Left Heart Disease Research Articles

Improved Prognostic Performance of Right Atrial Pressure-Corrected Cardiac Power Output in Pulmonary Hypertension and Heart Failure with Preserved Ejection Fraction.

Cardiac power output (CPO) is a powerful predictor of adverse outcomes in heart failure (HF). However, the original formula of CPO included the difference between mean arterial pressure and right atrial pressure (RAP). The prognostic performance of RAP-corrected CPO (CPORAP) remains unknown in heart failure with preserved ejection fraction (HFpEF). We studied 101 HF patients with a left ventricular ejection fraction > 40% who had pulmonary hypertension due to left heart disease. CPORAP was significantly more discriminating than CPO in predicting outcomes (Delong test, P = 0.004). Twenty-five (24.8%) patients presented with dis-concordantly high CPORAP and low CPO when stratified by the identified CPORAP threshold of 0.547 W and the accepted CPO threshold of 0.803 W. These patients had the lowest RAP, and their cumulative incidence was comparable with those with concordantly high CPO and CPORAP (P = 0.313). CPORAP might identify patients with right ventricular involvement, thereby providing better prognostic performance than CPO in HFpEF.

Echocardiographic Progression of Peak Tricuspid Regurgitant Velocity Among Medicare Beneficiaries

BackgroundPeak tricuspid regurgitant velocity (TRV) on transthoracic echocardiography (TTE) is a commonly obtained parameter and robust predictor of subsequent adverse clinical outcomes. ObjectivesThe purpose of this study was to determine the predictors and clinical significance of TRV progression. MethodsWe retrospectively linked consecutive outpatient TTE reports from our institution to 2005 to 2017 Medicare claims. Individuals with prior tricuspid surgery, endocarditis, tricuspid stenosis, missing TRV values, TTEs performed during inpatient hospitalization, or <2 TTEs were excluded. ResultsA total of 4,572 patients (mean age 67.8 ± 11.9 years, 50.4% female) received 13,273 TTEs over a median follow-up of 7.4 (IQR: 4.5-6.9) years. TRV increased by a mean of 0.23 (95% CI: 0.22 to 0.23 m/s/y, P < 0.001) (range, 0.01-0.80 m/s/y). Older age, depressed left ventricular ejection fraction, diabetes, hypertension, hyperlipidemia, atrial fibrillation, heart failure, and chronic kidney disease were associated with faster progression (all P < 0.05). Accounting for 23 demographic, clinical, and TTE variables, faster TRV progression was associated with a stepwise increased risk of all-cause mortality (TRV progression quartile 4 vs 1; adjusted HR: 2.17; 95% CI: 1.74-2.71; P < 0.001). Those with regression of TRV (n = 384 [8.4%]) had a lower mortality risk (adjusted HR: 0.40; 95% CI: 0.28-0.57; P < 0.001). ConclusionsIn this large, multidecade study of Medicare beneficiaries with serial TTEs performed in the outpatient setting, the mean rate of TRV progression was 0.23 m/s/y. Older age, left heart disease, and adverse metabolic features were associated with faster progression. Faster progression was associated with a graded risk for all-cause mortality.

Outcomes of pregnancy in women with different types of pulmonary hypertension

BackgroundPulmonary hypertension (PH) is considered to increase maternal and fetal risk, and we attempt to explore pregnancy outcomes in women with different types of PH.MethodsWe retrospectively analyzed the clinical data of pregnant women with PH who were admitted to Anzhen Hospital from January 2010 to December 2019, and followed up on these parturients and their offspring.ResultsThree hundred and sixty-six pregnant women with PH were collected, including 265 pulmonary arterial hypertension (PAH) associated with congenital heart disease (CHD), 65 PH caused by left heart disease, 12 idiopathic PH, and 24 PH associated with other diseases. Maternal mean age was 28.4 ± 4.4 years and 72.1% were nulliparous. The estimated systolic pulmonary artery pressure was < 50 mmHg in 40.2% of patients, 50–70 mmHg in 23.2%, and > 70 mmHg in 36.6%. In more than 94% of women, a diagnosis of PH was made before pregnancy. During pregnancy, heart failure occurred in 15% of patients. Cesarean section was performed in 90.5% (20.4% emergency). Complications included fetal mortality (0.5%), preterm delivery (40.4%), and low birth weight (37.7%). A total of 20 mothers died (5.5%). The highest mortality rate was found in patients with idiopathic PH (4/12, 33.3%). A total of 12 children died (3.3%), 5 (1.4%) of them after discharge from the hospital, and 7 (1.9%) were in hospital.ConclusionsAlthough most of these women are fertile, PH does increase maternal and fetal risk. Women with idiopathic PH and Eisenmenger syndrome are not recommended to have children.

