Invasive Hemodynamic Assessment Research Articles

Phenotyping and Hemodynamic Assessment in Cardiogenic Shock: From Physiology to Clinical Application.

There is growing interest in invasive hemodynamic assessment in cardiogenic shock, primarily due to the widespread adoption of mechanical circulatory support (MCS). Invasive hemodynamic assessment is central to two aspects of cardiogenic shock management: (1) the phenotyping of cardiogenic shock, and (2) the assessment of response to therapy. Phenotyping of cardiogenic shock serves to guide timely therapeutic intervention, and the assessment of hemodynamic response to therapy directs the escalation or de-escalation of therapy, including MCS. This review aims to discuss these two aspects of hemodynamic assessment in cardiogenic shock. Firstly, the physiologic underpinnings of a phenotyping schema, and the implication of the cardiogenic shock phenotype on the MCS strategy in cardiogenic shock will be discussed. Secondly, the concept of cardiac power output and 'effective' oxygen delivery will be discussed in relation to hemodynamic response to therapy in cardiogenic shock.

Non-invasive assessment of right ventricular function and pulmonary pressures in cardiogenic shock remains challenging: don't pack away the PAC just yet

Abstract Background Cardiogenic shock (CS) is associated with high levels of morbidity and mortality despite advances in treatment. Patients with right ventricle (RV) dysfunction have been shown to have poorer outcomes. It is suggested that invasive monitoring through pulmonary artery catheter (PAC) placement can assist in guiding management to improve survival, though they are associated with adverse events. Purpose This study assessed the utility of non-invasive, echocardiographic assessment of RV performance and pulmonary artery pressures (PAP) in patients with CS. Methods Consecutive patients admitted to a North American quaternary cardiac intensive care unit who had PAC placement were recruited into this study. Invasive haemodynamic assessment was followed by transthoracic echocardiography (TTE) performed by a critical care cardiologist, blinded to the invasive measurements. TTE images were later reported by a second cardiologist, blinded to the invasive measurements and the patient. Correlations between RV and pulmonary invasive and non-invasive parameters were evaluated using Pearson's correlation. Results Overall, 96 assessments of 60 patients were compared. Patients were predominantly male (73%), aged 58±14 years and SCAI stage C (55%) and D (22%) at the time of assessment. Invasive measurements of right heart and pulmonary function was possible in all patients. Mean RAP was 8.5±4.7 mmHg, systolic PAP 37.5±9.9 mmHg, diastolic PAP 18.1±6.5 mmHg, mean PAP 25.1±7.2 mmHg, pulmonary capillary wedge pressure (PCWP) 16.0±16.4 mmHg, pulmonary vascular resistance (PVR) 157±99dyn s cm–5, RV stroke work index (RVSWI) 7.0±3.9 g min/m2 and PAP index (PAPi) 2.9±4.2. When compared to non-invasive echocardiographic parameters, there was little correlation with invasive values (Table). RVSWI moderately correlated with peak tricuspid regurgitation (TR) velocity, tricuspid annular plane systolic excursion (TAPSE) and estimated systolic PAP; while peak TR velocity was mild-moderately correlated with PAP and PCWP. No single non-invasive parameter demonstrated strong prediction of invasive values. Conclusion Non-invasive assessment of right heart and pulmonary haemodynamic parameters is of limited validity when compared with invasive monitoring through PAC in patients with CS. PAC remains the most reliable method of assessing the RV haemodynamic profile in CS. Future studies should evaluate the clinical benefit of invasive haemodynamic monitoring in this population. Funding Acknowledgement Type of funding sources: None.

