Aim of this study is to investigate the impact of elevated pulmonary artery systolic pressure (PASP) on mortality and the clinical outcome after cardiac resynchronization therapy (CRT).
Ninety-three patients with heart failure were enrolled into this study, and all of them have been treated by CRT for more than 6 months. Based on the level of preoperative PASP, they were divided into three groups (Group I: PASP>50mmHg, n=29; Group II: 30mmHg
①Eight (28%), one (6%) and eight (17%) patients died in-group I, II and III respectively. Among those patients, 5 in group I and 1 in group III died of heart failure, while the patient in group II died of sudden death. ②In all three groups, CRT significantly improved heart function evaluated by NYHA heart function class and 6 minutes walking distance (6-MWT) (P<0.01). The improvement was more significant in group III than group I (P<0.01). ③At 3 months after CRT, Left ventricular ejection fraction (LVEF) increased significantly in Group III (P<0.01), but not in Group I or II (all P>0.05. At 6 months after CRT, LVEF increased significantly in all three groups (all P<0.05).
Elevated PASP has no prognostic effects on heart function improvement in patients undergone CRT. However, it was associated with worse LV remodeling and increased death due to aggravation of heart failure.
heart failure; cardiac resynchronization therapy; pulmonary artery systolic pressure; prognosis
To determine among community patients with heart failure (HF), whether pulmonary artery systolic pressure (PASP) assessed by Doppler echocardiography was associated with death and improved risk prediction over established factors, using the integrated discrimination improvement (IDI) and net reclassification improvement (NRI).
While several studies have focused on idiopathic pulmonary arterial hypertension, less is known about pulmonary hypertension among patients with HF, particularly on its prognostic value in the community.
Olmsted County residents with HF between 2003 and 2010 prospectively underwent assessment of ejection fraction (EF), diastolic function, and PASP by Doppler echocardiography.
PASP was recorded in 1049 of 1153 patients (mean age 76±13, 51% women). Median PASP was 48 mmHg (25th-75th percentile, 37.0-58.0). There were 489 deaths after a follow-up of 2.7±1.9 years. There was a strong positive graded association between PASP and mortality. Increasing PASP was associated with an increased risk of death (HR 1.45, 95%CI 1.13-1.85 for tertile 2; HR 2.07, 95%CI 1.62-2.64 for tertile 3, versus tertile 1), independently of age, sex, comorbidities, EF and diastolic function. Adding PASP to models including these clinical characteristics resulted in an increase in the c-statistic from 0.704 to 0.742 (p=0.007), an IDI gain of 4.2% (p<0.001), and an NRI of 14.1% (p=0.002), indicating that PASP improved prediction of death over traditional prognostic factors. All results were similar for CV death.
Among community patients with HF, PASP strongly predicts death and provides incremental and clinically relevant prognostic information independently of known predictors of outcomes.
heart failure; pulmonary hypertension; mortality; community
To define the prevalence, severity and significance of pulmonary hypertension (PH) in heart failure with preserved ejection fraction (HFpEF) in the general community.
While HFpEF is known to cause PH, its development is highly variable. Population-based data are lacking, and the relative contribution of pulmonary venous versus pulmonary arterial hypertension to PH in HFpEF is unknown. We hypothesized that PH would be a marker of symptomatic pulmonary congestion, distinguishing HFpEF from preclinical hypertensive heart disease (HTN).
Population-based study of 244 HFpEF patients (76±13y; 45%male) followed from Doppler echocardiography over 3 years. Controls were 719 adults with HTN without HF (66±10y; 44%male). Pulmonary artery systolic pressure (PASP) was derived from the tricuspid regurgitation velocity and PH defined as PASP>35 mmHg. Pulmonary capillary wedge pressure (PCWP) was estimated from E/e’.
