scholarly journals Hemodynamic changes after acute fluid loading in patients with systemic sclerosis without pulmonary hypertension

2018 ◽  
Vol 9 (1) ◽  
pp. 204589401881608 ◽  
Author(s):  
Michele D’Alto ◽  
Emanuele Romeo ◽  
Paola Argiento ◽  
Agostino Mattera Iacono ◽  
Serena Vettori ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Systemic Sclerosis ◽  
Pulmonary Artery ◽  
Diastolic Dysfunction ◽  
Fluid Challenge ◽  
Left Ventricular ◽  
Right Atrial ◽  
Volume Loading ◽  
Hemodynamic Changes

A fluid challenge with a rapid infusion of saline helps to discriminate between pre- and post-capillary pulmonary hypertension (PH) and allows unmasking hidden post-capillary PH. Systemic sclerosis (SSc) patients may present with biventricular systolic and diastolic dysfunction. The aim of this study was to evaluate the hemodynamic changes of the pulmonary circulation in SSc patients without PH after a fluid challenge. Twenty-five SSc patients and 25 controls underwent right heart catheterization in basal conditions and after volume loading with saline infusion of 7 mL/kg over 5–10 min. At baseline, there was no difference in hemodynamics between SSc patients and controls. Rapid volume loading resulted in a significant increase in pressures and flows in both groups. Increases in right atrial pressure (3 ± 1 vs. 2 ± 1 mmHg, P = 0.03), mean pulmonary artery pressure (5 ± 1 vs. 3 ± 1 mmHg, P < 0.001), and pulmonary artery wedge pressure (PAWP; 5 ± 2 vs. 3 ± 1 mmHg, P < 0.001) were larger in SSc patients than in controls. Conversely, cardiac index (0.4 ± 0.2 vs. 0.6 ± 0.3 L/min/m2, P = 0.005) increased less in SSc patients than in controls. Pulmonary vascular resistance did not differ between groups before and after volume loading. Four SSc patients and only one of the controls reached a PAWP > 18 mmHg suggesting latent left heart failure. Even if differences are small and not diagnostic for heart failure, SSc patients without PH have a larger increase in pulmonary vascular pressures and a smaller increase in cardiac output than controls after an acute volume loading, probably due to subclinical left ventricular diastolic dysfunction.

The Effect of Left Ventricular Assist Device Therapy in Patients with Heart Failure and Mixed Pulmonary Hypertension

2017 ◽  
Vol 40 (2) ◽  
pp. 67-73 ◽  
Author(s):  
Hoong S. Lim ◽  
Neil Howell ◽  
Aaron Ranasinghe
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Pulmonary Hypertension ◽  
Left Ventricular ◽  
Ventricular Assist Devices ◽  
Right Atrial ◽  
Pulmonary Hemodynamics ◽  
Ventricular Assist ◽  
Significant Difference ◽  
Left Ventricular Assist

Background Diastolic pressure gradient (DPG) of ≥7 mmHg has been proposed to distinguish mixed pulmonary hypertension from isolated post-capillary pulmonary hypertension in heart failure (HF). We evaluated the changes in pulmonary hemodynamics with left ventricular assist devices (LVADs) in patients with DPG of ≥7 or <7 mmHg, and effects on peak oxygen uptake (VO2) in patients with advanced HF. Methods Pre- and post-LVAD implant pulmonary hemodynamics (including right atrial (RA) pressures, DPG, pulmonary vascular resistance (PVR), pulmonary capacitance (PCap) and cardiac output), echocardiography, cardiopulmonary exercise test were measured in 38 consecutive patients. Results Ten of 38 patients had baseline DPG ≥7 mmHg. There were no significant difference in baseline characteristics, peak VO2 and ventilation slope, but PVR were higher, and PCap lower in patients with DPG ≥7 mmHg. Pulmonary artery pressures improved in all patients, but PVR and DPG remained higher and PCap lower in patients with baseline DPG ≥7 mmHg after a median follow-up of 181 (IQR 153–193) days. Peak VO2 increased and ventilation slope reduced post-LVAD, and these improvements were comparable between groups. Only RA pressure reduction and exercise increase in heart rate were significant predictors of peak VO2 increase on multivariate analysis. Conclusions Baseline DPG of ≥7 mmHg compared to DPG <7 mmHg have persistently lower PCap and higher PVR post-LVAD, but the increase in peak VO2 was comparable despite these residual pulmonary vascular abnormalities. The improvement in peak VO2 was related to reduction in right atrial pressure and exercise increase in heart rate.

