scholarly journals Echocardiographic and invasive measurements of pulmonary artery pressure correlate closely at high altitude

2000 ◽  
Vol 279 (4) ◽  
pp. H2013-H2016 ◽  
Author(s):  
Yves Allemann ◽  
Claudio Sartori ◽  
Mattia Lepori ◽  
Sébastien Pierre ◽  
Christian Mélot ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
High Altitude ◽  
Doppler Echocardiography ◽  
Systolic Pulmonary Arterial Pressure ◽  
Wide Range ◽  
High Altitude Pulmonary Edema ◽  
Reproducible Method ◽  
Pulmonary Arterial ◽  
Spearman Test ◽  
Invasive Measurement

Exaggerated hypoxia-induced pulmonary hypertension is a hallmark of high-altitude pulmonary edema (HAPE) and plays a major role in its pathogenesis. Many studies of HAPE have estimated systolic pulmonary arterial pressure (SPAP) with Doppler echocardiography. Whereas at low altitude, Doppler echocardiographic estimation of SPAP correlates closely with its invasive measurement, no such evidence exists for estimations obtained at high altitude, where alterations of blood viscosity may invalidate the simplified Bernoulli equation. We measured SPAP by Doppler echocardiography and invasively in 14 mountaineers prone to HAPE and in 14 mountaineers resistant to this condition at 4,559 m. Mountaineers prone to HAPE had more pronounced pulmonary hypertension (57 ± 12 and 58 ± 10 mmHg for noninvasive and invasive determination, respectively; means ± SD) than subjects resistant to HAPE (37 ± 8 and 37 ± 6 mmHg, respectively), and the values measured in the two groups as a whole covered a wide range of pulmonary arterial pressures (30–83 mmHg). Spearman test showed a highly significant correlation ( r = 0.89, P < 0.0001) between estimated and invasively measured SPAP values. The mean difference between invasively measured and Doppler-estimated SPAP was 0.5 ± 8 mmHg. At high altitude, estimation of SPAP by Doppler echocardiography is an accurate and reproducible method that correlates closely with its invasive measurement.

MO746CARDIAC REMODELING AND PULMONARY HYPERTENSION IN HEMODIALYSIS PATIENTS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Ekaterina Borodulina ◽  
Alexander M Shutov
Keyword(s):  
Pulmonary Hypertension ◽  
Left Ventricular Hypertrophy ◽  
Arterial Pressure ◽  
Ventricular Hypertrophy ◽  
Pulmonary Arterial Pressure ◽  
Hemodialysis Patients ◽  
Left Ventricular ◽  
Hemodialysis Treatment ◽  
Systolic Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Abstract Background and Aims An important predictor of cardiovascular mortality and morbidity in hemodialysis patients is left ventricular hypertrophy. Also, pulmonary hypertension is a risk factor for mortality and cardiovascular events in hemodialysis patients. The aim of this study was to investigate cardiac remodeling and the dynamics of pulmonary arterial pressure during a year-long hemodialysis treatment and to evaluate relationship between pulmonary arterial pressure and blood flow in arteriovenous fistula. Method Hemodialysis patients (n=88; 42 males, 46 females, mean age was 51.7±13.0 years) were studied. Echocardiography and Doppler echocardiography were performed in the beginning of hemodialysis treatment and after a year. Echocardiographic evaluation was carried out on the day after dialysis. Left ventricular mass index (LVMI) was calculated. Left ventricular ejection fraction (LVEF) was measured by the echocardiographic Simpson method. Arteriovenous fistula flow was determined by Doppler echocardiography. Pulmonary hypertension was diagnosed according to criteria of Guidelines for the diagnosis and treatment of pulmonary hypertension of the European Society of Cardiology. Results Pulmonary hypertension was diagnosed in 47 (53.4%) patients. Left ventricular hypertrophy was revealed in 71 (80.7%) patients. Only 2 (2.3%) patients had LVEF&lt;50%. At the beginning of hemodialysis correlation was detected between systolic pulmonary arterial pressure and LVMI (r=0.52; P&lt;0.001). Systolic pulmonary arterial pressure negatively correlated with left ventricular ejection fraction (r=-0.20; P=0.04). After a year of hemodialysis treatment LVMI decreased from 140.49±42.95 to 123.25±39.27 g/m2 (р=0.006) mainly due to a decrease in left ventricular end-diastolic dimension (from 50.23±6.48 to 45.13±5.24 mm, p=0.04) and systolic pulmonary arterial pressure decreased from 44.83±14.53 to 39.14±10.29 mmHg (р=0.002). Correlation wasn’t found between systolic pulmonary arterial pressure and arteriovenous fistula flow (r=0.17; p=0.4). Conclusion Pulmonary hypertension was diagnosed in half of patients at the beginning of hemodialysis treatment. Pulmonary hypertension in hemodialysis patients was associated with left ventricular hypertrophy, systolic left ventricular dysfunction. After a year-long hemodialysis treatment, a regress in left ventricular hypertrophy and a partial decrease in pulmonary arterial pressure were observed. There wasn’t correlation between arteriovenous fistula flow and systolic pulmonary arterial pressure.