Machine learning to differentiate pulmonary hypertension due to left heart disease from pulmonary arterial hypertension.

Pulmonary hypertension due to left heart disease (PH-LHD) is the most frequent form of PH. As differential diagnosis with pulmonary arterial hypertension (PAH) has therapeutic implications, it is important to accurately and noninvasively differentiate PH-LHD from PAH before referral to PH centres. The aim was to develop and validate a machine learning (ML) model to improve prediction of PH-LHD in a population of PAH and PH-LHD patients. Noninvasive PH-LHD predictors from 172 PAH and 172 PH-LHD patients from the PH centre database at the University Hospitals of Leuven (Leuven, Belgium) were used to develop an ML model. The Jacobs score was used as performance benchmark. The dataset was split into a training and test set (70:30) and the best model was selected after 10-fold cross-validation on the training dataset (n=240). The final model was externally validated using 165 patients (91 PAH, 74 PH-LHD) from Erasme Hospital (Brussels, Belgium). In the internal test dataset (n=104), a random forest-based model correctly diagnosed 70% of PH-LHD patients (sensitivity: n=35/50), with 100% positive predicted value, 78% negative predicted value and 100% specificity. The model outperformed the Jacobs score, which identified 18% (n=9/50) of the patients with PH-LHD without false positives. In external validation, the model had 64% sensitivity at 100% specificity, while the Jacobs score had a sensitivity of 3% for no false positives. ML significantly improves the sensitivity of PH-LHD prediction at 100% specificity. Such a model may substantially reduce the number of patients referred for invasive diagnostics without missing PAH diagnoses.

Elastin stabilization prevents impaired biomechanics in human pulmonary arteries and pulmonary hypertension in rats with left heart disease

Pulmonary hypertension worsens outcome in left heart disease. Stiffening of the pulmonary artery may drive this pathology by increasing right ventricular dysfunction and lung vascular remodeling. Here we show increased stiffness of pulmonary arteries from patients with left heart disease that correlates with impaired pulmonary hemodynamics. Extracellular matrix remodeling in the pulmonary arterial wall, manifested by dysregulated genes implicated in elastin degradation, precedes the onset of pulmonary hypertension. The resulting degradation of elastic fibers is paralleled by an accumulation of fibrillar collagens. Pentagalloyl glucose preserves arterial elastic fibers from elastolysis, reduces inflammation and collagen accumulation, improves pulmonary artery biomechanics, and normalizes right ventricular and pulmonary hemodynamics in a rat model of pulmonary hypertension due to left heart disease. Thus, targeting extracellular matrix remodeling may present a therapeutic approach for pulmonary hypertension due to left heart disease.

Group 2 pulmonary hypertension: from diagnosis to treatment.

Pulmonary hypertension associated with left heart disease (PHLHD) is common and associated with adverse prognosis. Proper diagnosis is critical to avoid inappropriate treatment. Practical approaches to noninvasive diagnosis are available, though invasive hemodynamics including volume loading or exercise are often necessary for definitive diagnosis. Treatment strategies and research in the field is rapidly evolving. Combined pre and post capillary pulmonary hypertension is associated with remodeling of the pulmonary vasculature that is proportional to the severity of the pulmonary hypertension. Even quite mild elevation of pulmonary vascular resistance (PVR), (greater than 2.0 Wood units (WU)) is associated with adverse outcome. Guideline-directed medical therapy (GDMT) for left heart failure has rapidly evolved, including approval of SGLT2 inhibitors for treatment of heart failure with preserved ejection fraction (HFpEF). However, full implementation of GDMT is lagging. Utilization of implanted pulmonary artery pressure monitoring can facilitate patient management in selected patient phenotypes and has been utilized to demonstrate improvement in pulmonary pressures with emerging therapies in HFpEF including SGLT2 inhibitors and sacubitril/valsartan. A variety of shunt devices to create a left-to-right shunt in order to decompress the left heart are available or undergoing clinical trials. There is concern that there could be adverse response to such devices in patients who have even mild elevation of pulmonary vascular resistance. Sleep disordered breathing is common in PHLHD and should be aggressively sought out and treated. Even mild elevation in pulmonary vascular resistance is associated with adverse outcome. A systematic approach to diagnosis of PHLHD is essential. Guideline-directed medical therapy for PHLHD prioritizes optimal management of the left heart disease. Pulmonary artery pressure sensors are useful in selected patients.