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 Speckle tracking assessment of the atrial function in patients with systemic sclerosis

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
G Stronati ◽  
F Ribichini ◽  
D Benfaremo ◽  
C Dichiara ◽  
M Casella ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Systemic Sclerosis ◽  
Mitral Valve ◽  
Speckle Tracking ◽  
Left Ventricular ◽  
Right Atrial ◽  
Contraction Function ◽  
Echocardiographic Parameters ◽  
Valve Opening ◽  
Conduit Function

Abstract Background Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by small vessel vasculopathy, autoantibodies production and exaggerated extracellular matrix deposition, leading to extensive tissue fibrosis. Cardiac involvement in SSc, albeit often asymptomatic, is frequent and represents a negative prognostic factor. Speckle tracking global longitudinal strain (GLS) has proved itself to be an effective tool to identify the presence and the progression of subclinical SSc-related cardiomyopathy. The aim of our study was to assess whether SSc-related cardiomyopathy affects not only the ventricles but also the right (RA) and left atria (LA) in patients with SSc and no overt cardiac disease nor pulmonary hypertension. Materials and methods Observational prospective study enrolling all consecutive patients with SSc age- and gender-matched 1:1 to healthy controls. Patients with structural heart disease, heart failure, atrial fibrillation and pulmonary hypertension were excluded. For every patient, standard echocardiographic parameters and speckle-tracking derived variables were registered. The reservoir function (from the end of ventricular contraction to mitral valve opening), conduit function (from mitral valve opening through the onset of atrium contraction) and contraction function (from the onset of atrium contraction to the end of ventricular diastole) were assessed via GLS. Zero strain reference was set at left ventricular end diastole. Results Fifty-two SSc patients and 52 matched controls were consecutively enrolled. Left ventricular ejection fraction (66.5%±7.4% vs. 66.1%±5.9%; p=ns) right fractional area change (49.4%±9.6% vs. 49.2%±9.2%; p=ns) and mean sPAP (29.0%±5.3% vs. 24.4%±4.1%; p=ns) were well within the normal range and similar between SSc patients and controls. Right atrial reservoir function (35.0%±7.3% vs. 42.3%±8.5%; p=.024) and contraction function (14.8%±4.3% vs. 18.5%±4.1%; p=.034) were significantly lower in SSc patients when compared to matched controls. No difference was seen in right atrial conduit function or left atrial strain. In patients with SSc, RA reservoir (r=.194; p=.033) and conduit function (r=.174; p=.036) were directly associated to right ventricular GLS. LA reservoir (r=.260; p=.008) and conduit function (r=.271; p=.006) were directly associated with left ventricular GLS. No association was observed between contraction function and GLS in both left and right chambers. Moreover, RA and LA reservoir (r=.358; p=.02), conduit (r=.525; p=.004) and contraction functions (r=.30; p=.0.18) were directly correlated. Conclusions While no significant difference was seen between cases and controls in terms of common echocardiographic parameters, RA reservoir and contraction function assessed through GLS were significantly impaired in patients with SSc. The correlation between impaired atrial and ventricular GLS in SSc may represent another indirect evidence of SSc-related heart global involvement. FUNDunding Acknowledgement Type of funding sources: None.

scholarly journals Validation of the 2016 ASE/EACVI Guideline for Diastolic Dysfunction in Patients With Unexplained Dyspnea and a Preserved Left Ventricular Ejection Fraction