In HFpEF, PH was present in 83% and median (25th, 75th percentile) PASP was 48 (37, 56) mmHg. PASP increased with PCWP (r=0.21; p<0.007). Adjusting for PCWP, PASP was higher in HFpEF than HTN (p<0.001). PASP distinguished HFpEF from HTN with an area under receiver-operating curve of 0.91 (p<0.001) and strongly predicted mortality in HFpEF (hazard ratio=1.3 per 10 mmHg; p<0.001).
PH is highly prevalent and often severe in HFpEF. While pulmonary venous hypertension contributes to PH, it does not fully account for the severity of PH in HFpEF, suggesting that a component of pulmonary arterial hypertension also contributes. The potent effect of PASP on mortality lends support for therapies aimed at pulmonary arterial hypertension in HFpEF.
pulmonary hypertension; diastolic heart failure; heart failure with preserved ejection fraction
Hypoxia is a major cause of pulmonary hypertension. Gene expression activated by the transcription factor hypoxia-inducible factor (HIF) is central to this process. The oxygen-sensing iron-dependent dioxygenase enzymes that regulate HIF are highly sensitive to varying iron availability. It is unknown whether iron similarly influences the pulmonary vasculature. This human physiology study aimed to determine whether varying iron availability affects pulmonary arterial pressure and the pulmonary vascular response to hypoxia, as predicted biochemically by the role of HIF. In a controlled crossover study, 16 healthy iron-replete volunteers undertook two separate protocols. The ‘Iron Protocol’ studied the effects of an intravenous infusion of iron on the pulmonary vascular response to 8 h of sustained hypoxia. The ‘Desferrioxamine Protocol’ examined the effects of an 8 h intravenous infusion of the iron chelator desferrioxamine on the pulmonary circulation. Primary outcome measures were pulmonary artery systolic pressure (PASP) and the PASP response to acute hypoxia (ΔPASP), assessed by Doppler echocardiography. In the Iron Protocol, infusion of iron abolished or greatly reduced both the elevation in baseline PASP (P < 0.001) and the enhanced sensitivity of the pulmonary vasculature to acute hypoxia (P = 0.002) that are induced by exposure to sustained hypoxia. In the Desferrioxamine Protocol, desferrioxamine significantly elevated both PASP (P < 0.001) and ΔPASP (P = 0.01). We conclude that iron availability modifies pulmonary arterial pressure and pulmonary vascular responses to hypoxia. Further research should investigate the potential for therapeutic manipulation of iron status in the management of hypoxic pulmonary hypertensive disease.
Hypoxia is a major cause of pulmonary hypertension. Gene expression activated by the transcription factor hypoxia-inducible factor (HIF) is central to this process. The oxygen-sensing iron-dependent dioxygenase enzymes that regulate HIF are highly sensitive to varying iron availability. It is unknown whether iron similarly influences the pulmonary vasculature. This human physiology study aimed to determine whether varying iron availability affects pulmonary arterial pressure and the pulmonary vascular response to hypoxia, as predicted biochemically by the role of HIF. In a controlled crossover study, 16 healthy iron-replete volunteers undertook two separate protocols. The ‘Iron Protocol’ studied the effects of an intravenous infusion of iron on the pulmonary vascular response to 8 h of sustained hypoxia. The ‘Desferrioxamine Protocol’ examined the effects of an 8 h intravenous infusion of the iron chelator desferrioxamine on the pulmonary circulation. Primary outcome measures were pulmonary artery systolic pressure (PASP) and the PASP response to acute hypoxia (ΔPASP), assessed by Doppler echocardiography. In the Iron Protocol, infusion of iron abolished or greatly reduced both the elevation in baseline PASP (P < 0.001) and the enhanced sensitivity of the pulmonary vasculature to acute hypoxia (P= 0.002) that are induced by exposure to sustained hypoxia. In the Desferrioxamine Protocol, desferrioxamine significantly elevated both PASP (P < 0.001) and ΔPASP (P= 0.01). We conclude that iron availability modifies pulmonary arterial pressure and pulmonary vascular responses to hypoxia. Further research should investigate the potential for therapeutic manipulation of iron status in the management of hypoxic pulmonary hypertensive disease.
