Sleep-Related Breathing Disorders

2016 ◽  
pp. 773-774
Author(s):  
Mithri R. Junna
Keyword(s):  
Systolic Pressure ◽  
Right Heart Catheterization ◽  
Heart Catheterization ◽  
Lower Extremity Edema ◽  
Right Ventricular Systolic Pressure ◽  
Sleep Related Breathing Disorders ◽  
Transthoracic Doppler Echocardiography ◽  
Ventricular Systolic Pressure ◽  
Progressive Dyspnea ◽  
The Many

Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure of at least 25 mm Hg at rest, as measured during right heart catheterization (RHC). The many causes of PH are classified into 5 groups. The clinical presentation of patients with PH is nonspecific: progressive dyspnea, chest pain, lower extremity edema, and fatigue. Typically, a diagnosis of PH is suggested by an increased right ventricular systolic pressure on transthoracic Doppler echocardiography and is confirmed with RHC.

Nerve growth factor receptor is involved in maintaining homeostasis of pulmonary arterial hypertension

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Goten ◽  
S Usui ◽  
O Inoue ◽  
H Okada ◽  
S Takashima ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Chronic Hypoxia ◽  
Systolic Pressure ◽  
Growth Factor Receptor ◽  
Right Heart Catheterization ◽  
Heart Catheterization ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Pulmonary Arterial ◽  
The Right

Abstract Introduction Pulmonary arterial hypertension (PAH), characterized by vascular remodeling, is still disease with poor prognosis although many pulmonary vasodilators have been developed, and new mechanism of treatment for PAH is desired. Nerve growth factor receptor (Ngfr) is known to relate to inflammatory reaction and repair process in the damaged tissue. We have reported that Ngfr is associated to vascular remodeling in patients with acute coronary syndrome. However, it is unclear how Ngfr is involved in the pathogenesis of PAH. Purpose In this study, we investigated whether Ngfr relate to pathophysiology in PAH. Methods We estimated the frequency of Ngfr positive cells (% Ngfr+) in peripheral blood mononuclear cells obtained from PAH and non-PAH patients using flowcytometric analysis. In PAH patients, the hemodynamic parameters such as mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR), and cardiac index (CI) were obtained by right heart catheterization, and evaluated for correlation with the % Ngfr+. Next, adult 8-week-old C57BL/6 (WT) mice and Ngfr knock out (KO) mice were exposed to chronic hypoxia (10% O2) or normoxia for 6 weeks. Then, mice were anesthetized and performed echocardiography and right heart catheterization. Then, mice were exsanguinated and blood sample was collected to evaluate the % Ngfr+ by flow cytometry. Right ventricular weight was measured and lung tissue was also collected for histological assessment and molecular pathway profiling. Results PAH (n=24) patients and non-PAH patients (n=17) were enrolled. The % Ngfr+ was significantly higher in PAH patients than that in non-PAH patients (0.056% versus 0.019%, p<0.0001). In PAH patients, the % Ngfr+ was correlated with severity of hemodynamic parameters such as mPAP (R=0.64 p<0.001), PVR (R=0.62 p<0.005), and CI (R=−0.48 p<0.05). In WT mice, chronic hypoxia significantly increased the right ventricular systolic pressure and induced vascular medial thickness and fibrosis around the pulmonary artery. Flow cytometry analysis revealed that the % Ngfr+ was significantly increased in the hypoxia compared to that in the normoxia. Under hypoxic conditions, the right ventricular systolic pressure was significantly increased in Ngfr KO mice compared to that in WT mice. In histological analysis, hypoxia-induced peripheral vascular fibrosis and medial thickness was more severe in Ngfr KO than that in WT mice. Conclusion Circulating Ngfr-positive cells are associated with severity of PAH in patients. In the hypoxia-induced PH model, gene deletion of Ngfr shows the progression of the pathogenesis of PAH. These results suggest that circulating Ngfr-positive cells have an important role in the pathogenesis of PAH and may be a novel target for PAH therapy. Funding Acknowledgement Type of funding source: None

scholarly journals Pulmonary Hypertension Assessment and Recognition of Outcomes in Scleroderma (PHAROS): Baseline Characteristics and Description of Study Population

