Introduction: Chronic heart disease (CHD) is a common comorbidity of patients receiving endovascular aneurysm repair (EVAR) for abdominal aortic aneurysms (AAA). The explicit relationship between ventricular systolic function and EVAR complication of thrombotic events is unknown.Methods: In this study, we proposed a three-dimensional numerical model coupled with the lumped-elements heart model, which is capable of simulating thrombus formation in diverse systolic functions. The relation of cardiac functions and the predicted risk of thrombus formation in the aorta and/or endograft of 4 patients who underwent EVAR was investigated. Relative risks for thrombus formation were identified using machine-learning algorithms.Results: The computational results demonstrate that thrombus tended to form on the interior side of the aorta arch and iliac branches, and cardiac function can affect blood flow field and affect thrombus formation, which is consistent with the four patients' post-operative imaging follow-up. We also found that RRT, OSI, TAWSS in thrombosis area are lower than whole average. In addition, we found that the thrombus formation has negative correlations with the maximum ventricular contractile force (r = −.281 ± .101) and positive correlations with the minimum ventricular contractile force (r = .238 ± .074), whereas the effect of heart rate (r = −.015 ± .121) on thrombus formation is not significant.Conclusion: In conclusion, changes in ventricular systolic function may alter the risk of thrombotic events after EVAR repair, which could provide insight into the selection of adjuvant therapy strategies for AAA patients with CHD. Abdominal aortic aneurysm (AAA) is one of the most common degenerative aortic diseases and is often complicated with various levels of cardiac dysfunction and cardiovascular comorbidities . For advß-blockers could be beneficial for AAA patients after EVAR in light of aneurysmal sac shrinking and clinical outcomes  and CRIMSON  were usesv(t) is the time function of ventricular pressure (mmHg), Vsv(t) is a time function of ventricular volume (mL), and V0 is the ventricular reference volume (mL), which is the theoretical volume relative to ventricular zero pressure. Boston  represents the normalized function of ventricular elasticity, which is described as the Hill equation as follows , which was induced by localized high concentration of activated platelets (APs), coagulation enzymes C), and prolonged flow residence time (RRT). The schematic of the thrombus formation is illustrated in The bounded platelets (BPs) attached to the reactive surface have neither convective nor diffusive motion; therefore, in this case, Eq. Considering the resistance of bounded platelets to blood flow, the momentum source term was added to the Navier-Stokes equations, and the viscosity coefficient was modified. Eq. max (end-systolic elastance), Emin (end-diastolic elastance), and T (heart rate) from 10% to -10% compared to the reference values and got the corresponding aortic blood flow velocity in different heart functions. Finally, we simulated the formation of thrombus in the 3D aorta under various cardiac functions, the boundary conditions of which are derived from the blood flow velocity at the boundary nodes in the lumped-elements model .Data were analyzed using Prism software . Statistical significance for samples was determined using two-tailed unpaired Student’s t-test. Data were considered statistically significant if The baseline information of 4 patients were shown in The hemodynamic parameters and BP levels at ROI were demonstrated in The impact of heart function alteration on thrombus formation in the ROI as well as the aortic inlet velocity were shown in max, Emin, and T. Then we analyzed the formation of thrombus, which was induced by the altered heart functions. First of all, the increased Emax  could maintain or alleviate thrombus formation levels in the ROI of four patients. However, the effects of decreased Emax are heterogeneous. For patient 1, a decrease in Emax would result in an increase in thrombus development at the iliac branches. However, for patients 2-4, the lower Emax would result in less thrombus development at the arch and descending aorta. In addition, the increased Emin, which represents ventricular compliance, would maintain or exacerbate the thrombus formation in the ROI of four patients. The decreased Emin would maintain or alleviate the thrombus formation in these regions. Furthermore, the influences of heart rate T) on thrombus formation are less significant.The aortic velocity profile demonstrated that the magnitude and shape of the blood flow profile are affected by the heart function parameters of Emax, Emin, T, and thrombus formation. We found that the BP concentration was negatively correlated with Emax , and was positively related with Emin (r = .238 ± .074)  of the four patients to quantitatively highlight the associations between heart function and thrombus formation in ROI. We discovered that TAWSS is largely affected by Emax level, while Emin and T have little impact by showing the Parallel coordinate charts classified by the heart function . In addition, we found that increasing Emax and decreasing Emin could reduce overall thrombus formation levels , which i ± .074) . HoweverEndograft mural thrombus accumulation had reported rates up to 33% and was detected as early as 1 week after EVAR . It mighThrombosis involves complex interlinked interactions between platelets, coagulation cascades, and the vascular wall . In thisPrevious works investigating the relationship between cardiac function and EVAR complications were mainly retrospective cohorts or reviews . To the min and t promoted thrombus formation, yet changes of Emax induced distinct results. It should be noted that BP levels in patients 1 and 3 were higher and more concentrated around the actual thrombus-forming area. Despite thrombus deposition in the local iliac stent, the BP in patients 2 and 4 had relatively low absolute value and occupied a more extensive spatial range. Morphological factors such as increasing diameter because of stent oversize may have a stronger influence on thrombosis in these patients, and the impact of cardiac parameter alteration should be cautiously interpreted. The heterogeneous results from different patients emphasized the importance of individualized analysis.Concerning the actual thrombus forming area, both elevated or reduced Emin was positively related. It has been reported that male AAA patients had reduced ventricular systolic and diastolic function  models with mass transport models of thrombus to more realistically predict thrombus formation in deformed vessels .In conclusion, changes in ventricular contractile force may alter the risk of thrombus formation for post-EVAR patients, whereas the effect of heart rate is not significant. Postoperative cardiac support recommends drugs that support maximum ventricular contractile force, maintain left ventricular pressure, and stabilize heart rate.


Background and Objectives: In addition to left ventricular (LV) functions, right ventricular (RV) functions and pulmonary arterial stiffness (PAS) may be adversely affected in patients with heart failure with reduced ejection fraction (HFrEF). Sodium-glucose co-transporter-2 (SGLT2) inhibitor therapy positively affects LV functions as well as having functional and symptomatic benefits in HFrEF patients. In this study, we aimed to evaluate the effects of SGLT2 inhibitor treatment on RV function and PAS in HFrEF patients. Materials andMethods: 168 HFrEF patients with New York Heart Association (NYHA) class ≥2 symptoms despite optimal medical treatment and who were started on SGLT2 inhibitor therapy were included in this retrospective study. NYHA classification, N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels, Minnesota Living with Heart Failure Questionnaire (MLWHFQ) scores, laboratory tests, and transthoracic echocardiography (TTE) measurements were recorded before treatment and at the end of the 6-month follow-up. Results: The mean age of the patients was 62.7 ± 11.4 years, and 38 (22.6%) were women. RV function  ; tricuspid annular plane systolic excursion (TAPSE) ; RV S’ (10 (8 − 13) cm/s vs. 13 (10 − 16) cm/s, p < 0.001); RV myocardial performance index (RV MPI) ; mean pulmonary artery pressure (mPAP) ) and PAS  values at the 6-month follow-up after SGLT2 inhibitor therapy significantly improved. It was found that SGLT2 inhibitor treatment provided significant improvement in NYHA classification, MLWHFQ scores, and NT-proBNP levels , and these functional and symptomatic positive changes in HFrEF patients were significantly correlated with positive changes in LVEF, PAS, and RV functional status. Conclusions: SGLT2 inhibitor treatment results in symptomatic and functional well-being in HFrEF patients, as well as positive changes in RV function and PAS. Heart failure (HF) is a chronic inflammatory syndrome with typical symptoms and signs, which reduces the quality of life and increases the risk of mortality and morbidity . In patiPulmonary arterial stiffness (PAS) is an index that is higher in HFrEF patients than in the healthy population and allows the evaluation of the structural and functional status of the pulmonary vascular bed ,5. DAPA-SGLT2 inhibitor therapy has been shown to increase LV ejection fraction and contractile reserve and improve LV adverse remodeling . However2). After applying the inclusion and exclusion criteria, a total of 168 HFrEF patients were included in our study. This study followed the principles stated in the Declaration of Helsinki and was approved by the local ethics committee . Written informed consent was taken from all participants.HFrEF patients with NYHA class ≥2 symptoms followed up from our cardiology clinic between January 2020 and April 2022 were evaluated for our single-center retrospective study. Inclusion criteria were: >18 years of age, LVEF ≤ 40%, and presence of NYHA class 2–4 symptoms despite optimal medical treatment. Exclusion criteria were determined as follows (in the last 6 months before the initiation of therapy and during the 6-month follow-up period): (i) implantation of a cardiac pacemaker, implantable cardioverter-defibrillator (ICD), or cardiac resynchronization therapy (CRT); (ii) coronary artery bypass graft surgery; (iii) surgical or percutaneous interventions for valve disease; (iv) percutaneous coronary intervention for acute coronary syndrome; (v) inflammatory, autoimmune and infectious diseases under follow-up and treatment; (vi) ongoing hematological diseases and malignancies; and (vii) advanced