Increase In Pulmonary Artery Wedge Pressure Research Articles

The relationship between mixed venous blood oxygen saturation and pulmonary arterial and venous pressures in patients with heart failure.

Recent discoveries have identified intrapulmonary bronchopulmonary anastomoses (IBAs) as a relatively common phenomenon forming intrapulmonary right-to-left shunts. This study hypothesizes that IBAs play a significant role in the pathophysiology of heart failure. We aim to investigate the impact of these intrapulmonary right-to-left shunts on pulmonary arterial and venous pressures in heart failure patients, utilizing mixed venous oxygen saturation (SvO₂) as a key measurement. This study included 237 patients with heart failure who underwent cardiac catheterization. The relationships between SvO₂ and pulmonary artery systolic pressure (sPAP), pulmonary artery wedge pressure (PAWP), and left ventricular end-diastolic pressure (LVEDP) were examined using various statistical methods (single regression analysis, partial correlation analysis, structural equation modeling, and Bayesian estimation). All statistical methods that we performed showed that SvO₂ was significantly and negatively correlated with both sPAP and PAWP (p < 0.01, respectively). However, SvO₂ did not significantly correlate with LVEDP. These results suggest that a decrease in SvO₂ leads to an increase in PAWP and sPAP, while LVEDP is only passively influenced by PAWP. This phenomenon likely reflects the impact of an intrapulmonary right-to-left shunt caused by IBAs. The decrease in SvO₂ causes an increase in sPAP and may also cause an increase in PAWP via IBAs.

Exercise postcapillary pulmonary hypertension in patients with chronic thromboembolism. Role of multimodal resting and exercise assessment

Abstract Introduction Chronic thromboembolic pulmonary disease refers to the presence of thrombotic material after a pulmonary embolism (PE), exercise limitation and the absence of resting pulmonary hypertension (PH) but impaired right ventricular and pulmonary vascular reserve during exercise causing exercise precapillary PH (exprecapPH). However, in some patients, PH arises from an abnormal increase in pulmonary arterial wedge pressure (PAWP) with exercise in relation to underlying diastolic dysfunction, with thrombotic material not playing a substantial role. Whether these patients present distinct non-invasive and resting invasive parameters remains largely unknown. Purpose To compare the different exercise hemodynamic profiles of patients with chronic thromboembolism to identify clinical, echocardiographic, functional and hemodynamic parameters associated with exercise postcapillary PH (expostcapPH). Methods Data come from a prospective cohort of 71 symptomatic patients with perfusion defects in lung scintigraphy and computed tomographic confirmation of chronic thrombi despite anticoagulation ≥3 months after PE without or mild resting PH, undergoing exercise cardiac catheterization via supine cycle ergometry. A multipoint mean pulmonary artery pressure (mPAP)/cardiac output (CO) and mean PAWP/CO slope were calculated. Simultaneous stress echocardiography was available in 43 patients. Cardiopulmonary exercise test (CPET) was performed 24 hours before catheterization. Results Mean age was 53±13.9 years, 46 (64.8%) were males. 37 patients showed normal exercise hemodynamics, while 26 developed exprecapPH and 8 expostcapPH. Mean mPAP/CO slope was 3.1±1.6 mmHg/L/min, mean PAWP/CO slope 1.5±0.9 mmHg/L/min. Patients with expostcapPH were older, had a higher body mass index and hypertension. Comparison of hemodynamics, CPET and resting echocardiography is depicted in the table. Patients with expostcapPH, similar to those without exercise PH, had significantly lower resting pulmonary pressures and pulmonary vascular resistance than those with exprecapPH. These differences remained at peak exercise; however, while resting PAWP did not differ between groups, a significant increase in PAWP was unmasked in patients with expostcapPH compared to the other groups, and accordingly a significant difference in the PAWP/CO slope. Regarding CPET, patients with expostcapPH had higher baseline systolic blood pressure and lower functional capacity (VO2 max, VO2 at VT1, O2 pulse, OUES). Resting TAPSE/PASP was higher in patients with expostcapPH compared to those with exprecapPH. Conclusions Patients with chronic thromboembolism and expostcapPH exhibit distinct clinical features and have lower functional capacity, while resting PAWP did not allow differentiation between groups. Further studies are warranted to delineate characteristic elements of patients with underlying diastolic dysfunction due to its distinct prognosis and treatment.

Can Inhaled Nitric Oxide Response Predict Tolerance to Therapies and Survival in Patients With Combined Precapillary and Postcapillary Pulmonary Hypertension?

Inhaled nitric oxide (iNO) relaxes the pulmonary circulation and variably increases the left ventricular preload and pulmonary artery wedge pressure (PAWP)-hemodynamic information that may help guide treatment decisions and assess prognosis in patients with combined precapillary and postcapillary pulmonary hypertension (PH). We included consecutive patients with combined precapillary and postcapillary PH (mean pulmonary artery pressure >20mm Hg, PAWP >15mm Hg, and pulmonary vascular resistance [PVR] >2 Woods unit [WU]) who underwent right-sided cardiac catheterization with iNO at the Cleveland Clinic Pulmonary Vascular Disease program between 2017 and 2022. We included 104 patients with baseline PAWP and PVR of 22.2 ± 4.2mm Hg and 6.1 ± 3.2 WU, respectively. Pulmonary arterial hypertension (PAH) with postcapillary component and PH left heart disease with precapillary component were identified in 27 (26%) and 77 patients (74%), respectively. No side effects were noted during the administration of iNO. During iNO, the PVR decreased 1.1 ± 1.4 WU and the PAWP increased 1.3 ± 3.7mm Hg. A more pronounced increase in PAWP with iNO was associated with a decrease in PVR (R -0.35, p <0.001) and increase in stroke volume (R 0.20, p=0.046). Tolerance to PAH-specific medications, overall survival, and heart failure hospitalizations were not significantly associated with the change in PAWP or PVR with iNO. In conclusion, in patients with combined precapillary and postcapillary PH, iNO challenge is safe and caused a significant decrease in PVR, with an increase in PAWP. The changes in PAWP and PVR during iNO administration were not associated with tolerance to PAH-specific medications, heart failure-related hospitalization, or survival.