2021 ◽  
Author(s):  
Arno A. van de Bovenkamp ◽  
Vidya Enait ◽  
Frances S. de Man ◽  
Frank T. P. Oosterveer ◽  
Harm Jan Bogaard ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Ejection Fraction ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Diagnostic Performance ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Preserved Ejection Fraction ◽  
Ventricular Ejection Fraction

Background Echocardiography is considered the cornerstone of the diagnostic workup of heart failure with preserved ejection fraction. Thus far, validation of the 2016 American Society of Echocardiography/European Association of Cardiovascular Imaging (ASE/EACVI) echo‐algorithm for evaluation of diastolic (dys)function in a patient suspected of heart failure with preserved ejection fraction has been limited. Methods and Results The diagnostic performance of the 2016 ASE/EACVI algorithm was assessed in 204 patients evaluated for unexplained dyspnea or pulmonary hypertension with echocardiogram and right heart catheterization. Invasively measured pulmonary capillary wedge pressure (PCWP) was used as the gold standard. In addition, the diagnostic performance of H 2 FPEF score and NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide) were evaluated. There was a poor correlation between indexed left atrial volume, E/e′ (septal and average) or early mitral inflow (E), and PCWP ( r =0.25–0.30, P values all <0.01). No correlation was found in our cohort between e′ (septal or lateral) or tricuspid valve regurgitation and PCWP. The correlation between diastolic function grades of the ASE/EACVI algorithm and PCWP was poor ( r =0.17, P <0.05). The ASE/EACVI algorithm had a sensitivity and specificity of 35% and 87%, respectively; an accuracy of 67% and an area under the curve of 0.56. Moreover, in 30% of cases the algorithm was not applicable or indeterminate. H 2 FPEF score had a modest correlation with PCWP ( r =0.44, P <0.0001), and accuracy was 73%; NT‐proBNP correlated weakly with PCWP ( r =0.24, P <0.001), and accuracy was 57%. Conclusions The 2016 ASE/EACVI algorithm for the assessment of diastolic function has a limited diagnostic accuracy in patients evaluated for unexplained dyspnea and/or pulmonary hypertension, and especially sensitivity to detect diastolic dysfunction was low.

The Serum Levels of N-Terminal Pro B-Type Natriuretic Peptide (NT-proBNP) Is a Strong Indicator of Pulmonary Hypertension in Patients with Sickle Cell/Beta Thalassemia.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1207-1207
Author(s):  
Ersi Voskaridou ◽  
Antonios Tsoutsias ◽  
George Tsetsos ◽  
Evgenia Spyropoulou ◽  
Evangelos Terpos
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Natriuretic Peptide ◽  
Sickle Cell ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Beta Thalassemia ◽  
Amino Terminal ◽  
Strong Indicator