scholarly journals Prognostic Relevance of Nonsustained Ventricular Tachycardia in Patients with Pulmonary Hypertension

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Dirk Bandorski ◽  
Harilaos Bogossian ◽  
Johanna Stempfl ◽  
Werner Seeger ◽  
Matthias Hecker ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Ventricular Tachycardia ◽  
Arterial Hypertension ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Holter Ecg ◽  
Nonsustained Ventricular Tachycardia ◽  
Prognostic Relevance ◽  
Systolic Pulmonary Arterial Pressure ◽  
Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Arterial

Background.Increased pulmonary vascular resistance in patients with pulmonary hypertension (PH) leads to an increased afterload of right heart and cardiac remodeling which could provide the substrate or trigger for arrhythmias. Supraventricular arrhythmias were associated with clinical deterioration but were not associated with sudden cardiac death (SCD). SCD has been reported to account for approximately 30% of deaths in patients with pulmonary arterial hypertension (PAH).Objective.The role of nonsustained ventricular tachycardia (nsVT) and its prognostic relevance in patients with PH remains unclear. This study evaluated the prognostic relevance of nsVT in patients with PAH and chronic thromboembolic pulmonary hypertension (CTEPH).Methods.Retrospectively, patients with PAH and CTEPH who underwent Holter ECG monitoring and available data of survival were investigated.Results.Seventy-eight (PAH: 55, CTEPH: 23) patients were evaluated. Holter ECG revealed nsVT in 12 patients. Twenty-one patients died during follow-up. In patients with nsVT, tricuspid annular plane systolic excursion was lower(p=0.001), and systolic pulmonary arterial pressure was higher(p=0.163). Mean survival of patients without/with nsVT was 155.2 ± 8.5/146.4 ± 21.4 months(p=0.690). The association between arrhythmias and survival was not confounded by age(p=0.681), gender(p=0.752), 6-MW distance(p=0.196), or arterial hypertension(p=0.238).Conclusions.In patients with PH, nsVT occurs more often than previously reported, and patients with PH group 1 seem to be more at risk.

scholarly journals Acute Lung Edema as a Presentation of Severe Acute Reentry High-Altitude Illness in a Pediatric Patient

2020 ◽  
Vol 2020 ◽  
pp. 1-3
Author(s):  
Alfredo Merino-Luna ◽  
Julio Vizcarra-Anaya
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Pediatric Patient ◽  
Lung Edema ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Illness ◽  
The City ◽  
Determining Factor

Acute high-altitude pulmonary edema (HAPE) is a pathology involving multifactorial triggers that are associated with ascents to altitudes over 2,500 meters above sea level (m). Here, we report two pediatric cases of reentry HAPE, from the city of Huaraz, Peru, located at 3,052 m. The characteristics of both cases were similar, wherein acclimatization to sea level and a subsequent return to the city of origin occurred, and we speculate that it was caused by activation of predisposing factors to HAPE. The diagnosis and management associated with pulmonary hypertension became a determining factor for therapy.

P6480Asymmetric dimethylarginine (ADMA) predicts altitude-associated hypoxic pulmonary arterial hypertension

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
R H Boeger ◽  
P Siques ◽  
J Brito ◽  
E Schwedhelm ◽  
E Pena ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Logistic Regression ◽  
Oxygen Saturation ◽  
High Altitude ◽  
Sea Level ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Arterial Blood ◽  
Pulmonary Arterial