The non-invasive estimation of pulmonary artery systolic pressure (PASP) has become a standard component of echocardiographic examination. Our aim was to evaluate the accuracy of this modality in a large series of unselected studies obtained in clinical practice. All right heart catheterizations (RHC) over a 4 year period were reviewed. Studies with echocardiography available within 48 hours were evaluated for agreement of PASP. In an effort to mirror clinical practice, RHC was used as the gold standard and values for PASP were taken directly from their respective clinical reports. Overall, 792 RHC-echocardiogram pairs were identified. Echocardiographic PASP could not be estimated in 174 of these studies (22.0%). Correlation between modalities was moderate, but agreement was poor (r=0.52, p<0.001, bias 9.0%, 95% limits of agreement −53.2% to 71.2%). Misclassification of clinical PASP categories occurred more often than not (54.4%). Multivariate analysis utilizing multiple potential sources of error could only account for 3.2% of the total variation in discrepancy between study modalities (p=0.003). In conclusion, non-invasively estimated pulmonary artery systolic pressure had limited agreement with invasively determined pressure and misclassification of PASP clinical categories occurred in the majority of cases. Given the widespread use of echocardiographically determined PASP these data are in need of replication in a large prospective study.
Non-invasive pulmonary artery systolic pressure; Echocardiographic pulmonary artery systolic pressure
To determine relationship of echocardiographic measures of pulmonary hypertension to lung function and inflammatory biomarkers in HIV-infected individuals.
Cross-sectional study of 116 HIV-infected outpatients.
Doppler-echocardiography and pulmonary function testing were performed. Induced sputum and plasma cytokines, sputum cell counts and differentials, markers of peripheral T cell activation, and serum N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured. Univariate and multivariate analyses determined relationship of echocardiographic variables to pulmonary function, inflammation, and NT-proBNP.
Mean estimated pulmonary artery systolic pressure (PASP) was 34.3 mmHg (SD 6.9) and mean tricuspid regurgitant jet velocity (TRV) was 2.5 m/sec (SD 0.32). Eighteen participants (15.5%) had PASP of at least 40 mmHg, and 9 (7.8%) had TRV of at least 3.0 m/sec. Elevated TRV was significantly associated with CD4 cell counts below 200 cells/μl and higher log HIV RNA levels. Forced expiratory volume in one second (FEV1) percent predicted, FEV1/forced vital capacity (FVC), and diffusing capacity for carbon monoxide (DLco) percent predicted were significantly lower in those with elevated PASP or TRV. Sputum interleukin-8, peripheral interleukin-8, peripheral interferon-γ levels, and CD8+ T-cell expression of CD69+ were associated increased with increasing PASP and TRV. Log NT-proBNP was significantly higher with increasing PASP and TRV. Left ventricular function was not associated with PASP or TRV.
Echocardiographic manifestations of pulmonary hypertension are common in HIV and are associated with respiratory symptoms, more advanced HIV disease, airway obstruction, abnormal DLco, and systemic and pulmonary inflammation. Pulmonary hypertension and COPD coexist in HIV and may arise secondary to common inflammatory mechanisms.
HIV; pulmonary hypertension; emphysema; COPD; inflammation
To determine whether HIV and HHV-8 infection are associated with pulmonary arterial hypertension (PAH)
Previous work has found a high prevalence of PAH in HIV-infected patients, but attempts to establish a causal relationship have been limited by the lack of a well-characterized contemporaneous HIV-uninfected comparison group. Among HIV-uninfected persons, human herpesvirus 8 (HHV-8) has also been recently linked to PAH, but whether this relationship is present or exaggerated among HIV-infected persons — who have among the highest prevalences of HHV-8 infection — has not been examined.
We echocardiographically estimated pulmonary artery systolic pressure (PASP) among HIV-infected and -uninfected adults in San Francisco.