Pulmonary arterial wedge pressure increase during exercise in patients diagnosed with pulmonary arterial or chronic thromboembolic pulmonary hypertension.

The course of pulmonary arterial wedge pressure (PAWP) during exercise in patients with pulmonary arterial or chronic thromboembolic pulmonary hypertension (PAH/CTEPH), further abbreviated as pulmonary vascular disease (PVD), is still unknown. The aim of the study was to describe PAWP during exercise in patients with PVD. In this cross-sectional study, right heart catheter (RHC) data including PAWP, recorded during semi-supine, stepwise cycle exercise in patients with PVD, were analysed retrospectively. We investigated PAWP changes during exercise until end-exercise. In 121 patients (59 female, 66 CTEPH, 55 PAH, 62±17 years) resting PAWP was 10.2±4.1 mmHg. Corresponding peak changes in PAWP during exercise were +2.9 mmHg (95% CI 2.1-3.7 mmHg, p<0.001). Patients ≥50 years had a significantly higher increase in PAWP during exercise compared with those <50 years (p<0.001). The PAWP/cardiac output (CO) slopes were 3.9 WU for all patients, and 1.6 WU for patients <50 years and 4.5 WU for those ≥50 years. In patients with PVD, PAWP increased slightly but significantly with the onset of exercise compared to resting values. The increase in PAWP during exercise was age-dependent, with patients ≥50 years showing a rapid PAWP increase even with minimal exercise. PAWP/CO slopes >2 WU are common in patients with PVD aged ≥50 years without exceeding the PAWP of 25 mmHg during exercise.

Hemodynamic Response to Oral Vasodilator Therapy in Systemic Sclerosis-Related Pulmonary Hypertension.

Although classified as group 1 pulmonary arterial hypertension (PAH), patients with systemic sclerosis-related pulmonary hypertension (SSc-PH) experience poorer clinical response to PAH therapy and increased mortality compared to those with idiopathic PAH. Due to heterogeneity in phenotypes, identifying patients likely to respond to therapy is challenging. The goal of this study was to determine clinical factors associated with hemodynamic response, defined by a > 20% reduction in pulmonary vascular resistance on repeat right heart catheterization. We applied a time-to-event model using a retrospective cohort of 39 patients with precapillary SSc-PH, defined by a mean pulmonary artery pressure of ≥ 25mmHg and pulmonary arterial wedge pressure (PAWP) ≤ 15mmHg on right heart catheterization. Patients with PAWP ≤ 8mmHg were nearly fourfold more likely to achieve a hemodynamic response compared to those with PAWP > 8mmHg (HR 3.88; 95% CI: 1.20, 12.57); each 1mmHg increase in PAWP was associated with a decreased hazard for hemodynamic response (HR 0.84; 95% CI: 0.70, 1.00). In patients with precapillary SSc-PH, PAWP was associated with time to hemodynamic response, suggesting the importance of subclinical cardiac disease in determining hemodynamic response to oral vasodilator therapy.

