Estimation of Right Atrial Pressure by Ultrasound-Assessed Jugular Vein Distensibility in Patients With Heart Failure.

BACKGROUND: Clinical evaluation of central venous pressure is difficult, depends on experience, and is often inaccurate in patients with chronic advanced heart failure. We assessed the ultrasound-assessed internal jugular vein (JV) distensibility by ultrasound as a noninvasive tool to identify patients with normal right atrial pressure (RAP ≤7 mm Hg) in this population. METHODS: We measured JV distensibility as the Valsalva-to-rest ratio of the vein diameter in a calibration cohort (N=100) and a validation cohort (N=101) of consecutive patients with chronic heart failure with reduced ejection fraction who underwent pulmonary artery catheterization for advanced heart failure therapies workup. RESULTS: A JV distensibility threshold of 1.6 was identified as the most accurate to discriminate between patients with RAP ≤7 versus >7 mm Hg (area under the receiver operating characteristic curve, 0.74 [95% CI, 0.64-0.84]) and confirmed in the validation cohort (receiver operating characteristic, 0.82 [95% CI, 0.73-0.92]). A JV distensibility ratio >1.6 had predictive positive values of 0.86 and 0.94, respectively, to identify patients with RAP ≤7 mm Hg in the calibration and validation cohorts. Compared with patients from the calibration cohort with a high JV distensibility ratio (>1.6; n=42; median RAP, 4 mm Hg; pulmonary capillary wedge pressure, 11 mm Hg), those with a low JV distensibility ratio (≤1.6; n=58; median RAP, 8 mm Hg; pulmonary capillary wedge pressure, 22 mm Hg; P<0.0001 for both) were more likely to die or undergo a left ventricular assist device implant or heart transplantation (event rate at 2 years: 42.7% versus 18.2%; log-rank P=0.034). CONCLUSIONS: Ultrasound-assessed JV distensibility identifies patients with chronic advanced heart failure with normal RAP and better outcomes. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03874312.

Mitral E-wave to stroke volume ratio displays stronger diagnostic performance to identify elevated left ventricular filling pressures than mitral E/e' during passive leg lift: A cross-sectional study employing simultaneous echocardiography and catheterization.

BACKGROUND: Elevated filling pressure is a hallmark of heart failure (HF) and portends poor prognosis. Accurate diagnosis is challenging, given that patients with normal filling pressure at rest develop disproportionate elevation with sudden preload increase. We aimed to test the accuracy of the ratio between mitral inflow velocity (E) and left ventricular stroke volume (SV) to identify patients with elevated filling pressure with passive leg lifting (PLL) and compare this with other echocardiographic surrogates of filling pressure. METHODS: Doppler echocardiography and right heart catheterization (RHC) were simultaneously performed in 37 patients (11 males, mean age 67 ± 12 years) with exertional dyspnea. Twenty-six healthy controls (14 males, mean age 60 ± 12 years) were added as reference. SV, cardiac output (CO), tricuspid regurgitation peak gradient (TRG), mitral E-wave (E) and early myocardial velocity (e') were obtained at rest and with PLL. E/SV, E/CO and E/e' were calculated and correlated with invasive pulmonary capillary wedge pressures (PCWP) with PLL. RESULTS: During PLL, E/SV (AUC = 0.94) displayed stronger diagnostic ability to identify PCWP >15 mmHg than E/e' (AUC = 0.81), mitral E/A ratio (0.76) and resting invasive PCWP (0.84). An E/SV cutoff of >1.0 showed 88% sensitivity and 75% specificity to identify elevated PCWP. Further, 10 patients (27%) were reassigned during PLL from normal to postcapillary pulmonary hypertension (postCPH), and 6 patients (16%) switched diagnosis from precapillary PH (preCPH) to postCPH. CONCLUSION: The novel E/SV ratio identifies patients with elevated PCWP with PLL and displays stronger diagnostic performance than routinely utilized echocardiographic measures such as E/e' in addition to resting, catheterization derived PCWP.

Left atrial reservoir pressure-volume relations during exercise in healthy older adults.