2011 ◽  
Vol 38 (10) ◽  
pp. 2172-2179 ◽  
Author(s):  
MONIQUE HINCHCLIFF ◽  
ARYEH FISCHER ◽  
ELENA SCHIOPU ◽  
VIRGINIA D. STEEN
Keyword(s):  
Pulmonary Hypertension ◽  
High Risk ◽  
Laboratory Data ◽  
Systolic Pressure ◽  
Right Heart Catheterization ◽  
Venous Hypertension ◽  
Heart Catheterization ◽  
Ventricular Systolic Pressure ◽  
Patient Reported ◽  
Baseline Characteristics

Objective.Pulmonary arterial hypertension (PAH) increases mortality in systemic sclerosis (SSc). The multicenter PHAROS registry (Pulmonary Hypertension Assessment and Recognition of Outcomes in Scleroderma) prospectively follows subjects with SSc at high risk for or with incident pulmonary hypertension (PH). We describe the registry design and baseline characteristics of subjects enrolled during the first 18 months since the start of the study.Methods.High-risk subjects are enrolled and classified as Pre-PAH if they have (1) carbon monoxide diffusing capacity (DLCO) < 55% predicted; (2) percentage of predicted forced vital capacity/DLCO ratio ≥ 1.6; or (3) an estimated right ventricular systolic pressure > 35 mm Hg on echocardiography. Subjects with right heart catheterization (RHC)-confirmed incident PH (mean pulmonary artery pressure ≥ 25 mm Hg within previous 6 months) are subclassified into PAH, pulmonary venous hypertension secondary to left-side heart disease (PVH), and PH due to interstitial lung disease (PH-ILD). Baseline and biannual demographic, clinical, and laboratory data and patient-reported health questionnaires are collected.Results.There are 237 subjects enrolled in PHAROS. The majority are white (73%) and women (87%). There are 166 Pre-PAH and 71 Definite PH subjects (49 PAH, 7 PVH, and 15 PH-ILD).Conclusion.PHAROS is the largest US and Canadian cohort of subjects with SSc at high risk for or with incident PAH. PAH-specific therapies are approved for 49/71 subjects with RHC-confirmed PAH. Analyses of PHAROS registry data will permit identification of risk factors for development of PAH among SSc patients at high risk for PAH and enhance understanding of the course of SSc-PAH.

Abstract 16574: Heart Failure Biomarkers (NT-proBNP, Gal-3, sST2) Correlate With Right Ventricular Systolic Pressure and Provide Insight to Poor CRT Response: A BIOCRT Substudy

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Roderick C Deaño ◽  
Jackie Szymonifka ◽  
Qing Zhou ◽  
Jigar H Contractor ◽  
Zachary Lavender ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Systolic Pressure ◽  
Fold Increase ◽  
Left Ventricular ◽  
Cardiac Resynchronization ◽  
Cardiac Transplant ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Crt Response

Objective: Patients with heart failure (HF) and pulmonary hypertension (PH) have worse outcomes after cardiac resynchronization therapy (CRT). The relationship of circulating HF biomarkers and right ventricular systolic pressure (RVSP) may provide insight to the mechanism between PH and poor CRT response. Methods: In 90 patients (age 65 ± 13, 78% male, EF 26 ± 8%, RVSP 44 ± 12 mmHg) undergoing CRT, we measured baseline RVSP by echocardiography and obtained peripheral blood samples drawn at the time of device implantation. We measured levels of established and emerging HF biomarkers (Table 1). CRT non-response was defined as no improvement of adjudicated HF Clinical Composite Score at 6 months. Major adverse cardiac event (MACE) was defined as composite endpoint of death, cardiac transplant, left ventricular assist device, and HF hospitalization within 2 years. Results: There were 34% CRT non-responders and 27% had MACE. Per 1 unit increase in log-transformed RVSP, there was an 11-fold increase risk of having CRT non-response (odd ratio [OR] 11.0, p=0.01) and over 5-fold increase of developing 2-year MACE (hazard ratio [HR] 5.8, p=0.02). When comparing patients with severe PH (RVSP>60 mmHg) to those without PH (RVSP < 35 mmHg), there was an 8-fold increase in CRT nonresponse (OR 8.4, p=0.03) but no difference in MACE (p=NS). RVSP was correlated with increased biomarker levels of myocardial stretch and fibrosis, but not myocardial necrosis (Table 1). Conclusions: Higher RVSP is associated with greater rates of CRT non-response and adverse clinical outcomes. The mechanistic association between severe PH and CRT nonresponse may be explained by the biomarker profile reflective of myocardial wall stretch and fibrosis.

