The effect of pulmonary hypertension
on left atrial mechanical functions in chronic obstructive lung disease.
Int J Cardiol. 2004 Nov;97(2):187-92
Acikel M, Yilmaz M, Gurlertop Y,
Kaynar H, Bozkurt E, Erol MK, Kose N, Meral M, Senocak H.
Faculty of Medicine, Department of Cardiology, Ataturk University, Erzurum,
Turkey. macikel@atauni.edu.tr
BACKGROUND: Left atrial (LA) function is an important determinant of left
ventricular (LV) filling. However, the effect of pulmonary hypertension (PH) on
LA mechanical function in chronic obstructive lung disease (COLD) has not been
studied, yet. METHODS: 49 patients with COLD and 25 controls were included in this
study. Patients were divided into two subgroups: patients without PH (group 1,
n=21) and with PH (group 2, n=28). LA volumes were determined at mitral valve
opening (Vmax), at onset of atrial systole (Vp) and at mitral valve closure
(Vmin) according to biplane area-length method. The following LA parameters
were calculated: passive emptying volume (PEV=Vmax-Vp), conduit volume [CV=LV
stroke volume-(Vmax-Vmin)], passive emptying fraction (PEF=PEV/Vmax), active
emptying volume (AEV=Vp-Vmin), active emptying fraction (AEF=AEV/Vp), total
emptying volume (TEV=Vmax-Vmin), percent contribution of PEV, CV and AEV to LV
stroke volume. RESULTS: Vmax (p<0.01), PEV (p<0.001) and TEV (p<0.05)
were lower in group 2 than in the controls, and the differences between group 1
and control group were insignificant (p>0.05). Vp, Vmin, CV and AEV did not
differ among three groups. Percent contribution to LV filling of the PEV was
decreased in group 2 when compared to group 1 (p<0.05) and the controls
(p<0.01). Percent contribution to LV filling of the AEV was increased in
group 2 when compared to the controls (p<0.05). There were inverse
correlations between pulmonary artery pressure and the following parameters: LV
stroke volume (r=-0.43, p<0.01), mitral E/A (r=-54, p<0.001), Vmax
(r=-0.35, p<0.05), PEV (r=-40, p<0.01) and PEF (r=-0.43, p<0.01).
CONCLUSION: This study shows that the alterations of LA mechanical functions in
patients with COLD are closely correlated to PH levels. Furthermore, these
results underline the importance of maintaining a sinus rhythm in these
patients.
PULMONARY HYPERTENSION IN NEONATES:
DOES THE CAUSE INFLUENCE THE OUTCOME ?
J Coll Physicians Surg Pak. 2004 Oct;14(10):612-614
Manzar S, Nair AK, Pai MG, Khusaiby
SM.
Department of Child Health, Royal Hospital, Muscat, Sultanate of Oman.
Objective: To determine the influence of the cause of pulmonary hypertension in
neonates on overall outcome. Design: Analytical study. Place and Duration of
Study: Special Care Baby Unit (SCBU) at Royal Hospital in Muscat, Sultanate of
Oman, from July 1998 to June 2003. Patients and Methods: All neonates with the
diagnosis of pulmonary hypertension, based on history, clinical examination and
2-D echocardiogram were reviewed with respect to the cause of hypertension
(primary or secondary), birth weight, Apgar score, gender, inborn/ outborn and
outcome. According to the outcome, neonates were divided into two groups, group
A (survived) and group B (expired). Both groups were compared for described
variables using Statistical Package for Social Sciences, version 7.5 for
Windows and Epi Info version 6. Results: Out of 37 neonates with pulmonary
hypertension, Group A comprised of 22 neonates while group B had 15 neonates,
giving a mortality of 40 % (15/37). The mean birth weight between the two
groups showed no significant differences, 3088 ± 479 gram and 2962 ± 454
gram, p =0.42, respectively. Similarly, no difference in the one and five Apgar
scores were noted, 4.9 ± 2.1 and 4.7 ± 1.3, p = 0.73 and 7.4 ± 1.5 and 6.7
± 1.4, p = 0.16, respectively. The place of birth had also no significant
influence on the outcome, however, the cause of pulmonary hypertension was noted
to be significantly associated with the outcome, p=0.004. Conclusion: The cause
of pulmonary hypertension in neonates does influence the survival. Primary
pulmonary hypertension in neonates was noted to be associated with poor outcome
as compared to secondary pulmonary hypertension.