Among the 196 HIV-infected participants, the median PASP was 27.5 mm Hg, and 35.2% had PASP > 30 mm Hg. This compared to a median of 22 mm Hg among 52 HIV-uninfected participants (p < 0.001) in whom 7.7% had a value > 30 (p < 0.001). After adjustment for injection drug use, stimulant use, smoking, age, and gender, HIV-infected participants had 5.1 mm Hg higher mean PASP (p < 0.001) and had 7.0-fold greater odds of having a PASP > 30 mm Hg (p < 0.001). While we found no evidence of an association between HHV-8 infection and PAH among all HIV-infected participants, a borderline relationship was present when restricting to those without other known risk factors for PAH.
HIV-infected persons have a high prevalence of elevated PASP, which is independent of other risk factors for PAH including injection drug use. This suggests a causal role of HIV in PAH and emphasizes the need to better understand the natural history of PAH in this setting. Evidence for a role for HHV-8 infection in PAH remains much less definitive.
pulmonary hypertension; AIDS; HIV infection; human herpesvirus 8 infection
The aim of the research reported here was to compare pulmonary artery systolic pressure (PASP) and 6-minute walk distance after 1 year of follow-up in hemoglobin E/β thalassemia (E/β-Thal) with pulmonary arterial hypertension (PAH) patients who received chronic blood transfusions versus those who received occasional transfusions.
A nonrandomized clinical trial was conducted at the Hematological Outpatient Clinic of Chiang Rai Hospital, Thailand. All adult cases of E/β-Thal with PAH (defined as PASP >35 mmHg by Doppler echocardiography) were evaluated and followed for the next 12 months. The patients were classified into two groups by patient preference. Group 1 patients received chronic blood transfusions – one to two units of leukocyte-poor packed red cells every 2–4 weeks – over 1 year to maintain pre-transfusion hemoglobin levels of ≥7.0 g/dL. Group 2 patients received occasional transfusions over the course of 1 year, with more than 4 weeks between transfusions. All patients were treated with iron chelation when serum ferritin levels were ≥1,000 μg/dL. PASP and the 6-minute walk distance were evaluated at baseline and at 6 and 12 months. Propensity score adjustment was used to control for confounding by indication and contraindication. Multivariable regression analysis was used to evaluate the effects of chronic blood transfusion.
There were 16 (53.3%) patients in Group 1 and 14 (46.7%) in Group 2. At 12 months, patients in Group 1 had a greater reduction in PASP than those in Group 1 (adjusted mean difference, −16.83; 95% confidence interval, −26.35 to −7.32; P=0.001). The 6-minute walk distance at 12 months in Group 1 patients was greater than that in Group 2 patients (adjusted mean difference, 46.55; 95% confidence interval, 18.08 to 75.02; P=0.001).
This study found evidence that chronic blood transfusions may have beneficial effects in PAH in thalassemia patients over 1 year.
pulmonary artery systolic pressure; Thailand; 6-minute walk distance; leukocyte-poor packed red cells
When advanced, heart failure (HF) with preserved ejection fraction (HFpEF) is readily apparent. However, diagnosis of earlier disease may be challenging, as exertional dyspnea is not specific for HF, and biomarkers and hemodynamic indicators of volume overload may be absent at rest.
Methods and Results
Patients with exertional dyspnea and EF>50% were referred for hemodynamic catheterization. Those with no significant coronary disease, normal BNP, and normal resting hemodynamics (mean pulmonary artery (PA) pressure<25 mmHg & PA wedge (PCWP) pressure <15 mmHg; n=55) underwent exercise study. The exercise PCWP was used to classify patients as having HFpEF (PCWP≥25 mmHg; n=32) or non-cardiac dyspnea (NCD, PCWP<25 mmHg; n=23). At rest, HFpEF patients displayed higher resting PA pressures and PCWP, though all values fell within normal limits. Exercise-induced elevation in PCWP in HFpEF was confirmed by greater increases in left ventricular end-diastolic pressure, and was associated with blunted increases in heart rate, systemic vasodilation and cardiac output. Exercise-induced pulmonary hypertension was present in 88% of HFpEF patients and was related principally to elevated PCWP, as pulmonary vascular resistances dropped similarly in both groups. Exercise PCWP and PASP were highly correlated. An exercise PASP≥45mmHg identified HFpEF with 96% sensitivity and 95% specificity.
