scholarly journals Predictive Modeling of Secondary Pulmonary Hypertension in Left Ventricular Diastolic Dysfunction

2021 ◽  
Vol 12 ◽  
Author(s):  
Karlyn K. Harrod ◽  
Jeffrey L. Rogers ◽  
Jeffrey A. Feinstein ◽  
Alison L. Marsden ◽  
Daniele E. Schiavazzi
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Diastolic Dysfunction ◽  
Diastolic Heart Failure ◽  
Circulation Model ◽  
Left Ventricular ◽  
Data Availability ◽  
Model Parameters ◽  
Ventricular Afterload

Diastolic dysfunction is a common pathology occurring in about one third of patients affected by heart failure. This condition may not be associated with a marked decrease in cardiac output or systemic pressure and therefore is more difficult to diagnose than its systolic counterpart. Compromised relaxation or increased stiffness of the left ventricle induces an increase in the upstream pulmonary pressures, and is classified as secondary or group II pulmonary hypertension (2018 Nice classification). This may result in an increase in the right ventricular afterload leading to right ventricular failure. Elevated pulmonary pressures are therefore an important clinical indicator of diastolic heart failure (sometimes referred to as heart failure with preserved ejection fraction, HFpEF), showing significant correlation with associated mortality. However, accurate measurements of this quantity are typically obtained through invasive catheterization and after the onset of symptoms. In this study, we use the hemodynamic consistency of a differential-algebraic circulation model to predict pulmonary pressures in adult patients from other, possibly non-invasive, clinical data. We investigate several aspects of the problem, including the ability of model outputs to represent a sufficiently wide pathologic spectrum, the identifiability of the model's parameters, and the accuracy of the predicted pulmonary pressures. We also find that a classifier using the assimilated model parameters as features is free from the problem of missing data and is able to detect pulmonary hypertension with sufficiently high accuracy. For a cohort of 82 patients suffering from various degrees of heart failure severity, we show that systolic, diastolic, and wedge pulmonary pressures can be estimated on average within 8, 6, and 6 mmHg, respectively. We also show that, in general, increased data availability leads to improved predictions.

scholarly journals Predictive modeling of secondary pulmonary hypertension in left ventricular diastolic dysfunction

2020 ◽  
Author(s):  
K. K. Harrod ◽  
J. L. Rogers ◽  
J. A. Feinstein ◽  
A. L. Marsden ◽  
D. E. Schiavazzi
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Diastolic Dysfunction ◽  
Diastolic Heart Failure ◽  
Circulation Model ◽  
Left Ventricular ◽  
Data Availability ◽  
Model Parameters ◽  
Ventricular Afterload

AbstractDiastolic dysfunction is a common pathology occurring in about one third of patients affected by heart failure. This condition is not associated with a marked decrease in cardiac output or systemic pressure and therefore is more difficult to diagnose then its systolic counterpart. Compromised relaxation or increased stiffness of the left ventricle with or without mitral valve stenosis induces an increase in the upstream pulmonary pressures, and classified as secondary or group II (2018 Nice classification) pulmonary hypertension. This may result in an increase in the right ventricular afterload leading to right ventricular failure. Elevated pulmonary pressures are therefore an important clinical indicator of diastolic heart failure (sometimes referred to as heart failure with preserved ejection fraction), showing significant correlation with associated mortality. Accurate measurements of this quantity, however, are typically obtained through invasive catheterization, and after the onset of symptoms. In this study, we use the hemodynamic consistency of a differential-algebraic circulation model to predict pulmonary pressures in adult patients from other, possibly non-invasive, clinical data. We investigate several aspects of the problem, including the well posedness of a modeling approach for this type of disease, identifiability of its parameters, to the accuracy of the predicted pulmonary pressures. We also find that a classifier using the assimilated model parameters as features is free from the problem of missing data and is able to detect pulmonary hypertension with sufficiently high accuracy. For a cohort of 82 patients suffering from various degrees of heart failure severity we show that systolic, diastolic and wedge pulmonary pressures can be estimated on average within 8, 6 and 6 mmHg, respectively. We also show that, in general, increased data availability leads to improved predictions.

scholarly journals Sickle cell disease: at the crossroads of pulmonary hypertension and diastolic heart failure