Sildenafil citrate alleviates
pulmonary hypertension after hypoxia and reoxygenation with cardiopulmonary
bypass.
J Am Coll Surg. 2004 Oct;199(4):607-14
Lyons JM, Duffy JY, Wagner CJ, Pearl
JM.
Division of Cardiothoracic Surgery, Cincinnati Children's Hospital Medical
Center, Cincinnati, OH 45229, USA.
BACKGROUND: Sudden reoxygenation of hypoxic neonates undergoing cardiac
operation exacerbates the systemic inflammatory response to cardiopulmonary
bypass secondary to reoxygenation injury, worsening cardiopulmonary
dysfunction. Reports suggest sildenafil decreases pulmonary hypertension and
may affect myocardial function. Sildenafil's efficacy for treating postbypass
cardiopulmonary dysfunction remains unknown. STUDY DESIGN: Fourteen neonatal
piglets (5 to 7 kg) underwent 90 minutes of hypoxia, 60 minutes of
reoxygenation with cardiopulmonary bypass, and 120 minutes of recovery. Six
animals received 50 mg oral sildenafil and eight received saline at hypoxia.
Data are presented as mean +/- SD. RESULTS: Sildenafil prevented the high
pulmonary vascular resistance observed in controls (controls baseline 81 +/- 37
dynes. s/cm(5) versus recovery 230 +/- 93 dynes. s/cm(5), p = 0.004; sildenafil
baseline 38 +/- 17 dynes. s/cm(5) versus recovery 101 +/- 60 dynes. s/cm(5), p
= 0.003). Despite lower pulmonary vascular resistance after sildenafil,
arterial endothelin-1 (ET-1) was increased in both groups (control baseline 1.3
+/- 0.5 pg/mL versus recovery 4.5 +/- 3.7 pg/mL, p = 0.01; sildenafil baseline
1.3 +/- 0.3 pg/mL versus recovery 9.8 +/- 4.9 pg/mL, p = 0.003). Intravenous
nitric oxide (NO) levels were preserved after sildenafil treatment (sildenafil
baseline 340 +/- 77 nM versus recovery 394 +/- 85 nM). IV NO levels in controls
were decreased when compared with baseline (control baseline 364 +/- 83 nM
versus recovery 257 +/- 97 nM, p = 0.028). Although levels of exhaled NO
decreased in both groups, the sildenafil-treated animals had higher levels of
exhaled NO when compared with controls at the end of recovery (0.6 +/- 0.4
parts per billion versus 1.8 +/- 0.9 parts per billion, respectively, p =
0.029). CONCLUSIONS: Sildenafil alleviated pulmonary hypertension after
reoxygenation with cardiopulmonary bypass. Despite increased ET-1 levels,
pulmonary vascular resistance was lower with sildenafil treatment, suggesting
sildenafil's effect on the pulmonary vasculature is capable of countering
vasoconstriction by ET-1. Further study into the role of sildenafil in perioperative
therapy and its interactions with ET-1 are warranted.
Increased pulmonary arterial
pressure in children with nephrotic syndrome.
Arch Dis Child. 2004 Sep;89(9):866-70
Du ZD, Cao L, Liang L, Chen D, Li
ZZ.
