Invasive Hemodynamic Assessment Research Articles

Pulmonary hypertension as a prognostic marker in low-flow low-gradient aortic stenosis: Insights from invasive hemodynamics and post-TAVR outcomes.

Pulmonary hypertension (PH) is a common and significant comorbidity in patients with low-flow low-gradient (LF-LG) aortic stenosis, impacting prognosis after transcatheter aortic valve replacement (TAVR). Non-invasive tools often fail to capture PH's full clinical impact due to inherent limitations. This study evaluates the prognostic significance of PH measured invasively and explores its implications on post-TAVR outcomes. This retrospective study analyzed 90 patients with symptomatic LF-LG aortic stenosis who underwent TAVR. Pulmonary artery systolic pressure (PASP) was categorized as mild (<35 mmHg), moderate (35-50 mmHg), or severe (>50 mmHg) using invasive right heart catheterization. Key endpoints included 12-month all-cause mortality and heart failure rehospitalization, assessed via Kaplan-Meier survival analysis and Cox proportional hazards modeling. PH was present in 50% of patients, with moderate-to-severe cases showing higher mortality (25% vs. 8%, p < 0.001) and rehospitalization rates (20% vs. 6%, p = 0.02). Baseline PASP emerged as an independent predictor of mortality (HR 1.07 per mmHg, p < 0.001) and rehospitalization (HR 1.04 per mmHg, p = 0.01). Subgroup analyses revealed that patients with concomitant COPD or advanced diastolic dysfunction exhibited worse outcomes, underscoring the role of systemic disease burden. Invasive hemodynamic assessment provides superior prognostic insight for PH in LF-LG aortic stenosis patients. The findings advocate for targeted PH management strategies to improve post-TAVR outcomes and challenge the sole reliance on non-invasive methods in high-risk cohorts.

Abstract 4138252: Association between Pressure-Adjusted Heart Rate and Mortality in Cardiogenic Shock

Introduction: Among patients with cardiogenic shock (CS), high right atrial pressure (RAP) and low mean arterial pressure (MAP) are associated with in-hospital mortality. Pressure-adjusted heart rate (PAHR), defined as heart rate * RAP-to-MAP ratio (HR * [RAP/MAP]), integrates these parameters and has been used to identify cardiovascular dysfunction in critical illness. Higher PAHR values associate with higher surgical ICU mortality, but the prognostic significance of PAHR has not been assessed in cardiac intensive care unit (CICU) patients with CS. Hypothesis: We hypothesized that higher PAHR values are associated with higher risk of in-hospital mortality in patients with CS. Methods: The Critical Care Cardiology Trials Network (CCCTN) is a multinational registry of CICUs coordinated by the TIMI Study Group. Among CS admissions (2018-2023) undergoing invasive hemodynamic assessment within 24h of CICU admission, we calculated PAHR (in bpm) and assessed its relationship with in-hospital mortality. Patients on temporary mechanical circulatory support were excluded. Odds ratios were adjusted for age, sex, vasoactive-inotropic score (VIS), SCAI stage, and preceding cardiac arrest. Subgroup analyses stratifying by CS subtype were performed. Results: Among the 1411 CS admissions in the analysis cohort (mean age 61 years, 31% women), 18% had AMI-CS, 75% had HF-CS, and 7% had secondary CS. At the time of assessment (median 1.4h after CICU admission), 75% were on vasoactive support (median VIS 3.8). Median HR was 92 (Q1-Q3 77-109) bpm, RAP 15 (Q1-Q3 10-19) mmHg, MAP 75 (Q1-Q3 67-87) mmHg, and PAHR 17 (Q1-Q3 11-24) bpm. A stepwise gradient of higher in-hospital mortality with increasing PAHR values (p-trend &lt;0.001; Fig ) was observed. In adjusted models, a higher PAHR was associated with higher in-hospital mortality (aOR per 10-bpm, 1.35 [95% CI, 1.15-1.58]), and had stronger prognostic associations with mortality than its individual hemodynamic components (Fig) . Conclusion: Higher PAHR is strongly associated with in-hospital mortality in CS patients. PAHR, a simple parameter which is readily calculable without needing a pulmonary artery catheter, may aid in identifying CS patients at higher risk of death.