The left atrium (LA) mediates cardiopulmonary interactions. During ventricular systole, the LA functions as a compliant reservoir that is coupled to the left ventricle (LV) and offloads volume from the pulmonary vasculature. We aimed to describe LA reservoir function using phasic relationships between pulmonary artery wedge pressure (PAWP) and LA volume events. We included healthy adults (7 M/6 F, 56 ± 8 yr) who were studied at rest and during semirecumbent cycle ergometry at a target of 100 beats/min heart rate. Right heart catheterization was performed to record the PAWP and two-dimensional (2-D) echocardiography was used to measure LA and LV volumes. We manually measured A-wave, x-trough, V-wave, and y-trough PAWP beat-by-beat, as well as minimal, maximal, and precontraction biplane LA volumes. Heart rate increased by 40 ± 7 beats/min with exercise; stroke volume and cardiac output also rose. Although all phasic PAWP measurements increased with exercise, the x-V pressure pulse during LA filling doubled from 4 ± 2 to 8 ± 4 mmHg (P = 0.001). LA minimal volume was unchanged but maximal volume increased from 39 ± 9 to 48 ± 9 mL (P < 0.001) with exercise, and so reservoir volume increased from 24 ± 5 to 32 ± 8 mL (P < 0.001). As such, calculated LA compliance decreased from 6.8 ± 3.4 to 4.8 ± 2.6 mL/mmHg (P = 0.029). The product of V-wave PAWP and LA maximal volume, a surrogate for LA wall stress, increased from 486 ± 193 to 953 ± 457 mmHg·mL (P < 0.001). In healthy older adults during submaximal exercise, the PAWP waveform shifts upward and its amplitude widens, LA filling increases, LA compliance decreases modestly, and LA wall stress may augment substantially.NEW & NOTEWORTHY We combined invasive estimates of left atrial pressure with noninvasive left atrial volume measurements made at rest and during exercise in healthy humans. Left atrial pressure and volume both increased with exercise, though the pressure increase was relatively greater, and calculated compliance decreased modestly while estimated peak wall stress nearly doubled. Our results demonstrate left atrial loading during exercise in healthy older adults and provide insight into how the left atrium mediates cardiopulmonary interactions.

[Diagnosis of heart failure with preserved ejection fraction]. / Diagnostik der Herzinsuffizienz mit erhaltener Pumpfunktion.

Heart failure with preserved ejection fraction (HFpEF) currently causes about half of the heart failure related hospitalizations. With the aging of the population and increasing prevalence of risk factors and comorbidities, such as arterial hypertension, diabetes mellitus and obesity, HFpEF prevalence is expected to increase as well. With regards to quality of life, overall morbidity, and mortality, HFpEF patients have a similarly adverse prognosis as patients with heart failure with reduced ejection fraction. The leading symptoms of exertional dyspnea and exercise intolerance with concomitant clinical signs of heart failure should, therefore, prompt diagnostic tests to exclude or confirm HFpEF. Considering the main pathophysiological mechanisms, echocardiography is crucial to non-invasively identify signs of left ventricular (LV) hypertrophy, impaired myocardial relaxation, and elevated filling pressures. Elevated NT-proBNP may furthermore indicate increased LV wall stress and volume overload. If the results of these investigations are inconclusive, parameters of elevated filling pressures can be measured invasively by right or left heart catheterization. High pulmonary capillary wedge pressure (PCWP) or left ventricular end-diastolic pressure (LVEDP) may confirm a HFpEF diagnosis. Ongoing studies are investigating potential distinct phenotypes within the HFpEF patient group.

Is Pulmonary Capillary Wedge Pressure a Reliable Indicator of Postcapillary Pulmonary Hypertension?

Although current pulmonary hypertension (PH) guidelines recommend a pulmonary capillary wedge pressure (PCWP) >15 mm Hg for the detection of a postcapillary component, the rationale of this recommendation may not be quite compatible with the peculiar hemodynamics of PH. We hypothesize that a high PCWP alone does not necessarily indicate left-sided disease, and this diagnosis can be improved using left ventricle transmural pressure difference (∆ PTM). In this 2-center, retrospective, observational study, we enrolled 1,070 patients with PH who underwent heart catheterization, with the final study population comprising 961 cases. ∆ PTM was calculated as PCWP minus right atrial pressure. The patients with group II PH had significantly higher ∆ PTM values (12.6 ± 6.6 mm Hg) compared with the other groups (1.1 ± 4.8 in group I, 12.4 ± 6.6 in group II, 2.5 ± 6.4 in group III, and 0.8 ± 8.0 in group IV, p <0.001) despite overlapping PCWP values. A ∆ PTM cutoff of 7 mm Hg identifies left heart disease when PCWP is >15 (area under curve 0.825, 95% confidence interval 0.784 to 0.866, p <0.001). Five-year mortality was significantly higher in patients with high ∆ PTM and PCWP subgroups compared with low ∆ PTM plus high PCWP (26.1% vs 18.5%, p = 0.027) and low ∆ PTM and PCWP subgroups (26.1% vs 15.6%, p <0.001). ∆ PTM has supplementary discriminatory power in distinguishing patients with and without postcapillary PH. In conclusion, a new approach utilizing ∆ PTM may improve our understanding of PH pathophysiology and may identify a subpopulation that may potentially benefit from PH-specific treatments.

