Clinical Course Of Patients With Pulmonary Hypertension Secondary To Diastolic Dysfunction, Obesity, And Sleep Apnea

2011 ◽  
Author(s):  
Krishna M. Sundar ◽  
Alika Willis ◽  
Douglas S. Ross
Keyword(s):  
Pulmonary Hypertension ◽  
Sleep Apnea ◽  
Diastolic Dysfunction ◽  
Clinical Course

THE CLINICAL COURSE OF MYOCARDIAL INFARCTION PECULIARITIES IN MEN UNDER 60 YEARS OLD WITH PULMONARY HYPERTENSION

2020 ◽  
pp. 64-68
Author(s):  
Gordienko A.V. ◽  
Men’shikova A.N. ◽  
Sotnikov A.V.
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Clinical Course ◽  
Comparative Assessment ◽  
Study Group ◽  
Routine Examination ◽  
Group Iii ◽  
Appropriate Treatment ◽  
Level Group

Relevance. Pulmonary hypertension (PH) negatively affects the prognosis of myocardial infarction (MI). Aim. To evaluate MI clinical features (CF) in men under 60 years old (y.o.) with PH, arising during MI to improve pre-vention and outcomes. Material and methods. The study included men 19-60 y.o. with MI and various dynamics of mean pulmonary artery pressure (MPAP), determined by echocardiography (A. Kitabatake) in first 48 hours (1) and completion of third week (2). Patients were divided into four groups: studied (I) included 67 patients (mean age 50.4±7.1 y.o) with PH (MPAP2 25 and more mm Hg) and normal of MPAP1 level. Group II included patients with a normal MPAP in both phases of study (70; 52.1±6.6 y.o); group III – with elevated MPAP at both study points (149; 51.2±5.5 y.o) and IV – with in-creased MPAP1 and normal MPAP2 (61, 50.5±6.8 y.o). A comparative assessment of the MI CF frequency in selected groups were performed. Results. The study group occupied intermediate place frequency in medical history presence: coronary heart disease (I: 59.5; II: 61.4; III: 63.6 and IV: 48.9%; p = 0.04), chronic heart failure (CHF) (35.7 ; 34.1; 51.1 and 24.5%, respec-tively; p=0.001), repeated (45.2; 42.0; 47.3 and 29.8%) and early recurrent (3.6; 3.4 ; 6.0 and 3.2%; pIII-IV=0.006) MI, Q-MI (44.0; 35.2; 58.7 and 56.4; p=0.001), anginal MI phenotype (75.0; 74.7; 54.3 and 77.7%; p˂0.0001) and acute HF (ACF) (45,2; 36,8; 50,5 и 48,9%; р=0,002). No pulmonary edema was detected in it (p˂0.0001). Conclusions. Men under 60 y.o. with PH resulting from MI occupy an intermediate place in frequency of complica-tions, ACF and CHF in first 56 days of MI during routine examination compared with other MPAP dynamics patients. This confirms the need for additional verification of PH genesis for the appropriate treatment.

HEMODYNAMIC CHARACTERISTICS OF PULMONARY HYPERTENSION IN SLEEP APNEA

CHEST Journal ◽  
2007 ◽  
Vol 132 (4) ◽  
pp. 665A
Author(s):  
Roop Kaw ◽  
Moustafa Hazin ◽  
Ribhi Hazin ◽  
Basma Ricuarte ◽  
Omar Minai
Keyword(s):  
Pulmonary Hypertension ◽  
Sleep Apnea ◽  
Hemodynamic Characteristics

scholarly journals DIPPERS AND NON DIPPERS DIASTOLIC DYSFUNCTION AND LEFT VENTRICULAR MASS IN PATIENTS WITH OBSTRUCTIVE SLEEP APNEA

2021 ◽  
Vol 77 (18) ◽  
pp. 1384
Author(s):  
Colin Gallagher ◽  
Jacob Grand ◽  
Ikuyo Imayama ◽  
Benjamin Follman ◽  
Bharati Prasad ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Diastolic Dysfunction ◽  
Left Ventricular Mass ◽  
Left Ventricular ◽  
Ventricular Mass ◽  
Obstructive Sleep

Prognostic relevance of sleep apnea syndrome in patients with pulmonary arterial hypertension

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Precek ◽  
K Vykoupil ◽  
F Kovacik ◽  
M Hutyra
Keyword(s):  
Pulmonary Hypertension ◽  
Sleep Apnea ◽  
Pulmonary Arterial Hypertension ◽  
General Population ◽  
Arterial Hypertension ◽  
Left Ventricular ◽  
Sleep Study ◽  
Prognostic Relevance ◽  
Obstructive Sleep ◽  
Pulmonary Arterial

