Iloprost
for chronic thromboembolic pulmonary hypertension.
[Article in English, Spanish]
Arch
Bronconeumol. 2004 Jul;40(7):326-8
Roig Figueroa V, Herrero Perez A, De La Torre Ferrera N,
Hernandez Garcia E, Aller Alvarez JL, Para Cabello J.
Servicio de Neumologia. Hospital Clinico Universitario de Valladolid.
Valladolid. Espana.
Chronic thromboembolic
pulmonary hypertension (CTPH) is an uncommon complication of pulmonary
embolism. The treatment of choice is thromboendarterectomy, a safe and
effective surgical procedure in expert hands. However, a fair number of
patients are not considered candidates for thromboendarterectomy or do not
accept the risk involved. Such patients may respond well to prostacyclin or its
derivatives. In recent years new vasodilator drugs administered by a variety of
routes have appeared on the market. These drugs have been studied mainly for
their effects on primary pulmonary hypertension or hypertension associated with
connective-tissue diseases. Few trials have assessed their efficacy in patients
with CTPH, however.We report 2 cases of CTPH in which thromboendarterectomy was
rejected. Neither of the patients responded to the conventional treatment of
anticoagulants, diuretics, calcium antagonists, and angiotensin-converting
enzyme inhibitors, but they did respond very well clinically, hemodynamically,
and functionally to an inhaled prostacyclin analog, iloprost. We discuss the
effects of iloprost in patients with CTPH, its mechanism of action, and its use
as a potential pharmacological alternative to thromboendarterectomy. We also
discuss new pulmonary vasodilators in general.
Prevalence of pulmonary hypertension and its association with respiratory
disturbances in obese patients living at moderately high altitude.
Int J Obes Relat Metab Disord. 2004 Jun 29
Valencia-Flores M,
Rebollar V, Santiago V, Orea A, Rodriguez C, Resendiz M, Castano A, Roblero J,
Campos RM, Oseguera J, Garcia-Ramos G, Bliwise DL.
[1] 1National Institute of Medical Science and Nutrition Salvador Zubiran,
Mexico, D.F. [2] 2National Autonomous University of Mexico, Mexico, D.F.
OBJECTIVE:: To determine the
point prevalence of pulmonary hypertension (PH) and its relationship with
respiratory disturbances in obese patients living at moderate altitude.
SUBJECTS:: A total of 57 obese patients comprised the final sample and
consisted of 34 women and 23 men, with a mean age of 42.7+/-12.1 ys and a mean
body mass index (BMI) 47.1+/-10.6 kg/m(2) (range from 30.1 to 76.1). The mean
living altitude was 2248.7 m, range 2100-2400 m above sea level. MEASUREMENTS:
Doppler echocardiography, pulmonary function tests, arterial blood gas
analysis, and polysomnography were performed. RESULTS: Data showed that 96.5%
of the studied sample had daytime PH defined as calculated systolic pulmonary
artery pressure (PSAP) >30 mmHg (mean PSAP=50, s.d.=13 mmHg). The severity
of diurnal PH was found to be related to the presence of alveolar
hypoventilation and BMI. The main risk factor for severity of diurnal PH was
hypoventilation with a significant odds ratio (OR) 7.96, 95% CI 1.35-46.84, BMI
was (OR 1.12, 95% CI 1.02-1.25) and apnea/hypopnea index was not a predictor of
pulmonary hypertension severity (OR 0.99, 95% CI 0.97-1.02). CONCLUSION: We
concluded that prevalence of diurnal PH is high in obese patients living at
moderate altitude, and that hypoventilation is the main risk factor associated
with the severity of pulmonary hypertension.International Journal of Obesity
advance online publication, 29 June 2004; doi:10.1038/sj.ijo.0802726
Increased oxidative stress following acute and chronic high altitude
exposure.
High Alt Med Biol. 2004 Spring;5(1):61-9
Jefferson JA, Simoni J, Escudero E, Hurtado ME, Swenson ER,
Wesson DE, Schreiner GF, Schoene RB, Johnson RJ, Hurtado A.
