Hemodynamic Evidence of Vascular Remodeling in Combined Post‐ and Precapillary Pulmonary Hypertension

Assad, Tufik R.; Brittain, Evan L.; Wells, Quinn S.; Farber‐Eger, Eric; Halliday, Stephen; Doss, Laura N.; Xu, Meng; Wang, Li; Harrell, Frank E.; Yu, Chang; Robbins, Ivan M.; Newman, John H.; Hemnes, Anna R.

doi:10.1086/688516

Cited by 39 publications

(69 citation statements)

References 54 publications

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“…However, we also included subjects who underwent echocardiography within 2 days after RHC, which somewhat mitigates indication bias. We are unable to manually review the RHC tracings for the accuracy of the computer‐generated pressure values, although we have previously reported that this difference is likely to be small in our population 10. A small minority of TTE studies performed at our institution are “limited” studies in which a full interrogation of the TRV may not have been attempted.…”

Section: Discussionmentioning

confidence: 94%

“…We extracted clinical and hemodynamic data from all adult patients undergoing RHC at Vanderbilt between 1998 and 2014. The method of data extraction has been described in detail elsewhere 9, 10, 11. We included only subjects who underwent a TTE within 2 calendar days before or after RHC.…”

Section: Methodsmentioning

confidence: 99%

“…Images were not reviewed by a core laboratory. Comorbidities were defined by a combination of International Classification of Diseases, Ninth Revision (ICD‐9) codes and laboratory data in the medical record before RHC or as defined by previously validated algorithms 10. Body mass index was extracted from TTE reports.…”

Section: Methodsmentioning

confidence: 99%

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Lack of a Tricuspid Regurgitation Doppler Signal and Pulmonary Hypertension by Invasive Measurement

O'Leary

Assad

et al. 2018

JAHA

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BackgroundTransthoracic echocardiography (TTE) is used to estimate pulmonary artery systolic pressure, but an adequate tricuspid regurgitation velocity (TRV) needed to calculate pulmonary artery systolic pressure is not always present. It is unknown whether the absence of a measurable TRV signifies normal pulmonary artery pressure.Methods and ResultsWe extracted hemodynamic, TTE, and clinical data from Vanderbilt's deidentified electronic medical record in all patients referred for right heart catheterization between 1998 and 2014. Pulmonary hypertension (PH) was defined as mean pulmonary artery pressure ≥25 mm Hg. We examined the prevalence and clinical correlates of PH in patients without a reported TRV. We identified 1262 patients with a TTE within 2 days of right heart catheterization. In total, 803/1262 (64%) had a reported TRV, whereas 459 (36%) had no reported TRV. Invasively confirmed PH was present in 47% of patients without a reported TRV versus 68% in those with a reported TRV (P<0.001). Absence of a TRV yielded a negative predictive value for excluding PH of 53%. Right ventricular dysfunction, left atrial dimension, elevated body mass index, higher brain natriuretic peptide, diabetes mellitus, and heart failure were independently associated with PH among patients without a reported TRV.Conclusions PH is present in almost half of patients without a measurable TRV who are referred for both TTE and right heart catheterization. Clinical and echocardiographic features of left heart disease are associated with invasively confirmed PH in subjects without a reported TRV. Clinicians should use caution when making assumptions about PH status in the absence of a measurable TRV on TTE.

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Section: Discussionmentioning

confidence: 94%

Section: Methodsmentioning

confidence: 99%

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Lack of a Tricuspid Regurgitation Doppler Signal and Pulmonary Hypertension by Invasive Measurement

O'Leary

Assad

et al. 2018

JAHA

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“…35 In another larger scale study, fluid challenge did not affect the time constant of the pulmonary circulation, or PVR×C PA , in Cpc-PH or in PAH, while it decreased it significantly in Ipc-PH, suggesting fixed pulmonary vascular remodeling in Cpc-PH. 36 Biological support for a Cpc-PH phenotype was recently provided by an analysis of a large database of 2817 PH patients from Vanderbilt University in Nashville. 37 In that study, patients with Cpc-PH were younger but with more severe pulmonary vascular disease than patients with Ipc-PH, despite similar comorbidities and prevalence, severity, and chronicity of LHD, and presented with 75 exonic single-nucleotide polymorphisms enriched in pathways involving cell structure, extracellular matrix, and immune function that were shared with PAH and not with Ipc-PH patients.…”