Euvolemic patients with exertional dyspnea, normal BNP and normal cardiac filling pressures at rest may have markedly abnormal hemodynamic responses during exercise, suggesting that chronic symptoms are related to heart failure. Earlier and more accurate diagnosis using exercise hemodynamics may allow better targeting of interventions to treat and prevent HFpEF progression.
heart failure; exercise; hemodynamics; diastole; diagnosis
Background. Pulmonary hypertension (PH) is an often complication of severe cystic fibrosis (CF); however, data on the presence and impact of pulmonary vasculopathy in adult CF patients with milder disease, is very limited. Aim. To investigate, for the first time, the impact of systolic pulmonary arterial pressure (PASP) on maximal exercise capacity in adults with mild-to-moderate cystic fibrosis, without PH at rest. Methods. This is a Case Control study. Seventeen adults with mild-to-moderate CF, without PH at rest (cases) and 10 healthy, nonsmoking, age, and height matched controls were studied. All subjects underwent maximal cardiopulmonary exercise testing and echocardiography before and within 1 minute after stopping exercise. Results. Exercise ventilation parameters were similar in the two groups; however, cases, compared to controls, had higher postexercise PASP and decreased exercise capacity, established with lower peak work rate, peak O2 uptake, anaerobic threshold, and peak O2 pulse. Furthermore, the change in PASP values before and after exercise was strongly correlated to the parameters of exercise capacity among cases but not among controls. Conclusions. CF adults with mild-to-moderate disease should be screened for the presence of pulmonary vasculopathy, since the elevation of PASP during exercise might contribute to impaired exercise capacity.
Hypertension is an important cardiovascular risk factor worldwide. It is associated with left ventricular hypertrophy (LVH). Both diastolic and systolic dysfunction may occur in hypertensive heart disease. The ventricles are structurally and functionally interdependent on each other. This was an echocardiographic study intended to describe the impact of left ventricular pressure overload and hypertrophy due to hypertension on right ventricular morphology and function.
One hundred subjects with systemic hypertension and 50 age- and gender-matched normotensive control subjects were used for this study. Two-dimensional (2-D), M-mode and Doppler echocardiographic studies were done to evaluate the structure and function of both ventricles. Data analysis was done using the SPSS 16.0 (Chicago, Ill). Statistical significance was taken as p < 0.05.
Age and gender were comparable between the two groups. Hypertensive subjects had significantly increased left ventricular end-diastolic dimensions, posterior wall thickness, interventricular septal thickness, left atrial dimensions and left ventricular mass and index. The mitral valve E/A ratio was reduced among hypertensive subjects when compared to normal controls (1.15 ± 0.75 vs 1.44 ± 0.31, respectively; p < 0.05). A similar pattern was found in the tricuspid E/A ratio (1.14 ± 0.36 vs 1.29 ± 0.30, respectively; p < 0.05). Hypertensive subjects also had reduced right ventricular internal dimensions (20.7 ± 8.0 vs 23.1 ± 3.1 mm, respectively; p < 0.001) but similar peak pulmonary systolic velocity. The mitral e/a ratio correlated well with the tricuspid e/a ratio.
Systemic hypertension is associated with right ventricular morphological and functional abnormalities. Right ventricular diastolic dysfunction may be an early clue to hypertensive heart disease.
hypertension; right ventricular function; echocardiography; systolic dysfunction; diastolic dysfunction
Background: Hypertrophic cardiomyopathy (HCM), an auto-somal dominant disorder due to mutation of genes encoding sarcomeric proteins, leads to left ventricular diastolic dysfunction. Recently, the research in this area suggests that systolic dysfunction exists in the patients with HCM even though traditional measures of systolic dysfunction are normal. So, we carried out this study to determine global systolic dysfunction in patients with HCM.
