 lesions, treated with BP-SES enrolled in the ULISSE registry were divided in two groups: DM (485 patients, 728 lesions) and non-DM (1,175 patients, 1,694 lesions). Primary endpoint was target lesion failure (TLF), a composite endpoint of cardiac-death, target-vessel myocardial infarction (TV-MI), and clinically driven target lesion revascularization (TLR) at 1-year. Secondary endpoint was TLR at 1-year. Results At 1-year follow-up TLF occurred in 5% overall patients and was significantly higher in DM patients (8 vs. 3.7%; p = .001), due to more cardiac deaths (3.4 vs. 1.1%; p = .002). TLR occurred in 3.2% overall patients, and it was not significantly higher in DM compared to non-DM patients (4.4 vs. 2.8%; p = .114). The incidence of stent thrombosis was low and similar between groups (0.4 vs. 0.9%; p = .526). Insulin-treated DM (ITDM) patients showed higher rate of TLF as compared to non-ITDM patients (13 vs. 6.5%; p = .041), but similar rate of TLR (6 vs. 4%; p = .405). After adjustment for relevant comorbidities, DM was not significantly associated with TLF or cardiac death in patients undergoing BP-SES implantation. Conclusions This study is the first all-comers evaluation of BP-SES in DM patients. Our findings show that DM patients, mostly those with ITDM, still represent a vulnerable population and experience significantly higher rate of TLF. Overall BP-SES efficacy is considerable, although not statistically significant higher rate of TLR is still present in DM compared to non-DM patients.

Introduction: Hypertrophic cardiomyopathy (HCM) is one of the most common genetic heart diseases and represents a leading cause of sudden cardiac death as well as a prevalent cause of heart failure and stroke. HCM is characterized by a very complex pathophysiology, consisting of heterogeneous clinical manifestations and natural history. Left ventricular outflow tract (LVOT) obstruction has been considered the most knowable feature of HCM since the initial clinical descriptions of the disease. Areas covered: In this review, the authors discuss the most recent reports on the pharmacological treatment of obstructive HCM, mainly based on three different levels of intervention: control of symptoms, cardiac metabolism modulation and disease-modifying approaches, including genetic preventive therapies. Expert opinion: There are presently limited data supporting pharmacological interventions for this complex disease. However, an improved understanding of HCM pathophysiology will allow the development of novel treatment options. Two important key messages are to further study drugs with negative but limited previous results and to design new and larger trials for those molecules that have already produced positive results in HCM, especially for pressure gradients and symptoms control.

BACKGROUND: Patients awaiting heart transplantation (HTx) often need bridging therapies to reduce worsening and progression of underlying disease. Limited data are available regarding the use of the MitraClip procedure in secondary mitral regurgitation for this clinical condition. METHODS: We evaluated an international, multicenter (17 centers) registry including 119 patients (median age: 58 years) with moderate-to-severe or severe secondary mitral regurgitation and advanced heart failure (HF) (median left ventricular ejection fraction: 26%) treated with MitraClip as a bridge strategy according to 1 of the following criteria: (1) patients active on HTx list (in list group) (n = 31); (2) patients suitable for HTx but awaiting clinical decision (bridge to decision group) (n = 54); or (3) patients not yet suitable for HTx because of potentially reversible relative contraindications (bridge to candidacy group) (n = 34). RESULTS: Procedural success was achieved in 87.5% of cases, and 30-day survival was 100%. At 1 year, Kaplan-Meier estimates of freedom from the composite primary end-point (death, urgent HTx or left ventricular assist device implantation, first rehospitalization for HF) was 64%. At the time of last available follow-up (median: 532 days), 15% of patients underwent elective transplant, 15.5% remained or could be included in the HTx waiting list, and 23.5% had no more indication to HTx because of clinical improvement. CONCLUSIONS: MitraClip procedure as a bridge strategy to HTx in patients with advanced HF with significant mitral regurgitation was safe, and two thirds of patients remained free from adverse events at 1 year. These findings should be considered exploratory and hypothesis-generating to guide further study for percutaneous intervention in high-risk patients with advanced HF. (C) 2020 International Society for Heart and Lung Transplantation. All rights reserved.

Prescription of cardiovascular drugs is aimed at preventing and treating morbid conditions affecting the cardiovascular system. However, apart from their primary therapeutic target, some of the ordinary drugs used in cardiology daily practice also have additional pharmacological actions. Among these ancillary actions, those primarily affecting global and cardiac metabolism deserve special attention. In fact, apart from primary cardiac metabolic diseases, most cardiovascular diseases are heavily influenced by the patient's metabolic status and adaptation to the disease itself. In this context, drugs affecting global and cardiovascular metabolism besides their recognized main mechanism of action may be of special interest, for both potential beneficial and deleterious effects, especially in the long-term period. In all cases, these effects should be well understood and known by all physicians managing patients with cardiovascular morbidities. The aim of this article is to describe the direct metabolic actions of some of the principal cardiovascular drugs.