stage liver and kidney failure , New York Heart Association (NYHA) classification, Minnesota Living with Heart Failure Questionnaire (MLWHFQ) scores, body mass index (BMI), electrocardiographic (ECG) and transthoracic echocardiographic (TTE) measurements of the patients included in our study were recorded. Patients who were given SGLT2 inhibitor therapy were invited to follow-up visits at the first, third, and sixth months to monitor for treatment compliance. Optimal medical treatment was restored according to the volume load, functional capacity and symptoms of the patients at the control visits. Diuretic doses were downregulated in patients with reduced volume load. Relevant measurements were repeated at each visit. In the analyses, baseline measurements before SGLT2 inhibitor treatment and at the six-month follow-up visit measurements were compared. Patients who did not attend or could not be reached at the control visits were excluded from the study. Tolerability of SGLT2 inhibitor therapy or its regular use for at least 6 months was considered to be one of the important conditions for inclusion in the study.2. The Minnesota Living with Heart Failure Questionnaire (MLWHFQ) contains 21 questions that assess the effects of heart failure symptoms and signs on social relationships, physical and sexual activity, work, and emotions. The answer to each question was chosen from a scale of 0  to 5 (very much); the higher the score, the worse or more restricted the quality of life [In line with the 2021 European Society of Cardiology (ESC) heart failure guidelines recommendations, optimal medical therapy (OMT) was defined as angiotensin converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARB)/sacubitril valsartan (SV) + beta-blocker + mineralocorticoid receptor antagonist (MRA) and SGLT2 inhibitors. The fact that the patients were symptomatic despite OMT was expressed after the maximum dose of the OMT drug group they could tolerate [ of life .Hypertension (HT) was defined as ongoing medication use with a previous diagnosis of HT, or systolic blood pressure (SBP) ≥ 140 mmHg or diastolic blood pressure (DBP) ≥ 90 mmHg (the mean of two consecutive measurements). Diabetes mellitus (DM) was defined as the use of anti-diabetic drugs or a fasting blood glucose level of ≥126 mg/dL or HbA1c ≥ 6.5% on at least two measurements. Hyperlipidemia was defined as low-density lipoprotein (LDL) cholesterol levels ≥130 mg/dL or ongoing statin use.All echocardiographic examinations were performed by experienced operators . Echocardiographic examinations were performed in the left lateral decubitus position after resting for at least 15 min. All measurements were taken in three consecutive cycles and mean values were calculated. Parasternal long and short axis views and apical views were used as standard viewing windows. All echocardiographic evaluations were performed according to the recommendations of the American Society of Echocardiography/European Association of Cardiovascular Imaging guidelines .2) was calculated with the formula (LVOT − VTI × LVOT area) × heart rate (beats/min)/BMI (kg/m2). RV end-diastolic diameters were calculated from the middle and basal segments in an apical four-chamber view. RV end-diastolic (RVEDa) and end-systolic areas (RVESa) were calculated from the apical four-chamber view. RV fractional area change (RV FAC) was calculated with the formula (RVEDa − RVESa)/RVEDa. Tricuspid annular plane systolic excursion (TAPSE) was measured as the displacement of the tricuspid lateral annulus between systole and diastole in M-mode. RV peak systolic S’ velocity was calculated by tissue Doppler velocity of the lateral tricuspid annulus. Mean pulmonary artery pressure (mPAP) was calculated from systolic PAP using the following formula: mPAP = 0.61 × sPAP + 2 mmHg [Left ventricular end-diastolic and end-systolic diameters  were measured from the parasternal long-axis view using M-mode. Left ventricular end-diastole and end-systole volumes were measured from the apical four-chamber and two-chamber views. Ejection fraction measurements were made using the Modified Simpson method. Left ventricular outflow tract (LVOT) diameter was measured in the parasternal long-axis view in systole. The left ventricular outflow tract velocity time integral (LVOT-VTI) was calculated using pulsed-wave (PW) Doppler on the LVOT. The cardiac index  of pulmonary flow was calculated by averaging at least three consecutive beat measurements. Again, the time from the onset of pulmonary flow ejection to the peak (pulmonary flow acceleration time = PAT) was calculated by averaging at least three consecutive pulse measurements . PAS . The continuous variables were tested for a normal distribution using the Kolmogorov-Smirnov test. Non-normally distributed data were presented as the median with an interquartile range and compared with Wilcoxon’s signed-rank test. Normally distributed data were expressed as mean ± standard deviation and compared with the Student’s The mean age of the 168 HFrEF patients included in our study was 62.7 ± 11.4, and 38 (22.6%) were women. In the study population, 58.3% of the etiology of heart failure was ischemic-based, 63.7% had HT, 32.1% had DM, 67.8% had a history of coronary artery disease, and 50% had dyslipidemia. It was observed that 92.8% of our study patients used β-blocker, 51.7% ACE inhibitor, 42.2% SV, and 63.1% spironolactone before SGLT2 inhibitor treatment. Baseline demographic and clinical data of the study patients are presented in p = 0.022)). While the mean NT-proBNP level was 2876 ± 401 pg/mL before treatment, it was observed to decrease to 1034 ± 361 pg/mL levels after treatment (p < 0.001). While the rate of patients with symptoms in NYHA class III and IV before treatment was calculated as 58.9%, this rate decreased to 21.4% in the sixth month of the controls after treatment (p < 0.001). It was determined that the MLWHFQ score decreased significantly in the 6-month control period compared with pre-treatment ).The comparison of baseline and 6-month control data before SGLT2 inhibitor therapy is presented in p < 0.001), cardiac index baseline: 2.34 ± 0.46 L/min/m2; and follow-up: 2.48 ± 0.42 L/min/m2 (p < 0.001)). It was observed that LVEDd, LVESd, left ventricular end-diastolic and end-systolic volumes  decreased significantly at the 6-month follow-up compared with pretreatment . The parameters we used in the functional evaluation of the right ventricle at the 6-month follow-up were compared to baseline and it was found that: (i) RV FAC , TAPSE  and RV S’ (10 (8 − 13) cm/s vs. 13 (10 − 16) cm/s, p < 0.001) significantly increased; (ii) RV MPI , mPAP  and PAS  significantly decreased (Baseline and 6-month follow-up TTE data are presented in ecreased .To the best of our knowledge, this is the first study to evaluate the effect of SGLT2 therapy on PAS and RV function in patients with HFrEF. A decrease in PAS values and improvement in RV function were detected at the end of the 6-month follow-up in patients who received SGLT2 treatment. When the pre-treatment and post-treatment 6-month control changes were compared; MLWHFQ score, NYHA classification, and NT-proBNP levels, which are the criteria we used to evaluate the functional, symptomatic and prognostic course of HFrEF patients, were found to be negatively correlated with LVEF, cardiac index, RV FAC, TAPSE and RV S’, and positively correlated with RV MPI and PAS values.Impaired LV functions also negatively affect RV function. The increase in pressure due to LV dysfunction is reflected in the pulmonary vascular system, and indirectly the increase in afterload worsens RV function . WorseniPAS is an index developed to evaluate the structural features and functions of the pulmonary vascular bed and indicates pulmonary artery elasticity . Clinica+/H+ exchanger [Many studies have shown that SGLT2 inhibitors reduce the risk of cardiovascular death and improve cardiovascular outcomes in type 2 DM patients ,28. In txchanger ,34,35,36SGLT2 inhibitors have direct effects on vascular cells. They positively affect the proliferation, migration, differentiation, and senescence of endothelial cells. They have powerful antioxidant and anti-inflammatory effects. They improve endothelium-dependent vasodilation by increasing the bioavailability of nitric oxide produced from the endothelium. They inhibit the molecular changes that cause early atherogenesis. They inhibit the contraction, proliferation and migration of vascular smooth muscle cells. As a result, vascular remodeling decreases arterial wall stiffness and vascular resistance decreases ,39,40,41Previously, there have been studies on the effect of SV, a new generation heart failure drug, on RV function and PAS. In the study of Landolfo et al. , an imprIn our study, a significant decrease was observed in the NYHA class, which is an indicator of HF symptomatic status and functional capacity, in the MLWHFQ score, which is an indicator of HF quality of life, and in the levels of NT-proBNP, which is the biochemical parameter of HF severity. There was an increase in RV FAC, TAPSE, and RV S’ values used in the evaluation of right ventricular functions, and a decrease in RV MPI values, and it was determined that right ventricular echocardiographic improvements correlated with clinical and biochemical improvement. Again, it was found that PAS values, which were strongly associated with RV function , decreasThere are some limitations of our study. In our study, no randomization was performed that compared the SGLT2 inhibitor and the placebo. It was conducted in a relatively small cohort and had a single-center retrospective design. Another important limitation was the lack of right heart catheterization or cardiac magnetic resonance imaging to evaluate pulmonary arterial stiffness, pulmonary artery pressure, and right ventricular function. In addition, patients who did not attend or could not be reached at control visits were excluded from the study. This might have influenced our results.As a result of the 6-month follow-up of HFrEF patients receiving SGLT2 inhibitor therapy, PAS, which is the evaluation criteria of the pulmonary vascular bed, and RV FAC, TAPSE, RV MPI, and RV S’, which are the RV functional evaluation criteria, showed a significant positive change. Positive changes in RV function and PAS are also significantly correlated with positive functional and symptomatic outcomes in HFrEF patients. SGLT2 inhibitor therapy not only results in symptomatic and functional well-being in HFrEF patients but also provides positive changes in RV function and pulmonary arterial stiffness, directly or indirectly.