University of Washington, Division of Nephrology, Seattle, WA 98195, USA.
jashleyj@u.washington.edu
The generation of reactive oxygen species is typically associated with
hyperoxia and ischemia reperfusion. Recent evidence has suggested that
increased oxidative stress may occur with hypoxia. We hypothesized that
oxidative stress would be increased in subjects exposed to high altitude
hypoxia. We studied 28 control subjects living in Lima, Peru (sea level), at
baseline and following 48 h exposure to high altitude (4300 m). To assess the
effects of chronic altitude exposure, we studied 25 adult males resident in
Cerro de Pasco, Peru (altitude 4300 m). We also studied 27 subjects living in
Cerro de Pasco who develop excessive erythrocytosis (hematocrit > 65%) and
chronic mountain sickness. Acute high altitude exposure led to increased
urinary F(2)-isoprostane, 8-iso PGF(2 alpha) (1.31 +/- 0.8 microg/g creatinine
versus 2.15 +/- 1.1, p = 0.001) and plasma total glutathione (1.29 +/- 0.10
micromol versus 1.37 +/- 0.09, p = 0.002), with a trend to increased plasma
thiobarbituric acid reactive substance (TBARS) (59.7 +/- 36 pmol/mg protein
versus 63.8 +/- 27, p = NS). High altitude residents had significantly elevated
levels of urinary 8-iso PGF(2 alpha) (1.3 +/- 0.8 microg/g creatinine versus
4.1 +/- 3.4, p = 0.007), plasma TBARS (59.7 +/- 36 pmol/mg protein versus 85
+/- 28, p = 0.008), and plasma total glutathione (1.29 +/- 0.10 micromol versus
1.55 +/- 0.19, p < 0.0001) compared to sea level. High altitude residents
with excessive erythrocytosis had higher levels of oxidative stress compared to
high altitude residents with normal hematological adaptation. In conclusion,
oxidative stress is increased following both acute exposure to high altitude
without exercise and with chronic residence at high altitude.
Publication Types:
● Clinical
Trial
Noninvasive Assessment of Fetal Pulmonary Blood Flow in
Experimental Pulmonary Hypertension in the Fetal Lamb.
Pediatr Res. 2004 Jul 7
Jouannic JM, Bonnet D, Hislop AA, Roussin R, Dinh-Xuan AT.
Service de Gynecologie-Obsterique, Hopital Rothschild, AP-HP
Paris XII, Paris, France; Cardiopediatrie, Hopital Necker-Enfants Malades,
AP-HP-Universite Paris V, 75015 Paris, France; Unit of Vascular Biology and
Pharmacology, Institute of Child Health, London, United Kingdom; Departement de
chirurgie cardiaque pediatrique, Hopital Marie Lannelongue, 92350 Le plessis
Robinson, France; and Service de Physiologie-Explorations Fonctionnelles
A.-T.D.-X.], Hopital Cochin, AP-HP-Universite Paris V, 75014 Paris, France.
The aim of this study was to assess pulmonary arterial blood flow changes
induced by the creation of a systemic arteriovenous fistula (120 d gestation)
in the fetal lamb using Doppler technique. Doppler echocardiographic assessment
of the pulmonary artery blood flow performed 1, 6, and 14 d after surgery showed
that mean pulmonary arterial blood flow in the left or right pulmonary artery
was 224 +/- 58 mL/min at day 1 in the fistula group, significantly higher than
in the control group (113 +/- 22 mL/min; p < 0.01, ANOVA test) whether no
difference was found at days 6 and 14. The mean inner diameter of the left
pulmonary artery measured on postmortem lung arteriograms compared favorably to
the one measured on day 14 at the same level on ultrasound. The mean left
pulmonary arterial blood flow, measured at birth on day 14 after surgery, using
ultrasonic flow transducer, was not statistically different from the one
measured by Doppler on day 14. Our data demonstrate that echocardiography
allows accurate assessment of pulmonary arterial blood flow in utero, providing
evidence suggesting transient high pulmonary blood flow that did not last >6
d after the creation of a systemic fistula.