Development and validation of non-invasive endothelial shear stress (ESS) estimations of coronary artery haemodynamics using computational modelling

Abstract Background Vascular remodelling is influenced by various biomechanical forces such as endothelial shear stress (ESS) and is associated with development and progression of coronary artery disease (CAD). ESS is the parallel frictional force exerted by blood flow on the endothelial luminal surface of the arterial wall. While ESS may not be the only cause of atherosclerosis, it is postulated that low ESS creates a pro-atherogenic environment and high ESS is athero-protective. Computational fluid dynamics (CFD) is an engineering method used to analyse fluid flow and has been increasingly applied to simulate ESS in cardiovascular research. However, current CFD-derived ESS estimates have never been validated and can display significant variability between research groups. Purpose This study aims to provide a comparative analysis of coronary flow using in-silico modelling of coronary flow and particle image velocimetry (PIV). Methods A proximal left anterior descending (pLAD) coronary phantom model was constructed from a patient who had received same day cardiac computed tomography angiography (CTCA) and invasive coronary haemodynamic (Combowire XT) assessment. Patient-specific coronary flow data was applied to CFD boundary conditions and a mock circulatory loop. CFD was validated using PIV under steady flow in a 4-times-scaled model. Same plane velocity field and flow patterns (at mid-luminal of pLAD) from both in-silico and in-vivo data were compared and analysed. Results Mean velocity contours and magnitude were analysed from CFD and PIV. Patient specific average peak velocity obtained from invasive assessment was 0.21m/s. Patient-specific velocity average from CFD was 0.22m/s. The approximated magnitude difference is 4.7%. Both same-axial average cross-sectional velocity estimated by CFD-pLAD and PIV-pLAD are 0.087m/s. Velocity contours and flow patterns simulated in the CFD were also comparable with the PIV results. Conclusion Simulation data from CFD correlate well with experimental PIV results. This early data allows for a non-invasive approach to determine patient-specific coronary haemodynamics (such as velocity profiling and ESS) and form the basis of personalising cardiovascular risk. Insights from this work may aid future development of a novel tool that incorporates CFD-derived ESS estimates with patient-specific risk factors to better predict rapid CAD progression. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Cardiac Society of Australia and New Zealand Monash Institute of Medical Engineering

Brain-type natriuretic peptide levels and invasive hemodynamic parameters in dialysis dependent patients

BackgroundPulmonary hypertension (PH) is associated with increased mortality in patients with end-stage renal disease (ESRD). The prevalence of PH within ESRD as measured by right heart catheterization (RHC) is poorly described, and the correlation of BNP to pulmonary artery pressure (PAP) is unknown. MethodsThe renal transplant database at our center was used to identify adult ESRD patients from July 2013 to July 2015 who had a plasma BNP level measurement and invasive hemodynamic assessment by RHC within a 1-month period. Pulmonary hypertension was defined as a mean pulmonary artery pressure (PAP) ≥ 25 mmHg. Multivariate linear regression analysis was used to identify correlations between BNP and RHC parameters. To estimate the utility of BNP in the screening of PH, a receiver-operating characteristic (ROC) curve was generated. ResultsEighty-eight patients were included in the study of which 43 had PH. Compared to patients without PH, BNP was significantly higher within the PH cohort (1619 ± 2602 pg/ml vs. 352 ± 491 pg/ml). A statistically significant association (r [86] = 0.60, p<0.001) between plasma BNP and mean PAP was identified. ROC curve indicated an acceptable predictive value of BNP in PH with a c-statistic of 0.800 (95% CI 0.708 – 0.892). ConclusionsIn ESRD patients being considered for renal transplantation, PH is highly prevalent and BNP levels are elevated and significantly correlated with higher PAP. BNP may be a useful non-invasive marker of PH in these patients.

The role of serial right heart catheterization in risk stratification and management of pulmonary arterial hypertension

Introduction Pulmonary arterial hypertension (PAH) is characterized by elevated pulmonary arterial blood pressure secondary to increased pulmonary vascular resistance. Despite the advances in medical therapy, PAH continues to be a significant cause of morbidity and mortality. Areas covered Invasive hemodynamic assessment by performing a right heart catheterization (RHC) remains the gold standard to confirm the diagnosis and further management of PAH. The RHC also helps to determine the severity of RV dysfunction and can be used to test for pulmonary vasoreactivity. After diagnosis and initiation of therapy, many PAH centers continue to perform RHC at regular intervals to monitor for disease progression and alter management. In this review, we discuss the importance of risk stratification in PAH, the role of RHC in the evaluation and treatment of these patients and compare non-invasive risk assessment tools to that of RHC. Expert opinion RHC is useful for diagnosis of PAH, assessing the risk of mortality and morbidity, directing the escalation and de-escalation of therapy, and monitoring for disease progression. In the current era of improved non-invasive cardiac hemodynamic assessment, the role for routine follow-up serial RHC in patients with PAH needs to be reassessed in future studies. With the availability of non-invasive risk assessment tools such as REVEAL Lite 2, it may be reasonable to reconsider the role of annual or protocoled RHC, and instead, move to an “as needed” and individual basis.