LINKS BETWEEN CORONARY MICROVASCULAR DYSFUNCTION AND EVIDENCE OF HEART FAILURE WITH PRESERVED EJECTIVE FRACTION

BackgroundIt has been hypothesized that coronary microvascular dysfunction (CMD) may be associated with the development of myocardial abnormalities associated with heart failure with preserved ejective fraction (HFpEF). Making a diagnosis of HFpEF is aided by exercise right heart catheterization (RHC) based on an abnormal pulmonary artery wedge pressure (PAWP) response during exercise. An exercise-associated increase in PAWP adjusted for the change in cardiac output (ΔPAWP/ΔCO) greater than 2 mmHg/L/min is a clinical predictor for HF outcomes and predicts exercise capacity. Although there is speculation that CMD may play a role in the development of early HFpEF, there is limited evidence that directly links CMD as assessed by an invasive coronary physiology study (ICPS) with HFpEF as measured by an exercise RHC.Methods and ResultsThis study was an exploratory, retrospective cohort analysis. The study population included patients experiencing unexplained cardiovascular symptoms including chest pain and dyspnea who were referred to our institution for a RHC with exercise who had also undergone an ICPS. Patients were classified hemodynamically based on a ΔPAWP/ΔCO ≤ or > 2 with exercise. Coronary physiology interventions included Doppler flow assessment after administration of intracoronary adenosine and acetylcholine, where coronary flow reserve (CFR) and the index of microvascular resistance (IMR) were quantified during hyperemia. To date, we identified a cohort of 20 patients who met the study’s inclusion criteria. Of these, 19 completed a RHC exercise study from which 9/19 (47%) had a ΔPAWP/ΔCO > 2. Characteristics of the patients are shown in Table 1. The mean index of microvascular resistance (IMR) for patients with abnormal exercise hemodynamics was 32.6 versus 20.9 (p=0.08).Conclusion BackgroundIt has been hypothesized that coronary microvascular dysfunction (CMD) may be associated with the development of myocardial abnormalities associated with heart failure with preserved ejective fraction (HFpEF). Making a diagnosis of HFpEF is aided by exercise right heart catheterization (RHC) based on an abnormal pulmonary artery wedge pressure (PAWP) response during exercise. An exercise-associated increase in PAWP adjusted for the change in cardiac output (ΔPAWP/ΔCO) greater than 2 mmHg/L/min is a clinical predictor for HF outcomes and predicts exercise capacity. Although there is speculation that CMD may play a role in the development of early HFpEF, there is limited evidence that directly links CMD as assessed by an invasive coronary physiology study (ICPS) with HFpEF as measured by an exercise RHC. It has been hypothesized that coronary microvascular dysfunction (CMD) may be associated with the development of myocardial abnormalities associated with heart failure with preserved ejective fraction (HFpEF). Making a diagnosis of HFpEF is aided by exercise right heart catheterization (RHC) based on an abnormal pulmonary artery wedge pressure (PAWP) response during exercise. An exercise-associated increase in PAWP adjusted for the change in cardiac output (ΔPAWP/ΔCO) greater than 2 mmHg/L/min is a clinical predictor for HF outcomes and predicts exercise capacity. Although there is speculation that CMD may play a role in the development of early HFpEF, there is limited evidence that directly links CMD as assessed by an invasive coronary physiology study (ICPS) with HFpEF as measured by an exercise RHC. Methods and ResultsThis study was an exploratory, retrospective cohort analysis. The study population included patients experiencing unexplained cardiovascular symptoms including chest pain and dyspnea who were referred to our institution for a RHC with exercise who had also undergone an ICPS. Patients were classified hemodynamically based on a ΔPAWP/ΔCO ≤ or > 2 with exercise. Coronary physiology interventions included Doppler flow assessment after administration of intracoronary adenosine and acetylcholine, where coronary flow reserve (CFR) and the index of microvascular resistance (IMR) were quantified during hyperemia. To date, we identified a cohort of 20 patients who met the study’s inclusion criteria. Of these, 19 completed a RHC exercise study from which 9/19 (47%) had a ΔPAWP/ΔCO > 2. Characteristics of the patients are shown in Table 1. The mean index of microvascular resistance (IMR) for patients with abnormal exercise hemodynamics was 32.6 versus 20.9 (p=0.08). This study was an exploratory, retrospective cohort analysis. The study population included patients experiencing unexplained cardiovascular symptoms including chest pain and dyspnea who were referred to our institution for a RHC with exercise who had also undergone an ICPS. Patients were classified hemodynamically based on a ΔPAWP/ΔCO ≤ or > 2 with exercise. Coronary physiology interventions included Doppler flow assessment after administration of intracoronary adenosine and acetylcholine, where coronary flow reserve (CFR) and the index of microvascular resistance (IMR) were quantified during hyperemia. To date, we identified a cohort of 20 patients who met the study’s inclusion criteria. Of these, 19 completed a RHC exercise study from which 9/19 (47%) had a ΔPAWP/ΔCO > 2. Characteristics of the patients are shown in Table 1. The mean index of microvascular resistance (IMR) for patients with abnormal exercise hemodynamics was 32.6 versus 20.9 (p=0.08). Conclusion

P283 PROGRESSION OF PULMONARY ARTERIAL HYPERTENSION OR LEFT HEART DISEASE? DO EXERCISE!

Abstract An 80–year–old man, diagnosed with idiopathic pulmonary arterial hypertension (PAH) in 2012 and treated with sildenafil, experienced his first hospitalization for heart failure in June 2019. He had several cardiovascular risk factors (overweight, hypertension, diabetes) and comorbidities (ischemic heart disease, and mild chronic obstructive pulmonary disease), whose progression was excluded. Since this event, he complained a progressive deterioration of the exertional dyspnea (NYHA III), with overt signs of fluid overload, right chambers dilation and high NTproBNP (1366 ng/L). However, the center taking care of this patient neither decided to fully re–evaluate him nor to escalate PAH–treatment due to his clinical profile (high suspicion of left heart disease, LHD). He then came to our pulmonary hypertension (PH) center where we decided to perform a cardiac catheterization, which showed the persistence of precapillary PH with high pulmonary vascular resistance, PVR (7.6 WU), low cardiac output, CO (2.2 L/min/m2), high right atrial pressure, RAP (12 mmHg). Pulmonary artery wedge pressure (PAWP) and left ventricular end–diastolic pressure (LVEDP) were at the upper limits of normal (13 mmHg and 16 mmHg, respectively) (Figure 1). Based on these “borderline” PAWP values, with an intermediate–high pre–test probability of left heart disease, we performed an exercise test with concomitant gas–exchange analysis on a cycle ergometer in the cath lab (Figure 2). Exercise induced a steep increase in pulmonary pressure (TPR 9 WU), unrelated to an exaggerate increase in PAWP or LVEDP (whose peak values reached 20 mmHg, with a PAWP/CO slope &amp;lt;2 mmHg/L/min), but entirely dependent on the precapillary component. Transpulmonary gradient (TPG)/CO slope was high, leading to an absent reduction in PVR (6.4 WU at peak), associated to severe increase in RAP (27 mmHg at peak, RAP/PAWP 1.4) (Figure 3). CO reserve was reduced (at peak 3.4 L/min/m2), due to both reduced increase in stroke volume and chronotropic incompetence. Accordingly, functional capacity was moderately–severely reduced (peak oxygen consumption was 8 ml/kg/min, 39% of predicted), with exercise hyperventilation. Once excluded LHD as the responsible of clinical worsening, and in consideration of the high–intermediate risk profile of this patient, we upgraded the PAH–specific therapy by adding macitentan, obtaining a subjective clinical improvement and a 3–years period of clinical stability.