Incident pulmonary hypertension in 13 488 cases investigated with repeat echocardiography: a clinical cohort study.

We addressed the paucity of data describing the characteristics and natural history of incident pulmonary hypertension. Adults (n=13 448) undergoing routine echocardiography without initial evidence of pulmonary hypertension (estimated right ventricular systolic pressure, eRVSP <30.0 mmHg) or left heart disease were studied. Incident pulmonary hypertension (eRVSP ≥30.0 mmHg) was detected on repeat echocardiogram a median of 4.1 years apart. Mortality was examined according to increasing eRVSP levels (30.0-39.9, 40.0-49.9 and ≥50.0 mmHg) indicative of mild-to-severe pulmonary hypertension. A total of 6169 men (45.9%, aged 61.4±16.7 years) and 7279 women (60.8±16.9 years) without evidence of pulmonary hypertension were identified (first echocardiogram). Subsequently, 5412 (40.2%) developed evidence of pulmonary hypertension, comprising 4125 (30.7%), 928 (6.9%) and 359 (2.7%) cases with an eRVSP of 30.0-39.9 mmHg, 40.0-49.9 mmHg and ≥50.0 mmHg, respectively (incidence 94.0 and 90.9 cases per 1000 men and women, respectively, per year). Median (interquartile range) eRVSP increased by +0.0 (-2.27 to +2.67) mmHg and +30.68 (+26.03 to +37.31) mmHg among those with eRVSP <30.0 mmHg versus ≥50.0 mmHg. During a median 8.1 years of follow-up, 2776 (20.6%) died from all causes. Compared to those with eRVSP <30.0 mmHg, the adjusted risk of all-cause mortality was 1.30-fold higher in 30.0-39.9 mmHg, 1.82-fold higher in 40.0-49.9 mmHg and 2.11-fold higher in ≥50.0 mmHg groups (all p<0.001). New-onset pulmonary hypertension, as indicated by elevated eRVSP, is a common finding among older patients without left heart disease followed-up with echocardiography. This phenomenon is associated with an increased morality risk even among those with mildly elevated eRVSP.

Long-term outcome of patients with combined post- and pre-capillary pulmonary hypertension.

Pulmonary hypertension (PH) is a complex clinical condition, and left heart disease is the leading cause. Little is known about the epidemiology and prognosis of combined post- and pre-capillary PH (CpcPH). This retrospective analysis of the Swiss PH Registry included incident patients with CpcPH registered from January 2001 to June 2019 at 13 Swiss hospitals. Patient baseline characteristics [age, sex, mean pulmonary artery pressure (mPAP), pulmonary artery wedge pressure (PAWP), pulmonary vascular resistance (PVR), and risk factors, including World Health Organization (WHO)-functional class (FC), 6 min walk distance (6MWD), and N-terminal pro-brain natriuretic peptide (NT-proBNP), treatment, days of follow-up, and events (death or loss to follow-up) at last visit] were analysed by Kaplan-Meier and Cox regression analyses. Two hundred and thirty-one patients (59.3% women, age 65 ± 12 years, mPAP 48 ± 11 mmHg, PAWP 21 ± 5 mmHg, PVR 7.2 ± 4.8 WU) were included. Survival analyses showed a significantly longer survival for women [hazard ratio (HR) 0.58 (0.38-0.89); P = 0.01] and a higher mortality risk for mPAP > 46 mmHg [HR 1.58 (1.03-2.43); P = 0.04] but no association with age or PVR. Patients stratified to high risk according to four-strata risk assessment had an increased mortality risk compared with patients stratified to low-intermediate risk [HR 2.44 (1.23-4.84); P = 0.01]. A total of 46.8% of CpcPH patients received PH-targeted pharmacotherapy; however, PH-targeted medication was not associated with longer survival. Among patients with CpcPH, women and patients with an mPAP ≤46 mmHg survived longer. Furthermore, risk stratification by using non-invasively assessed risk factors, such as WHO-FC, 6MWD, and NT-proBNP, as proposed for pulmonary arterial hypertension, stratified survival in CpcPH, and might be helpful in the management of these patients.