Section: The Diastolic Pulmonary Pressure Gradientmentioning

confidence: 99%

Hemodynamic Phenotyping of Pulmonary Hypertension in Left Heart Failure

Naeije

Gerges

Vachiéry

et al. 2017

Circ: Heart Failure

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ABSTRACT:Increased pulmonary venous pressure secondary to left heart disease is the most common cause of pulmonary hypertension (PH). The diagnosis of PH due to left heart disease relies on a clinical probability assessment followed by the invasive measurements of a mean pulmonary artery pressure (PAP) ≥25 mm Hg and mean wedged PAP (PAWP) >15 mm Hg. A combination of mean PAP and mean PAWP defines postcapillary PH. Postcapillary PH is generally associated with a diastolic pulmonary pressure gradient (diastolic PAP minus mean PAWP) <7 mm Hg, a transpulmonary pressure gradient (mean PAP minus mean PAWP) <12 mm Hg, and pulmonary vascular resistance ≤3 Wood units (WU). This combination of criteria defines isolated postcapillary PH. Postcapillary PH with elevated vascular gradients and pulmonary vascular resistance defines combined post-and precapillary PH (Cpc-PH). Postcapillary PH is associated with a decreased survival in proportion to increased pulmonary vascular gradients, decreased pulmonary arterial compliance, and reduced right ventricular function. The Cpc-PH subcategory occurs in 12% to 13% of patients with PH due to left heart disease. Patients with Cpc-PH have severe PH, with higher diastolic pulmonary pressure gradient, transpulmonary pressure gradient, and pulmonary vascular resistance and more pronounced ventilatory responses to exercise, lower pulmonary arterial compliance, depressed right ventricular ejection fraction, and shorter life expectancy than isolated postcapillary PH. Cpc-PH bears similarities to pulmonary arterial hypertension. Whether Cpc-PH is amenable to therapies targeting the pulmonary circulation remains to be tested by properly designed randomized controlled trials.

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“…We recently showed that pulmonary vascular physiology in Cpc-PH, as measured by the resistance-compliance relationship, resembles PAH more than Ipc-PH, suggesting a potential shared etiology (11). Although prior papers have provided valuable information (2,3,5,12–16), our understanding of Cpc-PH etiology and pathophysiology is limited, as no biological data have been reported in this population (17).…”

Section: Introductionmentioning

confidence: 99%

Clinical and Biological Insights Into Combined Post- and Pre-Capillary Pulmonary Hypertension

Assad

Hemnes

Larkin

et al. 2016

Journal of the American College of Cardiology

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201

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Background Pulmonary hypertension (PH) is a common and morbid complication of left heart disease with 2 subtypes: isolated post-capillary PH (Ipc-PH) and combined post-capillary and pre-capillary PH (Cpc-PH). Little is known about the clinical or physiological characteristics that distinguish these 2 subphenotypes, and if Cpc-PH shares molecular similarities to pulmonary arterial hypertension (PAH). Objectives We sought to test the hypothesis that the hemodynamic and genetic profile of Cpc-PH would more closely resemble PAH than Ipc-PH. Methods We used Vanderbilt’s electronic medical record linked to a DNA biorepository to extract demographics, clinical data, invasive hemodynamics, echocardiography, and vital status for all patients referred for right heart catheterization between 1998 and 2014. We identified shared genetic variants between PAH and Cpc-PH compared with Ipc-PH using pre-existing single-nucleotide polymorphism data. Results We identified 2,817 patients with PH (13% Cpc-PH, 52% Ipc-PH, and 20% PAH). Cpc-PH patients were on average 6 years younger, with more severe pulmonary vascular disease than Ipc-PH patients, despite similar comorbidities and prevalence, severity, and chronicity of left heart disease. After adjusting for relevant covariates, the risk of death was similar between Cpc-PH and Ipc-PH (HR: 1.14, 95% CI: 0.96 to 1.35, p = 0.15) when defined by diastolic pressure gradient. We identified 75 shared exonic single-nucleotide polymorphisms between Cpc-PH and PAH enriched in pathways involving cell structure, extracellular matrix, and immune function. These genes are expressed, on average, 32% higher in lungs relative to other tissues. Conclusions Cpc-PH patients develop pulmonary vascular disease similar to PAH patients, despite younger age and similar prevalence of obesity, diabetes mellitus, and left heart disease compared with Ipc-PH patients. An exploratory genetic analysis in Cpc-PH identified genes and biological pathways in the lung known to contribute to PAH pathophysiology, suggesting that Cpc-PH may be a distinct and highly morbid PH subphenotype.

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Hemodynamic Evidence of Vascular Remodeling in Combined Post‐ and Precapillary Pulmonary Hypertension

Cited by 39 publications

References 54 publications

Lack of a Tricuspid Regurgitation Doppler Signal and Pulmonary Hypertension by Invasive Measurement

Lack of a Tricuspid Regurgitation Doppler Signal and Pulmonary Hypertension by Invasive Measurement

Hemodynamic Phenotyping of Pulmonary Hypertension in Left Heart Failure

Clinical and Biological Insights Into Combined Post- and Pre-Capillary Pulmonary Hypertension

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