VEGFmRNA and eNOSmRNA expression in immature rabbits with
bleomycin-induced pulmonary hypertension.
J Zhejiang Univ Sci. 2004 Aug;5(8):995-1000
Gong FQ, Lin YM, Tang HF, Gu WZ, Wang W, Kang ML.
Affiliated Children's Hospital, College of Medicine, Zhejiang University,
Hangzhou 310003, China; gongfangqi@zju.edu.cn
Objective: To investigate the evolution of pulmonary hypertension, the
pathological changes of pulmonary arteries, and the expression of VEGFmRNA and
eNOSmRNA of pulmonary arterial endothelial cells in immature rabbits treated
with intratracheal bleomycin (BLM). Methods: Immature rabbits were divided into
control and BLM group. Two and four weeks after intratracheal normal saline or
BLM injection, the systolic, diastolic and mean pulmonary artery pressure
(PASP, PADP, MPAP) were measured by micro-catheter; the pathological changes
and the expression of VEGFmRNA and eNOSmRNA of endothelial cells in pulmonary
arteries were evaluated by HE and in situ hybridization. Results: Two and four
weeks after intratracheal injection of BLM, the PASP, PADP and MPAP increased
53%, 49%, 52% in 2 weeks, and 43%, 89%, 56% in 4 weeks; the wall thickness
increased and the cavity in middle and small pulmonary arteries became narrow;
the Thickness Index (TI) and Area Index (AI) increased 25%, 14% in 2 weeks, and
22%, 24% in 4 weeks; the level of VEGFmRNA and eNOSmRNA expression decreased
46%, 43% in 2 weeks, and 43%, 51% in 4 weeks. There was no significant difference
between 2 weeks and 4 weeks BLM groups. Conclusion: The pulmonary artery
pressure was elevated, the thickness of wall increased and the cavity became
narrow in middle and small pulmonary arteries, and the level of VEGFmRNA and
eNOSmRNA expression in pulmonary arterial endothelial cells decreased in
immature rabbits after 2 weeks and 4 weeks of intratracheal 4 U/kg BLM
injection.
Aortic dissection presenting with secondary pulmonary hypertension caused by
compression of the pulmonary artery by dissecting hematoma: a case report.
Korean J Radiol. 2004 Apr-Jun;5(2):139-42
Kim DH, Ryu SW, Choi YS, Ahn BH.
Department of Radiology, Soonchunhyang University Hospital, Seoul, Korea.
dhk1107@hanmail.net
The rupture of an acute dissection of the ascending aorta into the space
surrounding the pulmonary artery is an uncommon occurrence. No previous cases
of transient pulmonary hypertension caused by a hematoma surrounding the
pulmonary artery have been documented in the literature. Herein, we report a
case of acute aortic dissection presenting as secondary pulmonary hypertension.
Clinical and pathological
characterisation of primary pulmonary hypertension in a dog.
Vet Rec.
2004 Jun 19;154(25):786-9
Glaus TM, Soldati G, Maurer R,
Ehrensperger F.
Division of Cardiology, Department of
Small Animal Medicine, University of Zurich, Winterthurerstrasse 260, CH-8057
Zurich, Switzerland.
Primary pulmonary hypertension was diagnosed in an eight-year-old labrador
retriever on the basis of echocardiographic findings of severe right
ventricular eccentric hypertrophy, abnormally high systolic and diastolic
pulmonary arterial pressures calculated by applying the modified Bernoulli
equation to the tricuspid and pulmonary insufficiency peak velocities, and the absence
of any underlying disease known to cause secondary pulmonary hypertension. The
clinical abnormalities developed gradually, from exercise intolerance starting
early in life to terminal right-sided congestive heart failure. Consistent
histopathological findings were severe intimal and medial thickening of small
arteries and arterioles that led to vascular obliteration.
Publication Types:
● Case Reports
Systolic pulmonary artery pressure and serum uric acid levels in patients
with hyperthyroidism.
Arch Med Res. 2003 Jan-Feb;34(1):35-40
Yazar A, Doven O, Atis S, Gen R, Pata C, Yazar EE, Kanik A.