The adding value of fluid challenge and balloon occlusion tests in patients with atrial septal defect

Abstract Background Careful, step-wise assessment is required in all patients with an atrial septal defect (ASD) to exclude pre-existing pulmonary vascular disease or left ventricular disease. Fluid challenge test (FCT) and balloon occlusion testing (BOT) may unmask left ventricular disease and challenge the pulmonary circulation, but their complementary role in the evaluation of patients with “operable” ASD is not well established. Aim To evaluate the haemodynamic changes of the pulmonary circulation by FCT and BOT in ASD patients undergoing percutaneous closure according to the current guidelines. Methods Consecutive patients selected for percutaneous ASD closure underwent invasive hemodynamic assessment at baseline and after BOT, FCT and both. Results Fifty patients (mean age 47.3±11.7 years, 72% female) were included. All patients had a pulmonary-to-systemic flow ratio (QP/QS) ≥1.5, pulmonary vascular resistance (PVR) &amp;lt;5 WU and pulmonary arterial wedge pressure (PAWP) &amp;lt;15 mmHg. Individuals with a PVR ≥2 WU at baseline were older, more symptomatic, with a higher baseline systemic vascular resistance compared to the lower PVR group (PVR &amp;lt;2 WU; p&amp;lt;0.0001). The response of Qp/Qs to FCT was different between groups (p&amp;lt;0.0001, Figure 1). Patients with a lower baseline PVR experienced an increase in Qp/Qs, which remained above 1.5 in all patients, whereas in almost all (90%) patients with a higher baseline PVR, the Qp/Qs fell to below 1.5. FCT caused a marked increase in pulmonary blood flow of almost 2 liters (p&amp;lt;0.0001) accompanied by increases in PAWP (p&amp;lt;0.0001). BOT led to a modest increase in PAWP (Δ1.5 [−1.0–7.0] mmHg, p&amp;lt;0.0001). FCT added to BOT caused a further increase in PAWP and Qs (both p&amp;lt;0.0001), while PVR was unchanged (p&amp;gt;0.1). No difference was observed in the PAWP response to FCT, BOT or both between groups; no patients reached a PAWP ≥18 mmHg following FCT or BOT alone, but 4 (8%) patients did following the addition of FCT to BOT. No acute clinical adverse events were experienced by any patients. Conclusions None of the reported ASD patients presented with FCT criteria of post-capillary PH (that is a PAWP &amp;gt;18 mmHg). Even small rises in PVR may have significant implications on cardiovascular haemodynamics. In fact, patients with PVR &amp;lt;2 WU showed an increase in Qp/Qs, which remained above 1.5 in all patients, suggesting that they still had a distensible pulmonary circulation, whereas in almost all patients with a PVR ≥2 WU, the Qp/Qs fell to below 1.5. Funding Acknowledgement Type of funding sources: None. Figure 1

Passive leg raising: can it help in the diagnosis of pulmonary hypertension due to left heart disease

Abstract Pulmonary hypertension (PH) is a frequent hemodynamic condition that is highly prevalent in patients with left heart diseases (LHD). Patients with PH-LHD usually have post-capillary PH, which is now defined by a mean pulmonary arterial pressure (mPAP) of &amp;gt;20 mm Hg and a pulmonary arterial wedge pressure (PAWP) of &amp;gt;15 mm Hg. When assessing PAWP in LHD patients, it must also be acknowledged that pretreatment with diuretics leads to lowering of left-sided filling pressures and thus PAWP, and this bears the potential of misclassifying post- as pre-capillary PH if the PAWP should be lowered to a value below 15 mm Hg. In this context, in cases of borderline PAWP (13–15 mm Hg) a “volume challenge” (500 ml of saline within 5–10 min) has been proposed in order to reverse the diuretic effect and to uncover “occult HFpEF”, but the therapeutic consequences of such testing remain unclear. In acute circulatory failure, passive leg raising (PLR) is a test that predicts whether cardiac output will increase with volume expansion. By transferring a volume of around 300 mL of venous blood from the lower body toward the right heart, PLR mimics a fluid challenge. However, no fluid is infused and the hemodynamic effects are rapidly reversible, thereby avoiding the risks of fluid overload (safety). There are those who believe, that most PH in connective tissue diseases (CTD), espesially systemic sclerosis (SSc) is post-capillary and that many patients are receiving pulmonary vasodilator therapy inappropriately. The aim of this study to investigate possibility PLR test in the diagnosis of PH due to left heart disease. PLR test is applied during 77 catheterizations in 69 patients with CTD and PH, among them 14 patients with established PH-LHD and 55 patients with precapillary PH (45 with PAH, 10 with PH, associated with SSc interstitial lung diseases). The diagnosis of PH-LHD was established in the presence of lesions of the left heart (CHD or cardiomyopathy), identified using echocardiography, coronaroangiography and heart MRI. It was determined that despite approaching a valid difference between the PAWP 12 (7; 14) mm Hg and 8.5 (6; 12) mm Hg, p=0.06), in the PLR test, the level of PAWP increased significantly only in patients with PH-LHD (up to 17 (11; 19) mmHg than precapillary PH (9 (8; 13) mm Hg, p=0.00026). The increase of PAWP was 4 (3; 8) mm Hg and total 1 (0; 3) mm Hg, respectively, differences are valid (p=0.ehab724.19142). The PAWP was measured before the test, and on 5 and 10 minutes during test. It was found that the maximum increase in PAWP occurred 10 minutes from the start of the test. The ROC analysis of PAWP in this two groups showed the area under the curve was 0.837 (0.737; 0,937), p&amp;lt;0,0001. The cutt-off of the growth of PAWP was 4 mm Hg with a sensitivity of 82% and a specificity of 73%. Thus, an increase in PAWP more than 4 mm Hg can indicates the presence of PH-LHD in the patient with CTD. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Ministry of science and higher education, Russian Federation