Associated radiation exposure from medical imaging and excess lifetime risk of developing cancer in pediatric patients with pulmonary hypertension.

Pediatric patients with pulmonary hypertension (PH) receive imaging studies that use ionizing radiation (radiation) such as computed tomography (CT) and cardiac catheterization to guide clinical care. Radiation exposure is associated with increased cancer risk. It is unknown how much radiation pediatric PH patients receive. The objective of this study is to quantify radiation received from imaging and compute associated lifetime cancer risks for pediatric patients with PH. Electronic health records between 2012 and 2022 were reviewed and radiation dose data were extracted. Organ doses were estimated using Monte Carlo modeling. Cancer risks for each patient were calculated from accumulated exposures using National Cancer Institute tools. Two hundred and forty-ninepatients with PH comprised the study cohort; 97% of patients had pulmonary arterial hypertension, PH due to left heart disease, or PH due to chronic lung disease. Mean age at the time of the first imaging study was 2.5 years (standard deviation [SD] = 4.9 years). Patients underwent a mean of 12 studies per patient per year, SD = 32. Most (90%) exams were done in children <5 years of age. Radiation from CT and cardiac catheterization accounted for 88% of the total radiation dose received. Cumulative mean effective dose was 19 mSv per patient (SD = 30). Radiation dose exposure resulted in a mean increased estimated lifetime cancer risk of 7.6% (90% uncertainty interval 3.0%-14.2%) in females and 2.8% (1.2%-5.3%) in males. Careful consideration for the need of radiation-based imaging studies is warranted, especially in the youngest of children.

Pulmonary hypertension in ANCA-associated vasculitis: a retrospective analysis.

Little is known about pulmonary hypertension (PH) in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). The aims of this retrospective study, in which echocardiography was used for detection of PH, were to identify the potential causes of PH in AAV and to analyze the risk factors for mortality. We performed a retrospective descriptive review of 97 patients who had AAV with PH at our institution from January 1, 1997, through December 31, 2015. These patients with PH were compared with 558 patients who had AAV without PH. Demographic and clinical data were abstracted from electronic health records. Among the patients who had PH, 61% were men; mean (SD) age was 70.5 (14.1) years at the time of PH diagnosis. The majority of patients with PH (73.2%) had more than 1 potential cause of PH, with left heart disease and chronic lung disease being the most common causes. Older age, male sex, smoking history, and kidney involvement were associated with the presence of PH. PH was associated with an increased risk of death (hazard ratio, 3.15; 95% CI, 2.37-4.18). On multivariate analysis, PH, age, smoking status, and kidney involvement were independent risk factors for death. Median survival after the diagnosis of PH was 25.9 months (95% CI, 12.2-49.9). PH in AAV is often multifactorial, is commonly associated with left heart disease, and is associated with a poor prognosis.

Is it real that no idiopathic tricuspid regurgitation anymore after atrial tricuspid regurgitation regarded as a distinct entity?

Abstract Funding Acknowledgements Type of funding sources: None. Background We have recently found that idiopathic tricuspid regurgitation (TR) had unique characteristics after a systemic approach to strictly define it. Atrial TR has been proposed that TR caused by right atrial dilatation related to the atrial fibrillation and without other causes of TR. Some researchers suggested idiopathic TR was no longer existed. Methods We retrospectively recruit 978 subjects with significant (moderate and severe) TR during a period of 9 months. We carefully evaluated their echocardiography images and divided these subjects into different type of TR according to a step-by-step systemic approach which we have developed. The characteristics of these TR were compared. Results After a step-by-step diagnostic approach, we found that there were 105 subjects with primary TR (10.7%), 76 (7.8%) pacemaker or other intracardiac instrumentation related, 388 (39.7%) left heart disease related, 32 (3.3%) congenital heart disease related, 160 (16.3%) pulmonary hypertension related, 7 (0.7%) right ventricular myopathy, and 210 (21.5%) idiopathic TR. Among idiopathic TR, 81 (38.6%) men, mean age 74.4 ± 14.0 years, 35 (16.7%) severe TR, and 82 (39%) atrial fibrillation. Compared to the idiopathic TR in sinus rhythm, subjects with atrial fibrillation had older age (78.1 ± 10.4 vs. 72.0 ± 13.9 years, p = 0.001), more severe TR (32 vs. 7 %, p &amp;lt;0.001), higher pulmonary artery pressure (43.5 ± 9.8 vs. 38.9 ± 7.9 mmHg, p = 0.001), less fractional area fraction of right ventricle (44.9 ± 13.3 vs. 51.1 ± 10.8 %, p = 0.001), larger tricuspid annulus (3.4 ± 0.7 vs. 2.8 ± 0.6 cm, p &amp;lt;0.001), and large right atrial area (23.2 ± 7.6 vs. 13.6 ± 4.5 cm2, p &amp;lt;0.001). Conclusion There were only 39% atrial TR among idiopathic TR in our study. Many significant TR subjects without other causes were still in sinus rhythm with smaller annulus and right atrial size. Even atrial TR do a distinct entity, there are still have TR subjects without any obvious causes (idiopathic TR).

