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Aims To evaluate the prognostic impact of pre-procedural right ventricular longitudinal strain (RVLS) in patients with secondary mitral regurgitation (SMR) undergoing transcatheter edge-to-edge repair (TEER) in comparison with conventional echocardiographic parameters of RV function. Methods and results This is a retrospective study including 142 patients with SMR undergoing TEER at two Italian centres. At 1-year follow-up 45 patients reached the composite endpoint of all-cause death or heart failure hospitalization. The best cut-off value of RV free-wall longitudinal strain (RVFWLS) to predict outcome was −18% [sensitivity 72%, specificity of 71%, area under curve (AUC) 0.78, P < 0.001], whereas the best cut-off value of RV global longitudinal strain (RVGLS) was −15% (sensitivity 56%, specificity 76%, AUC 0.69, P < 0.001). Prognostic performance was suboptimal for tricuspid annular plane systolic excursion, Doppler tissue imaging-derived tricuspid lateral annular systolic velocity and fractional area change (FAC). Cumulative survival free from events was lower in patients with RVFWLS ≥ −18% vs. RVFWLS < −18% (44.0% vs. 85.4%; < 0.001) as well as in patients with RVGLS ≥ −15% vs. RVGLS < −15% (54.9% vs. 81.7%; P < 0.001). At multivariable analysis FAC, RVGLS and RVFWLS were independent predictors of events. The identified cut-off of RVFWLS and RVGLS both resulted independently associated with outcomes. Conclusion RVLS is a useful and reliable tool to identify patients with SMR undergoing TEER at high risk of mortality and HF hospitalization, on top of other clinical and echocardiographic parameters, with RVFWLS offering the best prognostic performance.

BACKGROUND Guideline-directed medical therapy (GDMT) optimization is mandatory before transcatheter edge-to-edge mitral valve repair (M-TEER) in patients with secondary mitral regurgitation (SMR) and heart failure (HF) with reduced ejection fraction (HFrEF). However, the effect of M-TEER on GDMT is unknown. OBJECTIVES The authors sought to evaluate frequency, prognostic implications and predictors of GDMT uptitration after M-TEER in patients with SMR and HFrEF. METHODS This is a retrospective analysis of prospectively collected data from the EuroSMR Registry. The primary events were all-cause death and the composite of all-cause death or HF hospitalization. RESULTS Among the 1,641 EuroSMR patients, 810 had full datasets regarding GDMT and were included in this study. GDMT uptitration occurred in 307 patients (38%) after M-TEER. Proportion of patients receiving angiotensin-converting enzyme inhibitors/angiotensin receptor blockers/angiotensin receptor-neprilysin inhibitors, beta-blockers, and mineralocorticoid receptor antagonists was 78%, 89%, and 62% before M-TEER and 84%, 91%, and 66% 6 months after M-TEER (all P < 0.001). Patients with GDMT uptitration had a lower risk of all-cause death (adjusted HR: 0.62; 95% CI: 0.41-0.93; P = 0.020) and of all-cause death or HF hospitalization (adjusted HR: 0.54; 95% CI: 0.38-0.76; P < 0.001) compared with those without. Degree of MR reduction between baseline and 6-month follow-up was an independent predictor of GDMT uptitration after M-TEER (adjusted OR: 1.71; 95% CI: 1.08-2.71; P = 0.022). CONCLUSIONS GDMT uptitration after M-TEER occurred in a considerable proportion of patients with SMR and HFrEF and is independently associated with lower rates for mortality and HF hospitalizations. A greater decrease in MR was associated with increased likelihood for GDMT uptitration.

