Myocardial edema, left ventricular function, and pulmonary hypertension

1995 ◽  
Vol 78 (1) ◽  
pp. 132-137 ◽  
Author(s):  
K. L. Davis ◽  
U. Mehlhorn ◽  
G. A. Laine ◽  
S. J. Allen
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Dry Weight ◽  
Left Ventricular ◽  
Interstitial Edema ◽  
Pulmonary Arterial

Left ventricular dysfunction has been reported in both experimentally induced and clinical pulmonary hypertension. However, the mechanism by which pulmonary hypertension causes left ventricular dysfunction is unknown. We hypothesized that acute pulmonary hypertension causes left ventricular myocardial interstitial edema and that it is this edema that causes left ventricular dysfunction. In pulmonary artery-banded or sham-operated dogs, left ventricular diameter (septal-free wall axis) and pressure were measured using sonomicrometry crystals and a micromanometer, respectively. These measurements were used to calculate preload recruitable stroke work (PRSW), an index of contractility, and the rate of active relaxation (tau) to assess systolic and diastolic left ventricular function, respectively. After 3 h of pulmonary arterial hypertension or control, the dogs were killed and the left ventricles were excised to determine wet-to-dry weight ratios. The wet-to-dry weight ratios were significantly higher in the pulmonary artery-banded dogs (3.57 +/- 0.12) than in the sham-operated dogs (3.41 +/- 0.17). PRSW decreased to 56.8 +/- 30.3% of control after 3 h of pulmonary hypertension. tau Slowed significantly from 29.8 +/- 5.8 ms at baseline to 63.6 +/- 30.4 ms after 3 h of pulmonary arterial hypertension. There were no differences in PRSW or tau in the sham-operated dogs. We conclude that pulmonary hypertension causes left ventricular myocardial interstitial edema, which results in both systolic and diastolic left ventricular dysfunction.

scholarly journals Pathophysiology and treatment of pulmonary hypertension in sickle cell disease

Blood ◽  
2016 ◽  
Vol 127 (7) ◽  
pp. 820-828 ◽  
Author(s):  
Victor R. Gordeuk ◽  
Oswaldo L. Castro ◽  
Roberto F. Machado
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Sickle Cell Disease ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Sickle Cell ◽  
Left Ventricular ◽  
Cell Disease ◽  
Pulmonary Pressure ◽  
Pulmonary Arterial

Abstract Pulmonary hypertension affects ∼10% of adult patients with sickle cell disease (SCD), particularly those with the homozygous genotype. An increase in pulmonary artery systolic pressure, estimated noninvasively by echocardiography, helps identify SCD patients at risk for pulmonary hypertension, but definitive diagnosis requires right-heart catheterization. About half of SCD-related pulmonary hypertension patients have precapillary pulmonary hypertension with potential etiologies of (1) a nitric oxide deficiency state and vasculopathy consequent to intravascular hemolysis, (2) chronic pulmonary thromboembolism, or (3) upregulated hypoxic responses secondary to anemia, low O2 saturation, and microvascular obstruction. The remainder have postcapillary pulmonary hypertension secondary to left ventricular dysfunction. Although the pulmonary artery pressure in SCD patients with pulmonary hypertension is only moderately elevated, they have a markedly higher risk of death than patients without pulmonary hypertension. Guidelines for diagnosis and management of SCD-related pulmonary hypertension were published recently by the American Thoracic Society. Management of adults with sickle-related pulmonary hypertension is based on anticoagulation for those with thromboembolism; oxygen therapy for those with low oxygen saturation; treatment of left ventricular failure in those with postcapillary pulmonary hypertension; and hydroxyurea or transfusions to raise the hemoglobin concentration, reduce hemolysis, and prevent vaso-occlusive events that cause additional increases in pulmonary pressure. Randomized trials have not identified drugs to lower pulmonary pressure in SCD patients with precapillary pulmonary hypertension. Patients with hemodynamics of pulmonary arterial hypertension should be referred to specialized centers and considered for treatments known to be effective in other forms of pulmonary arterial hypertension. There have been reports that some of these treatments improve SCD-related pulmonary hypertension.