Abstract Prolonged exposure to altitude-associated chronic hypoxia (CH) may cause high altitude pulmonary hypertension (HAPH). Chronic intermittent hypobaric hypoxia (CIH) occurs in individuals who commute between sea level and high altitude. CIH is associated with repetitive acute hypoxic acclimatization and conveys the long-term risk of HAPH. As nitric oxide (NO) is an important regulator of systemic and pulmonary vascular tone and asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthesis that increases in hypoxia, we aimed to investigate whether ADMA predicts the incidence of HAPH among Chilean frontiers personnel exposed to six months of CIH. We performed a prospective study of 123 healthy male subjects who were subjected to CIH (5 days at appr. 3,550 m, followed by 2 days at sea level) for six months. ADMA, SDMA, L-arginine, arterial oxygen saturation, systemic arterial blood pressure, and haematocrit were measured at baseline and at months 1, 4, and 6 at high altitude. Acclimatization to high altitude was determined using the Lake Louise Score and the presence of acute mountain sickness (AMS). Echocardiography was performed after six months of CIH in a subgroup of 43 individuals with either good (n=23) or poor (n=20) aclimatization to altitude, respectively. Logistic regression was used to assess the association of biomarkers with HAPH. 100 study participants aged 18.3±1.3 years with complete data sets were included in the final analysis. Arterial oxygen saturation decreased upon the first ascent to altitude and plateaued at about 90% during the further course of the study. Haematocrit increased to about 47% after one month and remained stable thereafter. ADMA continuously increased and SDMA decreased during the study course, whilst L-arginine levels showed no distinct pattern. The incidence of AMS and the Lake Louise Score were high after the first ascent (53 and 3.1±2.4, respectively) and at one month of CIH (47 and 3.0±2.6, respectively), but decreased to 20 and 1.4±2.0 at month 6, respectively (both p<0.001 for trend). In echocardiography, 18 participants (42%) showed a mean pulmonary arterial pressure (mPAP) greater than 25 mm Hg (mean ± SD, 30.4±3.9 mm Hg), out of which 9 (21%) were classified as HAPH (mPAP ≥30 mm Hg; mean ± SD, 33.9±2.2 mm Hg). Baseline ADMA, but not SDMA, was significantly associated with mPAP at month 6 in univariate logistic regression analysis (R = 0.413; p=0.007). In ROC analysis, a cut-off for baseline ADMA of 0.665 μmol/l was determined as the optimal cut-off level to predict HAPH (mPAP >30 mm Hg) with a sensitivity of 100% and a specificity of 63.6%. ADMA concentration increases during long-term CIH. It is an independent predictive biomarker for the incidence of HAPH. SDMA concentration decreases during CIH and shows no association with HAPH. Our data support a role of impaired NO-mediated pulmonary vasodilation in the pathogenesis of high altitude pulmonary hypertension. Acknowledgement/Funding CONICYT/FONDEF/FONIS Sa 09I20007; FIC Tarapaca BIP 30477541-0; BMBF grant 01DN17046 (DECIPHER); Georg & Jürgen Rickertsen Foundation, Hamburg

scholarly journals Stress Doppler echocardiography for identification of susceptibility to high altitude pulmonary edema

2000 ◽  
Vol 35 (4) ◽  
pp. 980-987 ◽  
Author(s):  
Ekkehard Grünig ◽  
Derliz Mereles ◽  
Wulf Hildebrandt ◽  
Erik R Swenson ◽  
Wolfgang Kübler ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Doppler Echocardiography ◽  
High Altitude Pulmonary Edema

Pulmonary arterial systolic pressure and susceptibility to high altitude pulmonary edema

2011 ◽  
Vol 179 (2-3) ◽  
pp. 294-299 ◽  
Author(s):  
Rémi Mounier ◽  
Aimé Amonchot ◽  
Nicolas Caillot ◽  
Cécile Gladine ◽  
Bernard Citron ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Systolic Pressure ◽  
Arterial Systolic Pressure ◽  
Pulmonary Arterial Systolic Pressure ◽  
High Altitude Pulmonary Edema ◽  
Pulmonary Arterial

scholarly journals The pathophysiology of pulmonary hypertension in left heart disease

2015 ◽  
Vol 309 (9) ◽  
pp. L924-L941 ◽  
Author(s):  
Siegfried Breitling ◽  
Krishnan Ravindran ◽  
Neil M. Goldenberg ◽  
Wolfgang M. Kuebler
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Heart Disease ◽  
Fluid Transport ◽  
Poor Response ◽  
Left Heart ◽  
Left Heart Disease ◽  
Wide Range ◽  
Pulmonary Arterial ◽  
Preclinical Animal Models

Pulmonary hypertension (PH) is characterized by elevated pulmonary arterial pressure leading to right-sided heart failure and can arise from a wide range of etiologies. The most common cause of PH, termed Group 2 PH, is left-sided heart failure and is commonly known as pulmonary hypertension with left heart disease (PH-LHD). Importantly, while sharing many clinical features with pulmonary arterial hypertension (PAH), PH-LHD differs significantly at the cellular and physiological levels. These fundamental pathophysiological differences largely account for the poor response to PAH therapies experienced by PH-LHD patients. The relatively high prevalence of this disease, coupled with its unique features compared with PAH, signal the importance of an in-depth understanding of the mechanistic details of PH-LHD. The present review will focus on the current state of knowledge regarding the pathomechanisms of PH-LHD, highlighting work carried out both in human trials and in preclinical animal models. Adaptive processes at the alveolocapillary barrier and in the pulmonary circulation, including alterations in alveolar fluid transport, endothelial junctional integrity, and vasoactive mediator secretion will be discussed in detail, highlighting the aspects that impact the response to, and development of, novel therapeutics.

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