Haut PDF Calcium dynamics and related alterations in pulmonary hypertension associated with heart failure

Calcium dynamics and related alterations in pulmonary hypertension associated with heart failure

Calcium dynamics and related alterations in pulmonary hypertension associated with heart failure

Vascular endothelium Pathophysiology Left heart diseases (LHD) represent the most prevalent cause of pulmonary hypertension (PH), yet there are still no approved therapies that selectively target the pulmonary circulation in LHD. The increase in pulmonary capillary pressure due to LHD is a triggering event leading to physical and biological alterations of the pulmonary circulation. Acutely, mechanosensitive endothelial dysfunction and increased capillary permeability combined with reduced fluid resorption lead to the development of interstitial and alveolar oedema. From repeated cycles of such capillary stress failure, originate more profound changes with pulmonary endothelial dysfunction causing increased basal and reactive pulmonary vascular tone. This contributes to pulmonary vascular remodelling with increased arterial wall thickness, but most prominently, to alveolar wall remodelling characterized by myofibroblasts proliferation with collagen and interstitial matrix deposition. Although protective against acute pulmonary oedema, alveolar wall thickening becomes maladaptive and is responsible for the development of a restrictive lung syndrome and impaired gas exchanges contributing to shortness of breath and PH. Increasing awareness of these processes is unraveling novel pathophysiologic processes that could represent selective therapeutic targets. Thus, the roles of caveolins, of the intermediate myofilament nestin and of endothelial calcium dyshomeostasis were recently evaluated in pre-clinical models. The pathophysiology of PH due to LHD (group II PH) is distinctive from other groups of PH. Therefore, therapies targeting PH due to LHD must be evaluated in that context.
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Resveratrol improves survival, hemodynamics and energetics in a rat model of hypertension leading to heart failure.

Resveratrol improves survival, hemodynamics and energetics in a rat model of hypertension leading to heart failure.

Figure 4. Cardiac mitochondrial function and biogenesis. (A) Maximal mitochondrial respiration of skinned fibers with 2 mM ADP, 4 mM malate, 0.1 mM palmitoylCoA, 0.15 mM palmitoylcarnitine, 1 mM pyruvate and 10 mM glutamate. (B) Citrate synthase (CS) and cytochrome oxidase (COX) activities, markers of mitochondrial mass. (C) mRNA levels of PGC-1a (peroxisome proliferator-activated receptor gamma coactivator 1a), Nrf2 (nuclear respiratory factor 2), mtTFA (mitochondrial transcription factor A), ERRa (estrogen-related receptor a), COX1 and IV (cytochrome c oxidase I and IV subunits). (D) mRNA levels of the fission protein Drp1 (dynamin-related protein 1) and the fusion proteins Mfn (mitofusin) 1 and 2 and OPA1 (optic atrophy 1). (E) Energetic coupling efficiency between sarcoplasmic reticulum ATPase and mitochondria or bound creatine kinases (CK) assessed by the ratio of calcium uptake under different energetic conditions (ATP+MITO+CK, ATP+MITO, ATP+CK, see Methods S1) to the uptake with ATP only. mRNA levels are normalized to LS group taken as 1. Between 6 and 9 animals per group. *P,0.05, **P,0.01, ***P,0.001 vs LS; $ P,0.05,
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Rehabilitation in patients with pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension: results from the Grenoble experience

Rehabilitation in patients with pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension: results from the Grenoble experience