Invasive haemodynamic assessment in heart failure with preserved ejection fraction.

Despite the increasing prevalence and substantial burden of heart failure with preserved ejection fraction (HFpEF), which constitutes up to 50% of all heart failure cases, significant challenges persist in its diagnostic and therapeutic strategies. These difficulties arise primarily from the heterogeneous nature of the condition, the presence of various comorbidities and a wide range of phenotypic variations. Considering these challenges, current international guidelines endorse the utilization of invasive haemodynamic assessments, including resting and exercise haemodynamics, as the gold standard for enhancing diagnostic accuracy in cases where traditional diagnostic methods yield inconclusive results. These assessments are crucial not only for confirming the diagnosis but also for delineating the complex underlying pathophysiology, enabling the development of personalized treatment strategies, and facilitating the precise classification of HFpEF phenotypes. In this review, we summarize the haemodynamic changes observed in patients with HFpEF, comparing resting and exercise-induced parameters to those of normal subjects. Additionally, we discuss the current role of invasive haemodynamics in HFpEF assessment and highlight its utility beyond diagnosis, such as identifying HFpEF comorbidities, guiding phenotype-based personalized therapies and characterizing prognostication. Finally, we address the challenges associated with utilizing invasive haemodynamics and propose future directions, focusing on integrating these assessments into routine HFpEF care.

Invasive testing leads to significantly altered (surgical) management strategy in coronary anomalies with interarterial course: 3 year interim analysis of MuSCAT

Abstract Introduction Diagnostic work-up of patients with an anomalous aortic origin of a coronary artery (AAOCA) includes an anatomical and functional assessment. The approach to functional evaluation currently varies widely and mainly includes noninvasive assessment. Intracoronary hemodynamic assessment can potentially enhance risk assessment for myocardial ischemia and sudden cardiac death and guide management of AAOCA patients. Hence, this study aims to evaluate invasive detection of ischemia on top of the standard of care diagnostic work-up for interarterial or intraseptal AAOCA and the impact on patient management. We report the first clinical outcomes. Methods In this multicenter prospective cohort study on AAOCA, all consecutive patients of 16 years and older with AAOCA with a newly diagnosed interarterial or intraseptal course in whom diagnostic work-up according to the protocol of the MuSCAT trial was performed between January 2021 and January 2024, were included for analysis. Exclusion comprised incomplete diagnostic evaluation, hemodynamically significant concomitant congenital heart disease or obstructive coronary artery disease in the AAOCA effluence. The work-up included invasive ischemia testing using fractional flow reserve (FFR) and or instantaneous wave-free ratio (iFR)/resting full-cycle ratio (RFR) at baseline and during pharmacological stress using adenosine, adrenaline and dobutamine. Results Fifty-eight patients (50% female, median age at AAOCA diagnosis 51.5 years (IQR 44.0-59.0)) were included, Table 1. The right coronary artery was anomalous in 88%, 93% patients had an interarterial and 69% an intramural course. Non-invasive ischemia detection was positive in 12%, negative in 84% and inconclusive in 4%. Invasive hemodynamic assessment was positive for ischemia in 22%, negative in 74% and inconclusive in 3%. Class of recommendation for surgery based on ESC guidelines was I or IIa in 28% patients and IIb, III or unclassified in 72%. Invasive hemodynamic assessment changed the treatment decision in 24% of the patients; 50% with initially recommended surgical treatment and 14% with initially a conservative treatment adjudication, Figure 1. Median follow-up after initial diagnosis was 20 [IQR 10-28] months and in 56% of all patients who completed 6 months follow-up the initial symptoms alleviated. One (2%) patient underwent a percutaneous re-intervention of the operated AAOCA. Conclusions This national prospective study of invasive hemodynamic assessment in patients with AAOCA showed clinically significant impact on the adjustment of initial management strategy in 24% of the patients. No cardiac death of myocardial infarction in the AAOCA supply area occurred during follow-up. Analysis of the complete follow-up of the MuSCAT trial can further substantiate the role of additional invasive functional imaging in AAOCA.