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

Pulmonary Hypertension

2013 ◽  
Author(s):  
George K Istaphanous ◽  
Andreas W Loepke
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Pulmonary Artery Pressure ◽  
Disease Process ◽  
Underlying Disease ◽  
Artery Pressure ◽  
Pulmonary Arterial ◽  
Made In

Pediatric pulmonary arterial hypertension (PAH) is characterized by a pathologically elevated pulmonary artery pressure in children. The etiology of PAH is multifactorial, and while its prognosis is closely related to the reversibility of the underlying disease process, much progress has recently been made in its diagnosis and treatment, significantly decreasing the associated morbidity and mortality.

scholarly journals Icariin Attenuates Monocrotaline-Induced Pulmonary Arterial Hypertension via the Inhibition of TGF-β1/Smads Pathway in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Yijia Xiang ◽  
Changhong Cai ◽  
Yonghui Wu ◽  
Lebing Yang ◽  
Shiyong Ye ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Western Blots ◽  
Pulmonary Arterial ◽  
The Right ◽  
Tgf Β1

Background. Pulmonary artery remodeling is important in the development of pulmonary artery hypertension. The TGF-β1/Smads signaling pathway is activated in pulmonary arterial hypertension (PAH) in rats. Icariin (ICA) suppresses the TGF-β1/Smad2 pathway in myocardial fibrosis in rats. Therefore, we investigated the role of icariin in PAH by inhibiting the TGF-β1/Smads pathway. Methods. Rats were randomly divided into control, monocrotaline (MCT), MCT + ICA-low, and MCT + ICA-high groups. MCT (60 mg/kg) was subcutaneously injected to induce PAH, and icariin (50 or 100 mg/kg.d) was orally administered for 2 weeks. At the end of the fourth week, right ventricular systolic pressure (RVSP) was obtained and the right ventricular hypertrophy index (RI) was determined as the ratio of the right ventricular weight to the left ventricular plus septal weight (RV/LV + S). Western blots were used to determine the expression of TGF-β1, Smad2/3, P-Smad2/3, and matrix metalloproteinase-2 (MMP2) in lung tissues. Results. Compared to the control group, RVSP and RI were increased in the MCT group (ρ < 0.05). Additionally, TGF-β1, Smad2/3, P-Smad2/3, and MMP2 expressions were obviously increased (ρ < 0.01). Compared to the MCT group, RVSP and RI were decreased in the MCT + ICA group (ρ < 0.05). TGF-β1, Smad2/3, P-Smad2/3, and MMP2 expressions were also inhibited in the icariin treatment groups (ρ < 0.05). Conclusions. Icariin may suppress MCT-induced PAH via the inhibition of the TGFβ1-Smad2/3 pathway.

scholarly journals Sex Differences in Pulmonary Hypertension

2021 ◽  
Vol 2 ◽  
Author(s):  
Juan José Rodriguez-Arias ◽  
Ana García-Álvarez
Keyword(s):  
Pulmonary Hypertension ◽  
Sex Differences ◽  
Pulmonary Arterial Hypertension ◽  
Animal Models ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Gender Bias ◽  
Response To Treatment ◽  
Experimental Animal Models ◽  
Pulmonary Arterial

Pulmonary hypertension (PH) includes multiple diseases that share as common characteristic an elevated pulmonary artery pressure and right ventricular involvement. Sex differences are observed in practically all causes of PH. The most studied type is pulmonary arterial hypertension (PAH) which presents a gender bias regarding its prevalence, prognosis, and response to treatment. Although this disease is more frequent in women, once affected they present a better prognosis compared to men. Even if estrogens seem to be the key to understand these differences, animal models have shown contradictory results leading to the birth of the estrogen paradox. In this review we will summarize the evidence regarding sex differences in experimental animal models and, very specially, in patients suffering from PAH or PH from other etiologies.

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