HIV status and survival of patients with pulmonary hypertension due to left heart disease: the Pan African Pulmonary Hypertension Cohort

In sub-Saharan Africa, little is known about pulmonary hypertension in left heart disease (PH-LHD). We used multivariate logistic and cox-hazard proportional regression models to examine factors associated with increased right ventricular systolic pressure (RVSP) and the effect of real-world HIV status scenarios on 6-month survival rate in the Pan African Pulmonary Hypertension Cohort (PAPUCO) study, a prospective cohort from four African countries. Exposure to biomass fuel smoke (aOR, 95%CI 3.07, 1.02–9.28), moderate to severe NYHA/FC III/IV (aOR, 95%CI 4.18, 1.01–17.38), and unknown HIV status (aOR, 95%CI 2.73, 0.96–7.73) predicted moderate to severe RVSP at the time of presentation. Six months later, HIV infection, moderate-to-severe NYHA/FC, and alcohol consumption were associated with decreased survival probabilities. Upon adjusting for HIV infection, it was observed that an incremental rise in RVSP (1 mmHg) and inter-ventricular septal thickness (1 mm) resulted in an 8% (aHR, 95%CI 1.08, 1.02–1.13) and 20% (aHR, 95%CI 1.2, 1.00–1.43) increase in the probability of mortality due to PH-LHD. In contrast, the risk of death from PH-LHD was reduced by 23% for each additional unit of BMI. (aHR, 95%CI 0.77, 0.59–1.00). In conclusion, the present study offers insights into the determinants that are notably linked to unfavorable survival outcomes in patients with pulmonary hypertension due to left heart disease. Certain factors identified in this study are readily evaluable and amenable to modification, even in settings with limited resources.

Anesthetic Management of an Unusual Case of Severe Pulmonary Hypertensive

The perioperative management of pulmonary hypertension continues to be a great challenge for anesthesiologists. Among the various types of pulmonary hypertension, pulmonary hypertension associated with left heart disease is the most common, while pulmonary hypertensive crisis is one of the causes of perioperative mortality in these patients. We present the case of a 54-year-old female with severe valvular heart disease complicated by severe pulmonary hypertension and massive hemothorax, who underwent emergency exploratory thoracotomy, mitral valve replacement, and tricuspid valvuloplasty. The patient was in critical condition and suspected to have a pulmonary hypertension crisis. The rationale for this case report is to learn about the anesthetic management of patients with severe pulmonary hypertension.

Pulmonary Hypertension in Left Heart Diseases: Pathophysiology, Hemodynamic Assessment and Therapeutic Management.

Pulmonary hypertension (PH) associated with left heart diseases (PH-LHD), also termed group 2 PH, represents the most common form of PH. It develops through the passive backward transmission of elevated left heart pressures in the setting of heart failure, either with preserved (HFpEF) or reduced (HFrEF) ejection fraction, which increases the pulsatile afterload of the right ventricle (RV) by reducing pulmonary artery (PA) compliance. In a subset of patients, progressive remodeling of the pulmonary circulation resulted in a pre-capillary phenotype of PH, with elevated pulmonary vascular resistance (PVR) further increasing the RV afterload, eventually leading to RV-PA uncoupling and RV failure. The primary therapeutic objective in PH-LHD is to reduce left-sided pressures through the appropriate use of diuretics and guideline-directed medical therapies for heart failure. When pulmonary vascular remodeling is established, targeted therapies aiming to reduce PVR are theoretically appealing. So far, such targeted therapies have mostly failed to show significant positive effects in patients with PH-LHD, in contrast to their proven efficacy in other forms of pre-capillary PH. Whether such therapies may benefit some specific subgroups of patients (HFrEF, HFpEF) with specific hemodynamic phenotypes (post- or pre-capillary PH) and various degrees of RV dysfunction still needs to be addressed.