SIGNIFICANCE OF THE PASSIVE LEG RAISING TEST IN THE DIAGNOSIS OF PULMONARY HYPERTENSION DUE TO LEFT HEART DISEASES IN SYSTEMIC SCLEROSIS

TOPIC: Pulmonary Vascular Disease TYPE: Original Investigations PURPOSE: The association between systemic sclerosis and pulmonary hypertension (PH) is well established. Patients with systemic sclerosis (SSc) are usually older than 50 years, therefore, along with pulmonary arterial hypertension (PAH), they often have PH due to left heart disease (PH-LHD). Some patients with left ventricular diastolic dysfunction may have normal resting pulmonary artery wedge pressure (PAWP) and this bears the potential of misclassifying post-as pre-capillary PH if the PAWP should be lowered to a value below 15 mm Hg. It is very important, that pulmonary vasodilator drugs approved for PAH may have deleterious effects or be ineffective if administered to patients with LHD. In this context, in cases of borderline PAWP (13–15 mm Hg) a "volume challenge" (500 ml of saline within 5–10 min) has been proposed to reverse the "occult LHD", but the therapeutic consequences of such testing remain unclear. In acute circulatory failure, passive leg raising (PLR) is a test that predicts whether the cardiac output will increase with volume expansion. By transferring a volume of around 300 mL of venous blood from the lower body toward the right heart, PLR mimics a fluid challenge.The aim of this study to investigate the possibility of PLR test in the differentiation between PAH and PH due to left heart disease in patients with "normal" PAWP. METHODS: PLR test is applied during 77 catheterizations in 69 patients with SSc and PH, among them 14 patients with established PH-LHD and 55 patients with precapillary PH (45 with PAH, 10 with PH, associated with SSc interstitial lung diseases). The hemodynamic parameters were measured before the test, and on 5 and 10 minutes during the test. It was found that the maximum increase in PAWP occurred 10 minutes from the start of the test. The diagnosis of PH-LHD was established in the presence of lesions of the left heart (CHD or subclinical cardiomyopathy), identified using echocardiography, coronary angiography, and heart MRI. RESULTS: PAWP level was 12 (7; 14) mm Hg at PH-LHD and 8.5 (6; 12) mm Hg, p = 0.06) at patients with PAH. Logistic regression analysis showed that the main differences between the groups were in the age of the patients (OR 1,06 95% CI 1,00-1,12, p 0,036), the PAWP level before the test (OR 1,15 95% CI 1,00 – 1,31, p=0,04), and the increase in PAWP during the test (OR 1,28 95% CI 1,10-1,47, p=0,001). The ROC analysis of PAWP increasing in these two groups showed the area under the curve was 0.837 (0.737; 0,937), p < 0,0001. The cut-off of the PAWP raise was 4 mm Hg with a sensitivity of 82% and a specificity of 73%. CONCLUSIONS: It is advisable to study the PLR ??test for differential diagnosis of PAH and PH-LHD, as a safer and more affordable method. CLINICAL IMPLICATIONS: none DISCLOSURES: No relevant relationships by Ildar Kurmukov, source=Web Response No relevant relationships by Eugene Nasonov, source=Web Response No relevant relationships by Ekaterina Nikolaeva, source=Web Response No relevant relationships by Alexander Volkov, source=Web Response

Physiologic Phenotype of Cardiogenic Shock Due to End-Stage Heart Failure and Acute Myocardial Infarction: Effect of ECLS

<h3>Purpose</h3> This study (i) models and compares the pathophysiology of cardiogenic shock (CS) due to end stage heart failure (ESHF) and acute myocardial infarction (AMI) using patient data and (ii) compares the effects extracorporeal life support (ECLS) in these 2 patient groups. <h3>Methods</h3> Data from consecutive patients with CS due to ESHF and AMI were used as the basis for simulating the hemodynamics with the computational model by Burkhoff et al. ESHF is defined as diagnosis of an ischemic or non-ischemic cardiomyopathy prior to CS. The effects of right atrial (RA) to femoral artery ECLS at 3.5L/min were simulated. <h3>Results</h3> Patient with ESHF had lower ejection fraction, more mitral regurgitation and higher right atrial pressure [TABLE]. Compared to AMI, CS due to ESHF is associated with (i) lower left (LV) and right ventricular (RV) diastolic pressure-volume relation (lower ‘stiffness') [FIGURE]; (ii) lower LV and RV end-systolic elastance (Ees) and (iii) larger pressure-volume loop area (PVA) corresponding to high myocardial oxygen consumption (MVO2), (iv) lower RV efficiency (ratio of stroke work to MVO2). ECLS increased systemic blood pressure and pulmonary artery wedge pressure (PAWP) in both groups, but patients with AMI had higher relative increase in PAWP due to the steeper diastolic pressure-volume relation compared to ESHF. <h3>Conclusion</h3> The hemodynamic phenotype in CS due to ESHF differs from AMI with higher LV and RV capacitance (lower 'stiffness'), lower LV and RV Ees (contractility) and lower RV efficiency in the former. ECLS increased systemic and pulmonary artery wedge pressure, which is more marked in AMI.