Side effects in specialist centres under expert supervision were relatively rare. Actually, no study has reported an increased incidence of major adverse events in PAH patients undergoing a monitored and personalised exercise training (105) Of the 6 RCTs analyzed by Morris et al., one study reported a single adverse event, where a participant stopped exercise training due to lightheadedness (101). In one of the largest studies (183 patients), a total of 13.6% of their participants had adverse events. Almost half of these patients suffered acute respiratory infections that had to be treated with antibiotics and forced the transitory suspension of the training programme. Severe adverse events, such as syncope/pre-syncope or supra-ventricular arrhythmias, occurred only in 4.4% of the patients. No signs of clinical worsening of right heart failure were detected during their hospitalisation, and no severe adverse episodes occurred when the patients continued the exercise training at home (between hospital discharge and the planned follow-up, 15 weeks later) (7). The meta- analysis including 16 prospective intervention studies with 469 PH patients, reported dizziness, presyncope, palpitation, hypotension and oxygen desaturation in 4,7% of training patients (one- third were not related to exercice). No major adverse events, such as progression of symptoms, right heart failure, or death, were observed among the patients during the training period. On median follow-up of 29.5 months (21–36 months), the survival rate was 91%, and the transplant-free survival rate was 89%. (99)
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Mortality Prediction in Severe Congestive Heart Failure Patients With Multifractal Point-Process Modeling of Heartbeat Dynamics

Mortality Prediction in Severe Congestive Heart Failure Patients With Multifractal Point-Process Modeling of Heartbeat Dynamics

of moments derived from probability density functions (PDFs) characterizing and predicting the time until the next heartbeat event occurs. To this extent, we proposed the use of inhomo- geneous point-processes to effectively characterize the proba- bilistic generative mechanism of heartbeat events, even con- sidering short recordings under nonstationary conditions [25]. The unevenly spaced heartbeat intervals are then represented as multiscale quantities of a state-space point process model defined at each moment in time, thus allowing to estimate in- stantaneous measures without using any interpolation method, therefore overcoming limitations i) and ii). We demonstrate how to capture fluctuations of regularity in heartbeat data by scan- ning all details finer than the chosen analysis scale [8], [11]. To compare our method against a more standard approach, we also investigate the use of a non-informative standard spline-based interpolation. Finally, we here study multiscale properties of heartbeat-derived series with high resolution in time, including long-term instantaneous mean heart rate, standard deviation, and low-frequency (LF) and high-frequency (HF) spectral powers, which correspond to time-varying vagal activity estimates [4], thus overcoming limitation iii). Application of these metrics is then performed on experimental data gathered from 94 CHF patients by evaluating the recognition accuracy in predicting survivor and non-survivor patients after a 4 years follow up, demonstrating how to overcome limitation iv). Of note, prelim- inary results associated with this study were presented in [27], [28], in which a wavelet leader-based multiscale representation was applied to instantaneous heartbeat series as well as to in- stantaneous vagal activity series. Here, we significantly expand on these results by generalizing the development of the method- ology to be suitable for generic inhomogeneous point process- derived heartbeat dynamics series defined in continuous time, as well as by increasing the number of patients involved in the ex- periment, and accounting for their clinical characteristics. Fur- thermore, the scale dependent features resulting from the pro- posed methodology have been exploited through nonlinear sup- port vector machines and related feature selection procedures.
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Pulmonary Vein-to-Pulmonary Artery Ratio is an Echocardiographic Index of Congestive Heart Failure in Dogs with Degenerative Mitral Valve Disease

Pulmonary Vein-to-Pulmonary Artery Ratio is an Echocardiographic Index of Congestive Heart Failure in Dogs with Degenerative Mitral Valve Disease

survival time 2,7,24 and to predict CHF. 16,24 A similar scenario might be expected for pulmonary vein size, but this has not been studied in dogs. We anticipate that in the absence of congenital heart disease (left-to-right shunt or pulmonic stenosis) and in the absence of pul- monary hypertension, the right pulmonary artery diam- eter should be relatively stable. Therefore, in uncomplicated DMVD, an increase of PV diameter (and PV/PA) is expected. In this study, PV/PA increased with increasing class of heart failure. Further- more, dogs identified to be in CHF by thoracic radiog- raphy had higher PV/PA values than did asymptomatic dogs. The increase of PV/PA is likely related to pul- monary vein enlargement. This variable had an AUC >0.9 indicating excellent diagnostic performance for CHF detection. A PV/PA value >1.7 in 2D predicted CHF with an accuracy >90%, a sensitivity of 96%, and a specificity of 91%. This variable had an AUC > 0.9, indicating excellent diagnostic performance for CHF detection. Theoretically, the presence of concurrent pul- monary hypertension could contribute to false negative results by decreasing the PV/PA ratio. In our study, the presence of pulmonary hypertension did not interfere with CHF diagnosis performed by echocardiographic
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Mortality Prediction in Severe Congestive Heart Failure Patients With Multifractal Point-Process Modeling of Heartbeat Dynamics