Children's Heart Center, Beijing Children's Hospital, No. 56, South Lishi Road,
Western District, 100045 Beijing, China. duzd@imicams.ac.cn
AIMS: To evaluate the pulmonary arterial pressure in children with nephrotic
syndrome (NS). METHODS: Doppler echocardiography was performed in 40 children
with NS (aged 1.5-13 years) at NS onset (n = 28) or relapse (n = 12), and 40
normal controls. Pulmonary pressure was estimated by: (1) measuring the
systolic transtricuspid gradient from tricuspid regurgitation; and (2)
measuring the time to peak velocity of pulmonary flow. RESULTS: Thirty five of
the 40 patients with NS had measurable tricuspid regurgitation with a pulmonary
systolic pressure ranging from 21 to 48 mm Hg. Pulmonary systolic pressure was
>40 mm Hg in seven patients. The pulmonary time to peak velocity was
shortened and the ratio of time to peak velocity and right ventricular ejection
time decreased compared with controls. The patients with increased pulmonary
pressure had a longer time since onset of NS. One patient developed thrombus in
the inferior vena cava during hospitalisation. CONCLUSION: Pulmonary arterial
pressure was increased in children with NS. Further work is needed to evaluate
the aetiology and clinical implications of this abnormality.
Aerosolized prostacyclins.
Respir Care. 2004 Jun;49(6):640-52
Siobal M.
Respiratory Care Services, San Francisco General Hospital, NH GA-2, 1001
Potrero Avenue, San Francisco, CA 94110, USA. msiobal@sfghsom.ucsf.edu.
Two prostacyclins (prostaglandin E(1) and prostaglandin I(2)) are potent
vasodilators. Aerosolized prostacyclins reduce pulmonary artery pressure,
improve right heart function, and increase arterial oxygenation by improving
ventilation/perfusion matching. This report describes aerosolized prostacyclins
and compares them to inhaled nitric oxide. I review the types of inhalable
prostacyclins and their indications, evidence of efficacy, delivery, and
adverse effects.
Publication Types:
·
Review
·
Review, Tutorial
Sildenafil alters calcium signaling
and vascular tone in pulmonary arteries from chronically hypoxic rats.
Am J Physiol Lung Cell Mol Physiol. 2004 Sep;287(3):L577-83
Pauvert O, Bonnet S,
Rousseau E, Marthan R, Savineau JP.
Laboratoire de Physiologie Cellulaire Respiratoire, INSERM (E 356 and IFR 4
Universite Bordeaux 2, 146 rue Leo Saignat, 33076 Bordeaux, France.
Sildenafil,
a potent type 5 nucleotide-dependent phosphodiesterase (PDE) inhibitor, has
been recently proposed as a therapeutic tool to treat or prevent pulmonary
artery hypertension (PAHT). We thus studied the effect of sildenafil on both
the calcium signaling of isolated pulmonary artery smooth muscle cells (PASMCs)
and the reactivity of pulmonary artery (PA) obtained from chronic hypoxia (CH)-induced
pulmonary hypertensive rats compared with control (normoxic) rats. CH rats were
maintained in an hypobaric chamber (50.5 kPa) for 3 wk leading to full
development of PAHT. Intracellular calcium concentration ([Ca2+]i) was measured
in PASMCs loaded with the calcium fluorophore indo 1. Unlike in control rats,
sildenafil (10-100 nM) decreased the resting [Ca2+]i value in PASMCs obtained
from CH rats. In PASMCs from both control and CH rats, sildenafil concentration
dependently inhibited the [Ca2+]i response induced by G-coupled membrane
receptor agonists such as angiotensin II and phenylephrine but had no effect on
the amplitude of the [Ca2+]i response induced by caffeine. Sildenafil (0.1 nM-1
microM) concentration dependently reduced basal PA tone that is present in CH
rats and relaxed PA rings precontracted with phenylephrine in both control and
CH rats. These data show that sildenafil is a potent pulmonary artery relaxant
in CH rats and that it normalizes CH-induced increases in resting [Ca2+]i and
basal tone. Consequently, pharmacological inhibition of sildenafil-sensitive
PDE5 downregulates the Ca2+ signaling pathway involved in this model of
pulmonary hypertension.