Invasive haemodynamic assessment shows the obesity-HFpEF phenotype is common amongst patients with symptomatic AF

Abstract Background The obesity-HFpEF phenotype is a unique form of heart failure associated with elevated LA and RA pressures, cardiac remodelling and poor exercise capacity. The influence of this HFpEF phenotype amongst patients with AF is unknown. Objective We sought to determine the influence of the obesity-HFpEF phenotype amongst patients with symptomatic AF, using invasive testing, imaging and cardiopulmonary exercise testing to assess haemodynamics, cardiac remodelling and exercise capacity in patients undergoing AF ablation. Methods Consecutive patients with symptomatic AF due to undergo an AF ablation procedure were recruited. Participants were grouped according to the presence of obesity if body mass index (BMI) exceeded 30kg/m2. Mean LA pressure (mLAP) and mean RA pressure (mRAP) were measured invasively at AF ablation and HFpEF was defined as mLAP&amp;gt;15mmHg at rest or after infusion of 500mls saline. Cardiac remodelling was assessed using transthoracic echocardiography. Exercise capacity was evaluated using cardiopulmonary exercise testing and AF symptoms and quality of life were assessed using the AF Symptom Severity Questionnaire. Results Of 120 participants, 44 (36.7%) were obese and 76 (63.3%) were non-obese (Table 1). Despite younger age (p=0.003), obese participants were more likely to have a coexistent diagnosis of HFpEF (84.1% vs 67.1%, p=0.043). In addition to higher mLAP (p&amp;lt;0.001), obesity was associated with higher mRAP (p&amp;lt;0.001) compared to non-obese patients. Obesity was not associated with differences in LV volume (p=0.559) or function (p=0.381) but was associated with larger LA volumes (p=0.032). On functional assessment, obese participants demonstrated a higher burden of AF symptoms (p=0.049), poorer quality of life (p=0.017) and a trend towards reduced exercise capacity (p=0.068). Conclusion Obese patients with AF demonstrate characteristic features of the obesity-HFpEF phenotype, including elevated LA and RA pressure, left atrial enlargement and poorer functional capacity. Novel treatments for the obesity-HFpEF phenotype, such as GLP-1 inhibitors, may be useful in obese patients with AF.

Definition, classification and diagnosis of pulmonary hypertension.

Pulmonary hypertension (PH) is a haemodynamic condition characterised by elevation of mean pulmonary arterial pressure (mPAP) >20 mmHg, assessed by right heart catheterisation. Pulmonary arterial wedge pressure (PAWP) and pulmonary vascular resistance (PVR) distinguish pre-capillary PH (PAWP ≤15 mmHg, PVR >2 Wood Units (WU)), isolated post-capillary PH (PAWP >15 mmHg, PVR ≤2 WU) and combined post- and pre-capillary PH (PAWP >15 mmHg, PVR >2 WU). Exercise PH is a haemodynamic condition describing a normal mPAP at rest with an abnormal increase of mPAP during exercise, defined as a mPAP/cardiac output slope >3 mmHg/L/min between rest and exercise. The core structure of the clinical classification of PH has been retained, including the five major groups. However, some changes are presented herewith, such as the re-introduction of "long-term responders to calcium channel blockers" as a subgroup of idiopathic pulmonary arterial hypertension, the addition of subgroups in group 2 PH and the differentiation of group 3 PH subgroups based on pulmonary diseases instead of functional abnormalities. Mitomycin-C and carfilzomib have been added to the list of drugs with "definite association" with PAH. For diagnosis of PH, we propose a stepwise approach with the main aim of discerning those patients who need to be referred to a PH centre and who should undergo invasive haemodynamic assessment. In case of high probability of severe pulmonary vascular disease, especially if there are signs of right heart failure, a fast-track referral to a PH centre is recommended at any point during the clinical workup.

Additive value of invasive haemodynamic assessment for predicting post-operative outcomes after Fontan.