The distinction between ‘acute’ and ‘chronic’ heart failure persists. Our review aims to explore whether reclassifying heart failure decompensation more accurately as an event within the natural history of chronic heart failure has the potential to improve outcomes.Although hospitalisation for worsening heart failure confers a poor prognosis, much of this reflects chronic disease severity. Most patients survive hospitalisation with most deaths occurring in the post-discharge ‘vulnerable phase’. Current evidence supports four classes of medications proven to reduce cardiovascular mortality for those who have heart failure with a reduced ejection fraction, with recent trials suggesting worsening heart failure events are opportunities to optimise these therapies.Abandoning the term ‘acute heart failure’ has the potential to give greater priority to initiating proven pharmacological and device therapies during decompensation episodes, in order to improve outcomes for those who are at the greatest risk. Is it the rapidity of deterioration? Acute implies a disease process occurring within minutes or hours, but in heart failure, this is seldom the case. Most patients are already known to have established chronic heart failure, and even when hospitalisation is the first time that cardiac structure and function are assessed, intravascular volume expansion and changes in left ventricular volumes are likely to have occurred over the preceding days or weeks. Furthermore, at what point does a patient with acute heart failure become a patient who has chronic heart failure? Should it be at discharge, or when the patient no longer requires intravenous diuretics, or perhaps when results of the echocardiogram are known since even in patients rendered asymptomatic, heart failure cannot be cured? . Al. Al12]. Hence, this framework has been superseded by criteria based on the pathophysiological mechanisms driving heart failure decompensations, which describes the four most commonly encountered clinical scenarios. Acute decompensated heart failure (ADHF) accounts for the majority of patients presenting with symptoms of worsening heart failure. Such patients have established chronic heart failure, which worsens gradually over days or weeks, most of whom are ‘wet and warm’. Acute pulmonary oedema typically presents more rapidly, is often a first presentation, and is usually not associated with peripheral oedema. Isolated right ventricular failure is another commonly encountered clinical presentation, the predominant symptom being systemic congestion, with or without hypoperfusion. Finally, cardiogenic shock accounts for a small number of patients who have a particularly poor prognosis. Cardiogenic shock is rarely simply ‘heart failure’ — more frequently, it is an acute presentation of a new event such as myocardial infarction, ventricular arrhythmia, fulfilment myocarditis, or Takotsubo cardiomyopathy. Patients presenting with a cardiogenic shock picture require specific therapies, intensification of therapies beyond intravenous diuretics, and typically have clinical signs of hypoperfusion and congestion.Not only is hospitalisation costly , it worsThe largest study of remote monitoring using implantable devices — the REmote Monitoring of Heart Failure (REM-HF) trial, assessed whether information gained from a protocolised remote monitoring strategy could improve outcomes for patients with established chronic heart failure . In a rep < 0.0001), but still only 4% within 30 days [A limitation of these approaches is poor specificity. The risk of hospitalisation in the Program to Access and Review Trending Information and Evaluate Correlation to Symptoms in Patients with Heart Failure (PARTNERS-HF) was 5.5-fold higher if combined heart failure device diagnostic criteria were fulfilled . Although the overall result of the trial was neutral, it was noted that the event rate in the active arm was lower during the COVID-19 pandemic than the period prior to this (pinteraction = 0.11). In a pre-specified analysis restricted to events prior to the pandemic, remote monitoring was associated with a reduction in the combined primary endpoint  [One potentially promising approach is remote haemodynamic assessment of pulmonary artery pressures by, for example, the CardioMEMs device . Although not originally designed to identify risk and avoid hospitalisation, rather to optimise the treatment of chronic heart failure, as we have suggested, these are one and the same aim. In the haemodynamic-GUIDEed management of Heart Failure (GUIDE-HF) trial, a responsive pulmonary artery pressure monitoring strategy was not associated with a lower rate of all-cause mortality or total heart failure events than usual care in patients at risk of hospitalisation   .Two key questions in preventing the primary (or repeat) hospitalisation are whether the response can be delivered in a timely manner in the community, where its use achieves clinical stability swiftly enough and secondly, whether in a population of patients receiving disease-modifying therapies, an effective intervention exists which has not yet been employed. Even in GUIDE-HF with direct congestion monitoring, the overall results of the trial were neutral, possibly as it enrolled a well-treated and low risk population  of whom the majority did not have elevated pulmonary artery pressures at baseline and therefore had little scope to improve . DespiteTherapies for worsening heart failure should stabilise haemodynamics and relieve symptoms. For this reason, loop diuretics remain the cornerstone of management. These agents increase renal excretion of sodium and water, alleviating congestion, the most common symptom of worsening heart failure. In doing so, they can improve cardiac contractility by moving left ventricular haemodynamics into a more favourable position of the Frank Starling curve. For patients at risk of hospitalisation, doses of these medications can be increased by the oral route, or administered intravenously in the community, although for many, hospitalisation will be necessary or more practical. Although studies defining the optimal dosing, frequency, and whether bolus or infusions are preferred are limited, what limited evidence there is suggests that these should be tailored to the individual patient . Clinicap < 0.001) and reduced length of hospital stay [Combination therapy can achieve additional diuresis with thiazide diuretics and mineralocorticoid receptor antagonists having been used alongside loop diuretics for decades. More recently, the ADVOR (Acetazolamide in Decompensated Heart Failure with Volume Overload) trial showed the addition of acetazolamide to intravenous loop diuretics resulted in more successful decongestion within 3 days  or non-invasive ventilation (NIV) rapidly correct respiratory distress, hypercapnaenia, and acidosis, when used alongside intravenous diuretic therapy although these have not been shown to improve survival .Patients presenting with cardiogenic shock require circulatory support using inotropes or vasopressors to maintain cardiac output, often used in combination. Inotropes increase cardiac contractility, thereby increasing cardiac output, whilst vasopressors increase peripheral vascular resistance, increasing end-organ perfusion but at the expense of increased afterload. Vasopressors, especially those with adrenergic mechanisms, can result in tachycardia, myocardial ischaemia, and arrythmia, and their use is associated with worse outcomes , whilst Therapies which improve acute haemodynamics or strategies to optimise the delivery of care for the decompensated patient have not translated into meaningful improvements in outcomes, suggesting that more completely treating the underlying syndrome should be our focus instead. For patients with heart failure with reduced ejection fraction (HFrEF), four classes of medications targeting the neurohormonal maladaptations of the syndrome are proven to reduce hospitalisations and improve survival . In clinOf particular relevance to hospitalised patients are sodium glucose co-transporter 2 inhibitors (SGLT2i) which are proven to improve symptoms, reduce hospitalisation, and extend longevity , 40. A cIn PARADIGM-HF , sacubitril-valsartan was shown to be superior to enalapril with respect to cardiovascular mortality and hospitalisations with heart failure  for ambulatory patients chronic heart failure and LVEF ≤ 40%   who had Whilst therapies have been mainly limited to patients with a reduced ejection fraction, there are now data showing reductions in hospitalisations for worsening heart failure for those with a preserved ejection fraction . AdditioCardiac resynchronisation therapy (CRT) is amongst the most effective treatments for HFrEF. For indicated patients who despite optimised medical therapy have persistently impaired left ventricular ejection fraction (LVEF), ongoing symptoms, and QRS duration ≥ 130 ms . ImplantImplantable cardioverter defibrillators (ICD) reduce the risk of sudden cardiac death and all-cause mortality for patients fulfilling similar criteria (with or without QRS ≥ 130 ms) . AlthougA possible compromise, especially for patients with new HFrEF as a consequence of myocardial infarction, wearable cardioverter-defibrillators may be considered although these have not been proven to reduce the risk of morality and carry a risk of inappropriate shocks . On the For patients hospitalised with worsening heart failure in whom the underlying pathophysiology is a primary valvular disorder, standard risk assessment and surgical procedures should be considered. However, many hospitalised patients, particularly those who have left ventricular systolic dysfunction are unlikely to be considered suitable for surgical treatments. Of particular relevance, severe aortic stenosis has a particularly poor prognosis in the presence of the heart failure syndrome or left ventricular systolic dysfunction. Non-surgical options for the management of aortic stenosis include balloon valvuloplasty and transcatheter aortic valve implantation (TAVI), with retrospective analyses suggesting the risk of re-hospitalisation and subsequent interventions is lower in those undergoing immediate rather than delayed TAVI, even after adjustment for relevant confounders .Many patients with HFrEF develop secondary mitral regurgitation, in which annular dilatation due to ventricular or atrial distension results in the failure of morphologically normal valve leaflets to coapt . PatientHeart failure is a chronic disease which cannot be cured , and so Various methods have been proposed to help clinicians identify patients who might benefit from such an approach. One such prompt is the ‘surprise question’ — “would you be surprised if this person were to die within the next 12 months?”. This question has been validated in a number of chronic diseases, including patients hospitalised with heart failure for whom it reliably identifies nearly all of those likely to die (sensitivity 85%), whilst also accuracy identifying who is unlikely to die  and can be used with similar levels of accuracy by a range of healthcare professionals in both inpatient and outpatient settings , 63. WhiMany patients discharged from hospital following an episode of worsening heart failure are not receiving all indicated classes of guideline-directed medical therapy . Even whWorsening heart failure events identify patients as being high risk for subsequent poor quality of life, re-hospitalisation, and mortality. Much of the adverse prognosis is related to the severity of underlying disease, rather than decompensation events themselves. Moving forwards, efforts to optimise disease modifying pharmacological therapies, devices, and structural interventions during decompensation episodes, have the potential to further improve outcomes for patients at the greatest risk. Those caring for those with chronic heart failure should be cognisant that for many, prognosis may be irreversible and the adoption of an early, palliative approach alongside active care may be most effective means by which to improve quality of life.