Chronic endothelin A receptor
blockade in lambs with increased pulmonary blood flow and pressure.
Am J Physiol Lung Cell Mol Physiol. 2004 Sep;287(3):L592-7
Fratz S, Meyrick B, Ovadia B,
Johengen MJ, Reinhartz O, Azakie A, Ross G, Fitzgerald R, Oishi P, Hess J,
Black SM, Fineman JR.
Dept. of Pediatric Cardiology and Congenital Heart Disease, Deutsches
Herzzentrum Munchen, Klinik an der Technischen Universitat Munchen,
Lazarettstr. 36, 80636 Munich, Germany. fratz@dhm.mhn.de
Endothelin receptor blockade is an emerging therapy for pulmonary hypertension.
However, hemodynamic and structural effects and potential changes in endogenous
nitric oxide (NO)-cGMP and endothelin-1 signaling of chronic endothelin A
receptor blockade in pulmonary hypertension secondary to congenital heart
disease are unknown. Therefore, the objectives of this study were to determine
hemodynamic and structural effects and potential changes in endogenous NO-cGMP
and endothelin-1 signaling of chronic endothelin A receptor blockade in a lamb
model of increased pulmonary blood flow following in utero placement of an
aortopulmonary shunt. Immediately after spontaneous birth, shunt lambs were treated
lifelong with either an endothelin A receptor antagonist (PD-156707) or
placebo. At 4 wk of age, PD-156707-treated shunt lambs (n = 6) had lower
pulmonary vascular resistance and right atrial pressure than placebo-treated
shunt lambs (n = 8, P < 0.05). Smooth muscle thickness or arterial number
per unit area was not different between the two groups. However, the number of
alveolar profiles per unit area was increased in the PD-156707-treated shunt
lambs (190.7 +/- 5.6 vs. 132.9 +/- 10.0, P < 0.05). Plasma endothelin-1 and
cGMP levels and lung NOS activity, cGMP, eNOS, preproendothelin-1,
endothelin-converting enzyme-1, endothelin A, and endothelin B receptor protein
levels were similar in both groups. We conclude that chronic endothelin A
receptor blockade attenuates the progression of pulmonary hypertension and
augments alveolar growth in lambs with increased pulmonary blood flow.
Magnetic resonance imaging analysis
of right ventricular pressure-volume loops: in vivo validation and clinical
application in patients with pulmonary hypertension.
Circulation. 2004 Oct 5;110(14):2010-6
Kuehne T, Yilmaz S, Steendijk P,
Moore P, Groenink M, Saaed M, Weber O, Higgins CB, Ewert P, Fleck E, Nagel E,
Schulze-Neick I, Lange P.
Department of Congenital Heart Diseases and Pediatric Cardiology, German Heart
Institute, Augustenburger Platz 1, Berlin 13353 Germany. titus.k@t-online.de.