Department of Internal Medicine, Mersin University Medical School, Mersin,
Turkey. azizyazar@yahoo.com
BACKGROUND: The aim of this study was to investigate systolic pulmonary artery
pressure (SPAP) and serum uric acid (SUA) levels in patients with
hyperthyroidism and after euthyroid state was reached. METHODS: Twenty five (10
male, 15 female, mean age 49.8 +/- 11.6 years) consecutive patients with hyperthyroidism
(18 due to toxic nodular goiter, seven to Graves' disease) and 25 (eight male,
17 female, mean age 48.7 +/- 8.7 years) healthy controls were included in the
study. Thyroid hormones, SUA, glucose, urea, creatinine, and transthoracic
echocardiography were performed in all patients. All tests were repeated after
treatment of hyperthyroidism. RESULTS: Mean SPAP and SUA levels in patients
with hyperthyroidism were significantly higher than in controls (30.4 +/- 8.5
vs. 22 +/- 3.7 mmHg, p <0.0001, and 5.1 +/- 1.1 vs. 4.3 +/- 0.5 mg/dL, p =
0.004, respectively). Elevated SPAP and SUA levels in patients with
hyperthyroidism decreased significantly after treatment to levels comparable
with controls (24.4 +/- 5.4 mmHg, p = 0.001 and 4.6 +/- 0.9 mg/dL, p = 0.002,
respectively). Correlation between SPAP and SUA levels, however, was not
significant in hyperthyroid population and after euthyroid stage was reached (r
= 0.34, p = 0.097, and r = 0.256, p = 0.216, respectively), possibly due to
relatively low number of patients (overall correlation of SPAPs and SUAs was r
= 0.4, p <0.0001). CONCLUSIONS: Hyperthyroidism should be included in
differential diagnosis of pulmonary arterial hypertension. However, further
investigations are needed to determine the exact mechanism between
hyperthyroidism and pulmonary hypertension.
Roles of Endothelin ETA and ETB Receptors in the Pathogenesis of
Monocrotaline-Induced Pulmonary Hypertension.
J Cardiovasc Pharmacol. 2004 Aug;44(2):187-91
Nishida M, Eshiro K, Okada Y, Takaoka M, Matsumura Y.
Department of Pharmacology, Osaka University of Pharmaceutical Sciences, Osaka,
Japan.
The functional roles of endothelin ETA and ETB receptors in the development of
monocrotaline (MCT)-induced pulmonary hypertension were investigated using
MCT-treated rats in the absence or presence of a daily administration of
A-192621, a selective ETB receptor antagonist, ABT-627, a selective ETA
receptor antagonist, or a combination of both drugs. Four weeks after the
injection of saline or MCT (60 mg/kg, s.c.), cardiac hypertrophy, right
ventricular systolic pressure and morphologic changes of pulmonary arteries
were evaluated. Compared with the control animals, MCT produced marked
pulmonary hypertension associated with increases in right ventricular pressure
and hypertrophy, and pulmonary arterial medial thickening. These MCT-induced
alterations were markedly suppressed by daily treatment with ABT-627 for 4
weeks (10 mg/kg/d, twice daily), whereas treatment with A-192621 significantly
aggravated the above MCT-induced pathologic changes. The blockade of both
receptor subtypes by a combination of A-192621 and ABT-627 also significantly
improved the MCT-induced pathologic changes, to the same extent as with ABT-627
administration. Thus, an exaggerated response to MCT during ETB receptor
blockade also seems to be mediated by ETA receptor activation, thereby suggesting
that ETA receptor-mediated action is exclusively contributive to the
pathogenesis of MCT-induced pulmonary hypertension, although we cannot rule out
a protective role of ETB receptor-mediated action.
HIV-related pulmonary hypertension. From pathogenesis to clinical aspects.
Acta Cardiol. 2004 Jun;59(3):323-30
Pellicellii AM,
D'Ambrosio C, Vizza CD, Borgia MC, Tanzi P, Pino P, Zachara E, Soccorsi F.