Routine pre-Fontan cardiac catheterization remains standard practice at most centres. However, with advances in non-invasive risk assessment, an invasive haemodynamic assessment may not be necessary for all patients.Using retrospective data from patients undergoing Fontan palliation at our institution, we developed a multivariable model to predict the likelihood of a composite adverse post-operative outcome including prolonged length of stay ≥ 30 days, hospital readmission within 6 months, and death and/or transplant within 6 months. Our baseline model included non-invasive risk factors obtained from clinical history and echocardiogram. We then incrementally incorporated invasive haemodynamic data to determine if these variables improved risk prediction.Our baseline model correctly predicted favourable versus adverse post-Fontan outcomes in 118/174 (68%) patients. Covariates associated with adverse outcomes included the presence of a systemic right ventricle (adjusted adds ratio [aOR] 2.9; 95% CI 1.4, 5.8; p = 0.004), earlier surgical era (aOR 3.1 for era 1 vs 2; 95% CI 1.5, 6.5; p = 0.002), and performance of concomitant surgical procedures at the time of Fontan surgery (aOR 2.5; 95% CI 1.1, 5.0; p = 0.026). Incremental addition of invasively acquired haemodynamic data did not improve model performance or percentage of outcomes predicted.Invasively acquired haemodynamic data does not add substantially to non-invasive risk stratification in the majority of patients. Pre-Fontan catheterization may still be beneficial for angiographic evaluation of anatomy, for therapeutic intervention, and in select patients with equivocal risk stratification.

Abstract Mo101: 3-Mercaptopyruvate Sulfurtransferase is a Critical Regulator of Branched-Chain Amino Acid Catabolism in Cardiometabolic HFpEF

Background: Heart failure with preserved ejection fraction (HFpEF) is among the leading causes of cardiovascular mortality and morbidity. Recent multi-omics data sets underscore severely impaired branched-chain amino acid (BCAA) catabolism in the failing hearts of HFpEF patients. 3-mercaptopyruvate sulfurtransferase (3-MST) is a mitochondrial hydrogen sulfide (H 2 S) synthase that regulates mitochondrial biogenesis, function, and substrate metabolism. Research Questions and Goals: In the current study, we aimed to elucidate the role of 3-MST in myocardial BCAA catabolism in cardiometabolic HFpEF. Methods: 3-MST knockout or wild-type (WT) mice were subjected to control or L-NAME and high fat diet - induced HFpEF. Echocardiographic measurements, invasive hemodynamic assessment, and exercise capacity testing were conducted to determine HFpEF severity. Metabolomic analysis was performed to study BCAA catabolism. Additionally, a H 2 S donor, SG1002 was administered to increase H 2 S bioavailability in the setting of 3-MST deficiency and HFpEF. Results: We observed progressive deterioration in left ventricular (LV) diastolic function and exercise performance from mice subjected to HFpEF. Genetic ablation of 3-MST further-exacerbated HFpEF severity as evidenced by significantly increased E/e’ ratio, elevated LV end-diastolic pressure, and reduced exercise performance. Metabolomic analysis revealed pathological accumulation of intermediate metabolites of BCAA in the HFpEF hearts, suggesting a major derangement in myocardial BCAA catabolism. 3-MST KO hearts exhibited further BCAA catabolic defects as compared to those from WT. Importantly, H 2 S donor treatment significantly attenuated BCAA catabolic defect and alleviated HFpEF severity in both WT and 3-MST KO HFpEF mice. Conclusion: Our results demonstrate that deficiency of 3-MST impairs myocardial BCAA catabolism, which results in exacerbated HFpEF severity in a “two-Hit” mouse model of HFpEF. These data suggest 3-MST is critically involved in physiological substrate metabolism within the mitochondria and exerts beneficial effects in HFpEF. Future experiments are underway to delineate the mechanisms by which 3-MST regulates BCAA catabolism.

Abstract Tu043: Gut Microbial Metabolite Phenylacetylglutamine Leads to Cardiomyocyte Hypercontractility and Vascular Endothelial Cell Activation