The mechanical complications of ST-segment elevation myocardial infarction (STEMI) include left ventricular free-wall rupture, ventricular septal rupture, acute mitral regurgitation due to rupture of chordae tendineae or papillary muscle, pseudo aneurysm, true aneurysm, cardiac tamponade, and dynamic left ventricular outflow tract (LVOT) obstruction.A 75-year-old postmenopausal woman presented to the emergency department with a history of easy fatigability for a duration of 6 hours. She had a significant history of diabetes mellitus and hypertension for a duration of 10 years and was on optimal medical treatment. She had no family history of cardiac illness or sudden cardiac death. At the time of admission, her pulse rate was 112 beats per minute (bpm), with blood pressure of 140/80 mm Hg and oxygen saturation of 98% at room air. The mean pressures of her jugular venous pulse were normal, and auscultation revealed a third heart sound (S3), grade 2/6 ejection systolic murmur in the left third intercostal area, and grade 3/6 pansystolic murmur in the mitral area. Normal vesicular breath sounds were heard equally in both lung fields, and there were no basal crepitations. The patient was in Killip class II heart failure at presentation. Examinations of other systems were unremarkable. Her electrocardiogram at admission showed ST-segment elevation in lead aVL and precordial leads V2-V6  suggesti2 body surface area, and a visually assessed ejection fraction of 70%  and discharged uneventfully 4 days after angioplasty. She was advised follow-up echocardiogram 3 months after the procedure with provocative maneuvers  or stress echocardiography to determine whether she had hypertrophic cardiomyopathy with LVOT obstruction before the STEMI. This patient discontinued her guideline-directed medical therapy after 1 month and presented 4 weeks later to the emergency department with pulmonary edema. An electrocardiogram was taken that showed QS complexes with ST-segment elevation and T-wave inversion in precordial leads V2-V6 . Since tIn a patient presenting with acute myocardial infarction, the causes for a systolic murmur in the apex include acute mitral regurgitation (due to papillary muscle dysfunction or rupture of chordae tendineae) in the left sternal border due to a ventricular septal rupture and acute tricuspid regurgitation (due to right ventricular infarction) in the left third intercostal space due to acute dynamic LVOT obstruction.The patient was advised follow-up evaluation with provocative maneuvers  or stress echocardiography,As age advances, dilatation and lengthening of the aorta push the septum downward and kink its upper portion, resulting in a more acute angle between the aortic root axis and the interventricular septum.The underlying mechanisms of acquired LVOT obstruction in acute STEMI are apical dysfunction and compensatory hypercontractility of the basal segments.The mechanisms leading to reversible dynamic LVOT obstruction in our patient could be categorized into anatomic and hemodynamic factors. Anatomic factors include sigmoid-shaped septum, long-standing hypertension with left ventricular hypertrophy, small left ventricular cavity, and a narrow aortoseptal angle. Hemodynamic factors include tachycardia, anterior wall STEMI resulting in left ventricular apical dysfunction, and compensatory basal hypercontractility leading to obstruction.P = 4V2).,Valve gradients are dynamic and vary considerably as a result of changes in heart rate, blood pressure, contractility, and volume status of the individual.Since the baseline hemodynamic status of the patient might significantly influence the inflow and outflow gradients, measuring vital parameters, particularly heart rate and blood pressure, is indispensable when performing an echocardiogram.,Treatment of dynamic left ventricular obstruction due to acute STEMI includes adequate intravenous fluids, early beta-blockers to reduce the basal hypercontractility, urgent revascularization to improve apical dysfunction,This case report highlights a rare mechanical complication of acute myocardial infarction—acquired dynamic LVOT obstruction—the role of an echocardiogram in therapeutic decision-making, the importance of measuring heart rate and blood pressure while performing an echocardiogram, and the role of early beta-blockers and revascularization in relieving dynamic LVOT obstruction.


To evaluate the great vessels in young children with complex congenital heart disease (CHD) using non-contrast cardiovascular magnetic resonance angiography (CMRA) based on three-dimensional relaxation-enhanced angiography without contrast (REACT) in comparison to contrast-enhanced steady-state CMRA.t-test, Pearson correlation, Bland–Altman analysis, Wilcoxon test, and intraclass correlation coefficients (ICC) were applied.In this retrospective study from April to July 2021, respiratory- and electrocardiogram-gated native REACT CMRA was compared to contrast-enhanced single-phase steady-state CMRA in children with CHD who underwent CMRA at 3T under deep sedation. Vascular assessment included image quality , vessel diameter, and diagnostic findings. For statistical analysis, paired Thirty-six young children with complex CHD  were included. Native REACT CMRA was obtained successfully in all patients (mean scan time: 4:22 ± 1:44 min). For all vessels assessed, diameters correlated strongly between both methods  with high interobserver reproducibility (ICC: 0.99 for both CMRAs). Native REACT CMRA demonstrated comparable overall image quality to contrast-enhanced CMRA . With REACT CMRA, better image quality was obtained at the ascending aorta , coronary roots , and inferior vena cava . In all patients, additional vascular findings were assessed equally with native REACT CMRA and the contrast-enhanced reference standard (n = 6).In young children with complex CHD, REACT CMRA can provide gadolinium-free high image quality, accurate vascular measurements, and equivalent diagnostic quality compared to standard contrast-enhanced CMRA. Cardiovascular magnetic resonance (CMR) is crucial for initial diagnosis, pre- and postoperative evaluation, and follow-up in children and adults with congenital heart disease (CHD) –3. CardiAlthough macrocyclic gadolinium-based contrast agents have an excellent safety profile, there are controversies regarding its retention in tissues after successive examinations . HoweverCurrent non-contrast CMRA techniques for assessing the great vessels are typically based on balanced steady-state free precession (bSSFP) , 11. AltThis study aimed to evaluate non-contrast REACT CMRA for assessment of the great vessels in young children with complex CHD in comparison to contrast-enhanced cardiac-gated steady-state CMRA as reference standard.This retrospective study was approved by the local institutional review board that waived informed consent. From April to July 2021, consecutive young children with complex CHD, who had undergone CMR were identified. Patients aged < 10 years who had undergone both contrast-enhanced CMRA and non-contrast CMRA (for comparability in upcoming non-contrast follow-up examinations) under deep sedation were included for analysis. No exclusion criteria were applied regarding the type of CHD or previously performed surgical or interventional procedures.All examinations were performed on a clinical whole-body 3T system . For signal reception, a 16-channel body array coil (35 patients) or a 12-channel array coil (1 patient) with digital interface were used. The CMR protocol for CHD evaluation consisted of ECG gated bSSFP cine imaging in standard orientations, phase contrast velocity-encoded flow imaging of vessels of interest, and late gadolinium enhancement (LGE) in standard orientations. The CMR protocol was individually extended according to the type of CHD or specific cardiovascular abnormalities.The imaging sequence applied was a 3D, magnetization-prepared, non-balanced, dual-echo acquisition with generalized Dixon for water and fat separation , 19. ForThe high-resolution single-phase steady-state CMRA was acquired during a slow infusion (flow rate: 0.1–0.3 ml/s) of a gadolinium-based contrast agent at a dose of 0.1 mmol per kg of body weight . Dual-echo Dixon readout was used to achieve fat removal in water images , 23. ResBoth CMRA methods were applied in the coronal plane covering the chest. Imaging parameters are given in Table Image quality assessment and vessel diameter measurements were performed independently by two radiologists in a blinded fashion for both CMRA methods  using a commercially available software . Water-only images were primarily used for image analysis of both CMRA techniques .The following great vessels of the heart were defined as vessels of interest: ascending aorta, main pulmonary artery, left pulmonary artery, right pulmonary artery, left superior pulmonary vein, right superior pulmonary vein, superior vena cava, inferior vena cava. The origin of the right and left coronary artery were also evaluated. Image quality assessment was performed visually. Qualitative ratings were based on a five-point Likert scale defined as follows: (5) excellent = no artifacts, good vessel border delineation, (4) good = minimal artifacts, minimal vessel blurring, (3) intermediate = some artifacts, some