Mortality Prediction in Severe Congestive Heart Failure Patients With Multifractal Point-Process Modeling of Heartbeat Dynamics

of moments derived from probability density functions (PDFs) characterizing and predicting the time until the next heartbeat event occurs. To this extent, we proposed the use of inhomo- geneous point-processes to effectively characterize the proba- bilistic generative mechanism of heartbeat events, even con- sidering short recordings under nonstationary conditions [25]. The unevenly spaced heartbeat intervals are then represented as multiscale quantities of a state-space point process model defined at each moment in time, thus allowing to estimate in- stantaneous measures without using any interpolation method, therefore overcoming limitations i) and ii). We demonstrate how to capture fluctuations of regularity in heartbeat data by scan- ning all details finer than the chosen analysis scale [8], [11]. To compare our method against a more standard approach, we also investigate the use of a non-informative standard spline-based interpolation. Finally, we here study multiscale properties of heartbeat-derived series with high resolution in time, including long-term instantaneous mean heart rate, standard deviation, and low-frequency (LF) and high-frequency (HF) spectral powers, which correspond to time-varying vagal activity estimates [4], thus overcoming limitation iii). Application of these metrics is then performed on experimental data gathered from 94 CHF patients by evaluating the recognition accuracy in predicting survivor and non-survivor patients after a 4 years follow up, demonstrating how to overcome limitation iv). Of note, prelim- inary results associated with this study were presented in [27], [28], in which a wavelet leader-based multiscale representation was applied to instantaneous heartbeat series as well as to in- stantaneous vagal activity series. Here, we significantly expand on these results by generalizing the development of the method- ology to be suitable for generic inhomogeneous point process- derived heartbeat dynamics series defined in continuous time, as well as by increasing the number of patients involved in the ex- periment, and accounting for their clinical characteristics. Fur- thermore, the scale dependent features resulting from the pro- posed methodology have been exploited through nonlinear sup- port vector machines and related feature selection procedures.
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Vasoreactive Pulmonary Arterial Hypertension Manifesting With Misleading Epileptic Seizure: Diagnostic and Treatment Pitfalls.

Vasoreactive Pulmonary Arterial Hypertension Manifesting With Misleading Epileptic Seizure: Diagnostic and Treatment Pitfalls.

Even if not completely elucidated, pathophysiology of this disease seems to be consecutive to intracellular pathway dysfunction resulting in a shift in the vasoactive balance toward an exaggerated vasoconstrictory response ( 8 – 11 , 20 ). In this particular form of reactive PAH, clinical manifestations may be related to acute pulmonary hypertensive crises triggered by several types of stimuli. Unlike other forms of PAH where the clinical manifestations are mainly due to RV failure and decreased of exercise capacity. These crises may result in acute life threatening decrease of cardiac output and syncope. The paroxysmal nature of vasoreactive PAH crisis renders the diagnosis challenging. For that reason, diagnosis needs invasive hemodynamic investigation with acute vasoreactivy testing. Recently it was suggested at the last PH world symposium to create a specific subgroup of vasoreactive PAH in the classification. It is of outmost importance to discriminate the vasoreactive responders because calcium channel blockers (CCB) therapy are correlated with an excellent prognosis ( 1 , 3 – 6 ).
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Cardiac arrhythmia mechanisms in rats with heart failure induced by pulmonary hypertension