Background: Numerous gut microbial metabolites including phenylacetylglutamine (PAGln) are associated with increased cardiovascular disease risk and mortality. However, little is known about the cellular-specific perturbations by which PAGln may drive cardiovascular dysfunction. Aims: To understand if elevated PAGln leads to cardiovascular dysfunction and what direct cardiac- and vascular-specific pathophysiology is occurring. Methods: Herein, we subject C57Bl/6N male mice to pharmacological increases in circulating PAGln (50mg/kg) or vehicle twice daily for 20 days. We performed echocardiography, invasive hemodynamics, and vascular reactivity assays. We also performed ex vivo cardiomyocyte cell physiology experiments in the presence or absence of PAGln. Moreover, to understand vascular effects we subjected endothelial cells to PAGln and looked at expression of proinflammatory and cell adhesion molecules. Results: We first performed LC-MS/MS analysis demonstrating significant elevation in PAGln levels in multiple tissues compared to vehicle. There was no significant alteration in cardiac structure and function through echocardiographic analysis. Invasive hemodynamic assessment of systemic blood pressure showed no change, however left ventricular filling pressures were significantly elevated in PAGln group. Aortic rings subjected to varying concentrations of acetylcholine in the PAGln-treated animals were significantly impaired compared to vehicle controls. Given the elevated filling pressures and aberrant vascular endothelial relaxation we measured nitrite levels. Nitrite was significantly reduced in the plasma, cardiac, and liver tissue in PAGln group. Cardiomyocyte fractional shortening was significantly increased compared to baseline and equivalent to b-adrenergic agonism. PAGln hypercontractility was not inhibited with adrenergic antagonism. Vascular endothelial cells which were exposed to PAGln had an increase in expression of proinflammatory and cell adhesion molecules versus vehicle. Conclusion: Our data demonstrates that PAGln drives cardiovascular dysfunction through cardiomyocyte hypercontractility and inducing vascular coronary endothelial cell activation in vitro .

Future of invasive and non-invasive hemodynamic assessment for coronary artery disease management.

Coronary artery disease represents a global health challenge. Accurate diagnosis and evaluation of hemodynamic parameters are crucial for optimizing patient management and outcomes. Nowadays a wide range of both non-invasive and invasive methods are available to assess the hemodynamic impact of both epicardial coronary stenosis and vasomotor disorders. In fact, over the years, important developments have reshaped the nature of both invasive and non-invasive diagnostic techniques, and the future holds promises for further innovation and integration. Non-invasive techniques have progressively evolved and currently a broad spectrum of methods are available, from cardiac magnetic resonance imaging with pharmacological stress and coronary computed tomography (CT) to the newer application of FFR-CT and perfusion CT. Invasive methods, on the contrary, have developed to a full-physiology approach, able not only to identify functionally significant lesions but also to evaluate microcirculation and vasospastic disease. The aim of this review is to summarize the current state-of-the-art of invasive and non-invasive hemodynamic assessment for CAD management.

A patient with pulmonary hypertension: a rare case of AL amyloidosis involving the heart and external auditory canal

The article presents a case of immunoglobulin light chain amyloidosis with cardiac involvement without typical noncardiac manifestations. A complex diagnostic search for the cause of newly diagnosed pulmonary hypertension is described. Aspects of differential diagnosis in invasive hemodynamic assessment of pulmonary circulation and echocardiographic data are discussed. A special case feature is involvement of the hearing organ, which is very rare.

Evaluating the hemodynamic impact of saddle versus non-saddle pulmonary embolism: insights from a thrombectomy cohort.

The aim of this study was to compare the hemodynamic impact and clinical outcomes of saddle vs non-saddle pulmonary embolism (PE). This was a retrospective analysis of clinical characteristics and outcomes among patients with saddle and non-saddle PE within a cohort referred for catheter-based thrombectomy (CBT) with invasive hemodynamic assessments. Patients who underwent CBT between August 2020 and January 2024 were included. The primary outcome was the proportion of patients with a low cardiac index (CI < 2.2 L/min/m²). Secondary outcomes included 30-day mortality, intensive care unit (ICU) length of stay (LOS), and hospital LOS. A total of 107 patients (84 intermediate risk, 23 high-risk; mean age 58 years, 47.6% female) were included in the study, with 44 patients having saddle PE and 63 having non-saddle PE. There were no significant differences in baseline demographics and clinical characteristics between saddle and non-saddle PE, including rates of high-risk PE (25% vs 16%, P = .24), rates of RV dysfunction, pulmonary artery systolic pressure (55 vs 53 mm Hg, P = .74), mean pulmonary artery pressure (34 mm Hg vs 33 mm Hg), low cardiac index (56% vs 51%, P = .64), rates of normotensive shock (27% vs 20%, P = .44), or Composite Pulmonary Embolism Shock scores (4.5 vs 4.7, P = .25). Additionally, 30-day mortality (6% vs 5%, P = .69), ICU LOS, and hospital LOS were similar between the groups. Among patients undergoing CBT, there were no significant differences in invasive hemodynamic parameters or clinical outcomes between those with saddle and non-saddle PE.