Prolonged Asynchronous Left Ventricular Isovolumic Relaxation Constant in Ascending Compared to Descending Thoracic Aortic Stenosis for Chronic Early Left Ventricular Afterload and Late Left Ventricular Afterload Increase.

Background: In arterial hypertension, left ventricular relaxation is affected early on in relation to a chronic difference in peak left ventricular afterload with early development of HF. Objective: in ascending compares to descending thoracic aortic stenosis, resulting in chronic late and early LV afterload increase, to assess the left ventricular isovolumic relaxation pressure decay constant through regression analysis, a parameter of left ventricular relaxation on the 4th and 8th week period from invasive left ventricular pressure measurements. Methods: fourteen pigs underwent posterolateral thoracotomy for ascending aortic stenosis, resulting in chronic early left ventricular afterload increase (EL = 6], or descending thoracic aortic stenosis creating chronic late systolic left ventricular load (LL = 8]. Exponential regression with nonzero asymptote for τ assessment, with linear and nonlinear regression were performed on isovolumic relaxation pressure decay from the left ventricular invasive pressure measurements on 4th and 8th week. Two-way repeated measurement ANOVA, post-hoc Tukey test and linear regression were performed for statistical analysis. Results presented are mean ± SEM or median (quartiles], with significance is at p < 0.05. Results: The ascending aortic stenosis associated with prolonged biexponential asynchronous τ, compared to the descending thoracic aorta stenosis, resulted in data that were different at the 8th week in presence of respirations (interaction p < 0.05]. Monoexponential and linear τ were not different in either respiration being preserved or suspended transitionally and in preload reduction. Preload sensitive response of τ was found in ascending compared to descending thoracic aortic banding that reduced in EL and in LL it increased with load reduction (p < 0.05]. These results indicated that τ is not different in and between LV afterloading conditions in a chronic setting, although it indicates that myocardial ischemia is present and that it is greater in ascending aortic banding, compared to descending thoracic aorta banding at the 8th week. Conclusion: In different sequence of the left ventricular afterload, ventricular relaxation is affected early on, having in EL compared to LL prolonged biexponential asynchronous left ventricular relaxation constant, thus indicating the development left ventricular myocardial ischemia and different elastic recoil in an invasive left ventricular hemodynamic assessment.

The Fontan Circulation: From Ideal to Failing Hemodynamics and Drug Therapies for Optimization.

Fontan palliation results in a hemodynamically complex circulation with multisystem consequences, which in the long term adversely affect many body processes. Systemic venous hypertension, nonpulsatilelow-shear pulmonary blood flow, and low cardiac output are the 3 main characteristics of a Fontan circulation, leading to unavoidableslowly progressive failure. An appreciation of how the hemodynamics of a Fontan circulation change with time and relate to the various modes of Fontan circulatory failure is important. Accurate hemodynamic assessment aid this understanding and may permit early identification of potentially treatable drivers of decline. While no evidence-based or guideline-directed pharmacologic management strategy has been established in Fontan patients, understanding the hemodynamics of Fontan circulation failure will assist in the rational selection of potentially helpful drug therapies for individual patients. In this review, we present hemodynamic concepts of the optimal Fontan physiology and Fontan circulatory failure, review practical aspects of invasive hemodynamic assessment, and discuss the role of drug therapies in increasing systemic venous blood flow return and decreasing ventricular filling pressures in Fontan circulation. Oftencomplementary to catheter-based or surgical interventions, pharmacologicmanagement aims at preserving patency of the circuit, adequate systolic and diastolic ventricular function, atrioventricular valve function, an unobstructed ventricular outflow tract, and pulmonary vascular integrity in order to maintain an acceptable cardiac output.