Infectious Diseases, San
Camillo Forlanini Hospital, Italy. apellicelli@scamilloforlanini.rm.it
HIV-related pulmonary hypertension (HIV-PH) is a cardiovascular complication of
HIV infection that has been recognized in the last years with increasing
frequency. HIV-related pulmonary hypertension is a clinical disorder which
carries a bad prognosis. While a direct HIV infection of the pulmonary vessels
in the pathogenesis of this disorder was not demonstrated, currently a
multifactorial pathogenesis of this disease could be hypothesized.
Echocardiography has been found to be the most useful screening imaging
modality for the diagnosis of HIV-PH, with a high predictive negative value and
a low positive predictive value. For this reason Doppler echocardiography is
not the gold standard in the diagnosis of HIV-PH. The treatment of HIV-PH is
complex and controversial. To date, no study determining the agent of choice
for the treatment of this disease exists. Different studies have shown variable
results in patiens with HIV-PH treated with highly active antiretroviral
therapy (HAART) but only HAART seems not to be effective in lowering pulmonary
hypertension in these patients, and in some patients, HIV-PH develops in spite
of a previous HAART. It seems reasonable in HIV-PH patients that a treatment
with oral vasodilator drugs can improve the adherence of a long-lasting and
complex antiretroviral therapy.
Postoperative hemodynamic parameter follow up in children with severe
pulmonary hypertension due to ventricular septal detect.
Chin Med Sci J. 2004 Jun;19(2):I
Zhu WH, Li JH, Zhu XK, Kang ML.
Department of Cardiology, Children's Hospital, Zhejiang University, Hangzhou
310003. zhuweihua54816@hotmail.com
Age-dependent likelihood of in situ thrombosis in secondary
pulmonary hypertension.
Clin Appl Thromb Hemost. 2004 Jul;10(3):217-23
Caramuru LH, Maeda NY, Bydlowski SP, Lopes AA.
Department of Pediatric Cardiology and Adult Congenital Heart Disease, Heart
Institute, University of Sao Paulo, Sao Paulo, Brazil.
SUMMARY: Pulmonary arterial thrombosis (PAT) may complicate the clinical course
of pulmonary hypertension associated with congenital heart disease (so-called
Eisenmenger syndrome, ES). In this study, variables were sought that could
represent risk factors for the occurrence of this complication. Twenty patients
aged 11 to 53 (median, 33) years were studied. The presence of PAT (spiral
computed tomography angiography) was correlated with age, gender group, PAP,
hematocrit, peripheral oxygen saturation (SpO(2)), and plasma levels of
endothelial and coagulation dysfunction markers: von Willebrand factor antigen
(vWF:Ag), tissue plasminogen activator (t-PA), and D-dimer (enzyme immunoassay).
Patients were classified according to the presence (group 1, N=7), or absence
(group 2, N=13) of PAT. Group 1 patients were older (42+/-8 vs. 27+/-10 years
in group 2, p=0.0051), had lower SpO(2) (82+/-7% vs. 89+/-6% in group 2,
p=0.0462) and increased D-dimer levels (637 vs. 149 ng/mL in group 2, median
values, p=0.0235). A trend was observed toward an increase in vWF:Ag (125+/-29
vs. 103+/-18 U/dL in group 2, p=0.0789) and t-PA (15.7 vs. 9.4 ng/mL in group
2, median values, p=0.0689). Age was the main variable influencing the
occurrence of PAT in multivariate analysis (p=0.0026), with odds ratio of 1.204
per year. The age of 35 years was 86% sensitive and 85% specific for occurrence
of PAT. Age correlated positively with t-PA (r=0.57, p=0.0111). Thus, PAT is
highly prevalent in ES as an age-dependent event, probably associated with
endothelial dysfunction. Prophylactic anticoagulation should be considered
before the age of 30 years, in particular in subjects with low SpO(2) and
increased D-dimer levels.
Pulmonary hypertension in autoimmune rheumatic diseases.
Autoimmun Rev. 2004 Jun;3(4):313-20
Carreira PE.