A multimodal approach to predict prosthesis-patient mismatch in patients undergoing valve-in-valve trans-catheter aortic valve implantation

AimsThe valve-in-valve transcatheter-aortic-valve-implantation (VIV-TAVI) represents an emerging procedure for the treatment of degenerated aortic bio-prostheses, and the occurrence of patient-prosthesis mismatch (PPM) after VIV-TAVI might affect its clinical efficacy. This study aimed to test a multimodal imaging approach to predict PPM risk during the TAVI planning phase and assess its clinical predictivity in VIV-TAVI procedures. MethodsConsecutive patients undergoing VIV-TAVI procedures at our Institution over 6 years were screened and those treated by self-expandable supra-annular valves were selected. The effective orifice area (EOA) was calculated with a hybrid Gorlin equation combining echocardiographic data with invasive hemodynamic assessment. Severe PPM was defined according to such original multimodality assessment as EOAi≤0.65 cm2/m2 (if BMI < 30 kg/m2) or < 0.55 cm2/m2 (if BMI ≥ 30 kg/m2). The primary endpoint was a composite of all-cause mortality and valve-related re-hospitalization during the clinical follow-up. ResultsA total of 40 VIV-TAVI was included in the analysis. According to the pre-specified multimodal imaging modality assessment, 18 patients (45.0 %) had severe PPM. Among all baseline clinical and anatomical characteristics, estimated glomerular filtration rate before VIV-TAVI (OR 0.872, 95%CI[0.765–0.994],p = 0.040), the echocardiographic pre-procedural ≥moderate AR (OR 0.023, 95%CI[0.001–0.964],p = 0.048), the MSCT-derived effective internal area (OR 0.958, 95%CI[0.919–0.999],p = 0.046) and the implantation depth (OR 2.050, 95%CI[1.028–4.086],p = 0.041) resulted as independent predictors of severe PPM at multivariable logistic analysis. At a mean follow-up of 630 days, patients with severe PPM showed a higher incidence of the primary endpoint (9.1%vs.44.4 %;p = 0.023). ConclusionIn VIV-TAVI using self-expandable supra-annular valves, a multimodal imaging approach might improve clinical outcome predicting severe PPM occurrence.

AORTIC REGURGITATION INDEX IDENTIFIES SIGNIFICANT AORTIC REGURGITATION DURING IMPELLA SUPPORT FOR CARDIOGENIC SHOCK

Abstract Background Aortic regurgitation (AR) significantly hampers the unloading effect and the antegrade flow enhancement expected from the micro–axial flow pump Impella (Abiomed, Danvers). To date, no dedicated hemodynamic index is available to inform on the severity of AR during Impella support. Methods We included 100 patients receiving Impella support for CS with invasive hemodynamic assessment with pulmonary artery catheter (PAC). PAC measures were obtained 48 hours after Impella support initiation. AR grading was performed by either trans–thoracic or trans–esophageal echocardiography in the following strata: 0–none; 1–mild; 2–moderate; 3–moderate–severe; 4–severe. Study cohort was dichotomized according to AR severity≥2+. Several relevant hemodynamic indexes were validated against echocardiographic AR assessment to identify those mostly associated with significant AR (AR severity≥2+), including: AR index [ARI, calculated as (diastolic arterial pressure – pulmonary artery wedge pressure)/systolic arterial pressure, abbreviated in (DAP–PAWP)/SAP], diastolic pulse pressure (DPP, calculated as DAP–PAWP), MAP–adjuster ARI [ARIMAP calculated as (diastolic arterial pressure – pulmonary artery wedge pressure)/mean arterial pressure, abbreviated in (DAP–PAWP)/MAP)]. Results Significant AR (≥2+) was found in 31% patients. Patients with AR≥2+ had higher values of pulmonary artery wedge pressure (PAWP) after 48 hours from support initiation [15 (12, 21) vs 12 (10, 16) mmHg; p&amp;lt;0.021]. Several invasive hemodynamic indexes differentiated AR≥2+ vs AR&amp;lt;2 patients, including: ARI [0.42 (0.36, 0.51) vs 0.50 (0.44, 0.61); p&amp;lt;0.001], DPP [47 (37, 58) vs 57 (48.00, 68) mmHg; p=0.003] and ARIMAP [0.62 (0.54, 0.70) vs 0.70 (0.64, 0.75); p=0.005] (Figure 1). ARI demonstrated the strongest association and the greatest accuracy in identifying AR≥2+ (area under the curve 0.73; 95%CI: 0.61–0.85; p=0.002). The threshold of ARI 0.39 had excellent specificity (88.0%) and moderate sensitivity (62.9%), Figure 2. Conclusions The easy–to–use ARI metric [(DAP–PAWP)/SAP] accurately identifies patients with significant AR during Impella support, at the optimal cutoff of ARI 0.39. This index may be complementary to echocardiography in the assessment of AR during Impella support.