Implications of Mean Pulmonary Arterial Wedge Pressure Trajectories in Pulmonary Arterial Hypertension.

Rationale: The mean pulmonary arterial wedge pressure (mPAWP) is the critical hemodynamic factor differentiating group 1 pulmonary arterial hypertension (PAH) from group 2 pulmonary hypertension associated with left heart disease. Despite the discrepancy between the mPAWP upper physiologic normal and current PAH definitions, the implications of the initial mPAWP for PAH clinical trajectory are poorly understood. Objectives: To model longitudinal mPAWP trajectories in PAH over 10 years and examine the clinical and hemodynamic factors associated with trajectory membership. Methods: Adult patients with PAH with two or more right heart catheterizations were identified from a multiinstitution healthcare system in eastern Massachusetts. mPAWP trajectories were constructed via group-based trajectory modeling. Feature selection was performed in least absolute shrinkage and selection operator regression. Logistic regression was used to assess associations between trajectory membership, baseline characteristics, and transplant-free survival. Measurements and Main Results: Among 301 patients with PAH, there were two distinct mPAWP trajectories, termed "mPAWP-high" (n = 71; 23.6%) and "mPAWP-low" (n = 230; 76.4%), based on the ultimate mPAWP value. Initial mPAWP clustered around median 12 mm Hg (interquartile range [IQR], 8-14 mm Hg) in the mPAWP-high and 9 mm Hg (IQR, 6-11 mm Hg) in the mPAWP-low trajectories (P < 0.001). After feature selection, initial mPAWP ⩾12 mm Hg predicted an mPAWP-high trajectory (odds ratio, 3.2; 95% confidence interval, 1.4-6.1; P = 0.0006). An mPAWP-high trajectory was associated with shorter transplant-free survival (vs. mPAWP-low, median, 7.8 vs. 11.3 yr; log-rank P = 0.017; age-adjusted P = 0.217). Conclusions: Over 10 years, the mPAWP followed two distinct trajectories, with 25% evolving into group 2 pulmonary hypertension physiology. Using routine baseline data, longitudinal mPAWP trajectory could be predicted accurately, with initial mPAWP ⩾12 mm Hg as one of the strongest predictors.

Systemic Arterial Oxygen Levels Differentiate Pre- and Post-capillary Predominant Hemodynamic Abnormalities During Exercise in Undifferentiated Dyspnea on Exertion.

BACKGROUND: Whether systemic oxygen levels (SaO2) during exercise can provide a window into invasively derived exercise hemodynamic profiles in patients with undifferentiated dyspnea on exertion is unknown. METHODS: We performed cardiopulmonary exercise testing with invasive hemodynamic monitoring and arterial blood gas sampling in individuals referred for dyspnea on exertion. Receiver operator analysis was performed to distinguish heart failure with preserved ejection fraction from pulmonary arterial hypertension. RESULTS: Among 253 patients (mean ± SD, age 63 ± 14 years, 55% female, arterial O2 [PaO2] 87 ± 14 mmHg, SaO2 96% ± 4%, resting pulmonary capillary wedge pressure [PCWP] 18 ± 4mmHg, and pulmonary vascular resistance [PVR] 2.7 ± 1.2 Wood units), there was no exercise PCWP threshold, measured up to 49 mmHg, above which hypoxemia was consistently observed. Exercise PaO2 was not correlated with exercise PCWP (rho = 0.04; P = 0.51) but did relate to exercise PVR (rho = -0.46; P < 0.001). Exercise PaO2 and SaO2 levels distinguished left-heart-predominant dysfunction from pulmonary-vascular-predominant dysfunction with an area under the curve of 0.89 and 0.89, respectively. CONCLUSION: Systemic O2 levels during exercise distinguish relative pre- and post-capillary pulmonary hemodynamic abnormalities in patients with undifferentiated dyspnea. Hypoxemia during upright exercise should not be attributed to isolated elevation in left heart filling pressures and should prompt consideration of pulmonary vascular dysfunction.