A severe secondary mitral regurgitation (SMR) can be found in a significant portion of patients affected by advanced heart failure (AHF). Conventional therapies (optimal medical therapy, devices, surgery) present restricted clinical efficacy in this stage of the left ventricle disease which is burdened by high mortality and morbidity rates. Although the treatment of choice is represented by heart transplantation (HTx), there is an unmet need related to the limited supply of donor hearts (as opposed to the growing prevalence of AHF) and the low eligibility of highly symptomatic patients. In case of concomitant severe SMR, transcatheter mitral valve therapies (repair and replacement) may play a crucial role in this setting. While a direct prognostic improvement after correction of SMR has yet to be proved, AHF patients can benefit from the following: hemodynamic stabilization, symptomatic relief, normalization of pulmonary arterial pressures, and reduction in hospitalizations for acute heart failure. Obtaining these results may lead to the clinical consequences of reaching the HTx in good enough clinical status (bridge to heart transplantation), becoming eligible for the HTx (bridge to HTx candidacy), and being delisted for clinical improvement (bridge to recovery). Therefore, achieving traditional secondary endpoints in patients with AHF and SMR can translate into significant clinical implications.

Background Patients with coronavirus disease 2019 (COVID-19) exhibit high thrombotic risk. The evidence on a potential independent prognostic role of antiplatelet treatment in those patients is limited. The aim of the study was to evaluate the prognostic impact of pre-admission low-dose acetylsalicylic acid (ASA) in a wide series of hospitalized patients with COVID-19. Methods This cohort study included 984 COVID-19 patients stratified according to ASA intake before hospitalization: ASA+ (n = 253) and ASA− (n = 731). Patients were included in ASA+ group if they received it daily in the 7 days before admission. 213 (83%) were on ASA 100 mg daily. Primary endpoint was a composite of in-hospital death and/or need for respiratory support upgrade, secondary endpoints were in-hospital death and need for respiratory support upgrade. Results Mean age was 72 [62; 81] with 69% of male patients. ASA+ patients were significantly older, with higher prevalence of comorbidities. No significant differences regarding the degree of respiratory dysfunction were observed. At 30-day Kaplan-Meier analysis, ASA+ patients had higher survival free from the primary endpoint and need for respiratory support upgrade, conversely in-hospital death did not significantly differ between groups. At multivariate analysis ASA intake was independently associated with a lower probability of reaching primary endpoint (HR 0.697, 95% C.I. 0.525–0.924; p = 0.012). Conclusions In COVID-19 patients undergoing hospitalization, pre-admission treatment with ASA is associated with better in-hospital outcome, mainly driven by less respiratory support upgrade.

BACKGROUND: Although heart failure (HF) is one of the most common conditions affecting the heart, little attention has been placed on the role of arteries in contributing to the progression of this disease. We sought to determine the hemodynamic change of arteries in HF patients subdivided according to left ventricular ejection fraction. The major goal was to establish the active compensatory role of arteries in HF. METHODS: Using sphygmography, we systematically studied a cohort of 228 HF patients and 52 healthy controls. We focused on the common carotid as the main elastic artery and the posterior tibial as the main muscular artery. Moreover, we categorized the three HF groups, HFrEF, HFmrEF, HFpEF, into two subgroups (A and B) according to the presence or absence of HF signs at baseline. RESULTS: We discovered that all the parameters of measured arterial kinetics, i.e., work, power, acceleration, and speed, were significantly increased (P

AIMS: The aim of this study was to evaluate the sensitivity of right ventricular endomyocardial biopsy (EMB) in myocarditis patients with cardiac magnetic resonance (CMR) and electroanatomical mapping (EAM) showing left ventricular abnormalities. METHODS: We performed right ventricular EMB in 144 consecutive patients (66% men, age 43 ± 15 years) with acute symptoms and CMR-proved diagnosis of left ventricular myocarditis. Right ventricular EMB sensitivity has been evaluated in patients with different localization and extension of abnormal substrate at both CMR and -- when performed -- EAM. Abnormal substrate was defined, respectively, by late gadolinium enhancement (LGE) and low-voltage areas (LVAs). RESULTS: Globally, right ventricular EMB sensitivity was 87.5%. EMB-negative cases had significantly smaller fragment sizes (cumulative area 2.8 ± 1.7 vs. 3.8 ± 1.8 mm2, P = 0.023), and lower LGE surface extension (24.7 ± 14.2 vs. 38.5 ± 20.2%, P = 0.006) and transmurality (32.0 ± 26.1 vs. 49.3 ± 22.6, P = 0.003). Right ventricular EMB sensitivity in patients with LGE involving both right ventricular and interventricular septum (IVS), isolated right ventricular or IVS, and remote left ventricular areas (n = 10, 49 and 67 cases) was 83.3, 84.4 and 90.5%, respectively (P = 0.522). Overall, 34 patients (23.6%) underwent EAM. On the basis of EAM, right ventricular EMB sensitivity was 85.3%: in detail, it was 50.0, 88.2 and 86.7% in patients with both right ventricular and IVS, isolated right ventricular/IVS and distant left ventricular involvement (n = 2, 17 and 15, respectively, P > 0.05). Sample size area was the only factor associated with right ventricular EMB sensitivity (hazard ratio = 1.6/mm2, 95% confidence interval 1.1-2.4, P = 0.013). CONCLUSION: Right ventricular EMB is still an accurate technique to confirm diagnosis in patients with CMR-proved left ventricular myocarditis. In particular, provided there is an adequate sample size, its sensitivity is comparable among patients with heterogeneous LGE or LVA localization.