Association between sarcopenia and exercise capacity in patients with pulmonary hypertension without left heart disease

BackgroundPulmonary hypertension (PH) has recently been described as a complex clinical syndrome affecting multiple organ systems, including the heart, lungs, and skeletal muscle, each of which plays an important role in exercise capacity. However, the relationship between exercise capacity and skeletal muscle abnormalities in patients with PH has not been fully elucidated. MethodsWe retrospectively analysed the exercise capacity and measures of skeletal muscle of 107 patients with PH without left heart disease (mean age 63 ± 15 years, 32.7% males, n = 30/6/66/5 in the clinical classification Group 1/3/4/5). ResultsSarcopenia, low appendicular skeletal muscle mass index, low grip strength, and slow gait speed, determined by international criteria, were found in 15 (14.0%), 16 (15.0%), 62 (57.9%), and 41 (38.3%) patients, respectively. The mean 6-min walk distance of all patients was 436 ± 134 m and was independently associated with sarcopenia (standardised β = −0.292, p < 0.001). All patients with sarcopenia showed reduced exercise capacity defined as 6-min walk distance < 440 m. Multivariable logistic regression analysis showed that each of the components of sarcopenia was associated with reduced exercise capacity (adjusted odds ratio and 95% confidence interval of appendicular skeletal muscle mass index: 0.39 [0.24–0.63] per 1 kg/m2, p = 0.006, grip strength: 0.83 [0.74–0.94] per 1 kg, p = 0.003, and gait speed: 0.31 [0.18–0.51] per 0.1 m/s, p < 0.001). ConclusionsSarcopenia and its components are associated with reduced exercise capacity in patients with PH. A multifaceted evaluation may be important in the management of reduced exercise capacity in patients with PH.

Pulmonary hypertension associated with left heart disease.

Pulmonary hypertension (PH) is acommon condition in patients with left heart disease (LHD) that is highly relevant for morbidity and mortality. While post-capillary in nature, the pathophysiology of PH in patients with LHD (heart failure/cardiomyopathy, valvular heart disease; other: congenital/acquired) is complex, and decisions about management strategies are challenging. Recently, the updated European Society of Cardiology/European Respiratory Society guidelines on the diagnosis and treatment of PH revisited hemodynamic definitions and the sub-classification of post-capillary PH, and provided numerous new recommendations on the diagnosis and management of PH associated with various types of LHD. Here, we review several novel aspects that focus on: (a)updated hemodynamic definitions, including the distinction between isolated post-capillary PH (IpcPH) and combined post- and pre-capillary PH (CpcPH); (b)the pathogenesis of PH-LHD, considering various components contributing to PH, such as pulmonary congestion, vasoconstriction, and vascular remodeling; (c)the prognostic relevance of PH and hemodynamic markers; (d)the diagnostic approach to PH-LHD; (e)management strategies in PH-LHD, distinguishing between targeting the underlying left heart condition, the pulmonary circulation, and/or impaired right ventricular function. In conclusion, precise clinical and hemodynamic characterization and detailed phenotyping are essential for prognostication and the management of patients with PH-LHD.

MicroRNA and lncRNA as the Future of Pulmonary Arterial Hypertension Treatment.

Pulmonary hypertension (PH) is characterized by a progressive increase in pulmonary arterial pressure and pulmonary vascular resistance. In a short time, it leads to right ventricular failure and, consequently, to death. The most common causes of PH include left heart disease and lung disease. Despite the significant development of medicine and related sciences observed in recent years, we still suffer from a lack of effective treatment that would significantly influence the prognosis and prolong life expectancy of patients with PH. One type of PH is pulmonary arterial hypertension (PAH). The pathophysiology of PAH is based on increased cell proliferation and resistance to apoptosis in the small pulmonary arteries, leading to pulmonary vascular remodeling. However, studies conducted in recent years have shown that epigenetic changes may also lie behind the pathogenesis of PAH. Epigenetics is the study of changes in gene expression that are not related to changes in the sequence of nucleotides in DNA. In addition to DNA methylation or histone modification, epigenetic research focuses on non-coding RNAs, which include microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). Preliminary research results give hope that targeting epigenetic regulators may lead to new, potential therapeutic possibilities in the treatment of PAH.