Hemodynamic Effects of Pulmonary Arterial Hypertension-Specific Therapy in Patients With Heart Failure With Preserved Ejection Fraction and With Combined Post- and Precapillay Pulmonary Hypertension

Drugs approved for pulmonary arterial hypertension have been considered for patients with heart failure with preserved ejection fraction and combined post- and precapillary pulmonary hypertension (Cpc-PH). We aimed to study changes in cardiac volumes, cardiac load and left ventricular (LV) filling pressures in patients with heart failure with preserved ejection fraction and Cpc-PH in response to pulmonary arterial hypertension-specific treatment. In this prospective study, 23 patients with heart failure with preserved ejection fraction and Cpc-PH underwent right-heart catheterization, including acute provocation testing (fluid loading and inhaled nitric oxide) and cardiac MRI at baseline. Right-heart catheterization and cardiac MRI were repeated after 4 months of treatment. At baseline, acutely increasing preload by fluid loading resulted in a significant increase in pulmonary arterial wedge pressure (PAWP), whereas reducing right ventricular (RV) afterload and increasing LV distensability by acute administration of inhaled nitric oxide had no effect on PAWP. After 4 months of treatment, we observed a significant reduction in RV and LV afterload and increased RV and LV stroke volume, but PAWP significantly increased. In patients with heart failure with preserved ejection fraction and Cpc-PH, 4 months of pulmonary arterial hypertension-specific treatment increased RV and LV stroke volume at the expense of increased PAWP. This increase in PAWP was similarly observed acutely after fluid loading.

Clinical and hemodynamic factors in predicting response to fluid challenge during right heart catheterization.

Fluid challenge during right heart catheterization has been used for unmasking pulmonary hypertension (PH) related to left-sided heart disease. We evaluated the clinical and hemodynamic factors affecting the response to fluid challenge and investigated the role of fluid challenge in the classification and management of PH patients. We reviewed the charts of 67 patients who underwent fluid challenge with a baseline pulmonary arterial wedge pressure (PAWP) of ≤ 18 mmHg. A positive fluid challenge (PFC) was defined as an increase in PAWP to > 18 mmHg after 500 mL saline infusion. Clinical characteristics and echocardiographic and hemodynamic parameters were compared between PFC and negative fluid challenge (NFC). PFC was associated with female sex, increased BMI, and hypertension. A greater rise in PAWP was observed in PFC (6.8 ± 2.3 vs. 3.8 ± 2.7 mmHg, P = 0.001). A larger increase in PAWP correlated with a lower transpulmonary gradient (r = –0.42, P < 0.001), diastolic pulmonary gradient (r = –0.42, P < 0.001), and pulmonary vascular resistance (r = –0.38, P < 0.001). We found 100% of the patients with PFC were classified as WHO group 2 PH compared to 49% of the NFC patients (P < 0.001). Fewer patients with PFC were started on advanced PH therapies and more were discharged from PH clinic. A PFC and the magnitude of PAWP increase after saline loading are associated with parameters related to left heart disease. In our population, fluid challenge appeared to influence the classification of PH and whether patients are started on therapy or discharged from clinic.

Left ventricular deformation at rest predicts exercise-induced elevation in pulmonary artery wedge pressure in patients with unexplained dyspnoea.

Impaired left ventricular (LV) deformation despite preserved LV ejection fraction (LVEF) is common and predicts outcomes in heart failure with preserved LVEF. We hypothesized that impaired LV deformation at rest is a marker of impaired cardiac systolic and diastolic reserve, and aimed to determine whether resting longitudinal (LS) and circumferential strain (CS) are associated with invasively measured haemodynamic response to exercise in patients with dyspnoea and a normal LVEF. We studied 85 patients with LVEF ≥50% and free of significant valvular disease who were referred for evaluation of dyspnoea. All patients underwent rest echocardiography followed by right heart catheterization and cardiopulmonary exercise testing with concomitant invasive haemodynamic monitoring. The LS, CS and CS/LS ratio were measured by two-dimensional speckle-tracking echocardiography at rest. Lower absolute LS at rest was associated with greater increase in pulmonary arterial wedge pressure (PAWP) from rest to peak exercise (r = 0.23, P = 0.034). In contrast, higher absolute CS at rest predicted a greater increase in PAWP (r = - 0.27, P = 0.032) and greater stroke volume augmentation with exercise (r = - 0.26, P = 0.021). Higher CS/LS ratio was most predictive of elevation in PAWP with exercise (r = 0.30, P = 0.015). Of the measures of LV systolic and diastolic function assessed, the CS/LS ratio resulted in the highest area under the curve and specificity for the presence of rest- or exercise-induced pulmonary venous hypertension. Left ventricular deformation at rest predicts exercise-induced rise in PAWP among patients with dyspnoea and a preserved LVEF. A pattern of rest deformation characterized by worse LS and exaggerated CS is most strongly associated with exercise-induced rise in PAWP.