Right ventricular pressure response to +GZ acceleration stress

1982 ◽  
Vol 53 (4) ◽  
pp. 908-913 ◽  
Author(s):  
J. E. Whinnery ◽  
M. H. Laughlin
Keyword(s):  
Right Ventricular ◽  
Diastolic Pressure ◽  
Vena Cava ◽  
Systolic Pressure ◽  
Ventricular Pressure ◽  
Miniature Swine ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
The Right ◽  
Acceleration Stress

Measurements of right ventricular pressure in miniature swine were made at +Gz levels from +1 through +9 Gz. Polyethylene catheters were chronically placed in the cranial vena cava of five 2-yr-old female miniature swine (35–50 kg). The catheters were large enough to allow the introduction of a Millar pressure transducer into the venous system for placement in the right heart. The animals were fitted with an abdominal anti-G suit, restrained in a fiberglass couch, and exposed to the various +Gz levels on a centrifuge while fully conscious and unanesthetized. Right ventricular pressure and heart rate were measured during and for 2 min following 30-s exposures to each level of +Gz stress. The maximum right ventricular systolic pressure observed during +Gz was 200 Torr at +5 Gz with the maximum diastolic pressure being 88 Torr observed at +5 Gz. Mean heart rates were 200–210 beats/min at all levels of +Gz greater than or equal to +3 Gz when the animal remained stable. Mean maximum right ventricular pressures during +Gz stress were observed to increase through +5 Gz (85 Torr) and to decrease at higher levels of +Gz, indicating that through +5 Gz there is at least a partial compensation during acceleration stress. Decompensation in response to the stress began to occur during acceleration above +5 Gz with all animals decompensating during +9 Gz.

The effect of endogenous estrogen on Doppler-estimated right ventricular systolic pressure during exercise

2012 ◽  
Vol 90 (10) ◽  
pp. 1364-1371
Author(s):  
Vicki N. Wang ◽  
Mavra Ahmed ◽  
Amelia Ciofani ◽  
Zion Sasson ◽  
John T. Granton ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Menstrual Cycle ◽  
Right Ventricular ◽  
Systolic Pressure ◽  
Rate Pressure Product ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Early Exercise ◽  
Endogenous Estrogen ◽  
Response To Exercise

We evaluated the effect of endogenous estrogen levels on exercise-related changes in right ventricular systolic pressure (RVSP) of healthy, eumenorrheic, sedentary women. Volunteers were studied at two separates phases of the menstrual cycle (LO and HI estrogen phases), exercised on a semi-supine ergometer with escalating workload and monitored continuously by 12-lead ECG and automated blood pressure cuff. At each exercise stage, Doppler echocardiography measurements were obtained and analyzed to determine RVSP. Fourteen subjects (age 24 ± 5) were studied. Exercise duration was significantly higher on the HI estrogen day, but no significant differences in hemodynamic response to exercise were found between the two study days. There were also no significant differences with respect to heart rate (HR) acceleration during early exercise, as well as resting and peak RVSP, HR, blood pressure, and rate pressure product. Doppler-estimated RVSP demonstrated a linear relationship to HR at a ratio of 1 mm Hg (1 mm Hg = 133.3224 Pa) for every 5 bpm (beats per minute) increase in HR. There were no differences in the slope of this relationship between HI and LO estrogen phases of the menstrual cycle. Our findings did not demonstrate any effect of endogenous estrogen levels on the modulation of the pulmonary vascular response to exercise in healthy women.

Abstract 14666: Association Between Right Ventricular Systolic Pressure and Health Status Following Transcatheter Aortic Valve Replacement

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Rahul Myadam ◽  
Ali O Malik ◽  
Matthew Pflederer ◽  
Kensey Gosch ◽  
Suzanne V Arnold ◽  
...  
Keyword(s):  
Health Status ◽  
Transcatheter Aortic Valve Replacement ◽  
Mixed Model ◽  
Linear Mixed Model ◽  
Systolic Pressure ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Transcatheter Aortic Valve ◽  
Increased Risk ◽  
Before And After