Early Real-World Experience Performing Invasive Hemodynamic Assessment of the Coronary Microvasculature

Early Real-World Experience Performing Invasive Hemodynamic Assessment of the Coronary Microvasculature

Invasive Cardiopulmonary Hemodynamic Assessment in Patients with Advanced Heart Failure: How to Interpret?

Invasive Cardiopulmonary Hemodynamic Assessment in Patients with Advanced Heart Failure: How to Interpret?

Dissecting the progression of cardiac dysfunction in tumor-bearing mice

Abstract Funding Acknowledgements Type of funding sources: None. Background Cancer patients undergoing heart-related complications result in high incidences of mortality. Nevertheless, it is still not fully understood whether localized tumors affect heart function prior to the onset of cachexia, hence, making the heart more vulnerable for functional abnormalities in later stages of the disease. In addition to analyse heart function, we focus on the expression BCL-2–associated athanogene 3 (BAG3), a co-chaperone protein and Hsp70, which are highly expressed in tumor but decrease in cardiomyocytes (CM) in heart failure (HF). Methods Colon-26 adenocarcinoma cells (C26; n=22) with/without shIL-6 (C26 shIL-6; n=22) were injected subcutaneously into the right flank of 10-11 weeks old BALB/c male mice. Control mice were injected with vehicle (PBS; n=8). Cardiac function was assessed by echocardiography and invasive hemodynamic measurements 10 (early) and 20 (late) days after the injection, respectively. In addition, the expression of BAG3 and Hsp70 were determined by Western blot as well as the extend of cardiac fibrosis was determined by Masson-Goldner's trichrome staining. Results The tumor size was comparable between the two injected groups. However, only C26 group showed a significant loss of subcutaneous fat and skeletal muscle (p&amp;lt;0.05, respectively), suggesting cachexia. Heart weight normalized to tibia length was not changed in the injected groups as compared to controls (day 20). However, left ventricular ejection fraction (LVEF) showed a tendency to decline in the early phase (p~0.08) in both injected group and it reached significance at late stage (p&amp;lt;0.05). Invasive hemodynamic assessment also confirmed the contractile dysfunction, resulting in a decrease in LV systolic pressure and increase of LV end-diastolic pressure (p&amp;lt;0.05, respectively). Importantly, these functional changes in the heart in tumor-bearing mice were associated with a marked reduction in both BAG3 and Hsp70 in the myocardium. Furthermore, there was no sign of cardiac fibrosis in the injected groups. Discussion Our study shows for the first time that tumor rather than cancer cachexia plays a significant maladaptive role in the progression of cardiac dysfunction in a mouse model of C26 injection-induced cachexia. The progression of cardiac contractile dysfunction was associated with a decline in BAG3 and Hsp70 in tumor-bearing mice, suggesting changes of BAG3/Hsp 70 signalling may be a critical component as well as target.

Invasive Hemodynamic Assessment and Procedural Success of Transcatheter Tricuspid Valve Repair-Important Factors for Right Ventricular Remodeling and Outcome.