Heart ◽  
2019 ◽  
Vol 106 (8) ◽  
pp. 562-568 ◽  
Author(s):  
Katherine C Wood ◽  
Mark T Gladwin ◽  
Adam C Straub
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Sickle Cell Disease ◽  
Ejection Fraction ◽  
Diastolic Dysfunction ◽  
Sickle Cell ◽  
Diastolic Heart Failure ◽  
Left Ventricular ◽  
Cell Disease ◽  
Lv Diastolic Dysfunction

Sickle cell disease (SCD) is caused by a single point mutation in the gene that codes for beta globin synthesis, causing haemoglobin polymerisation, red blood cell stiffening and haemolysis under low oxygen and pH conditions. Downstream effects include widespread vasculopathy due to recurring vaso-occlusive events and haemolytic anaemia, affecting all organ systems. Cardiopulmonary complications are the leading cause of death in patients with SCD, primarily resulting from diastolic heart failure (HF) and/or pulmonary hypertension (PH). HF in SCD often features biventricular cardiac hypertrophy and left ventricular (LV) diastolic dysfunction. Among HF cases in the general population, approximately half occur with preserved ejection fraction (HFpEF). The insidious evolution of HFpEF differs from the relatively acute evolution of HF with reduced ejection fraction. The PH of SCD has diverse origins, which can be pulmonary arterial (precapillary), pulmonary venous (postcapillary) or pulmonary thromboembolic. It is also appreciated that patients with SCD can develop both precapillary and postcapillary PH, with elevations in LV diastolic pressures, as well as elevations in transpulmonary pressure gradient and pulmonary vascular resistance. Regardless of the cause of PH in SCD, its presence significantly reduces functional capacity and increases mortality. PH that occurs in the presence of HFpEF is usually of postcapillary origin. This review aims to assemble what has been learnt from clinical and animal studies about the manifestation of PH-HFpEF in SCD, specifically the contributions of LV diastolic dysfunction and myocardial fibrosis, in an attempt to gain an understanding of its evolution.

Investigation of the Relationship Between Color M-Mode Early Diastolic Propagation Velocity and Left Ventricular Adverse Pressure Gradients

2010 ◽  
Author(s):  
Kelley C. Stewart ◽  
Rahul Kumar ◽  
John J. Charonko ◽  
Pavlos P. Vlachos ◽  
William C. Little
Keyword(s):  
Heart Failure ◽  
Diastolic Dysfunction ◽  
Diastolic Heart Failure ◽  
Diagnostic Techniques ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Pressure Gradients ◽  
Compensatory Mechanisms ◽  
Ventricular Diastolic Dysfunction ◽  
The Relationship

Left ventricular diastolic dysfunction (LVDD) and diastolic heart failure are conditions that affect the filling dynamics of the heart and affect 36% of patients diagnosed with congestive heart failure [1]. Although this condition is very prevalent, it currently remains difficult to diagnose due to inherent atrio-ventricular compensatory mechanisms including increased heart rate, increased left ventricular (LV) contractility, and increased left atrial pressure (LA). A greater comprehension of the governing flow physics in the left ventricle throughout the introduction of the heart’s compensatory mechanisms has great potential to substantially increase the understanding of the progression of diastolic dysfunction and in turn advance the diagnostic techniques.

Role of Diastole in Left Ventricular Function, II: Diagnosis and Treatment

2004 ◽  
Vol 13 (6) ◽  
pp. 453-466 ◽  
Author(s):  
Shannan K. Hamlin ◽  
Penelope S. Villars ◽  
Joseph T. Kanusky ◽  
Andrew D. Shaw
Keyword(s):  
Heart Failure ◽  
Diastolic Dysfunction ◽  
Left Atrial ◽  
Diastolic Heart Failure ◽  
Systolic Heart Failure ◽  
Clinical Signs ◽  
Left Ventricular ◽  
Exercise Intolerance ◽  
Radiographic Findings ◽  
Ventricular Compliance