BACKGROUND: The aims of this study were to validate MRI-derived right
ventricular (RV) pressure-volume loops for assessment of RV myocardial
contractility and then to apply this technique in patients with chronic RV
pressure overload for assessment of myocardial contractility, ventricular pump
function, and VA coupling. METHODS AND RESULTS: Flow-directed catheters were
guided under MR fluoroscopy (1.5 T) into the RV for invasive pressure
measurements. Simultaneously, ventricular volumes and myocardial mass were
assessed from cine MRI. From sampled data, RV pressure-volume loops were
constructed, and maximal ventricular elastance indexed to myocardial mass
(E(max_i)) was derived by use of a single-beat estimation method. This MRI
method was first validated in vivo (6 swine), with conductance techniques used
as reference. Bland-Altman test showed good agreement between methods
(E(max_i)=5.1+/-0.5 versus 5.8+/-0.7 mm Hg x mL(-1) x 100 g(-1), respectively;
P=0.08). Subsequently, the MRI method was applied in 12 subjects: 6 control
subjects and 6 patients with chronic RV pressure overload from pulmonary
hypertension. In these patients, indexes of RV pump function (cardiac index),
E(max_i), and VA coupling (E(max)/E(a)) were assessed. In patients with pulmonary
hypertension, RV pump function was decreased (cardiac index, 2.2+/-0.5 versus
2.9+/-0.4 L x min(-1) x m(-2); P<0.01), myocardial contractility was
enhanced (E(max_I), 9.2+/-1.1 versus 5.0+/-0.9 mm Hg x mL(-1) x 100 g(-1);
P<0.01), and VA coupling was inefficient (E(max)/E(a), 1.1+/-0.3 versus
1.9+/-0.4; P<0.01) compared with control subjects. CONCLUSIONS: RV
myocardial contractility can be determined from MRI-derived pressure-volume
loops. Chronic RV pressure overload was associated with reduced RV pump
function despite enhanced RV myocardial contractility. The proposed MRI
approach is a promising tool to assess RV contractility in the clinical
setting.
Reverse cardiac remodelling in
patients with primary pulmonary hypertension after isolated lung
transplantation.
Eur J Cardiothorac Surg. 2004 Oct;26(4):776-81
Kasimir MT, Seebacher G, Jaksch P,
Winkler G, Schmid K, Marta GM, Simon P, Klepetko W.
Department of Cardiothoracic and Vascular Anaesthesia and Intensive Care,
Medical University of Vienna, Vienna, Austria.
Objective: Pulmonary hypertension eventually leads to severe distortion of the
cardiac geometry with consequent impact on cardiac function. The purpose of
this study was to prove reverse cardiac remodelling after isolated bilateral
lung transplantation (LuTX) in patients with advanced primary pulmonary
hypertension (PPH) and severe alterations of cardiac morphology and function.
Methods: In the period of 2000-2002 17 (10 female, seven male) patients with
advanced PPH underwent isolated bilateral LuTX. Median age was 30 years (range
16-53). All patients were in NYHA III or IV, most of them with intractable
ascites, established renal impairment, malnutrition and immobility,
continuously deteriorating despite various forms of pharmacological treatment
including i.v. and inhalative prostacyclin, diuretics, Ca-antagonists, bosentan
and catecholamines. Echocardiography and Doppler echocardiography measurements
were performed before and 3 months after transplantation. Left and right
ventricular diameters and function were assessed and tricuspid valve
regurgitation was determined. Results: Mortality after 3 months was 17.5%
(cerebral bleeding, multi-organ failure and diffuse myocardial infarction in
one patient each). Three months after LuTX the 14 surviving patients were in
NYHA I or II. Echocardiography showed normal left ventricular function and markedly
improved right ventricular function with normal size of the RV. The leftward
shifted flattened interventricular septum had returned in its physiological
position and the high-grade tricuspid insufficiency had disappeared in all
patients. Conclusions: Advanced alterations of cardiac morphology and function
normalize completely and pre-existing tricuspid insufficiency disappears in PPH
patients after isolated bilateral LuTX. Quality of life is excellent.
Therefore, LuTX is preferred and safe in patients with advanced PPH even with
severe cardiac dysfunction.
Use of the AbioCor replacement heart
as destination therapy for end-stage heart failure with irreversible pulmonary
hypertension.
J Thorac Cardiovasc Surg. 2004 Oct;128(4):643-5
Samuels L, Entwistle J, Holmes E,
Fitzpatrick J, Wechsler A.
Lankenau Hospital, Department of Cardiothoracic Surgery, Wynnewood, PA 19096,
USA. SamuelsLE@aol.com
Successful thromboendarterectomy for
severe chronic thromboembolic pulmonary hypertension caused by primary
antiphospholipid syndrome.
J UOEH. 2004 Sep 1;26(3):287-94
Kamezaki F, Tasaki H, Yamanaka A,
Morishita T, Hirakawa N, Yamashita K, Okazaki M, Nakashima Y, Nakanishi N,
Ogino H.