Post-exercise left atrial conduit strain predicted hemodynamic change in heart failure with preserved ejection fraction.

OBJECTIVES: Left ventricle function directly impacts left atrial (LA) conduit function, and LA conduit strain is associated with exercise intolerance in patients with heart failure with preserved ejection fraction (HFpEF). Pulmonary capillary wedge pressure (PCWP) before and during exercise is the current gold standard for diagnosing HFpEF. Post-exercise ΔPCWP can lead to worse long-term outcomes. This study examined the correlation between LA strain and post-exercise ΔPCWP in patients with HFpEF. METHODS: We enrolled 100 subjects, including 74 with HFpEF and 26 with non-cardiac dyspnea, from November 2017 to December 2020. Subjects underwent echocardiography, invasive cardiac catheterization, and expired gas analysis at rest and during exercise. Arterial blood pressure, right atrial pressure, pulmonary artery pressure, and PCWP were recorded during cardiac catheterization. Cardiac output, stroke volume, pulmonary vascular resistance, pulmonary artery compliance, systemic vascular resistance, and LV stroke work were calculated using standard formulas. RESULTS: Exercise LA conduit strain significantly correlated with both post-exercise ΔPCWP (r = - 0.707, p < 0.001) and exercise PCWP (r = - 0.659; p < 0.001). Exercise LA conduit strain differentiated patients who did and did not meet the 2016 European Society of Cardiology HFpEF criteria with an area under the curve of 0.69 (95% confidence interval, 0.548-0.831) using a cutoff value of 14.25, with a sensitivity of 0.64 and a specificity of 0.68. CONCLUSIONS: Exercise LA conduit strain significantly correlates with post-exercise ΔPCWP and has a comparable power to identify patients with HFpEF. Additional studies are warranted to confirm the ability of LA conduit strain to predict long-term outcomes among patients with HFpEF. CLINICAL RELEVANCE STATEMENT: Exercise left atrial conduit strain was highly associated with the difference of post-exercise pulmonary capillary wedge pressure and may indicate increased mortality risk in patients with heart failure with preserved ejection fraction, and also has comparable diagnostic ability. KEY POINTS: • Left atrial conduit strain is associated with exercise intolerance in patients with heart failure with preserved ejection fraction. • Left atrial conduit strain during exercise can identify patients with heart failure with preserved ejection fraction. • Exercise left atrial conduit strain significantly correlates with the difference of pulmonary capillary wedge pressure during and before exercise which might predict the long-term outcomes of heart failure with preserved ejection fraction patients.

Pulmonary hemodynamics before and after pediatric heart transplantation.

BACKGROUND: Pulmonary hypertension (PH) may limit the outcome of pediatric heart transplantation (pHTx). We evaluated pulmonary hemodynamics in children undergoing pHTx. METHODS: Cross-sectional, single-center, observational study analyzing pulmonary hemodynamics in children undergoing pHTx. RESULTS: Twenty-three children (female 15) underwent pHTx at median (IQR) age of 3.9 (.9-8.2) years with a time interval between first clinical signs and pHTx of 1.1 (.4-3.2) years. Indications for pHTx included cardiomyopathy (CMP) (n = 17, 74%), congenital heart disease (CHD) (n = 5, 22%), and intracardiac tumor (n = 1, 4%). Before pHTx, pulmonary hemodynamics included elevated pulmonary artery pressure (PAP) 26 (18.5-30) mmHg, pulmonary capillary wedge pressure (PCWP) 19 (14-21) mmHg, left ventricular enddiastolic pressure (LVEDP) 17 (13-22) mmHg. Transpulmonary pressure gradient (TPG) was 6.5 (3.5-10) mmHg and pulmonary vascular resistance (Rp) 2.65 WU*m2 (1.87-3.19). After pHTx, at immediate evaluation 2 weeks after pHTx PAP decreased to 20.5 (17-24) mmHg, PCWP 14.5 (10.5-18) mmHg (p < .05), LVEDP 16 (12.5-18) mmHg, TPG 6.5 (4-12) mmHg, Rp 1.49 (1.08-2.74) WU*m2 resp.at last invasive follow up 4.0 (1.4-6) years after pHTx, to PAP 19.5 (17-21) mmHg (p < .05), PCWP 13 (10.5-14.5) mmHg (p < .05), LVEDP 13 (10.5-14) mmHg, TPG 7 (5-9.5) mmHg, Rp 1.58 (1.38-2.19) WU*m2 (p < .05). In CHD patients PAP increased (p < .05) after pHTx at immediate evaluation and decreased until last follow-up (p < .05), while in CMP patients there was a continuous decline of mean PAP values immediately after HTx (p < .05). CONCLUSIONS: While PH before pHTx is frequent, after pHTx the normalization of PH starts immediately in CMP patients but is delayed in CHD patients.