Pulmonary artery elastance as a predictor of hospital mortality in heart failure cardiogenic shock.

The initial bundle of cares strongly affects haemodynamics and outcomes in acute decompensated heart failure cardiogenic shock (ADHF-CS). We sought to characterize whether 24h haemodynamic profiling provides superior prognostic information as compared with admission assessment and which haemodynamic parameters best predict in-hospital death. All patients with ADHF-CS and with available admission and 24h invasive haemodynamic assessment from two academic institutions were considered for this study. The primary endpoint was in-hospital death. Regression analyses were run to identify relevant predictors of study outcome. We included 127 ADHF-CS patients [65 (inter-quartile range 52-72) years, 25.2% female]. Overall, in-hospital mortality occurred in 26.8%. Non-survivors were older, with greater CS severity. Among admission variables, age [odds ratio (OR)=1.06; 95% confidence interval (CI): 1.02-1.11; Padj=0.005] and CPIRAP (OR=0.62 for 0.1 increment; 95% CI: 0.39-0.95; Padj=0.034) were found significantly associated with in-hospital death. Among 24h haemodynamic univariate predictors of in-hospital death, pulmonary elastance (PaE) was the strongest (area under the curve of 0.77; 95% CI: 0.68-0.86). PaE (OR=5.98; 95% CI: 2.29-17.48; Padj<0.001), pulmonary artery pulsatility index (PAPi, OR=0.77; 95% CI: 0.62-0.92; Padj=0.013) and age (OR=1.06; 95% CI: 1.02-1.11; Padj=0.010) were independently associated with in-hospital death. Best cut-off for PaE was 0.85mmHg/mL and for PAPi was 2.95; cohort phenotyping based on these PaE and PAPi thresholds further increased in-hospital death risk stratification; patients with 24h high PaE and low PAPi exhibited the highest in-hospital mortality (56.2%). Pulmonary artery elastance has been found to be the most powerful 24h haemodynamic predictor of in-hospital death in patients with ADHF-CS. Age, 24h PaE, and PAPi are independently associated with hospital mortality. PaE captures ventricular (RV) afterload mismatch and PAPi provides a metric of RV adaptation, thus their combination generates four distinct haemodynamic phenotypes, enhancing in-hospital death risk stratification.

C-1 | "The Impact of Pulmonary Hypertension on Survival in Carcinoid Heart Disease: Insights from Invasive Hemodynamic Assessment"

C-1 | "The Impact of Pulmonary Hypertension on Survival in Carcinoid Heart Disease: Insights from Invasive Hemodynamic Assessment"

Novel Strategies in Diagnosing Heart Failure with Preserved Ejection Fraction: A Comprehensive Literature Review.

Heart failure (HF) with preserved ejection fraction (HFpEF) is a prevalent global condition affecting approximately 50% of the HF population. With the aging of the worldwide population, its incidence and prevalence are expected to rise even further. Unfortunately, until recently, no effective medications were available to reduce the high mortality and hospitalization rates associated with HFpEF, making it a significant unmet need in cardiovascular medicine. Although HFpEF is commonly defined as HF with normal ejection fraction and elevated left ventricular filling pressure, performing invasive hemodynamic assessments on every individual suspected of having HFpEF is neither feasible nor practical. Consequently, several clinical criteria and diagnostic tools have been proposed to aid in diagnosing HFpEF. Overall, these criteria and tools are designed to assist healthcare professionals in identifying and evaluating patients who may have HFpEF based on a combination of signs, symptoms, biomarkers, and non-invasive imaging findings. By employing these non-invasive diagnostic approaches, clinicians can make informed decisions regarding the best pharmacological and rehabilitation strategies for individuals with suspected HFpEF. This literature review aims to provide an overview of all currently available methods for diagnosing and monitoring this disabling condition.