IntroductionSevere tricuspid regurgitation (TR) is a common condition promoting right heart failure and is associated with a poor long-term prognosis. Transcatheter tricuspid valve repair (TTVR) emerged as a low-risk alternative to surgical repair techniques. However, patient selection remains controversial, particularly regarding the benefits of TTVR in patients with pulmonary hypertension (PH).AimWe aimed to investigate the impact of preprocedural invasive hemodynamic assessment and procedural success on right ventricular (RV) remodeling and outcome.MethodsAll patients undergoing TTVR with a TR reduction of ≥1 grade without precapillary or combined PH [mean pulmonary artery pressure (mPAP) ≥25 mmHg, mean pulmonary artery Wedge pressure ≤ 15 mmHg, pulmonary vascular resistance ≥3 Wood units] were assigned to the responder group. All patients with a TR reduction of ≥1 grade and precapillary or combined PH were classified as non-responders. Patients with a TR reduction ≥2 grade were directly classified as responders, and patients without TR reduction were directly assigned as non-responders.ResultsA total of 107 patients were enrolled, 75 were classified as responders and 32 as non-responders. We observed evidence of significant RV reverse remodeling in responders with a decrease in RV diameters (−2.9 mm, p = 0.001) at a mean follow-up of 229 days (±219 SD) after TTVR. RV function improved in responders [fractional area change (FAC) + 5.7%, p < 0.001, RV free wall strain +3.9%, p = 0.006], but interestingly further deteriorated in non-responders (FAC −4.5%, p = 0.003, RV free wall strain −3.9%, p = 0.007). Non-responders had more persistent symptoms than responders (NYHA ≥3, 72% vs. 11% at follow-up). Subsequently, non-response was associated with a poor long-term prognosis in terms of death, heart failure (HF) hospitalization, and re-intervention after 2 years (freedom of death, HF hospitalization, and reintervention at 2 years: 16% vs. 78%, log-rank: p < 0.001).ConclusionHemodynamic assessment before TTVR and procedural success are significant factors for patient prognosis. The hemodynamic profiling prior to intervention is an essential component in patient selection for TTVR. The window for edge-to-edge TTVR might be limited, but timely intervention is an important factor for a better outcome and successful right ventricular reverse remodeling.

Role of Exercise During Invasive Hemodynamic Assessment in Symptomatic Adults With a Systemic Right Ventricle

Role of Exercise During Invasive Hemodynamic Assessment in Symptomatic Adults With a Systemic Right Ventricle

Influence of anesthesia on hemodynamic assessment of mitral stenosis severity.

BackgroundThe treatment of choice for severe rheumatic mitral stenosis (MS) is balloon mitral valvuloplasty (BMV). Assessment of MS severity is usually performed by echocardiography. Before performing BMV, invasive hemodynamic assessment is also performed. The effect of anesthesia on the invasive assessment of MS severity has not been studied. The purpose of the present study was to assess changes in invasive hemodynamic measurement of MS severity before and after induction of general anesthesia.MethodsThe medical files of 22 patients who underwent BMV between 2014 and 2020 were reviewed. Medical history, laboratory, echocardiographic and invasive measurements were collected. Anesthesia induction was performed with etomidate or propofol. Pre-procedural echocardiographic measurements of valve area using pressure half time, and continuity correlated well with invasive measurements using the Gorlin formula.ResultsAfter induction of anesthesia the mean mitral valve gradient dropped by 2.4 mmHg (p = 0.153) and calculated mitral valve area (MVA) increased by 0.2 cm2 (p = 0.011). A wide variability in individual response was observed. While a drop in gradient was noted in 14 patients, it increased in 7. Gorlin derived MVA rose in most patients but dropped in 4. Assuming a calculated MVA of 1.5 cm2 and below to define clinically significant MS, 4 patients with pre-induction MVA of 1.5 cm2 or below had calculated MVA above 1.5 cm2 after induction.ConclusionsThe impact of general anesthesia on the hemodynamic assessment of MS is heterogeneous and may lead to misclassification of MS severity.

Invasive hemodynamic assessment of the effect of sildenafil treatment after Fontan operation