Servicio de reumatologia, Hospital 12 de Octubre, Avda. de Cordoba S/N, 28041
Madrid, Spain.
Arterial pulmonary
hypertension (PH) might be a complication of some autoimmune rheumatic
diseases, specially systemic sclerosis. This form of arterial PH is
indistinguishable from primary PH, characterised by the presence of plexiform
lesions. Although for many years plexiform lesions have been considered
end-stage scarring lesions, they are composed by actively proliferating
endothelial cells that share many features with cancer cells. Endothelial cells
within plexiform lesions in all forms of arterial PH show a decrease in the
expression of vasodilator and anti-proliferative factors, and an increase in
the expression of vasoconstrictor and angiogenic and mitogenic factors. These
cells also show important alterations in growth and apoptosis key regulatory
genes. Plexiform lesions are surrounded by inflammatory cell infiltrates,
probably providing cytokines that may contribute to the endothelial cell
proliferative process. All these data suggest that arterial PH might be seen as
a proliferative endothelial cell process, which would open new therapeutic approaches
for this devastating disease.
Pulmonary hypertension: diagnosis and treatment.
Clin Med. 2004 May-Jun;4(3):211-5
Elliot C, Kiely DG.
Sheffield Pulmonary Vascular Disease Unit, Royal Hallamshire Hospital,
Sheffield.
Use of oral endothelin-receptor antagonist bosentan in the
treatment of portopulmonary hypertension.
Transplantation. 2004 Jun 15;77(11):1775-6
Halank M, Miehlke S,
Hoeffken G, Schmeisser A, Schulze M, Strasser RH.
Publication Types:
Case Reports
Letter
|
|
Successful treatment of severe portopulmonary hypertension after liver
transplantation by bosentan.
Transplantation. 2004 Jun 15;77(11):1774-5
Clift PF, Townend JN, Bramhall S, Isaac JL.
Publication Types:
● Case
Reports
● Letter
Echocardiographic changes induced by moderate to marked hypobaric hypoxia in
dogs.
Vet Radiol Ultrasound. 2004 May-Jun;45(3):233-7
Glaus TM, Tomsa K, Hassig M, Reusch C.
Division of Cardiology, Department of Large Animal Medicine, Clinic for Small
Animal Internal Medicine, University of Zurich, Winterthurerstr. 260, CH-8057
Zurich, Switzerland. tglaus@vetclinics.unizh.ch
Hypobaric (high-altitude) hypoxia is a physiologic cause of pulmonary
hypertension, and alters left ventricular (LV) systolic and diastolic function.
In the presence of tricuspid regurgitation, systolic pulmonary artery pressure
can be measured noninvasively using the peak tricuspid regurgitation velocity
and the Bernoulli equation. In the absence of measurable tricuspid
regurgitation, severity of pulmonary hypertension may be estimated using
two-dimensional, M-mode, and Doppler-derived parameters. To evaluate the
usefulness of echocardiographic parameters for detecting mild-to-moderate
pulmonary hypertension caused by moderate-to-marked hypoxia and to study the
effect of high-altitude hypoxia on systolic and diastolic LV function in dogs,
19 Greenland dogs were examined at moderate altitude (2300 m) and high altitude
(3500 m), and 10 Greenland control dogs were examined at 700-900 m. Evaluated
parameters were pulmonary flow profile (shape, right ventricular acceleration
time (RVAT), ejection time (RVET), RVAT/ET), peak mitral inflow velocities
(LVE, LVA, LVE/A-ratio), LV % fractional shortening (FS), systolic time
intervals (LVPEP, LVPEP/ET), and stroke volume index (SVI). Notching during
deceleration was common in dogs at high altitude and in the control dogs, but
not in dogs at moderate altitude. RVAT was shorter in dogs at high altitude
compared with moderate altitude, but not compared with control dogs. Peak
A-velocity was higher and E/A-ratio was lower in dogs at high altitude compared
with moderate altitude and control dogs. FS was increased in dogs at high
altitude compared with moderate altitude, and LVPEP and LVPEP/ET were shorter
in the dogs at high altitude compared with moderate altitude and control dogs.