Materials and Methods: A total of 18 patients, diagnosed with HCM according to echocardiography parameters, that is thickness of interventricular septum/posterior wall thickness >1.3 or hypertrophy involving apex only with or without left ventricular outflow tract obstruction, were included in the study and were compared with normal age-matched controls. We measured torsion and strain imaging by 2-dimensional echocardiography as well as strain imaging by tissue Doppler echocardiography.
Result: The results of the study showed that there was considerable increased torsion in patients with HCM as compared to normal subjects (16.61±7.43 vs. 10.42±4.73, p=0.006). Tissue Doppler indices—systolic annular velocity (7.7±0.7 vs. 8.7±1.00, p=0.012) and lateral wall E/E’ (12.52±5.27 vs. 6.66±1.67, p<0.001) were significantly different in patients with HCM and normal subjects. The average systolic strain and strain rate as well as diastolic strain rate were significantly different in both the groups when strain imaging was performed by tissue Doppler echocardiography. We also observed significantly reduced global longitudinal, circumferential and radial strain in patients with HCM when strain analysis was carried out with 2-dimensional speckle tracking echocardiography.
Conclusion: The global subtle systolic dysfunction, as measured by left ventricular torsion and strain imaging, is present in patients with HCM even though traditional measure of systolic dysfunction is normal.
Global systolic dysfunction; Hypertrophic cardiomyopathy; Left-ventricular torsion; Strain imaging
Serum uric acid (UA) is emerging as a strong and independent marker for pulmonary arterial hypertension (PAH). PAH is well recognized as a life threatening complication of sickle cell disease (SCD). However, the association between UA and PAH in SCD is unknown. We reviewed electronic medical records (EMR) of 559 consecutive adult SCD patients from Kings County Hospital Center (KCHC) between January 2005 and February 2010. Patients (n = 96) with measurement of UA in close temporal proximity to the transthoracic echocardiography (TTE) were identified. PAH was defined as pulmonary artery systolic pressure (PASP) ≥30 mm Hg. Patients (n = 16) with other risk factors which may cause PAH and chronic renal insufficiency were excluded. In 18 patients, TTE could not measure PASP. Finally, 62 patients were selected. Statistical analysis was performed using Student t tests, Pearson correlation coefficient and multivariate regression analysis. Out of 62 patients, 30 had PAH. Patients with PAH had a higher UA level (8.67 ± 4.8 vs. 5.35 ± 2.1, P = 0.001). We found strong positive correlation between the UA level and PASP (r = 0.71; P < 0.0001). This correlation was independent of diuretic use. UA could be a potential marker for PAH in SCD. However, its’ prognostic and pathophysiologic role in SCD patients with PAH needs to be further investigated.
Pulmonary arterial hypertension;
Sickle cell disease;
Pulmonary hypertension; Hemoglobinopathy
Background and objectives
Sickle cell disease (SCD) is a chronic, inherited haemoglobin disorder, associated with recurrent vaso-occlusive and haemolytic crises and chronic tissue ischemia which may adversely affect any organ system. Our objectives were to evaluate the left ventricular (LV) systolic and diastolic functions in Saudi patients with SCD originally from the Eastern Province of Saudi Arabia.
Design and setting
Prospective hospital based echocardiography study on adolescent and adult patients with SCD.
Forty-five patients with SCD were recruited for echocardiographic study while 45 patients, matched for age and sex, served as controls. Left and right ventricular dimensions and LV wall thicknesses, LV mass index (LVMI) and LV contractility variables were obtained. Left atrial dimension and volume and pulmonary artery systolic pressure (PASP) were also estimated. We also evaluated parameters of LV diastolic function, including early and late mitral flow velocities (E and A wave respectively), E/A ratio, deceleration time (MVDT), A wave duration (MVA D), LV isovolumic relaxation time (IVRT), and tissue Doppler velocities, such as lateral annular e‘ wave, a‘ wave, e‘/a‘ ratio and E/e‘ ratio.