Background Guideline-directed medical therapy (GDMT) optimization is mandatory before transcatheter edge-to-edge mitral valve repair (M-TEER) in patients with secondary mitral regurgitation (SMR) and heart failure with reduced ejection fraction (HFrEF). However, the effect of M-TEER on GDMT is unknown. Objective To evaluate frequency and prognostic implications and predictors of GDMT optimization after M-TEER in patients with SMR and HFrEF. Methods This is a retrospective analysis of prospectively collected data from the EuroSMR Registry. The primary events were all-cause death and the composite of all-cause death or HF hospitalization. Results Among the 1641 EuroSMR patients, 810 had full datasets regarding GDMT and were included in this study. GDMT optimization occurred in 307 (38%) patients after M-TEER. Proportion of patients receiving ACEi/ARB/ARNI, betablockers and MRA was 78%, 89% and 62% before M-TEER and 84%, 91% and 66% 6-month after M-TEER (All p Conclusions GDMT optimization after M-TEER in HFrEF patients with SMR occurred in a considerable proportion of patients and is independently associated with lower rates for mortality and HF hospitalizations. A greater decrease in MR was associated with increased likelihood for GDMT optimization.

Prevalence of heart failure is increasing worldwide mainly due to the ageing of the population and the improvement in diagnosis and treatment. In recent years, huge progress has been made in the management of heart failure patients. A new definition of chronic heart failure based on left ventricular ejection fraction and its possible trajectories has been reported. New drug classes have been introduced for the treatment of chronic heart failure. In particular, the prognostic benefit of sodium glucose co-transporter 2 inhibitors was demonstrated across all the heart failure phenotypes. Therapies for patients with advanced heart failure (long-term mechanical circulatory supports and heart transplantation) are now indicated also in the case of mild-to-moderate symptoms but with high risk of progression. In patients with acute heart failure, monitoring of urinary sodium and the use of acetazolamide may lead to better decongestion. Importantly, pre- and postdischarge assessment should lead to optimal treatment. Devices and telemonitoring can also be of help. Cardiovascular and noncardiovascular comorbidities are major determinants of the clinical course and need proper management. This review will summarize these important advances.

Background: Preprocedural right ventricular–to–pulmonary artery (RV-PA) coupling is a major predictor of outcome in patients with secondary mitral regurgitation (SMR) undergoing transcatheter edge-to-edge mitral valve repair (M-TEER). However, clinical significance of changes in RV-PA coupling after M-TEER is unknown. Objectives: The aim of this study was to evaluate changes in RV-PA coupling after M-TEER, their prognostic value, and predictors of improvement. Methods: This was a retrospective observational study, including patients undergoing successful M-TEER (residual mitral regurgitation ≤2+ at discharge) for SMR at 13 European centers and with complete echocardiographic data at baseline and short-term follow-up (30-180 days). RV-PA coupling was assessed with the use of echocardiography as the ratio of tricuspid annular plane systolic excursion to pulmonary artery systolic pressure (TAPSE/PASP). All-cause death was assessed at the longest available follow-up starting from the time of the echocardiographic reassessment. Results: Among 501 patients included, 331 (66%) improved their TAPSE/PASP after M-TEER (responders) at short-term follow-up (median: 89 days; IQR: 43-159 days), whereas 170 (34%) did not (nonresponders). Lack of previous cardiac surgery, low postprocedural mitral mean gradient, low baseline TAPSE, high baseline PASP, and baseline tricuspid regurgitation were independently associated with TAPSE/PASP improvement after M-TEER. Compared with nonresponders, responders had lower New York Heart Association functional class and less heart failure hospitalizations at short-term follow-up. Improvement in TAPSE/PASP was independently associated with reduced risk of mortality at long-term follow-up (584 days; IQR: 191-1,243 days) (HR: 0.65 [95% CI: 0.42-0.92]; P = 0.017). Conclusions: In patients with SMR, improvement in TAPSE/PASP after successful M-TEER is predicted by baseline clinical and echocardiographic variables and postprocedural mitral gradient, and is associated with a better outcome.

