Prophylactic inhalation of a beta-adrenergic agonist reduces the risk of high-altitude pulmonary edema. Sodium-dependent absorption of liquid from the airways may be defective in patients who are susceptible to high-altitude pulmonary edema. These findings support the concept that sodium-driven clearance of alveolar fluid may have a pathogenic role in pulmonary edema in humans and therefore represent an appropriate target for therapy.
In pulmonary hypertension right ventricular pressure overload leads to abnormal left ventricular (LV) diastolic function. Acute high-altitude exposure is associated with hypoxia-induced elevation of pulmonary artery pressure particularly in the setting of high-altitude pulmonary edema. Tissue Doppler imaging (TDI) allows assessment of LV diastolic function by direct measurements of myocardial velocities independently of cardiac preload. We hypothesized that in healthy mountaineers, hypoxia-induced pulmonary artery hypertension at high altitude is quantitatively related to LV diastolic function as assessed by conventional and TDI Doppler methods. Forty-one healthy subjects (30 men and 11 women; mean age 41 +/- 12 yr) underwent transthoracic echocardiography at low altitude (550 m) and after a rapid ascent to high altitude (4,559 m). Measurements included the right ventricular to right atrial pressure gradient (DeltaP(RV-RA)), transmitral early (E) and late (A) diastolic flow velocities and mitral annular early (E(m)) and late (A(m)) diastolic velocities obtained by TDI at four locations: septal, inferior, lateral, and anterior. At a high altitude, DeltaP(RV-RA) increased from 16 +/- 7 to 44 +/- 15 mmHg (P < 0.0001), whereas the transmitral E-to-A ratio (E/A ratio) was significantly lower (1.11 +/- 0.27 vs. 1.41 +/- 0.35; P < 0.0001) due to a significant increase of A from 52 +/- 15 to 65 +/- 16 cm/s (P = 0.0001). DeltaP(RV-RA) and transmitral E/A ratio were inversely correlated (r(2) = 0.16; P = 0.0002) for the whole spectrum of measured values (low and high altitude). Diastolic mitral annular motion interrogation showed similar findings for spatially averaged (four locations) as well as for the inferior and septal locations: A(m) increased from low to high altitude (all P < 0.01); consequently, E(m)/A(m) ratio was lower at high versus low altitude (all P < 0.01). These intraindividual changes were reflected interindividually by an inverse correlation between DeltaP(RV-RA) and E(m)/A(m) (all P < 0.006) and a positive association between DeltaP(RV-RA) and A(m) (all P < 0.0009). In conclusion, high-altitude exposure led to a two- to threefold increase in pulmonary artery pressure in healthy mountaineers. This acute increase in pulmonary artery pressure led to a change in LV diastolic function that was directly correlated with the severity of pulmonary hypertension. However, in contrast to patients suffering from some form of cardiopulmonary disease and pulmonary hypertension, in these healthy subjects, overt LV diastolic dysfunction was not observed because it was prevented by augmented atrial contraction. We propose the new concept of compensated diastolic (dys)function.
is present in approximately 25% of the general population, but a higher prevalence has been reported in disease states known to be associated with pulmonary hypertension such as chronic obstructive pulmonary disease and sleep apnea syndrome.1,2 These observations could suggest that under conditions associated with elevated pulmonary vascular and right-sided cardiac pressures, some foramen ovale may reopen, implying a functional rather than an anatomical closing of these foramen. A reopened foramen ovale may contribute to systemic arterial oxygen desaturation from right-to-left intracardiac shunting under any condition that results in a higher right than left atrial pressure. [3][4][5] Exaggerated pulmonary hypertension is a hallmark of high-altitude pulmonary edema (HAPE) and plays an important role in its pathogenesis.6-8 Moreover, altitude-induced hypoxemia is more pronouncedinHAPE-susceptiblethanHAPEresistant individuals prior to onset of edema.9,10 Theunderlyingmechanismsare incompletelyunderstood.Inapreliminary report, Levine et al 11 demonstrated rightto-left intracardiac shunting across a PFO in a patient with HAPE and suggested that in persons with PFO a vicious cycle may beoperationalathighaltitudewhereinhypoxic pulmonary hypertension initiates right-to-left shunting, which in turn aggravates hypoxemia. We hypothesized that the frequency of PFO is greater in HAPE-susceptible than in HAPE-resistant individuals and, if so, may contribute to more severe hypoxemia at high altitude. To test this hypothesis, we searched for PFO by transesophageal echocardiography (TEE), estimated pulmonary artery pressure by Doppler echocardiography, and measured arterial oxygen saturation in 16 HAPE-susceptible and 19 HAPEresistant control participants at low and high altitude. METHODS Study Design and ParticipantsThirty-fivehealthymountaineerswereincluded in the study. Sixteen participants Context Individuals susceptible to high-altitude pulmonary edema (HAPE) are characterized by exaggerated pulmonary hypertension and arterial hypoxemia at high altitude, but the underlying mechanism is incompletely understood. Anecdotal evidence suggests that shunting across a patent foramen ovale (PFO) may exacerbate hypoxemia in HAPE.Objective We hypothesized that PFO is more frequent in HAPE-susceptible individuals and may contribute to more severe arterial hypoxemia at high altitude.Design, Setting, and Participants Case-control study of 16 HAPE-susceptible participants and 19 mountaineers resistant to this condition (repeated climbing to peaks above 4000 m and no symptoms of HAPE). Main Outcome MeasuresPresence of PFO determined by transesophageal echocardiography, estimated pulmonary artery pressure by Doppler echocardiography, and arterial oxygen saturation measured by pulse oximetry in HAPE-susceptible and HAPE-resistant participants at low (550 m) and high altitude (4559 m). ResultsThe frequency of PFO was more than 4 times higher in HAPE-susceptible than in HAPE-resistant participants, both at low altitude (56% vs 11%, P=.004; od...
Objective-To test the hypothesis that diastolic mitral annular motion velocity, as determined by Doppler tissue imaging and left ventricular diastolic flow propagation velocity, is related to the histological degree of heart transplant rejection according to the International Society of Heart and Lung Transplantation (ISHLT). Methods-In 41 heart transplant recipients undergoing 151 myocardial biopsies, the following Doppler echocardiographic measurements were performed within one hour of biopsy: transmitral and pulmonary vein flow indices; mitral annular motion velocity indices; left ventricular diastolic flow propagation velocity. Results-Late diastolic mitral annular motion velocity (A DTI ) and mitral annular systolic contraction velocity (SC DTI ) were higher in patients with ISHLT < IIIA than in those with ISHLT > IIIA (A DTI , 8.8 cm/s v 7.7 cm/s (p = 0.03); SC DTI , 19.3 cm/s v 9.3 cm/s (p < 0.05)). Sensitivity and specificity of A DTI < 8.7 cm/s (the best cut oV value) in predicting significant heart transplant rejection were 82% and 53%, respectively. Early diastolic mitral annular motion velocity (E DTI ) and flow propagation velocity were not related to the histological degree of heart transplant rejection. Conclusions-Doppler tissue imaging of the mitral annulus is useful in diagnosing heart transplant rejection because a high late diastolic mitral annular motion velocity can reliably exclude severe rejection. However, a reduced late diastolic mitral annular motion velocity cannot predict severe rejection reliably because it is not specific enough. (Heart 2001;86:432-437)
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