There is no pumping subpulmonary ventricle in patients with univentricular hemodynamics after Fontan type physiological correction of complex congenital heart defects (CHD). Hence the blood &amp;#64258; ow to the lungs is passive and depends on central venous pressure (CVP) and pulmonary vascular resistance (PVR) to provide adequate &amp;#64257; lling of the single ventricle. The increase in PVR leads to a reduction in ventricular &amp;#64257; lling and cardiac output, resulting in failure of the Fontan circulation (the so-called failing Fontan). Purpose. Invasive assessment of the hemodynamic effect of sildena&amp;#64257; l treatment in children with single ventricle Fontan circulation. Material and Methods. Twenty-six children (12 girls, 14 boys) with completed stages of Fontan type surgery in whom a selective pulmonary vasodilator (sildena&amp;#64257; l) has been administered during the follow-up have been investigated. An open-label, non-randomized, prospective invasive study of the hemodynamic effect of sildena&amp;#64257; l treatment in patients with completed Fontan surgery stages was performed. Results. A signi&amp;#64257; cant decrease in the cavopulmonary pressure (from 16.58 &amp;plusmn; 1.88 mm Hg to 13.80 &amp;plusmn; 2.20 mm Hg; p &lt; 0.001) and the pulmonary vascular resistance (from 2.02 &amp;plusmn; 0.72 WU to 1.42 &amp;plusmn; 0.41 WU; p = 0.001), increase of the pulmonary/systemic blood &amp;#64258; ow ratio (from 0.71 &amp;plusmn; 0.21 to 0.83 &amp;plusmn; 0.18; p &lt; 0.05), as well as increase in the systemic oxygen saturation (from 85.65 &amp;plusmn; 7.48% to 90.72 &amp;plusmn; 4.53%; p = 0.005) were found. No signi&amp;#64257; cant difference in hemodynamic parameters related to the ventricular morphology and the type of previous palliation was found. The only exception was the pulmonary blood &amp;#64258; ow after sildena&amp;#64257; l treatment,&amp;nbsp;&amp;nbsp;which was signi&amp;#64257; cantly higher in children with &amp;#1072; previous systemic to pulmonary shunt compared to children with &amp;#1072; previous banding (p &lt; 0.05). Conclusion. Our study showed signi&amp;#64257; cant bene&amp;#64257; cial changes in the main hemodynamic parameters after sildena&amp;#64257; l treatment. The pharmacological modulation of the pulmonary vascular status is an important component of the treatment of patients with Fontan circulation.

Correlation Between Venous Oxygen Saturations Obtained From Pulmonary Artery Catheter And Peripherally Inserted Central Catheter In Patients Receiving Inotrope Support

Correlation Between Venous Oxygen Saturations Obtained From Pulmonary Artery Catheter And Peripherally Inserted Central Catheter In Patients Receiving Inotrope Support

Right Ventricle Pressure-Volume Analysis During LVAD Explant Evaluation

<h3>Introduction</h3> Careful patient selection for left ventricular assist device (LVAD) explant after myocardial recovery involves echocardiographic and invasive hemodynamic assessment at safest minimal speed at rest and with exercise, indirect measures of cardiac function. Pressure-volume loop (PVL) analysis may supplement this process by directly assessing ventricular function. <h3>Case Report</h3> A 41 year old male underwent HeartMate3 LVAD placement 2.5 years prior for dilated cardiomyopathy. Post-LVAD, significant reverse remodeling on maximally tolerated guideline directed medical therapy (GDMT) was seen: left ventricular end diastolic diameter (LVEDD) was 4.2 cm (6.1cm pre-LVAD); ejection fraction (EF) was 40-45%. He was referred for exercise right heart catheterization for possible explant after developing incessant low flow LVAD alarms despite speed and medication adjustments. As part of an IRB-approved research protocol, PVLs of the resting right ventricle (RV) were obtained at multiple LVAD speeds. Clinical data were equivocal: chambers did not dilate, but rest cardiac index (CI) fell from 2.3 to 1.9 L/min/m² at a minimal speed of 4000 rpm. Filling pressures rose as speed decreased and increased to pathologic levels during exercise, which was reduced versus age- and sex-matched controls. Explant was not pursued given results and transplant was more aggressively pursued. Subsequent analysis of RV PVLs supported this decision (<b>Figure 1)</b>. RV-pulmonary artery (PA) relationship was preserved at initial speed of 5100 rpm. With speed decrease, summed afterload rose as a function of increased filling pressures, but Ees failed to augment. As a result, ventriculo-vascular coupling was lost. RV volumes increased as well, detected via PVL only and not by echo. Based on these results, poor RV contractile reserve may have contributed to predicted failure to thrive post LVAD explant. <h3>Summary</h3> PVL analysis may provide additional information to help assess ventricular reserve in LVAD patients being considered for explantation.