There were increases in the LV dimensions, LV volumes, stroke volume, and LVMI of the SCD patients. The preload was increased (LV diastolic volume) and afterload was decreased (low diastolic blood pressure). The LVEF was equivalent, though there was evidence of LV diastolic dysfunction in 24%, and pulmonary hypertension (PH) in 40% of the SCD patients. The mean left atrial volume (LAV) was also increased in the SCD patients.
LV diastolic dysfunction (heart failure with preserved ejection fraction) and PH may complicate cases of the Arab-Indian haplotype of SCD.
MVE vel, mitral valve flow E wave velocity (cm. sec); MVA vel, mitral valve flow A wave velocity (cm. sec); E/A, E wave/A wave ratio; MVDT, mitral valve deceleration time (ms); MVAD, mitral valve A wave duration (ms); TDI, tissue doppler imaging; Lat e‘, lateral annular e‘ wave velocity by TDI (cm. sec); Lat a‘, lateral annular a‘ wave velocity by TDI (cm. sec); e‘/a‘, e‘ wave/a‘ wave ratio; E/e‘, mitral flow E wave velocity/lateral annular e‘ wave velocity by TDI; Sickle cell disease; Left ventricular diastolic function; Left ventricular systolic function; Tissue doppler imaging
Ke, Tao, Jiye Wang, Erik R. Swenson, Xiangnan Zhang, Yunlong Hu, Yaoming Chen, Mingchao Liu, Wenbin Zhang, Feng Zhao, Xuefeng Shen, Qun Yang, Jingyuan Chen, and Wenjing Luo. Effect of acetazolamide and gingko biloba on the human pulmonary vascular response to an acute altitude ascent. High Alt Med Biol 14:162–167, 2013.—Acetazolamide and gingko biloba are the two most investigated drugs for the prevention of acute mountain sickness (AMS). Evidence suggests that they may also reduce pulmonary artery systolic pressure (PASP). To investigate whether these two drugs for AMS prevention also reduce PASP with rapid airlift ascent to high altitude, a randomized controlled trial was conducted on 28 healthy young men with acetazolamide (125 mg bid), gingko biloba (120 mg bid), or placebo for 3 days prior to airlift ascent (397 m) and for the first 3 days at high altitude (3658 m). PASP, AMS, arterial oxygen saturation (Sao2), mean arterial pressure (MAP), heart rate (HR), forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), and peak expiratory flow (PEF) were assessed both at 397 m and 3658 m. HR, PEF, and PASP increased with altitude exposure (p<0.05), and SaO2 decreased (p<0.05). PASP with acetazolamide (mean at 3658 m, 26.2 mm Hg; incremental change, 4.7 mm Hg, 95% CI., 2.6–6.9 mm Hg) was lower than that with ginkgo biloba (mean at 3658 m, 33.7 mm Hg, p=0.001; incremental change, 13.1 mm Hg, 95%CI., 9.6–16.5 mm Hg, p=0.002), and with placebo (mean at 3658 m, 34.7 mm Hg, p<0.001; 14.4 mm Hg, 95% CI., 8.8–20.0 mm Hg, p=0.001). The data show that a low prophylactic dosage of acetazolamide, but not gingko biloba, mitigates the early increase of PASP in a quick ascent profile.
acetazolamide; gingko Biloba; pulmonary artery systolic pressure; acute mountain sickness; randomized controlled trial
Pulmonary arterial systolic pressure (PASP) can be estimated with transthoracic echocardiography. However, the significance of raised PASP on routine echocardiography is uncertain. In this study, we evaluated the mortality and hospitalization rates of subjects with raised PASP in a cohort of patients referred directly by their general practitioners for routine outpatient (open access) echocardiography for further analysis of suspected heart failure.