Background. Myocarditis lacks systematic characterization in COVID-19 patients. Methods. We enrolled consecutive patients with newly diagnosed myocarditis in the context of COVID-19 infection. Diagnostic and treatment strategies were driven by a dedicated multidisciplinary disease unit for myocarditis. Multimodal outcomes were assessed during prospective follow-up. Results. Seven consecutive patients (57% males, age 51 ± 9 y) with acute COVID-19 infection received a de novo diagnosis of myocarditis. Endomyocardial biopsy was of choice in hemodynamically unstable patients (n = 4, mean left ventricular ejection fraction (LVEF) 25 ± 9%), whereas cardiac magnetic resonance constituted the first exam in stable patients (n = 3, mean LVEF 48 ± 10%). Polymerase chain reaction (PCR) analysis revealed an intra-myocardial SARS-CoV-2 genome in one of the six cases undergoing biopsy: in the remaining patients, myocarditis was either due to other viruses (n = 2) or virus-negative (n = 3). Hemodynamic support was needed for four unstable patients (57%), whereas a cardiac device implant was chosen in two of four cases showing ventricular arrhythmias. Medical treatment included immunosuppression (43%) and biological therapy (29%). By the 6-month median follow-up, no patient died or experienced malignant arrhythmias. However, two cases (29%) were screened for heart transplantation. Conclusions. Myocarditis associated with acute COVID-19 infection is a spectrum of clinical manifestations and underlying etiologies. A multidisciplinary approach is the cornerstone for tailored management.

Background The role of the target vessel in percutaneous revascularization of chronic total occlusion (CTO) is unclear. Objective We sought to assess the long-term results of percutaneous coronary intervention (PCI) for CTO lesions in each coronary artery and to investigate the impact of successful revascularization and previous myocardial infarction (MI) in the territory of the target vessel. Methods and results Cohort observational study on 1,124 patients who have undergone CTO PCI attempt: 371 on left anterior descending artery (LAD), 485 right coronary artery, and 268 left circumflex. Patients were further stratified by successfully revascularized and not-revascularized CTO (CTO-NR). Vessels affected by a previous MI were defined as infarct-related artery (IRA). The primary endpoint was cardiac death; the secondary endpoint was the combined rate of sudden cardiac-death and sustained ventricular-arrhythmias (SCD/SVAs). Propensity score-matching was performed to evaluate LAD versus NON-LAD CTO. Up to 12-year follow-up, the clinical benefit associated with successful PCI was consistent across the three groups. CTO-NR had the greatest association with cardiac death and SCD/SVAs in each coronary artery and in IRA-CTO patients. Conclusions Unsuccessful percutaneous CTO revascularization was associated with lower cardiac survival and freedom from SCD/SVAs, irrespective of the vessel treated. This result was mainly driven by patients with an IRA CTO.

OBJECTIVES Among patients undergoing transcatheter mitral valve repair with the MitraClip device, a relevant proportion (2–6%) requires open mitral valve surgery within 1 year after unsuccessful clip implantation. The goal of this review is to pool data from different reports to provide a comprehensive overview of mitral valve surgery outcomes after the MitraClip procedure and estimate in-hospital and follow-up mortality. METHODS All published clinical studies reporting on surgical intervention for a failed MitraClip procedure were evaluated for inclusion in this meta-analysis. The primary study outcome was in-hospital mortality. Secondary outcomes were in-hospital adverse events and follow-up mortality. Pooled estimate rates and 95% confidence intervals (CIs) of study outcomes were calculated using a DerSimionian–Laird binary random-effects model. To assess heterogeneity across studies, we used the Cochrane Q statistic to compute I2 values. RESULTS Overall, 20 reports were included, comprising 172 patients. Mean age was 70.5 years (95% CI 67.2–73.7 years). The underlying mitral valve disease was functional mitral regurgitation in 50% and degenerative mitral regurgitation in 49% of cases. The indication for surgery was persistent or recurrent mitral regurgitation (grade >2) in 93% of patients, whereas 6% of patients presented with mitral stenosis. At the time of the operation, 80% of patients presented in New York Heart Association functional class III–IV. Despite favourable intraoperative results, in-hospital mortality was 15%. The rate of periprocedural cerebrovascular accidents was 6%. At a mean follow-up of 12 months, all-cause death was 26.5%. Mitral valve replacement was most commonly required because the possibility of valve repair was jeopardized, likely due to severe valve injury after clip implantation. CONCLUSIONS Surgical intervention after failed transcatheter mitral valve intervention is burdened by high in-hospital and 1-year mortality, which reflects reflecting the high-risk baseline profile of the patients. Mitral valve replacement is usually required due to leaflet injury.