Decoupling Between Pulmonary Artery Diastolic and Wedge Pressure Following TAVR

<h3>Purpose</h3> Coexistent pulmonary hypertension with severe aortic stenosis confers a greater risk of mortality in undergoing TAVR. In this patient population, the impact of significant decoupling between pulmonary artery diastolic and pulmonary capillary wedge as it relates to clinical risk remained uncertain. <h3>Methods</h3> Patients with severe aortic stenosis who underwent TAVR and completed pre-procedural and post-procedural invasive hemodynamic assessments with right heart catheterization were retrospectively assessed. The impact of post-TAVR decoupling, defined as pressure difference ≥3 mmHg, on 2-year all-cause mortality or risk of heart failure admission was analyzed. <h3>Results</h3> Among 77 included patients (median 86 years old, 23 men), 16 had post-TAVR decoupling. The existence of post-TAVR decoupling was associated with a higher cumulative incidence of the primary endpoint (44% versus 7%, p = 0.001) with an adjusted hazard ratio of 5.87 (95% confidence interval 1.58-21.9, p = 0.008; Figure 1). <h3>Conclusion</h3> We observed a greater risk of worse outcomes in those with post-TAVR decoupling. Therapeutic strategy for the post-TAVR decoupling and its clinical implication remain the future concern.

Trends in Transcatheter Edge-to-Edge Mitral Valve Repair Over a Decade: Data From the MiTra ULM Registry.

ObjectiveThis study sought to determine the potential change in trends in the baseline characteristics of patients with symptomatic severe mitral regurgitation who underwent transcatheter edge-to-edge mitral valve repair (M-TEER) over the last decade in a high-volume center.MethodologyThe investigation included 942 symptomatic patients with moderate-to-severe and severe mitral regurgitation who underwent transcatheter edge-to-edge repair (TEER) at our institution between January 2010 and March 2021. Patients were divided into quintiles and compared separately.ResultsPatients treated in the last quintile had significantly lower surgical risk (Euro Score 7.2 ± 6.8% in the last quintile vs. 10.9 ± 9.4% in the first quintile, p < 0.001), better New York Heart Association (NYHA) status (NYHA IV 14% in the last quintile vs. 40% in the first quintile, p < 0.001), lower NT-pro-BNP, and smaller left ventricle diameter than patients who were treated in the first quintile. There was no difference in age between quintiles. However, an invasive hemodynamic assessment did not show significant changes over the last decade (sPAP 51.35 ± 16.2 mmHg in the first quintile vs. 51.02 ± 14.5 mmHg in the last quintile, p = 0.90, pulmonary capillary wedge V wave 30.7 ± 14.8 mmHg in the first quintile vs. 27.4 ± 10.3 mmHg in the last quintile, p = 0.40). There is a significant trend of a gradually increasing proportion of patients with degenerative mitral regurgitation (MR) over the last 10 years (p < 0.001). The experience gained in the M-TEER procedure brought a significant reduction in fluoroscopy time and hospitalization duration. Medical therapy significantly changed over the last decade in terms of higher use of angiotensin receptor blockers (ARBs), lower use of angiotensin-converting enzyme inhibitors (ACEIs), and the introduction of angiotensin receptor-neprilysin inhibitors (ARNIs).ConclusionPatients undergoing the M-TEER procedure nowadays have lower surgical risk and are treated before they develop a significant left ventricular (LV) remodeling than before. The increasing expertise on the procedure over the last decade led to a rising number of patients with complex degenerative pathology being treated.

Decoupling Between Pulmonary Artery Diastolic and Wedge Pressure Following Transcatheter Aortic Valve Replacement.

