RV Contractility and Exercise-Induced Pulmonary Hypertension in Chronic Mountain Sickness

Pratali, Lorenza; Allemann, Yves; Rimoldi, Stefano F.; Faita, Francesco; Hutter, Damian; Rexhaj, Emrush; Brenner, Roman; Bailey, Damian Miles; Sartori, Cláudio; Salmòn, Carlos Salinas; Villena, Mercedes; Scherrer, Urs; Picaño, Eugenio; Sicari, Rosa

doi:10.1016/j.jcmg.2013.08.007

Cited by 48 publications

(38 citation statements)

References 32 publications

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“…This may be compatible with some negative inotropic and lusitropic effects of hypoxia reported by in vitro studies, but is in contrast with trivial effects of hypoxic breathing on standard echocardiographic indices of ventricular function (Naeije & Dedobbeleer, 2013) and preserved RV contractile reserve in hypoxia (Pratali et al, 2013). This may be compatible with some negative inotropic and lusitropic effects of hypoxia reported by in vitro studies, but is in contrast with trivial effects of hypoxic breathing on standard echocardiographic indices of ventricular function (Naeije & Dedobbeleer, 2013) and preserved RV contractile reserve in hypoxia (Pratali et al, 2013).…”

Section: Discussionsupporting

confidence: 85%

Right ventricular dyssynchrony during hypoxic breathing but not during exercise in healthy subjects: a speckle tracking echocardiography study

Pezzuto

Forton

Badagliacca

et al. 2018

Experimental Physiology

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Pulmonary hypertension (PH) has been shown to be associated with regional inhomogeneity (or dyssynchrony) of right ventricular (RV) contraction. Right ventricular dyssynchrony is an independent predictor of decreased survival in advanced PH, but has also been reported in patients with only mildly elevated pulmonary artery pressure (PAP). The mechanisms of RV dyssynchrony in PH remain uncertain. Our aim was to evaluate RV regional function in healthy subjects during acute hypoxia and during exercise. Seventeen healthy subjects (24 ± 6 years) underwent a speckle tracking echocardiography of the RV at rest in normoxia and every 15 min during a 60 min exposure to hypoxic breathing ( 12%). Ten of the subjects also underwent an incremental cycle ergometry in normoxia to 100 W, with the same echocardiographic measurements. Dyssynchrony was measured as the SD of the times to peak systolic strain of the four basal and mid RV segments corrected for the heart rate (RV-SD4). RV-SD4 increased during hypoxia from 12 ± 7 to 22 ± 11 ms in spite of mild increases in mean PAP (mPAP) from 15 ± 2 to 20 ± 2 mmHg and pulmonary vascular resistance (PVR) from 1.18 ± 0.15 to 1.4 ± 0.15 Wood units (WU). During exercise RV-SD4 did not significantly change (from 12 ± 6 ms to 14 ± 6 ms), while mPAP increased to 25 ± 2 mmHg and PVR was unchanged. These data show that in healthy subjects, RV contraction is inhomogeneous in hypoxia but not during exercise. Since PAP increases more during exercise, RV dyssynchrony in hypoxia may be explained by a combination of mechanical (RV afterload) and systemic (hypoxia) factors.

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Section: Discussionsupporting

confidence: 85%

Right ventricular dyssynchrony during hypoxic breathing but not during exercise in healthy subjects: a speckle tracking echocardiography study

Pezzuto

Forton

Badagliacca

et al. 2018

Experimental Physiology

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“…Furthermore, our results highlight that the conventional interpretation of Z C as a measure of proximal artery stiffness is not valid in all physiological and pathological states. cardiopulmonary hemodynamics; chronic hypoxia; characteristic impedance; blood viscosity; pulmonary vascular impedance CHRONIC MOUNTAIN SICKNESS (CMS), also known as Monge's disease, occurs after chronic exposure to hypoxia at high altitudes and is characterized by increased pulmonary artery pressures and pulmonary vascular resistance (29) as well as increased hematocrit (19). Chronic hypoxia also contributes to worse outcomes in lung diseases such as chronic obstructive pulmonary disease, sleep apnea, and pulmonary fibrosis (1,10,15).…”

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confidence: 99%

Impact of increased hematocrit on right ventricular afterload in response to chronic hypoxia

