Cardiopulmonary Hemodynamics in Pulmonary Hypertension and Heart Failure

Maron, Bradley A.; Kovàcs, Gabór; Vaidya, Anjali; Bhatt, Deepak L.; Nishimura, Rick A.; Mak, Susanna; Guazzi, Marco; Tedford, Ryan J.

doi:10.1016/j.jacc.2020.10.007

Cited by 85 publications

(69 citation statements)

References 34 publications

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“…Idiopathic pulmonary arterial hypertension (IPAH) is a progressive and fatal disease in which functional and structural changes in the pulmonary vasculature lead to the increase in pulmonary vascular resistance (PVR) and pulmonary arterial pressure (PAP) [ 1 , 2 ]. Patients with IPAH, if untreated, die mainly because of progressive right heart failure, and the response of the right ventricle (RV) to the increased afterload is an important determinant of outcome in patients [ 3 , 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

mTOR Signaling in Pulmonary Vascular Disease: Pathogenic Role and Therapeutic Target

Babicheva

Makino

Yuan

2021

IJMS

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Pulmonary arterial hypertension (PAH) is a progressive and fatal disease without a cure. The exact pathogenic mechanisms of PAH are complex and poorly understood, yet a number of abnormally expressed genes and regulatory pathways contribute to sustained vasoconstriction and vascular remodeling of the distal pulmonary arteries. Mammalian target of rapamycin (mTOR) is one of the major signaling pathways implicated in regulating cell proliferation, migration, differentiation, and protein synthesis. Here we will describe the canonical mTOR pathway, structural and functional differences between mTOR complexes 1 and 2, as well as the crosstalk with other important signaling cascades in the development of PAH. The pathogenic role of mTOR in pulmonary vascular remodeling and sustained vasoconstriction due to its contribution to proliferation, migration, phenotypic transition, and gene regulation in pulmonary artery smooth muscle and endothelial cells will be discussed. Despite the progress in our elucidation of the etiology and pathogenesis of PAH over the two last decades, there is a lack of effective therapeutic agents to treat PAH patients representing a significant unmet clinical need. In this review, we will explore the possibility and therapeutic potential to use inhibitors of mTOR signaling cascade to treat PAH.

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Section: Introductionmentioning

confidence: 99%

mTOR Signaling in Pulmonary Vascular Disease: Pathogenic Role and Therapeutic Target

Babicheva

Makino

Yuan

2021

IJMS

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“…Estimation of peak systolic pulmonary arterial pressure (SPAP) is important in clinical practice (27)(28)(29). Most patients with ADHF had either passive or mixed pulmonary hypertension (30). There are two forms of pulmonary hypertension due to left-sided heart disease: postcapillary pulmonary hypertension, which is caused by the passive propagation of elevated left atrial or pulmonary venous pressures into the pulmonary arteries, and pre-capillary pulmonary hypertension, which is caused by pulmonary artery remodeling and further pulmonary artery pressure elevation.…”

Section: Evaluation Of Hemodynamicsmentioning

confidence: 99%

“…It has been suggested that therapeutic intervention is necessary for patients with reactive pulmonary hypertension, and it is critical to consider this diagnosis and subsequent management strategies for patients with acute heart failure. SPAP is estimated from the peak velocity of the tricuspid regurgitation jet and right atrial pressure ( 28 , 30 ). A correlation between echocardiographic and invasive assessment of SPAP in patients with acute HF has been reported, and echocardiography is used to assess SPAP in clinical practice ( 27 ).…”

Section: Evaluation Of Hemodynamicsmentioning

confidence: 99%

Value of Echocardiography in the Treatment of Patients With Acute Heart Failure

Izumo

2021

Front. Cardiovasc. Med.