Coexistent pulmonary hypertension with severe aortic stenosis confers a greater risk of mortality for patients undergoing transcatheter aortic valve replacement (TAVR). In this patient population, the impact of significant decoupling between pulmonary artery diastolic and pulmonary capillary wedge, as it relates to clinical risk, remained uncertain.Methods and Results:Patients with severe aortic stenosis who underwent TAVR and completed pre-procedural and post-procedural invasive hemodynamic assessments with right heart catheterization were retrospectively assessed. The impact of post-TAVR decoupling, defined as a pressure difference ≥3 mmHg, on 2-year all-cause mortality or risk of heart failure admission was analyzed. Among 77 included patients (median age 86 years, 23 men), 16 had post-TAVR decoupling. The existence of post-TAVR decoupling was associated with a higher cumulative incidence of the primary endpoint (44% vs. 7%, P=0.001), with an adjusted hazard ratio of 5.87 (95% confidence interval 1.58-21.9, P=0.008). A greater risk of worse outcomes in those with post-TAVR decoupling was observed. A therapeutic strategy for post-TAVR decoupling and its clinical implication need to be created and investigated in the future.

IMR or CFR - Which parameter is better suited to determine microvascular disease in patients with severe aortic stenosis?

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Research Foundation Flanders Background Chest pain in patients with severe aortic stenosis (AS) may result from the valve stenosis itself, a coronary atherosclerotic lesion or even microvascular dysfunction (MVD). MVD in severe AS may be purely functional or the consequence of structural left ventricular (LV) remodelling. Unfortunately, there is no data available about invasive quantification of MVD using the index of microvascular resistance (IMR) in this patient group. Purpose To study the microcirculation in patients with severe AS by means of IMR and coronary flow reserve (CFR) and to determine the relation between these indices and standard echocardiographic parameters. Methods Forty-five patients with severe AS (according to the focused 2017 EACVI/ASE update) were prospectively included and underwent invasive intracoronary hemodynamic assessment and dedicated transthoracic echocardiography (TTE). On TTE we measured LV ejection fraction (EF), diastolic function parameters (E/A, e’ septal and lateral, E/e’, TR velocity), left atrial volume (index) (LAV(I)), aortic valve (AV) pressure gradients, the aortic valve area (index) (AVA(I)) and LV mass (index). The invasive measurements compromised the calculation of the CFR and IMR via thermodilution with the use of an intracoronary guidewire with a dual pressure and temperature sensor and administration of IV adenosine. Results Mean IMR and CFR were 22.9 ± 14.2 and 2.5 ± 1.5, respectively (Fig. 1). When using the commonly used cut-offs (increased IMR ≥ 25; impaired CFR &amp;lt; 2.0), 29% of patients had high IMR and 33% had low CFR. Patients with normal and high IMR had similar LV EF (p = 0.54), grade of diastolic dysfunction (DD)(p = 0.18), AV peak (p = 0.80) and mean pressure gradient (p = 0.86), AVA (p= 0.80), AVAI (p = 0.92), E/e’ (p = 0.97), LAVI (p = 0.75), LV mass (p = 0.34) and LV mass index (p = 0.59). In contrast, patients with impaired CFR had significantly lower AVA (0.63 vs 0.80 cm2, p = 0.033) and AVAI (0.32 vs 0.43 cm2/m2, p = 0.035) (Fig. 2A). Moreover there was a significant negative correlation between CFR and LAV (r= -0.354, p= 0.019) as well as LAVI (r= -0.428, p= 0.004)(Fig. 2C). Similarly, patients with different DD grades had no significantly different IMR values (p= 0.71), while there was a significant difference with their CFR values (Grade I: 2.9 ± 1.6; Grade II: 3.1 ± 1.7; Grade III: 1.8 ± 0.6, undetermined DD (due to Atrial Fibrillation): 1.6 ± 0.7, ANOVA p= 0.033) (Fig. 2B). Conclusion Approximately 30% of patients with severe AS exhibit MVD as assessed by IMR and CFR. In contrast to CFR, IMR values were not related to the severity of valve disease or systolic and diastolic function of the LV. Interestingly, the IMR was also not related to LV hypertrophy. IMR may therefore be the more objective and independent marker of microvascular disease, better suited to evaluate MVD in severe AS patients with chest pain. Abstract Figure 1 Abstract Figure 2