Using pulsatility responses to breath-hold maneuvers to predict readmission rates in continuous-flow left ventricular assist device patients.

BACKGROUND: Dynamic respiratory maneuvers induce heterogenous changes to flow-pulsatility in continuous-flow left ventricular assist device patients. We evaluated the association of these pulsatility responses with patient hemodynamics and outcomes. METHODS: Responses obtained from HVAD (Medtronic) outpatients during successive weekly clinics were categorized into three ordinal groups according to the percentage reduction in flow-waveform pulsatility (peak-trough flow) upon inspiratory-breath-hold, (%∆P): (1) minimal change (%∆P ≤ 50), (2) reduced pulsatility (%∆P > 50 but <100), (3) flatline (%∆P = 100). Same-day echocardiography and right-heart-catheterization were performed. Readmissions were compared between patients with ≥1 flatline response (F-group) and those without (NF-group). RESULTS: Overall, 712 responses were obtained from 55 patients (82% male, age 56.4 ± 11.5). When compared to minimal change, reduced pulsatility and flatline responses were associated with lower central venous pressure (14.2 vs. 11.4 vs. 9.0 mm Hg, p = 0.08) and pulmonary capillary wedge pressure (19.8 vs. 14.3 vs. 13.0 mm Hg, p = 0.03), lower rates of ≥moderate mitral regurgitation (48% vs. 13% vs. 10%, p = 0.01), lower rates of ≥moderate right ventricular impairment (62% vs. 25% vs. 27%, p = 0.03), and increased rates of aortic valve opening (32% vs. 50% vs. 75%, p = 0.03). The F-group (n = 28) experienced numerically lower all-cause readmissions (1.51 vs. 2.79 events-per-patient-year [EPPY], hazard-ratio [HR] = 0.67, p = 0.12), reduced heart failure readmissions (0.07 vs. 0.57 EPPY, HR = 0.15, p = 0.008), and superior readmission-free survival (HR = 0.47, log-rank p = 0.04). Syncopal readmissions occurred exclusively in the F-group (0.20 vs. 0 EPPY, p = 0.01). CONCLUSION: Responses to inspiratory-breath-hold predicted hemodynamics and readmission risk. The impact of inspiratory-breath-hold on pulsatility can non-invasively guide hemodynamic management decisions, patient optimization, and readmission risk stratification.

Invasive haemodynamics at rest and exercise in cardiac amyloidosis.

AIMS: Our aim was to investigate haemodynamics at rest and during exercise in patients with transthyretin cardiomyopathy (ATTR-CM) in light of the 2022 European Society of Cardiology (ESC) and European Respiratory Society (ERS) guidelines on pulmonary hypertension (PH). METHODS AND RESULTS: We performed right heart catheterization (RHC) in 57 subjects with ATTR-CM. The proportion of patients with PH was 77% according to the 2022 guidelines versus 47% when applying the 2015 guidelines. Isolated post-capillary PH and combined pre- and post-capillary PH were most prevalent. Thirty-six patients underwent a supine bicycle cardiopulmonary exercise test during RHC. Exercise-induced PH was defined as an increase in mean pulmonary arterial pressure from rest to exercise per increase in cardiac output (ΔmPAP/ΔCO) of > 3 mmHg/L/min. An increase in pulmonary arterial wedge pressure per change in cardiac output (ΔPAWP/ΔCO) from rest to exercise >2 mmHg/L/min was considered suggestive of post-capillary exercise-induced PH. All but two patients who exercised during RHC developed exercise-induced PH. The median ΔmPAP/ΔCO was 7.2 mmHg/L/min and ΔPAWP/ΔCO was 5.1 mmHg/L/min. The median ΔRAP/ΔCO was 3.6 mmHg/L/min and ΔRAP/ΔPAWP was 0.6 mmHg/L/min. CONCLUSIONS: Most patients with ATTR-CM have isolated post-capillary or combined pre- and post-capillary PH at rest, and almost all patients develop exercise-induced PH with a large post-capillary component. There was a pronounced, but balanced increase in atrial pressures on exercise.