Background: The multiple beneficial effects of sacubitril/valsartan in the treatment of heart failure with reduced ejection fraction are vastly known, but still no or few mentions have been made regarding its effects on endothelial dysfunction and arterial stiffness. Patients and methods: To understand more deeply if sacubitril/valsartan may have a role on endothelial function and arterial stiffness, 15 patients with dilated cardiomyopathy with reduced left ventricular ejection fraction (LVEF) were evaluated through transthoracic echocardiography, peripheral arterial tonometry (EndoPAT(®)) and applanation tonometry (SphygmoCor(®) Px system). These noninvasive exams were performed at the beginning of the study and after 6 months of sacubitril/valsartan treatment. Results: Aortic stiffness parameters didn’t differ after 6 months of treatment. Augmentation pressure (P=0.889), augmentation index (P=0.906) and sphygmic wave velocity (P=0.263) increased slightly, but they weren’t found to be statistically significant. Systolic, diastolic, and differential central arterial pressure didn’t differ at the beginning and at the end of the study. RHI (reactive hyperemia index) increased significantly after 6 months (P=0.001) as well as augmentation index corrected for 75 bpm. Ejection fraction (32.21% ± 5.7 to 38.43% ± 8.4; P=0.010) and diastolic dysfunction degree (P=0.021) improved. There was an improvement in mitral regurgitation that wasn’t statistically significant (P=0.116). TAPSE didn’t change while pulmonary systolic arterial pressure increased, although not significantly (22.83 mmHg ± 4 to 27.33 mmHg ± 6; P=0.068) and within the normal range values. Conclusions: Even though in a study with a limited number of patients, sacubitril/valsartan improved endothelial function, left ventricular function, MR, and diastolic function significantly in patients with dilated cardiomyopathy and reduced LVEF. It showed no effects on vascular stiffness.

Aims To describe the characteristics of a cohort of patients with cardiac amyloidosis (CA) and to compare the two most common phenotypes of CA, transthyretin (ATTR) and immunoglobulin light-chain (AL). Methods and results One-hundred and eighty patients [n = 115 (64%) men, 74 ± 11 years] were retrospectively included from January 2013 to April 2021 in a single centre in Northern Italy. The majority [n = 102 (57%)] had ATTR-CA, whereas 78 patients (43%) had AL-CA. ATTR-CA patients were older (79 ± 7 vs. 66 ± 10 years, P Conclusions Despite ATTR-CA patients showed worse baseline characteristics, suggesting a more advanced disease at presentation, AL-CA phenotype was associated with a higher risk of all-cause death. Of note, CV mortality was comparable between the two groups.

Aims Severe acute respiratory syndrome coronavirus (SARS-CoV-2) is well described as being responsible for multi-organ involvement and SARS-CoV-2 cardiac involvement was observed since the beginning of the spread of the infection. However, there are no descriptions of acute myopericarditis in patient with previous myocarditis. Methods and results Cardiac involvement was assessed with electrocardiographic and echocardiographic changes and with increased levels of cardiac high-sensitivity troponin T (hs-cTnT). Diagnosis was confirmed with cardiac magnetic resonance imaging (CMR) and coronary artery disease (CAD) was excluded with coronary angiography. A 53-years-old woman with hypokinetic cardiomyopathy due to a previous myocarditis and recent COVID-19 pneumonia reached the Emergency Department with chest pain and tachycardia in December 2020. Twelve-lead ECG was not conclusive and after detection of significative increase of hs-cTnT she was admitted to the Cardiology Department. Transthoracic echocardiography showed reduction of left ventricle ejection fraction, subendocardial bright appearance and mild pericardial effusion. Coronary angiography excluded obstructive CAD and CMR confirmed diagnosis of recent myocarditis and worsening of left and right ventricular ejection fraction compared to a previous CMR. Patient was treated with evidence-based therapy for heart failure, prednisone, intravenous immunoglobulins, ibuprofen, and colchicine. Cardiac biomarkers reduced within the normal range, symptoms improved, and the patient was discharged asymptomatic and haemodynamically stable. Conclusions SARS-CoV-2, as already described in literature, can be associated with inflammatory cardiac involvement. This is the first report of SARS-CoV-2 associated myopericarditis in a patient with previous history of myocarditis and recent SARS-CoV-2 pneumonia. In our experience the patient was successfully treated with evidence-based therapy for heart failure and immunomodulation therapy.