In conclusion, significant differences in pulmonary flow profiles and systolic
and diastolic parameters can be observed echocardiographically in dogs at
different degrees of hypobaric hypoxia. However, overlap between the groups
compromises their usefulness for diagnosing and estimating the degree of
mild-to-moderate pulmonary hypertension in individual dogs.
Publication Types:
● Evaluation
Studies
In vitro hypoxia differentially affects constriction and relaxation
responses of isolated pulmonary arteries from broiler and leghorn chickens.
Poult Sci. 2004 May;83(5):835-41
Odom TW, Martinez-Lemus LA, Hester RK, Becker EJ, Jeffrey
JS, Meininger GA, Ramirez GA.
Department of Poultry Science, Texas A&M University System Health Science
Center, Texas Agricultural Experiment Station, College Station, Texas 77843,
USA. todom@poultry.tamu.edu
Under normoxic conditions in vitro, isolated pulmonary arteries from broilers
exhibit reduced endothelium-dependent relaxation responses when compared with
Leghorns. In vivo, hypoxia increases the susceptibility of broiler chickens to
pulmonary hypertension syndrome (PHS), whereas Leghorns are considered
resistant to PHS. Because L-arginine supplementation decreases the incidence of
PHS in vivo and improves the relaxation responses of broiler isolated pulmonary
arteries in vitro, we hypothesized that in vitro hypoxia would further reduce
the relaxation responses of broilers to endothelium-derived nitric oxide
(EDNO)-dependent vasodilators and that L-arginine supplementation would
alleviate this impairment. As a test of this hypothesis, pulmonary arteries
from broiler and Leghorn chickens were isolated and exposed to normoxia or
hypoxia in the presence or absence of L-arginine while their constriction and
relaxation responses to vasoactive compounds were recorded. In broilers,
hypoxia did not affect the constriction responses of isolated pulmonary
arteries but decreased EDNO-dependent acetylcholine-induced relaxation
responses. In contrast, in Leghorns hypoxia increased endothelin-1-induced
vasoconstriction responses and reduced the EDNO-dependent relaxation responses
only to the lowest concentration of acetylcholine used. L-Arginine
supplementation augmented the relaxation responses to acetylcholine in broilers
and Leghorns under normoxia but failed to augment them under hypoxia.
Relaxation responses to the NO donor, sodium nitroprusside, were not affected
by hypoxia in Leghorns but were increased by hypoxia in broilers. These results
suggest that the increased incidence of PHS in broiler chickens reared under hypoxia
may be associated with a hypoxia-induced reduction in the synthesis or activity
of EDNO in the pulmonary circulation.
Comparison of impedance cardiography to direct Fick and
thermodilution cardiac output determination in pulmonary arterial hypertension.
Congest Heart Fail. 2004 Mar-Apr;10(2 Suppl 2):7-10
Yung GL, Fedullo PF, Kinninger K, Johnson W, Channick RN.
Division of Pulmonary and Critical Care Medicine, University of California San
Diego Medical Center, San Diego, CA 92103-8373, USA. gyung@ucsd.edu
Cardiac output (CO) is an important diagnostic and prognostic tool for patients
with ventricular dysfunction. Pulmonary hypertension patients undergo invasive
right heart catheterization to determine pulmonary vascular and cardiac
hemodynamics. Thermodilution (TD) and direct Fick method are the most common
methods of CO determination but are costly and may be associated with
complications. The latest generation of impedance cardiography (ICG) provides
noninvasive estimation of CO and is now validated. The purpose of this study
was to compare ICG measurement of CO to TD and direct Fick in pulmonary
hypertension patients. Thirty-nine enrolled patients were analyzed: 44% were
male and average age was 50.8+/-17.4 years. Results for bias and precision of
cardiac index were as follows: ICG vs. Fick (-0.13 L/min/m2 and 0.46 L/min/m2),
TD vs. Fick (0.10 L/min/m2 and 0.41 L/min/m2), ICG vs. TD (respectively, with a
95% level of agreement between -0.72 and 0.92 L/min/m2; CO correlation of ICG
vs. Fick, TD vs. Fick, and ICG vs. TD was 0.84, 0.89, and 0.80, respectively).