Performance of DETECT Pulmonary Arterial Hypertension Algorithm According to the Hemodynamic Definition of Pulmonary Arterial Hypertension in the 2022 European Society of Cardiology and the European Respiratory Society Guidelines.

OBJECTIVE: The evidence-based DETECT pulmonary arterial hypertension (PAH) algorithm is frequently used in patients with systemic sclerosis (SSc) to help clinicians screen for PAH by using noninvasive data to recommend patient referral to echocardiography and, if applicable, for a diagnostic right-sided heart catheterization. However, the hemodynamic definition of PAH was recently updated in the 2022 European Society of Cardiology (ESC)/European Respiratory Society (ERS) guidelines. The performance of DETECT PAH in identifying patients with a high risk of PAH according to this new definition was assessed. METHODS: In this post hoc analysis of DETECT, which comprised 466 patients with SSc, the performance of the DETECT PAH algorithm in identifying patients with a high risk of PAH as defined in the 2022 ESC/ERS guidelines (mean pulmonary arterial pressure [mPAP] >20 mm Hg, pulmonary capillary wedge pressure [PCWP] ≤15 mm Hg, and pulmonary vascular resistance >2 Wood units) was assessed using summary statistics and was descriptively compared to the known performance of DETECT PAH as defined in 2014, when it was developed (mPAP ≥25 mm Hg and PCWP ≤15 mm Hg). RESULTS: The sensitivity of DETECT PAH in identifying patients with a high risk of PAH according to the 2022 ESC/ERS definition was lower (88.2%) compared to the 2014 definition (95.8%). Specificity improved from 47.8% to 50.8%. CONCLUSION: The performance of the DETECT algorithm to screen for PAH in patients with SSc is maintained when PAH is defined according to the 2022 ESC/ERS hemodynamic definition, indicating that DETECT remains applicable to screen for PAH in patients with SSc.

Haemodialysis patient with chronic kidney disease and pulmonary hypertension treated effectively with pulmonary vasodilators.

A male patient in his 70s on periodic haemodialysis complained of dysdialysis several months prior and was diagnosed subsequently with pulmonary hypertension (PH). To confirm this diagnosis, a catheter examination was performed after haemodialysis in the dry state. Pulmonary artery wedge pressure (PAWP), mean pulmonary artery (PA) pressure, cardiac index (CI) and pulmonary vascular resistance (PVR) were 9 mm Hg, 42 mm Hg, 2.63 L/min/m2 and 5.9 WU, respectively. The pathophysiological diagnosis was precapillary PH, which mimicked idiopathic PH. The pulmonary vasodilators were administered in a careful sequential manner. After initiation of therapy, dysdialysis disappeared within a few months, while mean PA pressure, CI and PVR improved to 24 mm Hg, 3.47 L/min/m2 and 2.3 WU, respectively. Although the cause of PH in haemodialysis patients is multifactorial, catheter examination in the dry state is useful for clarifying a patient's haemodynamic state. In a haemodialysis PH patient with precapillary PH, pulmonary vasodilators are an effective treatment option.

Revisiting Pulmonary Hypertension in the Era of Temporary Mechanical Circulatory Support - Literature Review and Case-Based Discussion.