Aims The SARS-CoV-2 infection is mostly characterized by acute lung injury. Yet, some COVID-19 patients showed also neurological signs, acute myocardial injury, heart failure, myocarditis, and hypercoagulability, such as pulmonary embolism. Cardiac biomarkers can play an essential role in the diagnosis, management, and prognosis of COVID-19. In fact, during hospitalization, these patients develop biochemical abnormalities, with increasing of all Troponins (TnT), B-type natriuretic peptide (NT-pro-BNP) and creatine kinase-myocardial band (CK-MB) levels. This situation helps us to predict adverse outcomes, especially in patients with cardiovascular comorbidities or risk factors. Data emerged demonstrated a myocardial involvement which determines a high risk of adverse events and increasing of mortality. Methods and results Lots of meta-analysis emphasize that a great number of hospitalized patients with moderate and severe forms of COVID-19 developed acute myocardial damage, defined as an increase of cardiac biomarkers, such NT-pro-BNP, CK-MB, and of all type of troponins. The highest mortality rate is related with progressively increasing biomarkers levels and with a history of cardiovascular disease. In fact, the biomarkers dosage should be considered as a prognostic marker in all patients with COVID-19 disease at admission, during hospitalization and in the case of clinical deterioration. Our purpose is to evaluate cardiovascular prognostic factors in COVID-19 disease throughout the analysis of cardiac biomarkers to early identify the most serious patients and to optimize their outcomes. Results of aforementioned studies underline how cardiac biomarkers are associated with severe form of COVID-19 infection. Above all, higher levels of these biomarkers are significantly associated with an increased risk of the mortality in COVID-19 infected patients. Therefore, has been demonstrated COVID-19 infection is more severe in those patients with a previous history of arterial hypertension, cardiovascular diseases. In addition to classical laboratory parameters evaluated in COVID-19 infection, such as C Reactive Protein (CRP), d-dimer, and lactate dehydrogenase (LDH), which are currently used in clinical practice, others biomarkers could potentially be useful for screening, clinical management, and prevention of serious complications. Therefore, it is clinically significant that fluctuating levels of myocardial biomarkers are closely monitored and patients with high levels of myocardial biomarkers are treated promptly to improve prognosis. At the end, on basis of symptoms and cardiac biomarkers patients could be divided in mild, severe and critical. Conclusions Biomarkers of acute myocardial injury play an important role in predicting worsening prognosis for COVID-19 patients with and without myocardial injury. They are not only predictive of disease severity, but are also helpful for therapeutic management, based on drugs preventing the activation of coagulation processes. It’s important, above all, to identify a laboratory score, made by haematological, inflammatory, biochemical, and immunological parameters, may help to stratify COVID-19 positive patients into risk categories for deciding therapeutic management, thus avoiding cardiac compromise which, as we have previously analysed, is an indication of a poor prognosis.

Aims It has already been demonstrated the efficacy of sacubitril/valsartan in the treatment of heart failure with reduced ejection fraction, but many of its properties are still unknown especially regarding its effects on endothelial dysfunction and arterial stiffness. Methods and results To this purpose, a longitudinal study involving 15 patients with dilated cardiomyopathy with reduced left ventricular ejection fraction (LVEF) was started; the purpose was collecting at the beginning and at the end of the study blood pressure measurements, transthoracic echocardiography images, parameters of endothelial function with peripheral arterial tonometry (EndoPAT®), and non-invasive evaluation of the aortic stiffness parameters by using applanation tonometry (SphygmoCor® Px system). Aortic stiffness parameters weren’t different at 6 months, compared to baseline. There was a slight, not significant increase in augmentation pressure (P = 0.889), augmentation index (P = 0.906), and sphygmic wave velocity (P = 0.263). Systolic, diastolic, and differential central arterial pressure didn’t change. RHI (reactive hyperaemia index) increased significantly after 6 months (P = 0.001) as well as augmentation index corrected for 75 b.p.m. Ejection fraction (32.21% ± 5.7 to 38.43% ± 8.4; P = 0.010) and diastolic dysfunction degree (P = 0.021) improved significantly. Mitral regurgitation improvement wasn’t statistically significant (P = 0.116). Tricuspid annular plane systolic excursion didn’t change while pulmonary systolic arterial pressure increased, although not significantly (22.83 mmHg ± 4 to 27.33 mmHg ± 6; P = 0.068) and within the normal range values. Conclusions Sacubitril/valsartan can improve endothelial function significantly in patients with dilated cardiomyopathy and reduced LVEF. It can also improve left ventricular function, mitral regurgitation, and diastolic function. Conversely, this drug seems to have no effects on vascular stiffness.