Prevalence of pulmonary hypertension in mitral regurgitation and its influence on outcomes

ObjectivePulmonary hypertension (PHT) commonly coexists with significant mitral regurgitation (MR), but its prevalence and prognostic importance have not been well characterised. In a large cohort of adults with moderate or...

A case report of pulmonary edema associated with left cardiac failure secondary with mitral insufficiency in dog

The cardiac left insufficiency with mitral dysfunction is a relevant cardiac pathology with importante repercussion in the lung, leads to pulmonary edema. Pulmonary edema corresponds to the accumulation of fluid in the lung parenchyma and alveoli, and can be classified as cardiogenic or non-cardiogenic. Clinical signs and symptoms include presence of dyspnea, cough, tachypnea, and alteration of normal sounds during lung auscultation. In this case report, a 16 year old female Lhasa Apso dog breed was presented to the clinical facility with signals of apathy, hyporexia, cough and dyspnea. After emergency treatment with oxygen therapy to stabilize the respiratory condition, imaging tests (radiography, Doppler echocardiography) were performed, confirming the suspicion of cardiogenic pulmonary edema due to left heart disease. The treatment of cardiac dysfunction was recommended through the use of pimobendan, which has a positive inotropic effect on the heart, and benzepril, an angiotensin-converting enzyme inhibitor. These drugs are important to control pulmonary vascular pressure, reducing the risk of developing pulmonary edema. Even though it is a veterinary clinical emergency, cardiogenic pulmonary edema when treated immediately and correctly tends to present a favorable prognosis in affected dogs.

Characteristics of cardiopulmonary exercise testing in patients with combined post- and pre-capillary pulmonary hypertension due to left heart disease.

Pulmonary hypertension (PH) is a common and morbid complication of left heart disease (LHD), comprising two subtypes: (1) isolated post-capillary pulmonary hypertension (Ipc-PH) and (2) combined post-capillary and pre-capillary pulmonary hypertension (Cpc-PH). Knowledge regarding the physiological characteristics that distinguish Cpc-PH, which has a worse prognosis, from Ipc-PH remains limited. Therefore, this study aimed to assess the utility of cardiopulmonary exercise testing (CPET) variables in detecting Cpc-PH. Among 105 consecutive patients with LHD (age: 55 ± 13 years; male/female = 79/26) who underwent right heart catheterization and CPET, 45 (43%) were classified as PH-LHD (mean pulmonary artery pressure >20 mmHg). Ipc-PH (n = 24) was defined as pulmonary vascular resistance (PVR) ≤ 3 WU and Cpc-PH (n = 21) as PVR > 3 WU. Patients with Cpc-PH had a significantly lower peak partial pressure of carbon dioxide (PETCO2) (Non-PH/Ipc-PH/Cpc-PH = 38.2 ± 6.6 vs. 38.3 ± 6.0 vs 33.0 ± 4.4 mmHg, p = 0.006), higher VE vs. VCO2 slope (Non-PH/Ipc-PH/Cpc-PH = 33.0 [28.3, 36.6] vs. 32.5 [28.1, 37.8] vs. 40.6 [33.6, 46.1], p = 0.007), and lower ΔVO2/ΔWR (Non-PH/Ipc-PH/Cpc-PH = 8.5 ± 1.4 vs. 8.0 ± 1.7 vs. 6.8 ± 2.0 mL/min/watt, p = 0.001) than those with Ipc-PH and non-PH. Using multivariable logistic regression analysis, CPET variables were found to be independent predictors of Cpc-PH (lower peak PETCO2: odds ratio, 0.728 [95% confidence interval {CI}: 0.616-0.840], p = 0.003 and lower ΔVO2/ΔWR: odds ratio, 0.747 [95% CI: 0.575-0.872], p = 0.003). From our exploratory analysis, CPET variables, especially in the lower peak PETCO2 and lower ΔVO2/ΔWR, were associated with Cpc-PH in patients with left heart disease.