Clinical Relevance of Fluid Challenge in Patients Evaluated for Pulmonary Hypertension

Fluid challenge may help in the differential diagnosis between pre- and postcapillary pulmonary hypertension (PH). However, the test is still in need of standardization and better defined clinical relevance. Two hundred twelve patients referred for PH underwent a right-sided heart catheterization with measurements before and after rapid infusion of 7mL/kg of saline. PH was defined as mean pulmonary artery pressure≥ 25mmHg, and postcapillary PH was defined as pulmonary artery wedge pressure (PAWP) > 15mmHg. An increase in PAWP≥ 18mmHg was considered diagnostic for postcapillary PH. At baseline, 66 patients received a diagnosis of no PH; 22, of postcapillary PH; and 124, of precapillary PH (mostly pulmonary arterial hypertension). After fluid challenge, five of 66 patients with no PH (8%) and eight of 124 with precapillary PH (6%) had the diagnosis reclassified as postcapillary PH. Fluid challenge was associated with an increase in PAWP by 7 ± 2mmHg in postcapillary PH and 3 ± 1mmHg in both precapillary PH and no-PH groups. Between-group differences were significant, but there was overlap. There were no adverse events related to fluid challenge. Prediction bands calculated from quadratic fits of the PAWP responses in pooled control subjects with no PH and patients with precapillary PH helped confirm 18mmHg as the cutoff for diagnosing postcapillary PH. Fluid challenge with 7mL/kg saline increases PAWP, more in postcapillary than in precapillary PH or in control subjects with no PH. A cutoff value of 18mmHg allows reclassification of 6%to 8%of patients with precapillary PH or normal hemodynamic characteristics at baseline.

The relationship of pulmonary vascular resistance and compliance to pulmonary artery wedge pressure during submaximal exercise in healthy older adults.

A consistent inverse hyperbolic relationship has been observed between pulmonary vascular resistance and compliance, although changes in pulmonary artery wedge pressure (PAWP) may modify this relationship. This relationship predicts that pulmonary artery systolic, diastolic and mean pressure maintain a consistent relationship relative to the PAWP. We show that, in healthy exercising human adults, both pulmonary vascular resistance and compliance decrease in relation to exercise-associated increases in PAWP. Pulmonary artery systolic, diastolic and mean pressures maintain a consistent relationship with one another, increasing linearly with increasing PAWP. Increases in PAWP in the setting of exercise are directly related to a decrease in pulmonary vascular compliance, despite small decreases in pulmonary vascular resistance, thereby increasing the pulsatile afterload to the right ventricle. The resistive and pulsatile components of right ventricular afterload (pulmonary vascular resistance, Rp; compliance, Cp) are related by an inverse hyperbolic function, expressed as their product known as RpCp-time. The RpCp-time exhibits a narrow range, although it may be altered by the pulmonary artery wedge pressure (PAWP). Identifying the determinants of RpCp-time should improve our understanding of the physiological behaviour of pulmonary arterial systolic (PASP), diastolic (PADP) and mean (mPAP) pressures in response to perturbations. We examined the effect of exercise in 28 healthy non-athletic adults (55±6years) who underwent right heart catheterization to assess haemodynamics and calculate Rp and Cp. Measurements were made at rest and during two consecutive 8-10min stages of cycle ergometry, at targeted heart-rates of 100beatsmin(-1) (Light) and 120beatsmin(-1) (Moderate). Cardiac output increased progressively during exercise. PASP, PADP, mPAP and PAWP increased for Light exercise, without any further rise for Moderate exercise. RpCp-time decreased for Light exercise (0.39±0.08 to 0.25±0.08, P<0.001) without any further change for Moderate exercise, and the decrease in RpCp-time was related to changes in PAWP (r(2) =0.26, P<0.001). Changes in PASP (r(2) =0.43, P<0.001), PADP (r(2) =0.47, P<0.001) and mPAP (r(2) =0.50, P<0.001) were linearly correlated with changes in PAWP, although they were not significantly related to changes in cardiac output. In healthy adults, exercise is associated with decreases in Cp and a resultant decline in RpCp-time, indicating increased pulsatile right ventricular afterload. Changes in RpCp-time, PASP, PADP and mPAP were systematically related to increases in PAWP.

The pulmonary artery wedge pressure response to sustained exercise is time-variant in healthy adults

ObjectivesThe clinical and prognostic significance of ‘exaggerated’ elevations in pulmonary artery wedge pressure (PAWP) during symptom-limited exercise testing is increasingly recognised. However, the paucity of normative data makes the identification...

Abstract 15435: Myocardial Deformation at Rest Predicts Exercise-induced Elevation in Left Ventricular Filling Pressure in Patients With Exertional Dyspnea

Background: An exaggerated rise in the pulmonary arterial wedge pressure (PAWP) with exercise is a hallmark of heart failure. However, conventional resting-state measures of cardiac structure and function poorly predict exercise hemodynamics. We determined whether LV longitudinal strain (LS) and circumferential strain (CS) predict exercise-induced rise in PAWP. Methods: We studied 85 patients referred for cardiopulmonary exercise testing with invasive hemodynamic monitoring for evaluation of dyspnea. Patients with an LVEF&lt;50% or moderate or greater valvular disease were excluded. All patients underwent rest echocardiography followed by exercise testing with invasive hemodynamic monitoring. Global longitudinal strain (LS), global circumferential strain (CS) and the CS/LS-ratio were measured by 2D speckle-tracking echocardiography. Results: Mean age was 53±18 years, 25% were male, 41% had hypertension, and 9% had diabetes mellitus. Lower absolute LS at rest was associated with greater increase in PAWP during exercise (r=0.23, p=0.033). In contrast, higher absolute CS at rest predicted a greater increase in PAWP (r=-0.27, p=0.025) and greater increase in stroke volume with exercise (r=-0.26, p=0.044). Higher CS/LS-ratio was most predictive of elevation in PAWP with exercise (r=0.27, p=0.023; Figure). Conclusion: Myocardial deformation at rest predicts exercise-induced rise in PAWP among patients with dyspnea and a preserved LVEF. A pattern of rest deformation characterized by worse LS and exaggerated CS is most strongly associated with exercise-induced rise in PAWP.