Cardiac arrhythmia mechanisms in rats with heart failure induced by pulmonary hypertension

alternans in FAIL animals could be traced from single myo- cytes to isolated whole hearts and to the ECG in vivo. Electrical restitution as a mechanism of alternans. Optical mapping was used to measure APD in isolated hearts (Fig. 5A). APD 80 was mapped across the whole RV epicardial surface (Fig. 5B). At a pacing frequency of 5 Hz, mean APD 80 at the midregion (asterisk in Fig. 5B) increased (with CON ) HYP ) FAIL hearts; Fig. 5C). We observed a significant correlation (R 2 " 0.83, P ) 0.001) between the degree of cardiac hyper- trophy (heart weight-to-body weight ratio) and APD 80 (data not shown). APD dispersion was also increased (CON ) HYP and FAIL; Fig. 5D). Pacing frequency was increased at inter- vals to 13 Hz to measure dynamic APD restitution (Fig. 5E); the slope of the APD restitution curve was significantly steeper in the FAIL group than in the CON and HYP groups (Fig. 5F). AP recordings from single myocytes revealed that steeper APD restitution was an intrinsic property of FAIL myocytes (Fig. 6, A–C ). Both increased APD dispersion and increased slope of APD restitution have been reported to be associated with an increased occurrence of alternans (see DISCUSSION ).
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Compromised cerebrovascular regulation and cerebral oxygenation in pulmonary arterial hypertension

Compromised cerebrovascular regulation and cerebral oxygenation in pulmonary arterial hypertension

CBF and central hemodynamics On visit 1, CBF was estimated by monitoring MCAv mean (mean flow velocity in the middle cerebral artery) with transcranial Doppler ultrasonography (2.0-MHz probe; Doppler Box) using a standardized searching method. 31,32 After obtaining the opti- mal signal/noise ratio, the probe was secured with a custom- made headband and adhesive probe conductive ultrasonic gel (Tensive). Cerebrovascular resistance index (mean arterial pressure [MAP]/MCAv mean ), cerebrovascular conductance index (MCAv mean /MAP), and Gosling pulsatility index ([systolic MCAv diastolic MCAv]/MCAv mean ) were calculated. A 3-lead ECG was used for heart rate monitoring. BP was measured noninvasively by finger photoplethysmography (Nexfin; BMEYE). The cuff was positioned to the midphalanx of the middle finger of the right hand and calibrated at heart level. CO was determined by using a 3-element model of arterial input impedance (Model flow method). Systemic pulsatility index was calculated as follows: (systolic AP diastolic AP)/MAP. Photo- plethysmographic and transcranial Doppler ultrasonographic data were simultaneously sampled at 1000 Hz via an analog-to- digital converter (Powerlab 16/30) and stored on an external disk for off-line computations (LabChart Pro version 7) (Data S1 provides further baseline analysis details).
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Pulmonary hypertension after pneumonectomy: a preclinical model in rats and human pulmonary endothelial cells

Pulmonary hypertension after pneumonectomy: a preclinical model in rats and human pulmonary endothelial cells

Pierre Sentenac, Gianluca Samarani, Patrice Bideaux, Pierre Sicard, Benjamin Bourdois, Sylvain Richard, Pascal Colson, Saadia Eddahibi. To cite this version:[r]

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Tumour biomarkers: association with heart failure outcomes.

Tumour biomarkers: association with heart failure outcomes.