Left ventricular diastolic dysfunction plays an important role in congestive heart failure. Although once thought to be lower, the mortality of diastolic heart failure may be as high as that of systolic heart failure. Diastolic heart failure is a clinical syndrome characterized by signs and symptoms of heart failure with preserved ejection fraction (0.50) and abnormal diastolic function. One of the earliest indications of diastolic heart failure is exercise intolerance followed by fatigue and, possibly, chest pain. Other clinical signs may include distended neck veins, atrial arrhythmias, and the presence of third and fourth heart sounds. Diastolic dysfunction is difficult to differentiate from systolic dysfunction on the basis of history, physical examination, and electrocardiographic and chest radiographic findings. Therefore, objective diagnostic testing with cardiac catheterization, Doppler echocardiography, and possibly measurement of serum levels of B-type natriuretic peptide is often required. Three stages of diastolic dysfunction are recognized. Stage I is characterized by reduced left ventricular filling in early diastole with normal left ventricular and left atrial pressures and normal compliance. Stage II or pseudonormalization is characterized by a normal Doppler echocardiographic transmitral flow pattern because of an opposing increase in left atrial pressures. This normalization pattern is a concern because marked diastolic dysfunction can easily be missed. Stage III, the final, most severe stage, is characterized by severe restrictive diastolic filling with a marked decrease in left ventricular compliance. Pharmacological therapy is tailored to the cause and type of diastolic dysfunction.

scholarly journals Right Ventricular Enlargement within Months of Arteriovenous Fistula Creation in 2 Hemodialysis Patients

2016 ◽  
Vol 43 (4) ◽  
pp. 350-353 ◽  
Author(s):  
Loheetha Ragupathi ◽  
Drew Johnson ◽  
Gregary D. Marhefka
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Diastolic Heart Failure ◽  
Ventricular Enlargement ◽  
Upper Arm ◽  
Echocardiographic Finding ◽  
Obstructive Sleep ◽  
Stage Renal Disease ◽  
End Stage

Surgically created arteriovenous fistulae (AVF) for hemodialysis can contribute to hemodynamic changes. We describe the cases of 2 male patients in whom new right ventricular enlargement developed after an AVF was created for hemodialysis. Patient 1 sustained high-output heart failure solely attributable to the AVF. After AVF banding and subsequent ligation, his heart failure and right ventricular enlargement resolved. In Patient 2, the AVF contributed to new-onset right ventricular enlargement, heart failure, and ascites. His severe pulmonary hypertension was caused by diastolic heart failure, diabetes mellitus, and obstructive sleep apnea. His right ventricular enlargement and heart failure symptoms did not improve after AVF ligation. We think that our report is the first to specifically correlate the echocardiographic finding of right ventricular enlargement with AVF sequelae. Clinicians who treat end-stage renal disease patients should be aware of this potential sequela of AVF creation, particularly in the upper arm. We recommend obtaining preoperative echocardiograms in all patients who will undergo upper-arm AVF creation, so that comparisons can be made postoperatively. Alternative consideration should be given to creating the AVF in the radial artery, because of less shunting and therefore less potential for right-sided heart failure and pulmonary hypertension. A multidisciplinary approach is optimal when selecting patients for AVF banding or ligation.

Link between diabetes and diastolic dysfunction and the diagnostic role of echocardiography

2009 ◽  
Vol 150 (45) ◽  
pp. 2060-2067 ◽  
Author(s):  
András Nagy ◽  
Zsuzsanna Cserép
Keyword(s):  
Heart Failure ◽  
Diastolic Dysfunction ◽  
Systolic Function ◽  
Diastolic Heart Failure ◽  
Systolic Dysfunction ◽  
Mitral Annulus ◽  
Left Ventricular ◽  
Diabetic Patients ◽  
Doppler Study

Diabetes mellitus, a disease that has been reaching epidemic proportions, is an important risk factor to the development of cardiovascular complication. The left ventricular diastolic dysfunction represents the earliest pre-clinical manifestation of diabetic cardiomyopathy, preceding systolic dysfunction and being able to evolve to symptomatic heart failure. In early stages, these changes appear reversible with tight metabolic control, but as pathologic processes become organized, the changes are irreversible and contribute to an excess risk of heart failure among diabetic patients. Doppler echocardiography provides reliable data in the stages of diastolic function, as well as for systolic function. Combination of pulsed tissue Doppler study of mitral annulus with transmitral inflow may be clinically valuable for obtaining information about left ventricular filling pressure and unmasking Doppler inflow pseudonormal pattern, a hinge point for the progression toward advanced heart failure. Subsequently we give an overview about diabetes and its complications, their clinical relevance and the role of echocardiography in detection of diastolic heart failure in diabetes.

scholarly journals Transitioning from Preclinical to Clinical Heart Failure with Preserved Ejection Fraction: A Mechanistic Approach