BACKGROUND: Pulmonary arterial hypertension (PAH) is characterized by persistently increased pressure in the pulmonary arteries. New defining criteria for the different hemodynamic types of pulmonary hypertension (PH) that occur with left heart disease have been proposed by the task force on PH. After consideration of the changes in the general definition of PH in left heart disease, the proposed hemodynamic definition was: (1) isolated postcapillary PH: pulmonary artery wedge pressure >15 mm Hg and mean pulmonary arterial pressure (mPAP) >20 mm Hg and pulmonary vascular resistance (PVR) <3 Woods units (WU); and (2) combined post- and precapillary PH: pulmonary artery wedge pressure >15 mm Hg, mPAP >20 mm Hg, and PVR ≥3 WU. Secondary PH is initially reversible, but eventually, it can become fixed because of the remodeling process of the pulmonary vascular system. Limitations in defining both the time for and amount of reversibility lack clarity. We discuss a case of PH as a framework to better understand these key principles in addressing patients' candidacy for heart or heart-lung transplantation. METHODS: We performed a literature search for all available contemporary data with the following terms: "pulmonary hypertension," "reversal," "Impella 5.5," "temporary mechanical support," and "LVAD" using the National Library of Medicine - PubMed and PubMed Central between 2019 and 2023. A total of 14 published papers were found with these search. From these, 3 addressed the issue of PH and reversibility in the setting of LHD after durable LVAD placement. No papers were found using Impella 5.5 and PH during this timeframe. Given the paucity of data in the field regarding temporary mechanical circulatory support and pulmonary hypertension, we present a case-based discussion to guide the reader in understanding the potential impact of this method in patients with WHO Class 2 Pulmonary hypertension. CASE: A 49-year-old woman with a medical history of acute on chronic biventricular systolic and diastolic heart failure, American College of Cardiology stage D, Stevenson profile C, New York Heart Association class IV (ejection fraction 18%) secondary to nonischemic cardiomyopathy after cardiac resynchronization therapy, pulmonary hypertension, bilateral deep vein thrombosis, and segmental pulmonary embolism presented for heart transplant evaluation. Her cardiac output and central hemodynamics were measured, and she was found to have a pulmonary artery (PA) pressure of 78/38 with a mean PA pressure of 51, pulmonary capillary wedge pressure (PCWP) 30, transpulmonary pressure gradient (TPG) 21, thermodilution cardiac output (CO) 3.35 L/min, and cardiac input (CI) 1.75 L/min/m2. Her PVR was 6.2 WU. Provocative pharmacologic testing for reversibility of PH was performed using sodium nitroprusside, which resulted in a blood pressure of 83/57 (92), heart rate 92/min, and PA pressure of 71/31, with a mean PA pressure of 44 PCWP 22, TPG 22, CO 4.8 L/min, and CI of 2.48 L/min/m2 with a PVR of 4.5 WU. Following this, the patient underwent Impella 5.5 placement through the right axillary artery to optimize afterload reduction and improve end-organ perfusion. Post-Impella hemodynamics on milrinone 0.5 mcg/kg/min demonstrated the following: blood pressure 90/66 (74), heart rate 53/min, and PA pressure of 56/29, with a mean PA pressure of 38, PCWP 24, TPG 14, CO 6 L/min, and CI of 2.9 L/min/m2 with a PVR of 2.3 WU. CONCLUSION: Left ventricular assist device support with Impella 5.5 is associated with a reduction in mPAP and PVR over weeks to months and thus plays a crucial role as a bridge to transplant. Our case and this review highlights the characteristics of PH resulting from heart failure with reduced ejection fraction and discusses the important clinical issues related to the treatment of these patients. We have shown that left ventricular assist device therapy with Impella 5.5 can effectively reduce left-sided filling pressures and lead to PH improvement. We demonstrate the potential benefits of Impella 5.5 in the management of patients with WHO 2 PH and cardiogenic shock with impaired hemodynamics.

Left atrial expansion index measured with cardiovascular magnetic resonance estimates pulmonary capillary wedge pressure in dilated cardiomyopathy.

BACKGROUND: Pulmonary capillary wedge pressure (PCWP) assessment is fundamental for managing dilated cardiomyopathy (DCM) patients. Although cardiovascular magnetic resonance (CMR) has become the gold-standard imaging technique for evaluating cardiac chamber volume and function, PCWP is not routinely assessed with CMR. Therefore, this study aimed to validate the left atrial expansion index (LAEI), a LA reservoir function parameter able to estimate filling pressure with echocardiography, as a novel CMR-measured parameter for non-invasive PCWP estimation in DCM patients. METHODS: We performed a retrospective, single-center, cross-sectional study. We included electively admitted DCM patients referred to our tertiary center for further diagnostic evaluation that underwent a clinically indicated right heart catheterization (RHC) and CMR within 24 h. PCWP invasively measured during RHC was used as the reference. LAEI was calculated from CMR-measured LA maximal and minimal volumes as LAEI = ( (LAVmax-LAVmin)/LAVmin) × 100. RESULTS: We enrolled 126 patients (47 ± 14 years; 68% male; PCWP = 17 ± 9.3 mmHg) randomly divided into derivation (n = 92) and validation (n = 34) cohorts with comparable characteristics. In the derivation cohort, the log-transformed (ln) LAEI showed a strong linear correlation with PCWP (r = 0.81, p < 0.001) and remained a strong independent PCWP determinant over clinical and conventional CMR parameters. Moreover, lnLAEI accurately identified PCWP ≥ 15 mmHg (AUC = 0.939, p < 0.001), and the optimal cut-off identified (lnLAEI ≤ 3.85) in the derivation cohort discriminated PCWP ≥ 15 mmHg with 82.4% sensitivity, 88.2% specificity, and 85.3% accuracy in the validation cohort. Finally, the equation PCWP = 52.33- (9.17xlnLAEI) obtained from the derivation cohort predicted PCWP (-0.1 ± 5.7 mmHg) in the validation cohort. CONCLUSIONS: In this cohort of DCM patients, CMR-measured LAEI resulted in a novel and useful parameter for non-invasive PCWP evaluation.