Second Department of Internal Medicine, School of Medicine, University of
Occupational and Environmental Health, Yahatanishi-ku, Kitakyushu 807-8555,
Japan.
Pulmonary hypertension is one of the lethal complications in the antiphospholipid
syndrome due to chronic recurrence of embolism or thrombosis. We experienced a
19-year-old man suffering from severe chronic thromboembolic pulmonary
hypertension (CTEPH) caused by primary antiphospholipid syndrome. According to
the guideline, pulmonary thromboendarterectomy was decided on after combined
therapy with warfarin, beraprost and oxygen inhalation had not been effective
enough to improve severe CTEPH. By an operation, the mean pressure of the
pulmonary artery was decreased from 50 mmHg to 16 mmHg, while his New York
Heart Association (NYHA) functional class classification significantly improved
from class III to class I. We concluded that pulmonary thromboendarterectomy
could dramatically improve hemodynamic indices, NYHA functional status and
quality of life in patients with CTEPH.
Reduced pulmonary clearance of
endothelin in congestive heart failure: A marker of secondary pulmonary
hypertension.
J Card Fail. 2004 Oct;10(5):427-32
Staniloae C, Dupuis J, White M,
Gosselin G, Dyrda I, Bois M, Crepeau J, Bonan R, Caron A, Lavoie J.
Department of Medicine and Research Center, Montreal Heart Institute, Montreal,
Quebec, Canada.
BACKGROUND: Endothelin-1 (ET-1) levels are elevated in congestive heart failure
(CHF) in relation with the severity of pulmonary hypertension. We evaluated
whether a reduced pulmonary ET-1 clearance could contribute to this
elevation.Methods and results We determined pulmonary ET-1 clearance in 24
patients with CHF in relation with hemodynamics, plasma ET-1, and N-terminal
pro-brain natriuretic peptide (NT-proBNP) levels. Pulmonary ET-1 extraction,
measured by the single bolus indicator-dilution technique, was reduced to
32+/-14% in comparison to historic controls (47+/-7%). Plasma ET-1 clearance by
the lungs (924+/-588 mL/min) was also much lower than in controls (1424+/-79
mL/min). Clearance correlated inversely with mean pulmonary artery pressure
(PAP, r=-.47, P=.017) and pulmonary capillary wedge pressure (r=-.47, P=.017)
and positively with the rate of left ventricular (LV) relaxation LV -dP/dt
(r=.593, P=.004). After multivariate analysis, only mean PAP and LV -dP/dt were
independently correlated with ET-1 clearance (r=-.40, P=.03, and r=.55, P=.005,
respectively). Plasma ET-1 levels did not correlate with clearance (r=.038,
P=.86), and there was no significant arteriovenous ET-1 gradient. There was a
mild nonsignificant correlation between plasma ET-1 and pulmonary artery
systolic pressure (r=.38, P=.06), but a strong correlation with right atrial
pressure (r=.696, P < .0001) and NT-proBNP levels (r=.51, P=.001), which
were maintained after multivariate linear regression (r=.60, P=.001, and r=.32,
P=.04, respectively). CONCLUSION: Pulmonary ET-1 clearance is reduced in CHF in
relation with the severity of pulmonary hypertension. This reduced clearance
does not significantly modulate plasma ET-1 levels. Whether this is only a
marker of secondary pulmonary hypertension or could modulate pulmonary vascular
tone will require further studies.
Pulmonary vasodilator effects of
norepinephrine during the development of chronic pulmonary hypertension in
neonatal lambs.
Br J Anaesth. 2004 Oct 1
Jaillard S, Elbaz F, Bresson-Just S,
Riou Y, Houfflin-Debarge V, Rakza T, Larrue B, Storme L.