vessel blurring, (2) poor = severe artifacts, severe vessel blurring, (1) non-diagnostic = vessels are not identifiable. The overall image quality score included ratings for all predefined vessels.For quantitative analysis, following vessels were analyzed: ascending aorta and descending aorta (at pulmonary bifurcation level), main pulmonary artery or conduit , left and right pulmonary artery , left and right inferior, as well as superior pulmonary veins . Measurements were performed independently by both readers at the same predefined landmarks according to recent CMR guidelines for adults and children . For eacThe presence of artifacts compromising the great vessels was reviewed by both readers in consensus agreement. The evaluation included susceptibility artifacts , flow artifacts , and fat-water swap artifacts  .Most patients referred for CMR had complex cardiovascular anomalies, most of which were already known based on medical history and previous examinations . Final diagnosis of all vascular abnormalities and all accompanying clinically relevant findings based on CMRA was made in consensus by experienced, board-certified CMR readers (JAL with 10 years of CMR experience and CH with 17 years of CMR experience).t-test, Pearson correlation, and Bland–Altman analysis. Differences in image quality ratings were tested using the Wilcoxon signed-rank test. The McNemar test was used to compare the frequency of occurring artifacts between both CMRA techniques. Intraclass correlation coefficients (ICC) were applied to analyze interobserver reproducibility [Commercially available software  was used for statistical analysis. Data are presented as mean ± standard deviation or as absolute frequency. The Shapiro–Wilk test was applied to check for normal distribution of continuous data. Quantitative measurements between both CMRA methods were compared using the paired cibility .Thirty-six pediatric patients with CHD were included in this study  . The mean total scan time was 4:22 ± 1:44 min for REACT CMRA and 1:51 ± 0:18 min for contrast-enhanced steady-state CMRA (P < 0.001). A representative imaging example of both CMRA methods is shown in Fig. In total, image quality was assessed by each reader for 330 vessels on REACT CMRA and contrast-enhanced steady-state CMRA, respectively . 30 vessels (8%) were not assessable on both CMRA methods due to pronounced susceptibility artifacts or congenital or postoperative absence of vessel structures. The overall image quality score was slightly higher for REACT CMRA compared to steady-state CMRA  Fig. A. The imMeasurements of vessel diameter were performed for 285 landmarks by each reader . 39 landmarks (12%) could not be assessed on both CMRA due to severe artifacts or aberrant cardiovascular anatomy. Vessel diameter measurements strongly correlated between both CMRA techniques and showed close intermethod agreement . All of them were related to surgical or interventional material. Fat-water swapping artifacts occurred more frequently on REACT CMRA than on contrast-enhanced CMRA . They were predominantly observed within the pulmonary veins . However, compensation for fat-water swapping was possible in all cases by reconstruction of in-phase and out-of-phase images , both CMRA sequences showed stable vascular conditions in most patients . Both CMRA techniques detected stable moderate proximal pulmonary artery stenosis in 7 of these 32 patients (22%). Eleven of these 32 patients (34%) showed stable aorto-pulmonary collaterals on both CMRA methods , there was no difference in final diagnosis between the two CMRA techniques. However, visualization of a partial anomalous pulmonary venous connection was limited in one patient on REACT CMRA compared to contrast-enhanced CMRA. In another patient a partial anomalous pulmonary venous connection could be excluded with both CMRA methods. Two patients with known CHD who were primarily referred for evaluation of progressive heart failure, did not present relevant vascular abnormalities on both CMRA methods.In 3/36 patients 8%), the main pulmonary arteries could not be evaluated on REACT CMRA due to distinct flow artifacts caused by severe pulmonal insufficiency . However, in one patient stenosis of a right ventricular outflow tract graft was more clearly assessable on REACT CMRA compared to contrast-enhanced CMRA  with complex CHD, compared to contrast-enhanced steady-state CMRA. Improved image quality at the ascending aorta including the proximal coronary arteries and at the inferior vena cava underline that native REACT CMRA can be implemented for clinical use in CHD.Due to the ongoing debate on CMR contrast deposit in the human body, efforts to reduce the use of gadolinium contrast media have been intensified over the recent years. So far there is no standard approach for gadolinium-free CMRA in children with complex CHD. To accurately assess vessel diameter and clearly visualize even small vessels and vascular connections in CHD, high spatial resolution cardiac and respiratory gated CMRA is often complementary performed to time resolved multiphase CMRA . HoweverREACT-CMRA provided accurate and reliable measurements of vessel diameter comparable to contrast-enhanced CMRA. Although there was a small difference between both methods in the vessel diameter of the inferior pulmonary veins , the difference was still within an acceptable range. The overall image quality score of REACT CMRA was comparable to contrast-enhanced CMRA. Major benefits in image quality were achieved at the ascending aorta including the proximal coronary arteries and at the inferior vena cava.Excellent diagnostic quality of the ascending aorta on non-contrast REACT CMRA allowed for accurate detection of aortic ectasia at pre- or postsurgical follow-up (two patients). Because of the high prevalence in CHD, concomitant assessment of aberrant coronary anatomy is of particular value . In clinThe slightly impaired image quality for the pulmonary arteries and the intermediate image quality for the pulmonary veins were mainly contributed to artifacts caused by high and turbulent pulmonary flow . However, clinically relevant abnormalities such as dilatation or stenosis of the pulmonary arteries were adequately assessed compared to contrast-enhanced CMRA. Turbulent flow effects occurred particularly in highly pulsatile circulations like in patients with repaired tetralogy of Fallot. It is known from previous whole heart imaging studies that these effects can be reduced or even compensated by data acquisition in different cardiac phases . Our resAs most patients in our cohort were referred for pre- or postsurgical follow-up with known CHD, most findings of vascular abnormalities were stable. However, all additional vascular findings diagnosed with contrast-enhanced CMRA could also be visualized with REACT-CMRA . There was no difference in the detection of aorto-pulmonary collateral arteries or signs of venous collateralization between both CMRA techniques. In two patients (6%) the use of REACT CMRA was beneficial compared to contrast-enhanced CMRA . However, in three patients (8%) with severe pulmonary insufficiency, the main pulmonary arteries could not be adequately assessed on REACT CMRA because of distinct flow artifacts. In one patient (3%) a partial anomalous pulmonary venous connection was better depicted on contrast-enhanced CMRA.CMR is particularly well suited for contrast reduction because it is usually based on double dose contrast administration owing to LGE imaging. The assessment of disease- or surgery-related myocardial fibrosis by LGE imaging may improve risk stratification, especially in grown-up patients with CHD –35. As tOur study has several limitations. The number of patients in the current study is relatively small. However, a wide range of complex CHD types with postoperative conditions were included, suggesting applicability in pre- and postoperative follow-up. Nevertheless, studies with larger patient cohorts are needed to provide subgroup analyses of different age groups and CHD types to further standardize the approach in different clinical settings. There might be an observer bias, as readers could not be blinded to the CMRA techniques for qualitative and quantitative analyses. In this study, only morphological vascular findings could be assessed with REACT and single-phase contrast-enhanced CMRA, but not functional findings detectable with cine and flow imaging or time-resolved CMRA. Signal and contrast to noise analysis were not performed due to different acceleration factors. Furthermore, comparison of REACT CMRA to other non-contrast techniques such as bSSFP-based or Quiescent-Interval Single Shot (QISS) CMRA was beyond the scope of this study. However, bSSFP CMRA is generally limited at 3T due to predominant off-resonance artifacts caused by field inhomogeneity.In conclusion, non-contrast REACT CMRA provides high image quality, accurate vascular measurements, and equivalent diagnostic certainty compared to high-resolution contrast-enhanced steady-state CMRA in a challenging cohort of young children with complex CHD. As part of a standard CMR protocol, REACT CMRA can enable gadolinium-free examinations without compromises in diagnostic quality for children with CHD undergoing pre- or postsurgical follow-up.