Emerging evidences prove that the ongoing pandemic of coronavirus disease 2019 (COVID-19) is strictly linked to coagulopathy even if pneumonia appears as the major clinical manifestation. The exact incidence of thromboembolic events is largely unknown, so that a relative significant number of studies have been performed in order to explore thrombotic risk in COVID-19 patients. Cytokine storm, mediated by pro-inflammatory interleukins, tumor necrosis factor α and elevated acute phase reactants, is primarily responsible for COVID-19-associated hypercoagulopathy. Also comorbidities, promoting endothelial dysfunction, contribute to a higher thromboembolic risk. In this review we aim to investigate epidemiology and clarify the pathophysiological pathways underlying hypercoagulability in COVID-19 patients, providing indications on the prevention of thromboembolic events in COVID-19. Furthermore we aim to reassume the pathophysiological paths involved in COVID-19 infection.

A close and intriguing relationship has been suggested between heart failure (HF) and coronavirus disease 2019 (COVID-19). First, COVID-19 pandemic represented a global public health emergency in the last year and had a catastrophic impact on health systems worldwide. Several studies showed a reduction in HF hospitalizations, ranging from 30 to 66% in different countries and leading to a subsequent increase in HF mortality. Second, pre-existing HF is a risk factor for a more severe clinical course of COVID-19 and an independent predictor of in-hospital mortality. Third, patients hospitalized for COVID-19 may develop both an acute decompensation of chronic HF andde-novoHF as a consequence of myocardial injury and cardiovascular (CV) complications. Myocardial injury occurred in at least 10% of unselected COVID-19 cases and up to 41% in critically ill patients or in those with concomitant CV comorbidities. Few cases of COVID-19-related acute myocarditis, presenting with severe reduction in the left ventricular (LV) ejection fraction and peculiar histopathological findings, were described. However, recent data suggested that COVID-19 may be associated with both systolic and diastolic LV dysfunction, with LV diastolic impairment, pulmonary hypertension, and right ventricular dysfunction representing the most frequent findings in echocardiographic studies. An overview of available data and the potential mechanisms behind myocardial injury, possibly leading to HF, will be presented in this review. Beyond the acute phase, HF as a possible long-term consequence of cardiac involvement in COVID-19 patients has been supposed and need to be investigated yet.

Mitral annular disjunction (MAD) is a structural abnormality of the mitral annulus, defined by a detachment of the atrial wall-mitral valvular junction from the left ventricular (LV) free wall. This structural abnormality in mitral annulus fibrosus is significantly associated with the presence of mitral valve prolapse (MVP) [1], but it can be also detected in normal cases as an anatomical variation of the mitral annulus fibrosus [2]. The main tools to detect MAD are echocardiography and cardiac magnetic resonance. Prevalence of MAD in the general population ranges from 7% [1] to 9% [2]. Several studies proved an association between MAD and arrhythmic events, independently of concomitant mitral valve abnormalities, suggesting the existence of a novel entity: MAD arrhythmic syndrome [3]. Herein we describe a case report of a middle age man with MAD who experienced ventricular arrhythmias and placement of an implantable cardioverter-defibrillator (ICD).