Department
of Anesthesiology and Cardio-thoracic Surgery, Centre Hospitalier et
Universitaire, Lille, France; EA1049, Department of Biophysics, Centre
Hospitalier et Universitaire, Lille, France; Departement
Hospitalo-Universitaire de Recherche Experimentale, Centre Hospitalier et
Universitaire, Lille, France.
BACKGROUND:
This experimental study was performed to determine the effects of
norepinephrine on: (i) the pulmonary vascular tone during the development of
pulmonary hypertension (PH) in the fetus and (ii) the circulatory adaptation at
birth after chronic intrauterine PH. METHODS: Chronically instrumented fetal
lambs were randomized into two groups: (i) a group with PH obtained by
antenatal partial ligation of the ductus arteriosus (DA) (n=9) and (ii) a
control group without DA ligation (n=6). Pulmonary vascular responses to
norepinephrine (1.5 microg min(-1)) were measured in utero 7 days after
surgery. At day 8 post-surgery, after delivery, animals were ventilated for 3 h
with oxygen 100%. The group with PH was randomly assigned to receive
norepinephrine or saline. RESULTS: Mean pulmonary artery pressure (PAP) and
pulmonary vascular resistance (PVR) were higher in the PH group (P<0.01).
Norepinephrine-induced decrease in PVR was more pronounced in the PH group than
in the control group (63 vs 35%, respectively; P<0.01). In the PH group, the
decrease in PVR during mechanical ventilation was greater in the animals
receiving norepinephrine than in the animal receiving saline (from 1.05 (0.12)
to 0.1 (0.02) vs from 1.04 (0.1) to 0.2 (0.04) mm Hg ml(-1) min(-1),
respectively; P<0.01). After 3 h of ventilation, mean PVR in the PH lambs
treated by norepinephrine was similar to those measured in the control lambs.
Aortic pressure was higher in the group treated with norepinephrine.
CONCLUSION: The data suggest that norepinephrine may improve post-natal
pulmonary adaptation in the newborn with persistent PH both by increasing
systemic vascular pressure and by increasing pulmonary blood flow.
Syndromes of subacute mountain
sickness.
High Alt Med Biol. 2004 Summer;5(2):156-70
Anand IS, Wu T.
Heart Failure Program, VA Medical Center, and University of Minnesota Medical
School, Minneapolis, 55417, USA. anand001@umn.edu
Two clinical syndromes, acute and chronic mountain sickness, have traditionally
been associated with high altitude. Recently, two separate entities of subacute
nature have been described in infants and adults. In this paper, we review the
published literature on these conditions. Subacute infantile mountain sickness
is a condition seen predominantly in Han Chinese infants living in Tibet,
although it has been described in other high altitude communities as well. It
came into prominence only after the large-scale migration of Chinese population
from the low altitude of mainland China to the high altitudes of the
Qinghai-Tibetan plateau. The condition is characterized by features of severe
hypoxic pulmonary hypertension and heart failure. Pulmonary histology is consistent
with muscularization of the pulmonary arterioles, but no intimal proliferation
or plexiform lesions are seen. The second syndrome, adult subacute mountain
sickness, has been described almost exclusively in Indian soldiers living at
extreme altitude for prolonged periods of time. In this condition also, hypoxic
pulmonary hypertension appears to be the dominant factor responsible for severe
congestive heart failure. Both these conditions have several similarities with
brisket disease in cattle; hypoxic pulmonary vasoconstriction plays an
important role in the pathogenesis, and removal from high altitude results in
complete resolution. Thus, it appears that both these syndromes are human
counterparts of brisket disease in cattle.
Publication Types:
·
Review
·
Review, Tutorial
Unraveling the mechanism of high altitude
pulmonary edema.
High Alt Med Biol. 2004 Summer;5(2):125-35
Schoene RB.
University of California, San Diego School of Medicine, 92103, USA.
rschoen@ucsd.edu
During the last decade, major advances in the understanding of the mechanism of
high altitude pulmonary edema (HAPE) have supplemented the landmark work don