Abstract 17885: Pulmonary Vascular Compliance Predicts Mortality in the Acute Respiratory Distress Syndrome

Introduction: Novel markers of prognosis in the acute respiratory distress syndrome (ARDS) are needed. Hypothesis: We hypothesized that pulmonary vascular compliance would predict outcome in ARDS, and that higher left heart filling pressure would be associated with increased pulsatile loading of the right ventricle manifested as reduced RC time. Methods: We performed a retrospective analysis of 392 subjects with a complete hemodynamic data set on trial day 0 in the ARDS Network Fluid and Catheter Treatment Trial of PA catheter use in ARDS. Pulmonary vascular compliance (Cpa) was calculated as stroke volume divided by PA pulse pressure. Pulmonary vascular resistance (PVR) was calculated as mean PA pressure minus pulmonary artery wedge pressure (PAWP) divided by cardiac output. The RC time was calculated as the product of PVR and Cpa. Cox proportional hazard modeling and Kaplan-Meier survival analysis were performed with primary outcome of death. Results: The mean age was 50 ± 16 years. Mean PA pressure and PAWP were both elevated (29 ± 8 mmHg and 15 ± 5 mmHg, respectively) as was cardiac output (7.7 ± 2.7 L/m). The mean PVR was 2.1 ± 1.2 Wood units and Cpa 4.6 ± 2.5 ml/mmHg. Mean RC time was 0.47 ± 0.24 seconds (s). With each 5 mmHg increase in PAWP, RC time decreased by 0.06 s (p&lt;0.0001 for slope). There was increased hazard of death per quartile decrease in Cp (HR 1.28, 95% CI 1.08-1.52; p = 0.004) and per quartile increase in PVR (HR 1.23, 95% CI 1.04-1.46; p = 0.02). Adjusted for APACHE III score, there remained a trend towards increased hazard of death per quartile increase in PVR (HR 1.2 95% CI 1.03-1.4, p = 0.02) and per quartile decrease in Cp (HR 1.18 95% CI 1.0-1.4, p = 0.055). Kaplan-Meier survival curves per quartile of Cp are shown in the Figure. Conclusion: Pulmonary vascular compliance predicts mortality in ARDS. Higher wedge pressure is associated with lower RC time in ARDS consistent with increased RV pulsatile loading.

THE RISE AND FALL OF PULMONARY ARTERY WEDGE PRESSURE: TIME-DEPENDENT PRESSURE DECAY MAINTAINS LOW PULMONARY PRESSURES DURING SUBMAXIMAL EXERCISE

It is now widely accepted that pulmonary arterial wedge pressure (PAWP) can rise significantly with exercise, even in health. The utility of exercise as a probe for hemodynamic abnormalities is an area of emerging interest, but has had limited success to date, in part due to low specificity of proposed ‘normal’ cut-off values. Recent works have identified ‘exaggerated’ patterns of PAWP responses to exercise as a marker of poor prognosis in heart failure cohorts. A detailed understanding of the ‘normal’ pattern of PAWP response to exercise may aid in the design of diagnostic protocols with appropriate normative data. The purpose of our study was to describe the PAWP response to submaximal exercise in healthy older adults. We hypothesized that PAWP would transiently increase during escalating work-rate, but subsequently decay as submaximal exercise is sustained. Twenty-eight healthy volunteers (17M/11F; mean age = 55±6 years) were studied at rest and during two consecutive stages of cycle-ergometry, with individualized work-rates designed to elicit heart rates (HR) of 100 bpm (Light Exercise) and 120 bpm (Moderate Exercise). Right heart catheterization was performed to directly measure pulmonary pressures. Pulmonary arterial and wedge pressures were measured early (2 minutes) and after sustained (7 minutes) exercise at each intensity. At control, HR was 63 ± 8 bpm, and mean right atrial pressure and PAWP were 6 ± 3 mmHg and 10 ± 3 mmHg, respectively. Pulmonary arterial systolic pressure was 25 ± 4 mmHg. Exercise data are presented in Table 1. With initiation of Light Exercise, target HR was achieved at approximately 2 minutes and then maintained. At 2 minutes of Light Exercise, PAWP increased from control by 100±34% and by 7 minutes of sustained exercise, PAWP then decayed by 57±26%. A further increase of exercise intensity (Moderate Exercise) failed to elicit a further increase in PAWP at 2 minutes, and by 7 minutes of Moderate Exercise, PAWP decayed further, matching resting Control measures despite significantly elevated HR and cardiac output. PAWP increases acutely and substantially with the initiation of exercise, but decays significantly within a period of minutes to that observed at rest. This time-dependent accommodation may be related to left-sided diastolic function, which may vary accordingly with age. Our data indicates that during sustained submaximal exercise, pressure across the pulmonary vasculature remains relatively low in health. Pulmonary hemodynamic response patterns to exercise may provide insight into hemodynamic abnormalities in clinical populations.