Abstract Introduction Sleep disordered breathing (SDB) is a group of ventilatory disorders during sleep which includes obstructive sleep apnea (OSA), central sleep apnea (CSA), and sleep related hypoventilation. In patients with SDB, the prevalence of pulmonary hypertension (PH) ranges from 17% to 52%. While SDB is prevalent in the general population with recent estimates of 20% to 30%, in those with cardiovascular disease, particularly left ventricular failure, there is a higher reported prevalence of 47%. Aims The aims of this study were to determine the prevalence and prognostic relevance of sleep apnea in a cohort of patients with newly diagnosed pulmonary arterial hypertension (ESC/WHO Group 1 pulmonary hypertension). Methods We evaluated prospectively 76 patients with the pulmonary arterial hypertension (mean age 54±16 years; 45% male). All patients underwent right heart catheterisation, clinical assessments, sleep study, standard laboratory testing and evaluation of subjective sleepiness by the Epworth Sleepiness Scale. Sleep test was provided with an ApneaLink Plus, consisting of nasal pressure sensor, respiratory effort band, and pulse oximeter worn on the finger. Subjects previously treated for or diagnosed with SDB were excluded from the study. Results Sleep apnea (SA) – defined as apnea-hypopnea index (AHI) ≥5/h – was found in 59 (77.6%) of the pulmonary arterial hypertension (PAH) patients. Mean AHI in the cohort of PAH patients with SA was 26.1±16.6/h. Mean follow-up was 24 months, during which 15 (19.7%) patients died. Characteristics of parameters related to SA in groups of survivors and deceased are in table 1. From the sleep apnea-related parameters, only time with O2Sat <90% – T90 was significantly associated with mortality (AUC 0.856; 95% CI 0.693 – 1.019; p<0.001). Conclusions The presence of sleep apnea in pulmonary arterial hypertension patients is high. The prevalence of sleep apnea is higher in PAH patients than in the general population. The presence of sleep apnea in patients with PAH was not associated with worse prognosis, but noctural hypoxemia (time with O2Sat <90%) was related to poor prognosis. Sleep apnea in patients with PAH should be screened for systematically. Funding Acknowledgement Type of funding source: None

Diastolic dysfunction in controlled hypertensive patients with mild–moderate obstructive sleep apnea

2015 ◽  
Vol 187 ◽  
pp. 686-692 ◽  
Author(s):  
Elisabetta Lisi ◽  
Andrea Faini ◽  
Grzegorz Bilo ◽  
Laura Maria Lonati ◽  
Miriam Revera ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Diastolic Dysfunction ◽  
Hypertensive Patients ◽  
Obstructive Sleep

Fenestrated Transcatheter ASD Closure in Adults with Diastolic Dysfunction and/or Pulmonary Hypertension: Case Series and Review of the Literature

2016 ◽  
Vol 11 (6) ◽  
pp. 663-671 ◽  
Author(s):  
Ayman Abdelkarim ◽  
Daniel S. Levi ◽  
Bao Tran ◽  
Joanna Ghobrial ◽  
Jamil Aboulhosn
Keyword(s):  
Pulmonary Hypertension ◽  
Diastolic Dysfunction ◽  
Case Series ◽  
Review Of The Literature ◽  
Asd Closure

Abstract P428: A New Mouse Model Of Myocardial Lipids, Fibrosis, Arrhythmia And Diastolic Dysfunction Induced By Hyperlipidemia And Cardiac LDLR

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Monique Williams ◽  
Camila Iansen Irion ◽  
Jose Manuel Condor Capcha ◽  
Guerline Lambert ◽  
Grace Seo ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Function ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Lipid Accumulation ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Poloxamer 407 ◽  
Whole Body ◽  
Subsequent Increase

Background: Hyperlipidemia is a major risk factor for CVD. Patients with HF with preserved ejection fraction (HFpEF) have more myocardial lipid accumulation than patients with reduced EF (HFrEF). RNASeq data from cardiac biopsies showed downregulation of the gene for lipoprotein lipase (LPL) that degrades triglycerides, in HFpEF patients compared to healthy and HFrEF controls. Poloxamer-407 (p407) induces hyperlipidemia by blocking LPL and subsequent increase in plasma triglycerides and low-density lipoprotein (LDL) cholesterol. We hypothesized that mice treated with p407 and cardiac LDL-Receptor (LDLR) over-expression (OE) develop hyperlipidemia, myocardial lipid accumulation, and diastolic dysfunction resulting in HFpEF and arrhythmias. Methods: Baseline cardiac function was assessed by echo for male and female C57Bl6 mice (n=9) for 2 groups: 4wk biweekly i.p. p407-injections with (n=4) or without (n=3) single i.v. injection with AAV9-cTnT-LDLR. Cardiac function was assessed by echocardiography at 3 and 4 wks. Blood Pressure (BP) and Whole Body Plethysmography (WBP) were assessed during wk4. Ttest was used for statistics. PR and ORO staining and telemetry were performed at wk4. Results: At wk3, P407 and LDLR OE led to alterations in diastolic function (increased IVCT, IVRT, MV E/E’, MPI, and NFT) and increased LV wall thickness, p<0.05. At wk4, there was pulmonary hypertension (increased mean pulmonary arterial pressure, decreased pulmonary acceleration time p <.05).Histology showed excessive myocardial lipids and fibrosis, and telemetry showed incidents of second-degree and higher-degree AV block. The group injected solely with p407 show e d alterations in diastolic function (increased IVCT, IVRT, NFT, LVMPI, LVMPI NFT p<.05 ) and decreased EDV, ESV, EDLVM, ESLVM, p<.05 at wk4. All groups had preserved %EF and no abnormalities in BP or WBP. Conclusions: P407 and cardiac LDLR OE induce a drastic decline in cardiac diastolic function over a shorter period of time compared to p407 alone. Diastolic dysfunction was observed in wk3 followed by pulmonary hypertension, arrhythmia, myocardial lipid accumulation and fibrosis in wk4. This new model may allow for more rapid investigations of cardiac abnormalities seen in HFpEF patients.

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