Schreier

Hacker²,

Hunter

et al. 2014

Journal of Applied Physiology

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Chesler N. Impact of increased hematocrit on right ventricular afterload in response to chronic hypoxia. J Appl Physiol 117: 833-839, 2014. First published August 28, 2014 doi:10.1152/japplphysiol.00059.2014.-Chronic hypoxia causes chronic mountain sickness through hypoxiainduced pulmonary hypertension (HPH) and increased hematocrit. Here, we investigated the impact of increased hematocrit and HPH on right ventricular (RV) afterload via pulmonary vascular impedance. Mice were exposed to chronic normobaric hypoxia (10% oxygen) for 10 (10H) or 21 days (21H). After baseline hemodynamic measurements, ϳ500 l of blood were extracted and replaced with an equal volume of hydroxyethylstarch to normalize hematocrit and all hemodynamic measurements were repeated. In addition, ϳ500 l of blood were extracted and replaced in control mice with an equal volume of 90% hematocrit blood. Chronic hypoxia increased input resistance (Z 0 increased 82% in 10H and 138% in 21H vs. CTL; P Ͻ 0.05) and characteristic impedance (Z C increased 76% in 10H and 109% in 21H vs. CTL; P Ͻ 0.05). Hematocrit normalization did not decrease mean pulmonary artery pressure but did increase cardiac output such that both Z 0 and ZC decreased toward control levels. Increased hematocrit in control mice did not increase pressure but did decrease cardiac output such that Z 0 increased. The paradoxical decrease in ZC with an acute drop in hematocrit and no change in pressure are likely due to inertial effects secondary to the increase in cardiac output. A novel finding of this study is that an increase in hematocrit affects the pulsatile RV afterload in addition to the steady RV afterload (Z 0). Furthermore, our results highlight that the conventional interpretation of Z C as a measure of proximal artery stiffness is not valid in all physiological and pathological states. cardiopulmonary hemodynamics; chronic hypoxia; characteristic impedance; blood viscosity; pulmonary vascular impedance CHRONIC MOUNTAIN SICKNESS (CMS), also known as Monge's disease, occurs after chronic exposure to hypoxia at high altitudes and is characterized by increased pulmonary artery pressures and pulmonary vascular resistance (29) as well as increased hematocrit (19). Chronic hypoxia also contributes to worse outcomes in lung diseases such as chronic obstructive pulmonary disease, sleep apnea, and pulmonary fibrosis (1,10,15). In preclinical animal models of pulmonary arterial hypertension (PAH), chronic hypoxia is often used to generate hypoxia-induced pulmonary hypertension (HPH). PAH is a debilitating disease with a low median survival of 2.8 yr (6,17) and is characterized by remodeling throughout the pulmonary vasculature, including distal arterial narrowing and proximal and distal pulmonary artery stiffening, leading to right ventricular (RV) dysfunction that progresses to RV failure as the cause of death (28). HPH in rodents recapitulates the pulmonary vascular remodeling and RV hypertrophy that occur in patients with PAH but also increases hematocrit. Indeed, the increase in ...

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“…Further details on the methodology of signal processing and experimental setup can be found in [6,7], and in [2][3][4], respectively.…”

Section: Methodsmentioning

confidence: 99%

“…Chronic Mountain Sickness (CMS), also known as Monge's disease, is defined as a persistent combination of polycythemia (an abnormally increased concentration of hemoglobin in the blood) in associations with hypoxemia impairment in cerebral function, and, in some cases, moderate or severe pulmonary hypertension that may evolve to cor pulmonale, leading to congestive heart failure [1][2][3][4]. Usually, this disease begins during adult life in high altitude regions, and its marked systemic vascular dysfunction may predispose CMS patients to premature cardiovascular disease [1,2,4].…”

Section: Introductionmentioning

confidence: 99%

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Changes in instantaneous complex dynamics during exercise in Chronic Mountain Sickness

Valenza

Faita

Pratali

et al. 2015

2015 Computing in Cardiology Conference (CinC)

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The combination of persistent polycythemia with decreased physical and cognitive performances while living in high-altitude is defined as 'Chronic Mountain Sickness' (CMS). To date, the role of the autonomic nervous system in CMS is still unknown. In this study, we analyze instantaneous tracking of cardiovascular complexity in order to increase the knowledge on CMS physio-pathology. To this extent, we processed heartbeat dynamics gathered from 13 CMS males and 7 high-altitude male dwellers, taken as healthy controls (HC), during semi-supine bicycle tasks performed at 25W, 50W, and 100W, along with a recovery session. Instantaneous Dominant Lyapunov exponents (IDLE), as estimated through point-process nonlinear models with Laguerre and Volterra expansions, were evaluated from such series. Results showed that instantaneous heartbeat complex dynamics was significantly altered in CMS. In particular, IDLE increases were associated to CMS, with respect to HC, during the 25W and 50W exercise sessions (p < 0.01). Conversely, no statistical differences were found when analyzing the 100W session, and first recovery after exercise.

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RV Contractility and Exercise-Induced Pulmonary Hypertension in Chronic Mountain Sickness

Abstract: Comparable RV contractile reserve in CMS and HA suggests that the lower resting values of RV function in CMS may represent a physiological adaptation to chronic hypoxic conditions rather than impaired RV function. (Chronic Mountain Sickness, Systemic Vascular Function [CMS]; NCT01182792).

Cited by 48 publications

References 32 publications

Right ventricular dyssynchrony during hypoxic breathing but not during exercise in healthy subjects: a speckle tracking echocardiography study

Right ventricular dyssynchrony during hypoxic breathing but not during exercise in healthy subjects: a speckle tracking echocardiography study

Impact of increased hematocrit on right ventricular afterload in response to chronic hypoxia

Changes in instantaneous complex dynamics during exercise in Chronic Mountain Sickness

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