Abstract Echocardiography studies have reported that approximately 30% of screened adult patients with sickle cell disease (SCD) have pulmonary hypertension (PH) defined as systolic pulmonary artery pressures of ≥ 35 mm Hg or regurgitant jet velocity value (TRV) of ≥ 2.5 m/sec. PH is increasingly observed in SCD and thalassemia. B-type natriuretic peptide (BNP) and the putatively inactive amino-terminal fragment of proBNP (NT-proBNP) are produced by the cleavage of proBNP, which is secreted from the ventricles during pressure strain. The serum concentration of NT-proBNP is considered as one of the strongest independent predictors for survival in patients with left ventricular dysfunction. The aim of this study was to evaluate the prevalence of PH in correlation with hemolytic findings and NT-proBNP levels in 73 patients with HbS/beta-thalassemia (HbS/β-thal; thal 0: 44 pts and thal +: 29 pts). The presence of PH was evaluated by using Doppler echocardiography and applying the modified Bernoulli equation (pulmonary artery systolic pressure=4V2 +right atrial pressure). Exclusion criteria of this study include: evidence of left ventricular failure, vaso-occlussive crisis during the last 15 days, atrial fibrillation or ventricular tachycardia, mitral value regurtitation (MVR) &gt;2/4+ or mitral value stenosis, and severe pericardial perfusion. In all pts we measured Hb, leukocyte, platelet, and reticulocyte counts, LDH, bilirubin, ferritin, creatinine, and Hb F. NT-proBNP levels were evaluated using an electrochemiluminescence immunoassay (Roche Diagnostics GmbH, Mannheim, Germany). Thirty-six patients (49%) were on hydroxyurea administration for a median time of 9 years. Nineteen patients (26%) had PH and experienced mild symptoms, such as fatigue or dyspnea on slight exertion. The administration of hydroxyurea did not affect the presence of PH. Patients with PH had elevated values of NT-pro BNP, reticulocyte counts and serum ferritin and a borderline increase of HbF compared with non PH patients (table). Even patients without PH had elevated concentrations of NT-proBNP compared with 20 controls of similar age and gender (mean±SD for controls: 48.1±22.1 pg/mL; p&lt;0.0001). The results of this ongoing study have shown that the frequency of PH in our cohort of HbS/beta-thal patients is similar with that observed in patients with SCD. Serum NT-proBNP is a strong indicator of PH in this cohort of hemoglobinopathy patients. Furthermore, the correlation between PH with reticulocyte counts and ferritin suggests that the degree of hemolysis and iron overload is implicated in the pathogenesis of PH in HbS/beta-thal. Parameter Patients with PH (n=19) Patients without PH (n=54) p-value Age (median; range) 40 ± 10.4 38 ± 12.6 Gender (n) 11M/8F 17M/37F On hydroxyurea (n) 12 (33.3%) 24 (66.6%) 0.23 NT-proBNP (pg/mL; mean ± SD) 486.8 ± 126.8 261.7 ± 139.6 &lt;0.01 Hb (g/dL; mean ± SD) 9.0 ± 1.5 8.9 ± 1.6 0.31 Retics (x1000/mm3) (mean ± SD) 239 ± 88 170 ± 61 0.01 LDH (U/L; mean ± SD) 779.6 ± 378.1 780.7 ± 352.9 0.76 Bilirubin (mg/dL; mean ± SD) 2.3 ± 1.8 2.4 ± 1.6 0.51 Creatinine (mg/dL; mean ± SD) 0.8 ± 0.1 0.8 ± 0.3 0.37 Ferritin (μg/L; mean ± SD) 1204.5 ± 1159.7 508.7 ± 599.1 0.02 HbF (%) 16.2 ± 8.0 13.5 ± 10.1 0.07

Pulmonary Hypertension after Thalidomide Administration in Multiple Myeloma Patients. Pilot Study.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4846-4846 ◽  
Author(s):  
Christos Lafaras ◽  
Eudokia Mandala ◽  
Eugenia Verrou ◽  
Dimitrios Platogiannis ◽  
Kostas Zervas ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Pulmonary Hypertension ◽  
Diastolic Dysfunction ◽  
Functional Status ◽  
Left Ventricular ◽  
Diagnostic Methods ◽  
Right Atrial ◽  
Biventricular Function ◽  
Increased Risk ◽  
Thalidomide Treatment