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Heart failure (HF) is a burden in pandemic medicine resulting in high mortality and morbidity. Because acute HF is a life-threatening event, its diagnosis and choice of optimal treatment are important to improve outcomes. Furthermore, understanding the cause and hemodynamics of acute HF is important in selecting the optimal treatment for these patients. Echocardiography is widely used in daily clinical practice because of its non-invasive nature and excellent portability to understand cardiac function and hemodynamics. Echocardiography is highly recommended by guidelines in the practice of HF, but evidence is limited. In this review, I would like to share clinical value of echocardiography in the treatment of patients with acute HF and discuss the usefulness of echocardiography.

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“…Understanding the biochemical, electrocardiographic, and echocardiographic patterns during the course of PAH may guide clinical management of patients with PAH and help identify patients at an early stage of the disease when therapies could potentially be more effective ( 8 ). Furthermore, recent change in the clinical diagnosis of PAH using a threshold of mean pulmonary artery pressure (mPAP) from >25 to >20 mmHg underscores the efforts in diagnosing PAH at an early stage ( 9 , 10 ).…”

Section: Introductionmentioning

confidence: 99%

Echocardiographic, Biochemical, and Electrocardiographic Correlates Associated With Progressive Pulmonary Arterial Hypertension

Zaky

Zafar

Masjoan-Juncos

et al. 2021

Front. Cardiovasc. Med.

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Background: Pulmonary arterial hypertension (PAH) is a progressive proliferative vasculopathy associated with mechanical and electrical changes, culminating in increased vascular resistance, right ventricular (RV) failure, and death. With a main focus on invasive tools, there has been an underutilization of echocardiography, electrocardiography, and biomarkers to non-invasively assess the changes in myocardial and pulmonary vascular structure and function during the course of PAH.Methods: A SU5416-hypoxia rat model was used for inducing PAH. Biventricular functions were measured using transthoracic two-dimensional (2D) echocardiography/Doppler (echo/Doppler) at disease onset (0 week), during progression (3 weeks), and establishment (5 weeks). Similarly, electrocardiography was performed at 0, 3, and 5 weeks. Invasive hemodynamic measurements and markers of cardiac injury in plasma were assessed at 0, 3, and 5 weeks.Results: Increased RV systolic pressure (RVSP) and rate of isovolumic pressure rise and decline were observed at 0, 3, and 5 weeks in PAH animals. EKG showed a steady increase in QT-interval with progression of PAH, whereas P-wave height and RS width were increased only during the initial stages of PAH progression. Echocardiographic markers of PAH progression and severity were also identified. Three echocardiographic patterns were observed: a steady pattern (0–5 weeks) in which echo parameter changed progressively with severity [inferior vena cava (IVC) expiratory diameter and pulmonary artery acceleration time (PAAT)], an early pattern (0–3 weeks) where there is an early change in parameters [RV fractional area change (RV-FAC), transmitral flow, left ventricle (LV) output, estimated mean PA pressure, RV performance index, and LV systolic eccentricity index], and a late pattern (3–5 weeks) in which there is only a late rise at advanced stages of PAH (LV diastolic eccentricity index). RVSP correlated with PAAT, PAAT/PA ejection times, IVC diameters, RV-FAC, tricuspid systolic excursion, LV systolic eccentricity and output, and transmitral flow. Plasma myosin light chain (Myl-3) and cardiac troponin I (cTnI) increased progressively across the three time points. Cardiac troponin T (cTnT) and fatty acid-binding protein-3 (FABP-3) were significantly elevated only at the 5-week time point.Conclusion: Distinct electrocardiographic and echocardiographic patterns along with plasma biomarkers were identified as useful non-invasive tools for monitoring PAH progression.

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Cardiopulmonary Hemodynamics in Pulmonary Hypertension and Heart Failure

Cited by 85 publications

References 34 publications

mTOR Signaling in Pulmonary Vascular Disease: Pathogenic Role and Therapeutic Target

mTOR Signaling in Pulmonary Vascular Disease: Pathogenic Role and Therapeutic Target

Value of Echocardiography in the Treatment of Patients With Acute Heart Failure

Echocardiographic, Biochemical, and Electrocardiographic Correlates Associated With Progressive Pulmonary Arterial Hypertension

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