Introduction: Pulmonary hypertension (PH) was shown in multiple studies to be associated with an increased risk of mortality after transcatheter aortic valve replacement (TAVR). However, it is unclear if echocardiogram derived right ventricular systolic pressure (RVSP) is associated with health status outcomes in surviving patients after TAVR. We explored for an association between baseline RVSP and quality of life in patients before and after undergoing TAVR. Methods: We estimated RVSP by echocardiography using the modified Bernoulli equation in a single-center cohort of patients undergoing TAVR from 2012-2017 . Disease-specific health status was assessed at baseline and 1-month and 12-months after TAVR with the Kansas City Cardiomyopathy Questionnaire-Overall Summary Score (KCCQ-OS). We then explored the association between baseline RVSP and KCCQ-OS before and after TAVR using a linear mixed model with an interaction for time and baseline RVSP and adjusted for baseline mitral valve regurgitation and systolic blood pressure. Results: Among 485 patients who underwent TAVR (mean age 81.7±7.9 years, 54.8% men), baseline RVSP was 42±15 mmHg, and 73% had RVSP >34 mmHg. After TAVR, mean RVSP decreased to 37±13 mmHg at 1 month and 36±14 mmHg at 12 months. Baseline KCCQ-OS was 46±25 and improved to 66.9±23.6 at 1 month and 69.5± 22.6 at 12 months. In the linear mixed model, there was a significant cross-sectional association between baseline RVSP and baseline KCCQ-OS, with higher RVSP associated with worse health status. However, baseline RVSP was not significantly associated with KCCQ-OS at 1 month or 12 months (Figure). Conclusions: RVSP is not associated with worse health status after TAVR. This suggests that while patients with high RVSP are at an increased risk for mortality after TAVR, surviving patients appear to have similar health status as those with normal RVSP.

Abstract 17168: Myocardial Natriuretic Peptide Expression in Heart Failure With Preserved Ejection Fraction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Virginia S Hahn ◽  
Hildur Knutsdottir ◽  
Kenneth C Bedi ◽  
Kenneth B Margulies ◽  
Saptarsi M Haldar ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Renal Function ◽  
Ejection Fraction ◽  
Systolic Pressure ◽  
Principal Component ◽  
Serum Levels ◽  
Right Heart Catheterization ◽  
Heart Catheterization ◽  
Preserved Ejection Fraction

Introduction: Serum natriuretic peptides (NP) are reduced in heart failure with preserved ejection fraction (HFpEF) compared to HFrEF; however, myocardial NP expression in HFpEF is unknown. We analyzed serum NTproBNP and myocardial RNAseq data to test the hypothesis that 1) lower myocardial NP expression in HFpEF drives the difference in serum levels, and 2) HFpEF with higher NP expression have transcriptomic signatures more similar to HFrEF. Methods: HFpEF patients (n=41) with clinical HF, LVEF≥50%, and meeting current consensus criteria for HFpEF underwent right heart catheterization and right ventricular (RV) endomyocardial biopsy. We performed differential gene expression analysis of RV septal tissue from HFpEF and compared to explanted HFrEF (n=30) and unused donor hearts (n=24, Control). Results: Myocardial NPPB expression was 5-fold higher in HFrEF vs Control (p<0.001) and unchanged in HFpEF vs Control, while NPPA expression was 9-fold higher in HFrEF and 5-fold higher in HFpEF vs Control (p<0.0001 for both comparisons). After adjustment for renal function and BMI, myocardial NPPB expression was significantly associated with serum NTproBNP in HFpEF (R 2 0.68; p<0.0001 for renal function, NPPB expression; p=0.03 for BMI). Pulmonary artery (PA) systolic pressure and PA wedge pressure correlated with myocardial NPPB expression (PASP R 2 0.45, p<0.0001; PAWP R 2 0.25, p=0.01), even after adjustment for comorbidities. HFpEF patients with high (≥ median NPPB expression in HFpEF) vs low NPPB expression had transcriptomic signatures more similar to HFrEF using ~13,000 genes in a Principal Component Analysis (Figure), quantified by vector distance from HFrEF (p=0.017). Conclusions: HFpEF patients have reduced serum NTproBNP due to lower myocardial NPPB gene expression. HFpEF patients with higher NPPB expression have transcriptomic signatures more similar to HFrEF, highlighting a HFpEF subgroup that may benefit from targeted therapies.

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