ICG provides an accurate, useful, and cost-effective method for determining CO
in pulmonary hypertension patients, and is a potential tool for following
responses to therapeutic interventions.
Methodology and grading for pulmonary hypertension evidence review and
guideline development.
Chest. 2004 Jul;126(1 Suppl):11S-13S
McCrory DC, Lewis SZ.
Department of Medicine and the Center for Clinical Health Policy Research, Duke
University Medical Center, Department of Veterans Affairs Medical Center,
Durham, NC, USA. douglas.mccrory@duke.edu
The American College of Chest Physicians assembled a multidisciplinary,
geographically diverse panel of experts in the treatment of pulmonary
hypertension to develop clinically relevant practice guidelines for the
diagnosis and treatment of pulmonary hypertension in its many variations. That
group of experts produced recommendations covering five topic areas, each
related to a distinct set of patient-management decisions. This article
describes the approach used to develop the guidelines, including identifying,
evaluating, and synthesizing the evidence, assessing the strength of evidence
pertinent to individual guidelines, and grading guideline recommendations.
Nesiritide in pulmonary hypertension.
Chest. 2004 Jul;126(1):302-5
Kurian DC, Wagner IJ, Klapholz M.
Saint Vincent Catholic Medical Centers, New York, NY 10011, USA.
We present the case of a patient with severe symptomatic pulmonary hypertension
due to rheumatic mitral valve disease who was refractory to traditional
therapies, including prostacyclin. Therapy with continuous nesiritide infusion
resulted in significant and sustained decreases in pulmonary vascular
resistance, an improvement in renal function, and the maintenance of euvolemia.
Prolonged nitric oxide inhalation fails to regress hypoxic vascular
remodeling in rat lung.
Chest. 2004 Jun;125(6):2247-52
Jiang BH, Maruyama J, Yokochi A, Iwasaki M, Amano H, Mitani
Y, Maruyama K.
Department of Anesthesiology and the Intensive Care Unit, Faculty of Medicine,
University of Mie, Japan.
STUDY OBJECTIVE: The purpose of present study was to investigate whether long-term
nitric oxide (NO) inhalation during the recovery in air might improve the
regression of chronic hypoxic pulmonary hypertension (PH) and vascular changes.
MATERIALS AND METHODS: The rats were exposed to 10 ppm of NO in air for 10 days
(n = 12) and 30 days (n = 4), or 40 ppm of NO in air for 10 days (n = 6) and 30
days (n = 12) following 10 days of hypobaric hypoxia (380 mm Hg, 10% oxygen).
For each NO group, air control rats following hypoxic exposure were studied at
the same time (n = 13, 11, 9, and 11, respectively). Normal air rats (n = 6)
without hypoxic exposure and rats (n = 7) following 10 days of hypoxic exposure
were used as normal and chronic hypoxic control groups, respectively.
Muscularization of normally nonmuscular peripheral arteries and medial
hypertrophy of normally muscular arteries were assessed by light microscopy. An
additional 16 rats were used to investigate the recovery of pulmonary artery
pressure with (n = 8) and without NO inhalation (n = 8) after 10 days of
hypobaric hypoxia. RESULTS: Long-term hypoxia-induced PH, right ventricular
hypertrophy (RVH), and hypertensive pulmonary vascular changes, each of which
regressed partly after recovery in room air. There were no differences among
rats with and without NO during each recovery period in RVH, medial wall
thickness of muscular artery, and the percentages of muscularized arteries at
the alveolar wall and duct levels. Continuous inhaled 40 ppm NO decreased
pulmonary artery pressure from 40.1 +/- 1.1 to 29.9 +/- 3.8 mm Hg (mean +/- SE)
[n = 8], which was not different in the rats without NO inhalation (n = 8).
Urine nitrate level was higher in rats that had inhaled NO. CONCLUSION:
Continuous NO inhalation showed no effect on regression of pulmonary vascular
remodeling in chronic hypoxic PH after returning to room air.