Statistical analyses Data are presented as means  standard deviation (SD) when data were normally distributed, or as medians with interquartile ranges (IQR), when data were non-normally distributed. Continuous nor- mally distributed variables were compared using Student’s independent t-test or ANOVA, whereas skewed variables were compared using Mann– Whitney U-test or Kruskal–Wallis H-test. The dis- tribution of tumour biomarker levels was observed according to NT-proBNP levels (ng/L) quintiles. Trends of the tumour biomarkers over NT-proBNP quintiles were statistically tested with an extension of the Wilcoxon rank-sum test. The assumption of normal distribution was checked before linear regression analysis. If necessary, skewed variables were log-transformed (using natural logarithm). Univariable and multivariable regression analyses were conducted to analyse the association between tumour biomarkers and variables, in which all variables associated with tumour biomarkers with P < 0.10 in univariable analysis were included in multivariable regression models and were sub- jected to the backward elimination method. Cox proportional hazard regression analysis was performed for all end-points to evaluate the inde- pendent prognostic value of each tumour biomar- ker and NT-proBNP. All-cause mortality, HF hospitalization and the composite end-point of both were corrected for their respective BIOSTAT risk model (including age, blood urea nitrogen [BUN], NT-proBNP, haemoglobin and beta blocker use at baseline), as previously published [12, 14]. The models for CV mortality were corrected for age, BUN, NT-proBNP, troponin T and sodium, while non-CV mortality models included age, haemoglo- bin, C-reactive protein and history of malignancy. These correction factors were selected using a regression model, including all factors that were univariably significantly associated with CV and non-CV mortality, respectively. Receiver operating characteristic (ROC) curve analysis was used to determine the predictive performance of each tumour biomarker. The area under the curve (AUC) was calculated as the diagnostic measure of the test. A 2-tailed P-value < 0.05 was consid- ered to denote statistically significant differences, while for interaction testing a P-value < 0.1 was used. For our primary and prespecified secondary analyses, we present Bonferroni-corrected P-val- ues. The non-prespecified, exploratory secondary analyses in the supplement were not corrected,
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en
                                                                    fr

en fr Vascular alterations, hypertension and cognitive decline Altération vasculaire, hypertension et troubles cognitifs

hypertension artérielle, et plus de 91% des sujets étaient sous antihypertenseurs, ainsi que 51% des hypertendus traités ont été bien contrôlés (PA systolique <140 mmHg) 93 . Cependant ce résultat n’exclut pas cette relation surtout pour cette période de suivi de 1 an. Cette absence de corrélation entre la PA et le déclin cognitif a été également constatée chez la population de l’étude Bilan Senior. Nous avons étudié la relation entre la pression artérielle et la fonction cognitive évaluée par le MMSE, et nos résultats ont montré l’absence de telle relation dans l’analyse univariée ayant comparé les deux groupes selon leurs scores MMSE (≤ 25 et > 25). Du même contexte, l’absence de cette relation persiste dans la comparaison des scores MMSE des différentes classes de la PA (tableau 6) chez l’ensemble de la population ainsi que chez les sujets avec ou sans traitement antihypertensif analysés séparément.
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Transcatheter Mitral-Valve Repair in Patients with Heart Failure.

Transcatheter Mitral-Valve Repair in Patients with Heart Failure.

T h e ne w e ngl a nd jou r na l o f m e dicine n engl j med 380;20 nejm.org May 16, 2019 1980 Why is there an absence of benefit in the MITRA-FR trial and a dramatic improvement in clinical out- comes in the COAPT trial? The left ventricular dimension was, on average, greater among pa- tients in the MITRA-FR trial, which reflects more advanced disease. Perhaps more important, in the COAPT trial, nearly 60% of screened patients (911 of 1576) did not undergo randomization. The success of the MitraClip device is critically dependent on whether strict echocardiographic criteria are met. Enrollment was supervised by the sponsor (Abbott) in the COAPT trial and was physician-led and independent of industry in the MITRA-FR trial. The results of the COAPT trial suggest that transcatheter mitral-valve repair may be beneficial in highly selected patients with heart failure who have secondary mitral regurgitation. However, we are concerned that the real-world effect of this therapy may prove to be more like the results presented in the MITRA-FR trial.
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In vitro study of carbon black nanoparticles on human pulmonary artery endothelial cells: effects on calcium signaling and mitochondrial alterations