Left ventricular myocardial work (MW) assessed by echocardiography has recently been introduced as a new index of global and regional myocardial performance. The presence of microvascular obstruction after revascularization in ST-segment elevation myocardial infarction (STEMI) patients predicts poor clinical outcomes. This study aimed to explore the usefulness of MW in identifying impaired microvascular perfusion (MVP) in the patients with STEMI after revascularization.One hundred and sixty STEMI patients who underwent myocardial contrast echocardiography (MCE) within 48 h after percutaneous coronary intervention (PCI) were included. Patients were divided into normal MVP and impaired MVP groups according to the myocardial perfusion score. The clinical data, coronary angiography results and echocardiographic data including Global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE) were collected.P = 0.004), final TIMI flow ≤ 2 , left ventricular end-diastolic volume index (LVEDVi) , and GWI  were independently associated with impaired MVP. GWI showed a good sensitivity (86.8%) but low specificity (53.7%) in identifying impaired MVP . Combination with GWI can improve the diagnostic value of TNI or LVEVi for impaired MVP.Impaired MVP was found in 60% of patients. Compared with the normal MVP group, GWI (909.2 ± 287.6 mmHg% vs. 1191.2 ± 378.2 mmHg%), GCW (1198.3 ± 339.6 mmHg% vs. 1525.9 ± 420.5 mmHg%), GWE (82.7 ± 7.8% vs. 86.8 ± 5.6%) and GLS (− 11.0 ± 3.4% vs. − 14.4 ± 3.8%) were significantly reduced in the impaired MVP group. Whereas there was no statistically significant difference in left ventricular ejection fraction (LVEF) and GWW, multivariate logistic regression analysis showed that peak troponin I (OR 1.017, 95% CI 1.006–1.029; Impaired MVP is relatively common in STEMI patients after revascularization and independently associated with left ventricular GWI assessed by echocardiography. GWI confer incremental value to MVP assessment in STEMI patients. Acute myocardial infarction, especially ST-segment elevation myocardial infarction (STEMI), has always occupied the primary position in cardiovascular disease due to its acute onset and high mortality. Percutaneous coronary intervention (PCI) is the main therapeutic strategy to improve the prognosis . HoweverMyocardial contrast echocardiography (MCE) is a noninvasive and convenient technique using echocardiography combined with ultrasound microbubbles, which allow a real time evaluation of local MVP by bedside , 5. NoniPatients admitted with acute STEMI who had completed MCE examination within 48 h after PCI from June 2016 to January 2022 in our hospital were enrolled in this study. Demographic information, medical history, and details of clinical data were obtained from medical records and retrospectively analyzed. Patients younger than 18 years of age or combined with known congenital heart disease, significant valvular heart disease, valve prosthesis, paced rhythm or significant variation in R-R intervals, those who had poor image quality or missing blood pressure measurements, did not provide informed consent, or were allergic to sulfur hexafluoride (SonoVue) were excluded from the study. This study was approved by the local Ethics Committee and the informed consent was obtained from all subjects.Transthoracic echocardiographic (TTE) examinations were performed in all subjects with an M5S 3.5-MHz transducer . Patients were scanned in the left lateral decubitus position with synchronous ECG monitoring. Blood pressure was measured at the beginning of the echo exam. Standard two-dimensional echocardiography with Doppler examination was performed and measurements were obtained according to the guidelines of the American Society of Echocardiography  at admission when compared with those in normal MVP group. As for angiographic data, the rate of three-vessel disease was lower  but the incidence of intraoperative slow flow/no reflow  was significantly higher in impaired MVP group. The culprit artery in the impaired MVP group was frequently LAD but the rate of RCA as the culprit artery was higher in the normal MVP group (both P < 0.001).The clinical characteristics including angiographic data at admission and differences between the normal and impaired MVP group were summarized in Table 2 vs. 54.1 ± 15.6 ml/m2; P = 0.006) and lower SBP  prior to echo examination. GLS was significantly reduced in the impaired MVP group , but there was no difference in LVEF between the two groups. Significant differences were observed in GWI, GCW and GWE between the two groups. The patients with impaired MVP had much lower values in the above indices .The echocardiographic characteristics and the global values of LVMW indices between the two groups were illustrated in Table P < 0.2 in the univariate analysis were subsequently entered into multivariate model. Only incomplete revascularization , peak TNI , LVEDVi  and GWI  were independent predictors of impaired MVP.Logistic regression analysis was performed to identify predictors of impaired MVP Table . In the P < 0.001]. Combination of GWI can increase the diagnostic value of TNI (AUC increased from 0.643 to 0.755) and LVEDVi (AUC increased from 0.633 to 0.712) for impaired MVP . Systolic blood pressure was significantly reduced in impaired MVP group either at admission or at echo examination. As for echocardiographic data, left ventricular volume was significantly increased and GLS was decreased in the patients with impaired MVP, but LVEF showed no difference between the two groups. In addition, LVMW indices including GWI, GCW and GWE were significantly reduced, suggesting an early LV remodeling and myocardial dysfunction in CMD.There are many tools to assess microvascular function including coronary flow reserve, fractional flow reserve and index of microcirculatory resistance using invasive angiographic method, echocardiography or cardiac magnetic resonance , 14, 15.Currently, LVEF is still the most important indicator of heart function. However, LVEF measurement has great variability due to a variety of influencing factors , 7 and cNoninvasive LVMW seems to be a potentially valuable method to detect early and subtle myocardial dysfunction, which was first introduced by Russell et al.  using brSince LVMW assessed by echocardiography can identify early myocardial dysfunction and detect impaired MVP in STEMI patients, this non-invasive, safe and easy-to-operate tool should be promoted more widely in clinical practice.This study has several limitations. (1) This was a retrospective single-center study. (2) The study population was still insufficient, further research with a larger sample size is needed in the future. (3) Follow-up clinical and echocardiographic data should be collected to further investigate the influences of LVMW on prognosis. (4) We did not explore the effects of different coronary lesion location and severity on MW indices. More patients need to be enrolled and further studies should be done to clarify this point. (5) MCE is still not a well validated method to assess CMD, and further comparative study with MRI is needed.In conclusion, the present study had shown that the incidence of impaired MVP is relatively high after revascularization in STEMI patients. LVMW is a potential tool to detect microvascular dysfunction and early myocardial performance impairment.


Tricuspid regurgitation (TR) is a common finding in patients with end stage heart failure referred for implantation of left ventricular assist devices. While functional TR frequently resolves after left ventricular unloading, patients with residual and progressive TR demonstrate increased rates of RV dysfunction and poor survival. Criteria for intervention on the tricuspid valve have focused on the degree of tricuspid annular dilatation and the severity of tricuspid regurgitant volume. The surgical decision making regarding intervention on the tricuspid valve remains obscure and historical cohort data cannot distinguish cause from effect. Even if the degree of regurgitation is determined, the clinical significance and optimal therapeutic intervention  remain difficult to determine, primarily because tricuspid regurgitation is most often secondary to, or accompanied by, another disease process. The relative contribution of the regurgitant blood flow to the clinical situation may be difficult to assess in the face of right ventricular failure or elevated pulmonary arterial pressure.” .“The role of surgical intervention in the pathophysiology of functional tricuspid regurgitation (TR) is obscure. While moderate to severe tricuspid regurgitation is associated with high mortality , indicatTricuspid regurgitation secondary to left sided heart failure is a consequence of RV dilatation , caudal displacement of the anterior papillary muscle, leaflet tethering, and valvular deformation. While there is minimal annular dilatation early in the natural history of the pressure loaded right ventricle, increasing right ventricular (RV) diastolic volume worsens the coaptation defect as the tricuspid annulus dilates along the anterolateral axis. Progressive interventricular septal shift toward the left ventricle increases LV diastolic pressure with increased RV afterload and “TR begets more TR.” Chronic volume overload results in right ventricular remodeling, variously defined by the changes in ventricular geometry and compliance which describe RV dysfunction.Despite the reduction in RV pressure overload that accompanies implantation of a left ventricular assist device, residual TR can persist. Fixed pulmonary vascular resistance, residual mitral regurgitation, and inadequate decompression of the left ventricle  can all contribute to right sided atrioventricular incompetence. Acute unloading of the dilated LV causes a leftward shit of the interventricular septum, decreasing the septal contribution to RV contraction and altering RV geometry with exacerbation of antero-septal tricuspid leaflet tethering. Early RV failure after LVAD is defined by an inability to separate from cardiopulmonary bypass  and is likely a distinct physiology from the progressive RV failure seen in postoperative LVAD patients. Tricuspid regurgitation is common to the distorted geometry of both acute and chronic RV failure after LVAD implantation.p = 0.033) among patients with residual TR and from 38.7 to 41.1 mm (p = 0.017) among patients without residual TR. Most importantly, multivariate logistic regression identified residual MR as the most significant predictor of residual TR (OR 4.5).Nakanishi et al.  examinedIn an analysis of the EUROMACS database, Veen et al.  observedIn a single institution study, Zadok et al.  found thConfounding is the situation in which the epidemiologic difference in the risk of the outcome between exposed  and unexposed (no tricuspid surgery) can be explained by other differences in the contrasted groups  is preferentially prescribed to groups of patients based on their underlying risk profile . Consequently, patients exposed or not exposed to intervention might not be comparable, precluding any causal inference between tricuspid valve repair and outcome. This is selection bias, best described as a potential fundamental difference among the patients in the treatment arm (tricuspid intervention) due to the way in which patients were allocated to the treatment group.d groups . The vasd groups –15. Thermisclassification bias in the published observational studies. Significant TR can—and frequently does—resolve after isolated LVAD implantation. Tricuspid valve repair in a patient with significant preoperative TR that would have resolved after isolated left ventricular unloading is misclassified as the tricuspid intervention is redundant, valvular intervention did not impact TR. Differential misclassification bias skews the data toward the null hypothesis , making historical cohort studies an unlikely source of information for surgical decision making.Far more important is the question of Another confounder is the relationship between tricuspid regurgitation and RV failure. Significant tricuspid regurgitation is well-tolerated in LVAD patients without RV dysfunction  and RV dP = 0.026). Despite significantly less moderate to severe TR immediately after surgery in the tricuspid intervention group, differences in the probability of TR disappeared during the follow up period suggesting that concomitant TV surgery is not associated with improved clinical outcome.Propensity scoring, wherein the likelihood of being exposed to the intervention  is used to match patients can account for confounding. Veen et al.  in an exn = 28) or LVAD implantation with concomitant tricuspid valve surgery . At 6 months there was no difference in the incidence of moderate or severe right heart failure (46% in the LVAD only group and 44% in the group with LVAD and concomitant tricuspid intervention).To avoid the confounding relationship between TR and ventricular function, the TVVAD trial (NCT03775759) stratified patients by pre-operative right ventricular dysfunction (none/mild vs. moderate vs. severe) at the time of randomization. Sixty patients with moderate or severe TR on pre-operative echocardiography were randomized to either LVAD implantation alone  and late right heart failure . However2, and need for inotropic support at 6 months), higher mean pulmonary artery pressures, and elevated pulmonary capillary wedge pressure  .Given the high incidence of recurrent TR after annuloplasty, is repair the wrong approach? Would valve replacement alter the mechanics of RV dysfunction and subsequent RV failure? AICD leads and biventricular pacing wires are nearly ubiquitous in the end stage heart population and “pinning” of tricuspid leaflets by trans-annular EP device leads is a common observation (25% in our patient population). Annuloplasty is unlikely to significantly impact the tethered leaflet. Is reduction annuloplasty with a flexible band or remodeling annuloplasty with a rigid ring relevant to the conversation regarding concomitant surgery and TV repair? Does annuloplasty ring size impact durability and ventricular pathophysiology, or does a “one size 28 mm reduction annuloplasty fit all”? Given the importance of RV geometry and the impact of pump speed on septal and posterior leaflet displacement, is preservation of the pericardium and passive ventricular constraint more important than preservation of annular dimensions? Many of us embrace the reduction in RV failure seen with the thoracotomy approach as more than case selection bias . Are theSurgeons looking to the aggregate data of historical population studies for surgical decision making will be frustrated by differences in study design, variable definitions and descriptions of RV dysfunction, and most significantly by the remarkable complexity of right ventricular failure. Despite enormous amounts of data, there is little information, and even less knowledge as to the “correct” surgical decision. What is clear is that no “once size fits all” approach to TR at the time of LVAD implantation will be effective therapy for all patients. While there may be patients who would benefit from TV procedures at the time of LVAD implant, defining a population cohort for whom evidence based data can recommend intervention seems unlikely given the dynamic complexity of functional TR. It is more likely that biomarker and functional imaging data will define a patient cohort in which TV intervention is ill advised and unlikely to contribute to reverse remodeling. As noted by McGee , effectiThe author confirms being the sole contributor of this work and has approved it for publication.The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.