Coronary Microvascular Disease Registry (CMDR): Study design and rationale

BackgroundCoronary microvascular dysfunction (CMD) is a prevalent condition among patients with cardiovascular risk factors, leading to a reduced quality of life and an increased risk of major adverse cardiovascular events. Novel invasive techniques have emerged to more accurately diagnose CMD. However, CMD's natural history remains poorly understood due to limited data. To address this knowledge gap, the Coronary Microvascular Disease Registry (CMDR) was established with the primary aim of standardizing comprehensive coronary functional testing and understanding of CMD. DesignCMDR is a prospective, multicenter registry enrolling an unlimited number of consecutive subjects who undergo comprehensive invasive hemodynamic assessment of the entire coronary arterial vasculature. Patients undergoing acetylcholine provocation test for coronary vasospasm will also be included. Follow-up assessments will be conducted at 30 days and annually for up to 5 years. The primary endpoint is Canadian Cardiovascular Society angina grade over time. Secondary endpoints, including all-cause mortality, cardiovascular death, acute myocardial infarction, stroke, hospitalizations, medication changes, and subsequent coronary interventions, will be analyzed to establish long-term safety and clinical outcomes in patients undergoing invasive CMD assessment. SummaryCMDR aims to characterize the clinical and physiologic profile of patients undergoing comprehensive invasive coronary functional testing, simultaneously providing crucial longitudinal information on the natural history and outcomes of these patients. This will shed light on CMD's course and clinical implications, which, in turn, holds the potential to significantly improve diagnostic and treatment strategies for CMD patients, ultimately leading to the enhancement of their overall prognosis and quality of life. Clinical trial registrationclinicaltrials.gov, NCT05960474

Mitral Annulus Calcium Score in Patients With Calcific Mitral Stenosis Undergoing Invasive Hemodynamic Assessment.

Aortic valve calcium score is associated with hemodynamic severity of aortic stenosis. Whether this association is present in calcific mitral stenosis remains unknown. This study was a retrospective analysis of consecutive patients with mitral stenosis secondary to mitral annular calcification (MAC) undergoing transseptal catheterization. All patients underwent invasive mitral valve assessment via direct left atrial and left ventricular pressure measurement. Computed tomography within 1 year of cardiac catheterization and with adequate visualization of the mitral annulus was included. MAC calcium score quantification by Agatston method was obtained offline using dedicated software (Aquarius, TeraRecon, V.4). Median patient age was 66.9±11.2 years, 47% of patients were women, 50% had coronary artery disease, 40% had atrial fibrillation, 47% had prior cardiac surgery, and 33% had prior chest radiation. Median diastolic mitral valve gradient was 9.4±3.4 mm Hg on echocardiography and 8.5±4 mm Hg invasively. Invasive median mitral valve area using the Gorlin formula was 1.87±0.9 cm2. Median MAC calcium score for the cohort was 7280±7937 Hounsfield units. MAC calcium score correlated with the presence of atrial fibrillation (P=0.02) but was not associated with other comorbidities. There was no correlation between MAC calcium score and mitral valve area (r=0.07; P=0.6) or mitral valve gradient (r=-0.03; P=0.8). MAC calcium score did not correlate with invasively measured mitral valve gradient and mitral valve area in patients with MAC-related mitral stenosis, suggesting that calcium score should not be used as a surrogate for invasive hemodynamic parameters.

Lead Dislodgement Post Invasive Hemodynamic Assessment after Atrioventricular Node Ablation and Biventricular Pacemaker

A man with history of Heart Failure with preserved Ejection Fraction (HFpEF), Atrioventricular (AV) node ablation followed by biventricular pacemaker placement was hospitalized for dyspnea. During invasive hemodynamic assessment patient had brief episode of asystole due to lead displacement. Right catheterization should be cautiously performed in patients with intracardiac devices, when done safety protocols should be followed.