In vitro study of carbon black nanoparticles on human pulmonary artery endothelial cells: effects on calcium signaling and mitochondrial alterations

induces mitochondrial membrane depolarization (West- ermann 2010 ). Moreover, cellular uptake and trafficking of NPs play a key role in NPs-induced toxicity. Despite the fact that FW2 NPs were not observed in mitochondria and nucleus after internalization, large aggregates of FW2 NPs were present very close to mitochondria, and could critically interfere with mitochondrial functions. Some studies have reported that NPs (SiO 2 , Fe 2 O 3 ) cause mito- chondrial swelling, cristae disruption or disappearance and mitochondria vacuolization in several cell types (Faisal et al. 2016 ). Regarding mitochondria biogenesis and dynamic, this study provides evidence that FW2 NPs induce morphological and structural alterations (Fig.  8 ). The fact that mitochondrial dynamics alterations (fusion/ fission equilibrium perturbation) do alter mitochondrial morphology (Zamponi et al. 2018 ) supports the present findings (Fig.  9 ). Overall results are summarized in Fig.  11 .
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Calcium homeostasis alterations in a mouse model of the Dynamin 2-related centronuclear myopathy

Calcium homeostasis alterations in a mouse model of the Dynamin 2-related centronuclear myopathy

One central question for the DNM2-related diseases is to understand why mutations of the ubiquitously expressed DNM2 lead to a tissue-specific phenotype only affecting skeletal muscles in AD-CNM (Bitoun et al., 2005) or peripheral nervous system in rare form of Charcot –Marie–Tooth neuropathy (Zuchner et al., 2005). Moreover, all the muscles are not similarly affected in AD- CNM since a temporal and spatial muscle involvement has been described in patients (Fischer et al., 2006). In this context, the correlation between calcium defects and muscle weakness is of particular importance. Indeed, these results suggest that calcium homeostasis impairment might be involved in the development of the tissue-specific phenotype in DNM2-related CNM and may also participate to the spatial pattern of muscle involvement. Two mechanisms may underlie the uneven spatial involvement in response to DNM2 mutations as illustrated here through the different impacts on EDL and soleus muscles in HTZ mice. First, DMN2 mutation may impair cytosolic calcium concentration depending on the type and the amount of channels participating in SPCa initially expressed at the plasma membrane of a given muscle. Accordingly, the sarcolemmal calcium channels TRPC1 and TRPC3, two modulators of SPCa and cytosolic calcium, are differently expressed in EDL and soleus. In this context, it is interesting to note that TRPV4, known to be regulated by DNM2, may form a heteromeric channel with TRPC1 (Fraysse et al., 2003; Garcia-Elias et al., 2013; Rosenberg et al., 2004; Woo et al., 2014; Zhang et al., 2016). The second mechanism may be related to the different calcium handling mechanisms occurring in fast- and slow- twitch muscles fibers in relation to their contractile phenotype (Dowling et al., 2016; Schiaffino and Reggiani, 2011). In particular, EDL and soleus muscles differ in regard to expression of specific SR Ca 2+ -ATPase SERCA isoforms, mitochondrial content, and development of SR, the main intracellular calcium compartment. Resulting from these differences, we found that [Ca2+] c is significantly higher in soleus than in EDL (ANOVA and Bonferroni post-hoc test, P<0.05) as previously reported (Carroll et al., 1999; Fraysse et al., 2003, 2006; Gailly et al., 1993). A similar trend is observed for SPCa, although not significant. One may hypothesize that soleus muscle is less sensitive to DNM2 mutations due to its naturally higher SPCa and cytosolic
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Empagliflozin and health-related quality of life outcomes in patients with heart failure with reduced ejection fraction: the EMPEROR-Reduced trial

Empagliflozin and health-related quality of life outcomes in patients with heart failure with reduced ejection fraction: the EMPEROR-Reduced trial