Background and aim: The left atrium contributes significantly to the left ventricular filling as it functions as a reservoir, conduit, and pump. These functions are referred to as the phasic function of the left atrium and they are assessed using left atrial volumes. The left atrial function index on the other hand is a rhythmic independent composite index which is a better marker of left atrial function. The study therefore aimed at comparing left atrial function  among hypertensive heart failure patients, patients with hypertension but not in heart failure, and normotensive patients.p < 0.05.Method: The study was a cross-sectional analytical study that was carried out at Delta State University Teaching Hospital, Nigeria. A total of 80 hypertensive heart failure patients, 80 hypertensive, and 40 normotensive patients who met the inclusion criteria were recruited from the cardiology clinics using the convenience sampling method. The left atrial function index was determined using the volumetric method. Significance was assessed at p = 0.001) of the hypertensive heart failure group was significantly lowest when compared with the hypertensive (p < 0.001) and normotensive (p < 0.001) groups. Although the left atrial function index of the hypertensive group (42.28 ± 10.40) was lower than the normotensive group (50.47 ± 14.37), it was however not found to be significant (p = 0.12). Also, the left atrial function index was significantly (p = 0.001) worse among the patients with heart failure with reduced ejection fraction (13.5 ± 5.94) compared to heart failure with preserved ejection fraction (40.81 ± 12.12).Result: The left atrial function index (21.13 ± 8.83 versus 42.28 ± 10.40 versus 50.47 ± 14.37, Conclusion: Left atrial function index was lowest among hypertensive heart failure patients compared with hypertensive and normotensive cohorts, and it was worse among heart failure with reduced ejection fraction patients. However, there was no significant difference between the left atrial function index of the hypertensive and normotensive groups. As a result, we recommend that the left atrial function index should be incorporated into the routine echocardiographic assessment of patients in our day-to-day clinical practice and large studies should be carried out to determine the cut-off value for the left atrial function. In heart failure (HF), left atrium (LA) dysfunction is a mediator of impaired cardiac dynamics, and its structural and functional changes have different clinical implications ,2. The dThe LA serves as a reservoir, conduit, and pump and it exerts a profound effect on left ventricular (LV) filling and overall cardiovascular function . These rIn Africa, some efforts have been made to assess LA function using phasic LA volumes. However, studies on LA function using LAFI are lacking even though it better represents a marker of pathological LA remodeling when compared to LA phasic volumes . In addiThe study was a comparative, cross-sectional, and analytical study carried out at Delta State University Teaching Hospital (DELSUTH), Oghara, Delta State, Nigeria, between June 2020 and June 2021.2), chronic obstructive pulmonary disease, valvular heart disease, diabetic mellitus, retroviral disease), or cancer and autoimmune disorders  were excluded.The study population includes 80 patients who presented consecutively to the cardiology outpatient clinic for HHF (group 1), and this was age- and sex-matched with the hypertensive patient without HF (group 2), and normotensive patient (group 3). The inclusion criteria for the group 1 population were patients that are 18 years old and above who gave consent, irrespective of their left ventricular ejection fraction (LVEF), functional class, and whether they presented with acute or chronic HF. For group 2, inclusion criteria include those that are 18 years old and above who gave consent, irrespective of their blood pressure (BP) duration and control. The inclusion criteria for group 3 include healthy individuals aged 18 years or above who gave consent and are without any known medical or cardiovascular disease. For all the groups, those with suboptimal echocardiographic images , atrial fibrillation, atrial flutter, who refused or are unable to give consent, comorbidities . Informed consent was obtained from participants and was duly signed/thumb-printed before they were recruited for the study. Confidentiality and the right to exit from the study at any time were maintained.A semi-structured interviewer-administered questionnaire was used to obtain and record information on biodata, medical history, electrocardiography, and echocardiography. A transthoracic echocardiogram  with electrocardiography (ECG) gating was performed by the researcher at the time of recruiting patients.LA function was assessed by the LAFI. To assess the LA function by the volumetric method, LA volumes were measured at different time points of the cardiac cycle: maximal LA volume (LAVmax) at the end of the T-wave on ECG, just before the opening of the mitral valve; minimal LA volume (LAVmin) at beginning of QRS-complex, just at the closure of the mitral valve; and preceding LA contraction volume (LAVpreA) at the beginning of P-wave . The velLAFI = (LA emptying fraction x LVOT-VTI)/LAESV indexed to BSAwhere;LAFI = left atrial function indexLVOT-VTI = velocity time integral of the left ventricular outflow tract (cm),LAESV = maximal left atrial volume in end-systole (cc)2)BSA = body surface area (ml/mLA emptying fraction = (LAESV-LAEDV)/LAESVLA conduit function: the LA conduit function was assessed as follows:LA passive emptying volume = LA maximum volume-LA pre ‘A’ wave volume;LA passive emptying fraction = passive emptying volume/LA maximum volume x 100%;p < 0.05.Data was collated and analyzed with Statistical Product and Service Solutions (SPSS)  . The queBaseline characteristics of study participantsAmong the three groups, the hypertensive individuals had significantly higher weight  and BMI  but the waist circumference  and waist-hip ratio  were not statistically significantly different. The pulse rate  was significantly higher among the HHF patients. However, the systolic blood pressure , diastolic blood pressure , pulse pressure , and mean arterial pressure  were significantly higher among the hypertensive group. Table LAFI of study participantsLAFI  was significantly lower among the HHF group compared to the other groups. Left atrial total emptying volume (LAtEV)  and left atrial total emptying fraction (LatEF)  were significantly lower among the HHF group. Although the left atrial passive emptying volume (LApEV)  was not significantly lower among the three groups of patients, left atrial passive emptying fraction (LApEF)  and LA conduit volume (LA CV)  were significantly lower among the HHF. The left atrial active emptying volume (LAaEV)  and left atrial active emptying fraction (LAaEF)  were significantly lower among the HHF compared to the other groups. Table Post hoc analysis of LAFI among study participantsFigure LAFI of HHF based on LVEFThe LAFI was significantly lower among the HF with reduced ejection fraction (HFrEF) group compared to the HFpEF . Among HHF patients, the LA reservoir function of HFrEF was significantly lower compared to HFpEF . The LA conduit function was found to be lower among the HFrEF compared to HFpEF  but these findings were not significant. The LAaEV  and LAaEF  were significantly lower among the HFrEF compared to HFpEF. Table In our study, the LAFI of HHF and hypertensive patients differ significantly, being worse in HHF patients. The hypertensive group had lower LAFI compared to the normotensive group, but this finding was not of statistical significance. The reduced level of LAFI among HHF may be attributed to progressive LA dilation, poor LA contractile function, and impaired atrial compliance which occurs as hypertensive patients progressively develop hypertensive heart disease. In other words, HF symptoms develop among hypertensive individuals when the LA losses its compensatory mechanism and becomes dysfunctional leading to pulmonary congestion. The Framingham offspring study  reportedA Chinese study  that evaAnother study  stated tLimitation of studyTransthoracic echocardiography was used for the assessment of left atrial function instead of transoesophageal echocardiography which better assesses left atrial function.There were limited funds for carrying out specific tests to rule cofounders and as such results were retrospectively obtained from patients' case notes.The LAFI is inversely related to hypertensive heart disease categories making it an excellent tool for assessing individuals with HHF. We recommended that LAFI should be incorporated into the routine assessment of patients in our day-to-day clinical practice. We also propose that large prospective studies on LAFI should be carried out to determine partition value for the assessment of left atrial function and HF prognostication.