A total of 485 subjects were referred for open access echocardiography at our hospital in 2002. A cohort of 209/485 (43%) consecutive subjects with measurable tricuspid regurgitation were followed for a minimum of five years investigating hospitalization rates and survival. Some 62 of 209 (30%) subjects had pulmonary hypertension (PH). Subjects with PH were significantly more likely to have four or more hospital admissions (22% vs. 8%; P < 0.01) and > 30 days of cumulative hospital stay over five years (29% vs. 13%; P < 0.01). PH was significantly associated with mortality (P = 0.003), while moderate to severe PH was an independent predictor of mortality (hazard ratio: 4.31; 95% confidence interval (95% CI): 1.51–12.30). Records from the Office of National Statistics revealed that subjects with PH were more likely to have chronic lung diseases recorded as immediate or contributory causes of death (50% vs. 14%; P < 0.05).
PASP ≥ 36 mmHg on routine echocardiography is associated with recurrent hospital admissions, prolonged hospitalizations and increased cause of mortality. Therefore, the diagnosis of PH on echocardiography deserves further clinical evaluation, with future studies designed at defining a suitable diagnostic strategy.
Dyspnoea; Pulmonary hypertension; Transthoracic echocardiography; Chronic lung disease; Heart failure
Hyperadrenocorticism (HAC) is associated with an increased prevalence of hypertension. This study investigated the left ventricular function using two-dimensional speckle-tracking echocardiography (2D-STE) in small breed dogs affected with spontaneous HAC.
Age-matched healthy controls (n = 9), dogs with pituitary-dependent hyperadrenocorticism (PDH, n = 10), and dogs with adrenal-dependent hyperadrenocorticism (ADH, n = 9) were included in this study. Conventional echocardiography, global longitudinal and circumferential strain, and strain rate were assessed.
On group-wise comparison, left ventricular free wall (LVFWd) and interventricular septal thickness in diastole (IVSd) were thickest in the ADH group, followed by the PDH and controls (P = 0.014 and P = 0.001, respectively). Neither LVFWd nor IVSd was correlated with systemic blood pressure (P = 0.238 and P = 0.113, respectively). The values of all variables derived from the global strain and strain rate in longitudinal and circumferential directions followed the same pattern: highest in the controls, followed by PDH and then ADH (all P < 0.05, respectively). On multiple regression analyses, global longitudinal strain, global longitudinal strain rate in systole and early diastole, and global circumferential strain all decreased linearly with increased IVSd (all P < 0.05).
Left ventricular hypertrophy (LVH) was more prevalent in the HAC group compared to the control group. Association between hypertension and development of LVH was not identified. Decreased global longitudinal and circumferential strains were associated with increased IVSd. 2D-STE revealed significant decreases in systolic functions that were undetected using conventional echocardiography in the ADH and PDH groups.
Canine; Left ventricular deformation; Hypercortisolism; Hypertension; Hypertrophic cardiomyopathy
We describe a case of a 25-year-old pregnant woman who presented with severe primary pulmonary hypertension (PPH). Her echocardiogram showed severe right ventricular hypertrophy with dilatation and Moderate right ventricular systolic dysfunction. Right ventricle systolic pressure (RVSP) was estimated to be 125 mmHg. She had an elective caesarean section under general anaesthesia at 32 weeks of gestation. Pulmonary artery pressures measured by a pulmonary artery catheter before anaesthesia were 102 mmHg and pulmonary vascular resistance was 429. Intraoperative nitric oxide was used to reduce pulmonary artery systolic pressure (PASP). After the delivery of a healthy infant, PASP was controlled with nebulized iloprost and silandifil. Five days later she was transferred from intensive care unit after she was started on silandifil 50 mg three times daily and a small dose of warfarin.
Primary pulmonary hypertension; Pregnancy; General anaesthesia; Pulmonary vasodilators