[Vaskuläre Dyspnoe: Pulmonale Hypertonie]. / Vaskuläre Dyspnoe: Pulmonale Hypertonie.

INTRODUCTION: Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure > 20 mmHg [1] [2]. Echocardiography is used to screen for pulmonary hypertension, but right heart catheterization is required to confirm the diagnosis. Right heart catheterization is used to measure hemodynamic parameters such as pulmonary arterial pressures and pulmonary artery wedge pressure (PAWP), which normally corresponds to the left ventricular end-diastolic pressure. In addition, cardiac output (CO) is measured using the direct Fick method or thermodilution. The pulmonary vascular resistance (PVR) can be derived from these values. Precapillary PH is defined by PAWP ≤15 mmHg and PVR >2 WU (wood units), postcapillary PH is defined by increased PAWP > 15 mmHg with PVR 2 WU due to passive backflow [3]. However, there are also combined pre- and post-capillary PH with a PAWP > 15 mmHg and elevated PVR > 2 WU. Supportive therapies for all forms of PH include diuretics, supplemental oxygen in case of hypoxemia, gentle exercise under specialized supervision, and anticoagulants for some forms. Specific drug or interventional therapies are available only for pulmonary vascular disease subgroups pulmonary arterial hypertension (group 1) and chronic thromboembolic PH (CTEPH, group 4), while for PH due to heart and lung diseases (groups 2 and 3) as well as mixed forms the therapy of the underlying disease is of major importance. Drug therapy for pulmonary vascular diseases includes endothelin receptor antagonists, phosphodiesterase-5 inhibitors and prostanoids. CTEPH requires clarification regarding surgical pulmonary endarterectomy or interventional balloon angioplasty [4]. Since the diagnosis and therapy of PH is very complex, it must be carried out in an experienced center.

Long-Term Natural Course of Patients with Pulmonary Artery Pressures in the Range of 21-24 mmHg: Insights from a Single-Center Study.

OBJECTIVE: Slightly elevated mean pulmonary artery pressure (mPAP) was previously termed as ''borderline pulmonary hypertension (PH)''. We examined the long-term prognosis of patients with mPAP values between 21 and 24 mmHg, who were referred with the suspicion of pulmonary hypertension. METHODS: Our retrospective study included patients with moderate-to-high echocardiographic risk who underwent right heart catheterization (RHC) between 2008 and 2021 and were followed for at least 1 year. Patients with mPAP <21 mmHg and mPAP 21-24 mmHg were compared. Demographic and clinical characteristics and prognoses of the groups were compared. All-cause mortality over a mean follow-up of 5 years (min 1-max 13 years) was evaluated. RESULTS: A total of 140 patients (mean age 53.1 ± 14.8 years, female 74.5%) with mPAP values <25 mmHg measured of the 395 diagnostic RHCs. Mean follow-up was 4.92 ± 3.13 years. NT-pro-BNP and 6-min walking distance were better in patients with mPAP <21 mmHg. Echocardiographic findings suggestive of PH were more common in mPAP 21-24 mmHg group (P < 0.05). Both the pulmonary artery wedge pressure and cardiac index values were significantly deteriorated in individuals with mPAP 21-24 mmHg (P = 0.001). All-cause mortality tended to be higher in the borderline PH group but did not reach to statistical significance. CONCLUSION: Our single-center observational study revealed that the individuals with an mPAP of 21-24 mmHg tended to have a worser prognosis than those with mPAP of <21 mmHg for up to 13-year follow-up.