The change in right-ventricular function (RVF) after transcatheter mitral valve repair is still poorly understood. We assessed the early response of RVF to the MitraClip procedure and its clinical relevance.We analyzed consecutive patients who underwent a MitraClip procedure to treat MR between August 2010 and March 2019 in the Heart Failure Network Rhineland registry. RVF was assessed before and after the procedure. Impaired RVF was defined as an RV fractional area change (RVFAC) < 35% or tricuspid annular plane systolic excursion (TAPSE) < 16 mm.n = 274), normalized in 17% (n = 140), deteriorated in 15% (n = 125), and was persistently impaired in 34% (n = 277) of patients. The RVF response was significantly associated with a composite outcome of all-cause mortality and hospitalization due to heart failure within a 2-year follow-up. Compared to stable/normal RVF, the adjusted hazard ratios for the outcome were 1.78 (95% CI 1.10–2.86) for normalized RVF, 1.89 (95% CI 1.34–3.15) for deteriorated RVF, and 2.25 (95% CI 1.47–3.44) for persistently impaired RVF. Changes in TAPSE and RVFAC as continuous variables were significantly correlated with the outcome.816 eligible patients  were included in the analysis. Baseline values of RVF were: RVFAC 38.6 (IQR 29.7–46.7) % and TAPSE 17.0 (IQR 14.0–21.0) mm. At a median time of 3 (IQR 2–5) days after the procedure, the RVF remained normal in 34% (An early change in RVF following transcatheter mitral valve repair is predictive of mortality and hospitalization due to heart failure during follow-up.Early response of RVF after MitraClip and its clinical significance. An acute, early change in RVF can be observed following the MitraClip procedure, which is associated with the risk of mortality and hospitalization for HF.The online version contains supplementary material available at 10.1007/s00392-021-01951-7. Mitral regurgitation (MR) is the most common valvular heart disease , which iTreating MR may promote RV unloading and eventually recovery of function, with a potential prognostic benefit. Transcatheter edge-to-edge mitral valve repair using the MitraClip system is a less invasive therapeutic option for patients with MR who are at a high risk of surgical complications . BecauseWe conducted a retrospective analysis of data from the Heart Failure Network Rhineland registry—a multicenter, prospective, consecutive database that includes information for patients treated at university hospitals in Bonn, Cologne, and Duesseldorf . We reviThis study was approved by the ethics committees of the individual centers and was conducted in accordance with the Declaration of Helsinki. All patients provided written informed consent to participate in the registry.Echocardiographic assessments were performed in accordance with current guidelines , 7. All The primary outcome was a composite of all-cause mortality and hospitalization due to HF within 2 years. Outcomes were prospectively assessed during scheduled hospital visits or via telephone interviews with the patients’ general practitioners and families.t tests or Wilcoxon signed-rank tests.Categorical variables are reported as percentages and were compared using Fisher’s exact tests. Continuous variables are reported as the mean ± standard deviation (SD) or as medians and interquartile ranges (IQRs), as appropriate. Analyses of variance (ANOVAs) were used to compare continuous variables across groups. Changes in RVF before and after MitraClip (within a few days) were assessed using paired The Kaplan–Meier method was used to generate event-free survival curves according to an acute response of RVF. The unadjusted and adjusted Cox proportional hazard models were conducted to estimate the association of the RVF response with outcomes , 9. The To examine the robustness of our inference, we performed several sensitivity analyses. Cox proportional hazard models were conducted to determine the clinical relevance of the changes in TAPSE (model 1) and in RVFAC (model 2). The models were adjusted for the aforementioned variables and baseline RVF. In addition, we performed a landmark-analysis during two periods, from discharge to 3 months and from 3 months to 2 years. Finally, associations between the response of RVF and clinical outcomes were assessed separately, according to MR etiology or residual MR.p values < 0.05 were considered statistically significant. All statistical analyses were performed using EZR version 1.37  and SPSS Statistics version 25.0 .Two-tailed Baseline and postprocedural RVF data were available for 816 patients during the study period , while there was no significant change in TAPSE . Patients were divided into groups according to their change in RVF. Among the study population, after the procedure, 274 (34%) patients showed stable/normal RVF, 140 (17%) patients showed normalization of RVF, 125 patients (15%) exhibited deterioration of RVF, while 277 (34%) patients exhibited persistently impaired RVF  days after the procedure. Overall, RVFAC increased significantly . As compared to patients with stable/normal or normalized RVF, patients with deteriorated RVF or persistently impaired RVF showed slightly higher pulmonary arterial pressure (p = 0.02) and more severe TR (p < 0.001) after the procedure. Changes in the main echocardiographic variables are depicted in Fig. r = 0.14, p < 0.001). However, there was no significant difference with regard to a reduction in systolic pulmonary arterial pressure among the groups, and the LV ejection fraction tended to decrease in patients with deteriorated RVF.The echocardiographic parameters following MitraClip are summarized in Supplemental Table 1. A reduction in MR was consistently observed among the groups (e p = 0.0 and morep = 0.001). In addition, patients with normalized RVF had a numerically lower incidence of the primary endpoint than patients with persistently impaired RVF , although the difference did not reach statistical significance at the 2-year follow-up. Similarly, the incidence of all-cause mortality , 149 patients had died and 114 patients had been hospitalized due to HF. This means that in total 230 patients (28.2%) experienced the predefined primary endpoint within 2 years after MitraClip. The incidence of the primary outcome differed significantly according to the RVF response  for normalized RVF, 2.14 (1.38–3.31) for deteriorated RVF, and 2.66 (1.87–3.77) for persistently impaired RVF, all with a Multivariable models were calculated using the change in TAPSE and that in RVFAC, as shown in Table We also evaluated the primary outcome during two distinct time periods, from discharge to 3 months and from 3 months to 2 years  .This is the first study assessing the response of RVF in the acute phase following the MitraClip procedure and its clinical implications for patients with MR. The main findings can be summarized as follows:Impairment of RVF often coincides with MR because of pulmonary hypertension and increased RV afterload. Decreases in MR can reduce the volume overload of the LA and LV, thereby decreasing RV afterload . PreviouWe found that 17% of patients showed a normalization of RVF after MitraClip. Conversely, 15% of the study population showed an acute deterioration of RVF. Such early variation of RVF is novel but consistent with a prior study showing that 20% of patients undergoing MitraClip showed worsening RVF over a median of 4.9-months follow-up . Such de]. Our results could contribute to a reconciliation of these conflicting data.Impairment of RVF has been shown to be associated with unfavorable outcomes in the setting of HF. However, conflicting data exist for transcatheter edge-to-edge mitral valve repair , 19. Kan 18]. In the current study, acute increases in TAPSE or RVFAC were correlated with a lower risk of the composite outcome at 2 years. Nevertheless, patients with normalized RVF still had a worse outcome compared to patients with stable/normal RVF at 2 years. The worse clinical prognosis of patients with acute normalized RVF after MitraClip might be explained by having more highly impaired kidney function, a higher prevalence of coronary artery disease, and a lower LV ejection fraction. Our findings suggest that baseline comorbidities could attenuate the benefits of RVF improvement over the long-term follow-up.Unloading the RV may promote RV recovery, with a potential prognostic benefit . In the Rapid worsening of RVF was also found to be detrimental. Acute changes in TAPSE or RVFAC were negatively associated with the risk of outcomes by a Cox regression analysis, independent of baseline RVF. Our findings not only highlight that we should focus on patients who could be at a higher risk for adverse outcomes but also imply that certain adjunctive therapies after transcatheter edge-to-edge mitral valve repair could be beneficial. Closure of the iASD has been linked to reducing the right-heart volume overload , 21. YetNot surprisingly, persistently impaired RVF was associated with the worst outcome. In this subgroup, the RVF impairment may be the consequence of long-lasting RV afterload. Thus, it could be representative of the ‘epiphenomenon’ of intrinsic myocardial damage . TherefoSeveral limitations have to be considered when interpreting our findings. The present study was retrospective in nature, which may have introduced a selection bias. Furthermore, although the present cohort of patients undergoing MitraClip with the assessment of RVF is the largest study of its kind so far, the sample size is still limited. Therefore, the correlation of the primary outcome with RVF response may not have been fully adjusted. Nevertheless, the associations we found were significant across several sensitivity analyses.Following transcatheter edge-to-edge mitral valve repair, there can be an acute change in RVF, even after a few days. In this study, the early RVF response was associated with the primary composite outcome of all-cause mortality and hospitalization due to HF. Our findings highlight that RVF should be carefully assessed shortly after transcatheter edge-to-edge mitral valve repair, as well as left-side heart function and MR. Strategies to improve post-procedural hemodynamics need to be explored further.Supplementary file1 (DOCX 18 KB)Supplementary file2 (DOCX 16 KB)Supplementary file3 (DOCX 17 KB)Supplementary file4 Supplemental Figure 1. Subgroup analyses stratified by MR etiology and LV ejection fraction. Shown are Kaplan–Meier curves according to the etiolgy of MR and LV ejection fraction. An association of the RVF response with the primary outcome was consistently observed in patients with (A) primary MR and (B) secondary MR or patients with LV ejection fraction across the subgroups by MR etiology or by (C) LV ejection fraction ≥50% and (D) <50%. Abbreviations: LV, left ventricular; MR, mitral regurgitation; RVF, right-ventricular function (PDF 154 KB)Supplementary file5 (XLSX 2989 KB)Below is the link to the electronic supplementary material.


This guideline recommended patients with heart failure with type 2 diabetes sodium‑glucose co-transporter‑2 inhibitors for the management of hyperglycemia and to reduce heart failure-related morbidity and mortality . It is important to note that the source of evidence based on this recommendation is from EMPEROR-Reduced, DAPA-HF, and DECLARE-TIMI 58 and does not include newly published PRESERVED-HF, CHIEF-HF, and EMPEROR-Preserved. Here we reviewed these important trials in order to provide more clinical references for patients with diabetes and heart failure, especially heart failure with preserved ejection fraction. Recently, the 2022 AHA/ACC/HFSA guideline for the management of heart failure was released . The 202Collectively, our current evidence mainly focuses on empagliflozin/dapagliflozin in the treatment of diabetes with heart failure with reduced ejection fraction  and empa