2020 ◽  
Vol 9 (4) ◽  
pp. 1110 ◽  
Author(s):  
Antoni Bayes-Genis ◽  
Felipe Bisbal ◽  
Julio Núñez ◽  
Enrique Santas ◽  
Josep Lupón ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Ejection Fraction ◽  
Right Ventricular ◽  
Left Atrial ◽  
Interstitial Fibrosis ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Preserved Ejection Fraction ◽  
Ventricular Ejection Fraction

To better understand heart failure with preserved ejection fraction (HFpEF), we need to better characterize the transition from asymptomatic pre-HFpEF to symptomatic HFpEF. The current emphasis on left ventricular diastolic dysfunction must be redirected to microvascular inflammation and endothelial dysfunction that leads to cardiomyocyte remodeling and enhanced interstitial collagen deposition. A pre-HFpEF patient lacks signs or symptoms of heart failure (HF), has preserved left ventricular ejection fraction (LVEF) with incipient structural changes similar to HFpEF, and possesses elevated biomarkers of cardiac dysfunction. The transition from pre-HFpEF to symptomatic HFpEF also involves left atrial failure, pulmonary hypertension and right ventricular dysfunction, and renal failure. This review focuses on the non-left ventricular mechanisms in this transition, involving the atria, right heart cavities, kidneys, and ultimately the currently accepted driver—systemic inflammation. Impaired atrial function may decrease ventricular hemodynamics and significantly increase left atrial and pulmonary pressure, leading to HF symptoms, irrespective of left ventricle (LV) systolic function. Pulmonary hypertension and low right-ventricular function are associated with the incidence of HF. Interstitial fibrosis in the heart, large arteries, and kidneys is key to the pathophysiology of the cardiorenal syndrome continuum. By understanding each of these processes, we may be able to halt disease progression and eventually extend the time a patient remains in the asymptomatic pre-HFpEF stage.

P5370Pulmonary pressure overload stimulates cardiac stem or progenitor cell-derived cardiac regeneration in the right ventricular area

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Kanda ◽  
T Nagai ◽  
N Kondou ◽  
K Tateno ◽  
M Hirose ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Progenitor Cell ◽  
Pressure Overload ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Free Wall ◽  
Right Heart ◽  
The Right

Abstract Introduction and purpose The number of patients with right heart failure due to pulmonary hypertension has been increasing. Although several drugs have reportedly improved pulmonary hypertension, no treatments have been established for decompensated right heart failure. The heart has an innate ability to regenerate, and cardiac stem or progenitor cells (e.g., side population [SP] cells) have been reported to contribute to the regeneration process. However, their contribution to right ventricular pressure overload has not been clarified. Here, this regeneration process was evaluated using a genetic fate-mapping model. Methods and results We used Cre-LacZ mice, in which more than 99.9% of the cardiomyocytes in the left ventricular field were positive for 5-bromo-4-chloro-3-indolyl-β-D-galactoside (X-gal) staining immediately after tamoxifen injection. Then, we performed either a pulmonary binding (PAB) or sham operation on the main pulmonary tract. In the PAB-treated mice, the right ventricular cavity was significantly enlarged (right-to-left ventricular [RV/LV] ratio, 0.24±0.04 in the sham group and 0.68±0.04 in the PAB group). Increased peak flow velocity in the PAB group (1021±80 vs 1351±62 mm/sec) was confirmed by echocardiography. One month after the PAB, the PAB-treated mice had more X-gal-negative (newly generated) cells than the sham mice (94.8±34.2 cells/mm2 vs 23.1±10.5 cells/mm2; p<0.01). The regeneration was biased in the RV free wall (RV free wall, 225.5±198.7 cells/mm2; septal area, 88.9±56.5/mm2; LV lateral area, 46.8±22.0/mm2; p<0.05). To examine the direct effects of PAB on the cardiac progenitor cells, bromodeoxyuridine was administered to the mice daily until 1 week after the PAB operation. Then, the hearts were isolated and SP cells were harvested. The SP cell population increased from 0.65±0.23% in the sham mice to 1.87% ± 1.18% in the PAB-treated mice. Immunostaining analysis revealed a significant increase in the number of BrdU-positive SP cells, from 11.6±2.0% to 44.0±18%, therefore showing SP cell proliferation. Conclusions Pulmonary pressure overload stimulated cardiac stem or progenitor cell-derived regeneration with a RV bias, and SP cell proliferation may partially contribute to this process. Acknowledgement/Funding JSPS KAKENHI Grant Number JP 17K17636, GSK Japan Research Grant 2016

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