Abstract Multiple myeloma (MM) is thrombogenic as a consequence of multiple hemostatic effects and endothelial damage. Thalidomide is effective (anti-inflammatory, immunomodulatory and anti-angiogenic) both in advanced MM and as first-line therapy in combination with dexamethasone or other cytotoxic chemotherapy. It has been associated with an increased risk of thromboembolic pulmonary hypertension (PH). PH in the absence of thromboembolism has been also described in MM patients during thalidomide treatment. Aim: detection of clinical and subclinical PH in MM patients after thalidomide treatment. 82 patients, 46–82 years (median age 61), 41 females, were studied. They underwent echocardiographic study at baseline, one month thearafter, six months later and whenever symptoms indicating deterioration of cardiac function were appeared. Echocardiographic signs of PH were especially identified: Right atrial and ventricular enlargement, hypokinesia or hypertrophy, systolic flattening of intraventricular septum as a result of the right ventricular pressure overload, pulmonary artery dilatation and septal displacement. Doppler echocardiographic quantitation of systolic arterial PH was obtained by measuring velocity of the tricuspid regurgitant jet using the Bernoulli formula and summing central venous pressure evaluated by inferior vena cava diameter and its alteration during inspiration as it enters right atrium. Clinical and echocardiographic evaluation revealed four patients (4/82, 4.87%) with PH. One patient had clinical signs and symptoms of right heart failure three months after thalidomide administration with progressive deterioration. He was a 59 year- old man with multiple myeloma IgG λ and 85% diffuse bone marrow infiltration. Echocardiogram performed at baseline, revealed mild aortic regurgitation due tocalcification of non coronary cusp, good biventricular function, mild left ventricular hypertrophy, diastolic dysfunction of impaired relaxation, no evidence of PH and no signs of amyloid cardiac infiltration. He had no history of obstructive pulmonary disease and his functional status was Class I (NYHA). The second patient was a 62 years old woman with IgG κ MM. Echocardiogram at baseline identified good biventricular function and left ventricular diastolic dysfunction of impaired relaxation. Echocardiogram six months after thalidomide administration detected mild pulmonary hypertension without clinical symptoms of functional status deterioration. Her medical history was unremarkable except for arterial hypertension. The other two patients (72 and 76 years) had coronary artery disease and developed subclinical PH 1 and 3 months after thalidomide administration. A significant corelation between structural heart disease, age and PH was observed. Nonimaging (plasma D-Dimer,ECG) and imaging (chest roentgenography, lung scanning and chest computed tomography) diagnostic methods excluded deep venous thrombosis and pulmonary embolism. Vascular involvement seems to be a plausible mechanism in the pathophysiology of PH. Pre-existed endothelial dysfunction due to structural cardiac disease enhances the vasoactive substances release (nitric oxide, endothelin) causing increased pulmonary vascular resistance. Thalidomide causes a vasodilator and vasoconstriction impalance which may cause abnormal pulmonary vascular response interfering to a vicious circle perpetuating PH.

scholarly journals Acute and Long-Term Hemodynamic Effects of MitraClip Implantation on a Preexisting Secondary Right Heart Failure

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
M. Hünlich ◽  
E. Lubos ◽  
B. E. Beuthner ◽  
M. Puls ◽  
A. Bleckmann ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Tricuspid Regurgitation ◽  
Right Heart Failure ◽  
Right Atrial ◽  
Right Heart ◽  
Artery Pressure

Positive results of MitraClip in terms of improvement in clinical and left ventricular parameters have been described in detail. However, long-term effects on secondary pulmonary hypertension were not investigated in a larger patient cohort to date. 70 patients with severe mitral regurgitation, additional pulmonary hypertension, and right heart failure as a result of left heart disease were treated in the heart centers Hamburg and Göttingen. Immediately after successful MitraClip implantation, a reduction of the RVOT diameter from 3.52 cm to 3.44 cm was observed reaching a statistically significant value of 3.39 cm after 12 months. In contrast, there was a significant reduction in the velocity of the tricuspid regurgitation (TR) from 4.17 m/s to 3.11 m/s, the gradient of the TR from 48.5 mmHg to 39.3 mmHg, and the systolic pulmonary artery pressure (PAPsyst) from 58.6 mmHg to 50.0 mmHg. This decline continued in the following months (Vmax TR 3.09 m/s, peak TR 38.6 mmHg, and PAPsyst 47.4 mmHg). The tricuspid annular plane systolic excursion (TAPSE) increased from 16.5 mm to 18.9 mm after 12 months. MitraClip implantation improves pulmonary artery pressure, tricuspid regurgitation, and TAPSE after 12 months. At the same time, there is a decrease in the RVOT diameter without significant changes in other right ventricular and right atrial dimensions.

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