Introduction Besides the risk for mortality and recurrent hospitalizations, patients with heart failure with reduced ejection fraction HFrEF also suffer from impaired health status.1,2 I[r]

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Patiromer versus placebo to enable spironolactone use in patients with resistant hypertension and chronic kidney disease (AMBER): results in the pre-specified subgroup with heart failure

Patiromer versus placebo to enable spironolactone use in patients with resistant hypertension and chronic kidney disease (AMBER): results in the pre-specified subgroup with heart failure

Briefly, eligible patients were aged ≥18 years with an eGFR of 25–45 mL/min/1.73 m 2 , and had serum K + between 4.3 and 5.1 mmol/L. All patients had resistant hypertension, defined as unattended systolic automated office blood pressure (AOBP) of 135–160 mmHg despite taking ≥3 antihypertensives, includ- ing a diuretic, and an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker (unless not tolerated or con- traindicated) during screening. Reasons for exclusion included untreated secondary causes of hypertension (other than CKD), recent cardiovascular event (e.g. myocardial infarction, unstable angina, hospitalization for HF), and clinically significant ventricular arrhythmia or atrial fibrillation with heart rate >100 bpm. Based on investigator reporting of clinical history, the following informa- tion was recorded in the case report form to accurately describe this pre-specified subgroup: HF (presence/absence), type of HF ...............................................................
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Heart Failure with preserved Ejection Fraction: Defining phenotypes

Heart Failure with preserved Ejection Fraction: Defining phenotypes

Heart failure with preserved ejection (HFpEF) has been increasingly recognized as an epidemic and various phenotypes have now been suggested (1). The clinical presentation as well as medical history may vary in this condition. Some patients experience multifold hospitalizations, and others complain of breathlessness and have a similar decrease in quality of life, but have never been hospitalized. Some patients have severe, recurrent congestion, and others are essentially symptomatic only when exercising.
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The Right Heart-Pulmonary Circulation Unit and Left Heart Valve Disease.

The Right Heart-Pulmonary Circulation Unit and Left Heart Valve Disease.

patients can remain asymptomatic for a pro- longed period of time at early stages of VHD and develop either exercise-related symptoms, such as dyspnea, before displaying heart failure. Symptoms at exercise are related to increased sPAP secondary to the increment of LV filling pressure in relation to advanced grade of diastolic dysfunction, severity of VHD, and RV function adaptation capacity and pulmonary vascular function. 2 Exercise echocardiography should therefore contribute to unmask patients with hid- den symptoms, revealing moderate or severe VHD. It has been suggested that exercise echo- cardiography was a useful tool to screen exercise-induced PH (EIPH) and to identify pa- tients with asymptomatic VHD at rest and higher risk of further worsening. 25 Previous study also
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Three-dimensional right-ventricular regional deformation and survival in pulmonary hypertension

Three-dimensional right-ventricular regional deformation and survival in pulmonary hypertension

Our patients’ population included 65 (62.5%) group 1 pulmonary arterial hypertension (PAH) patients (detailed below), 26 (25.0%) group 3 PH patients, 11 (10.6%) group 4 PH patients and 2 (1.9%) group 5 PH patients according to the most recent PH classification (26). PAH aetiology was idiopathic PAH in 17 patients (26.2% of group 1 PAH patients), heritable PAH in 1 patient (1.5%), 4 drug- and toxin-induced PAH (6.2%), PAH associated with connective tissue disease in 16 patients (24.6%), associated with congenital heart disease in 13 patients (20%) (including 4 ventricular septal defects, 4 atrial septal defects, 1 complete atrio-ventricular septal defect and 4 closed left-to-right shunts), associated with portal hypertension in 12 (18.5%) patients, and HIV-associated PAH in 2 patients (3.1%). All group 1, 4 and 5 patients as well as 9 patients from group 3 PH were treated with advanced targeted PAH therapy at baseline.
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