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1.  The value of hepatic diffusion-weighted MR imaging in demonstrating hepatic congestion secondary to pulmonary hypertension 
Congestive hepatomegaly might be the first sign for pulmonary hypertension. Apparent diffusion coefficient (ADC) value obtained with quantitative diffusion-weighted magnetic resonance imaging (DW-MRI) is affected by liver fibrosis and perfusion. We aimed to evaluate the diagnostic value of DW-MRI in cooperation with biochemical markers, ultrasonography (US) and echocardiography (TTE) in determining the degree of hepatic congestion secondary to pulmonary hypertension (PHT).
35 patients with PHT and 26 control subjects were included in the study. PHT was diagnosed if pulmonary artery systolic pressure (PASP) was measured above 35 mmHg with TTE. Study group was classified into mild and moderate PHT. DW-MRI was performed with b-factors of 0, 500 and 1000 sec/mm². Mean ADC, ADC-II (Average of the ADC values of right lobe anterior and posterior segments), US, TTE and blood biochemical parameters of both groups were compared.
There exists a positive correlation between liver size and the diameters of vena cava inferior, right atrium, right hepatic vein(RHV), mid-hepatic vein(MHV), left hepatic vein(LHV) (p < 0.01). There was a positive correlation between PASP and RHV, MHV, LHV. The patients had lower ejection fractions (p < 0.01) and higher LDH (p < 0.01) and ALP (p < 0.05) levels than the control group. The ADC values of the patients with moderate PASP were higher than those with a mild PASP (p < 0.05). Mean ADC was higher in patients with moderate PHT compared to control group (p = 0.009). There was a positive correlation between PASP and ADC values of right lobe posterior segment of the liver (p < 0.05). The ADC-II and mean ADC values of the patients with moderate PASP were higher than those of the control group (p < 0.01).
Congestion due to moderate PHT might be diagnosed with DW-MRI. As PASP increase; mean ADC and ADC-II values increase.
PMCID: PMC2920852  PMID: 20663149
2.  Prognostic Value of Emergency Physician Performed Echocardiography in Patients with Acute Pulmonary Thromboembolism 
Pulmonary embolism (PE) is a life-threatening illness with high morbidity and mortality. Echocardiography (ECG) plays an important role in the early identification of right ventricular (RV) dysfunction, making it a helpful tool in identifying hemodynamically stable patients affected by PE with a higher mortality risk. The purpose of this study was to evaluate if one or more ECG indexes could predict a short-term evolution towards RV dysfunction.
We selected all patients consecutively admitted to the Careggi Hospital Emergency Department with the clinical suspicion of PE, confirmed by computed tomography angiography prior to enrollment. Subsequently, properly trained emergency physicians acquired a complete ECG to measure RV morphological and functional indices. For each patient, we recorded if he or she received a fibrinolytic treatment, a surgical embolectomy or heparin therapy during the emergency department (ED) stay. Then, every patient was re-evaluated with ECG, by the same physician, after 1 week in our intensive observation unit and 1 month as outpatient in our ED regional referral center for PE.
From 2002 to 2007, 120 consecutive patients affected by PE were evaluated by echocardiography at the Careggi Hospital ED. Nine patients (8%) were treated with thrombolytic therapy. Six died within 1 week and 4 abandoned the study, while the remaining 110 survived and were re-evaluated by ECG after 1 week and 1 month. The majority of the echocardiographic RV indexes improve mostly in the first 7 days: Acceleration Time (AT) from 78±14 ms to 117±14 ms (p<0.001), Diameter of Inferior Vena Cava (DIVC) from 25±6 mm to 19±5 mm (p<0.001), Tricuspid Annular Plane Systolic Excursion (TAPSE) from 16±6 mm to 20±6 mm (p<0.001). Pulmonary Artery Systolic Pressure (PASP) showed a remarkable decrease from 59±26 mmHg to 37±9 mmHg, (p<0.001). The measurements of the transverse diameters of both ventricles and the respective ratio showed a progressive normalization with a reduction of RV diameter, an increase of Left Ventricular (LV) diameter and a decrease of RV/LV ratio over time. To evaluate the RV function, the study population was divided into 3 groups based on the TAPSE and PASP mean values at the admission: Group 1 (68 patients) (TAPSE+/ PASP−), Group 2 (12 patients) (TAPSE−/PASP−), and Group 3 (30 patients) (TAPSE−/PASP+). Greater values of AT, minor RV diameter, greater LV diameter and a lesser RV/LV ratio were associated with a short-term improvement of TAPSE in the Group 2. Instead, in Group 3 the only parameter associated with short-term improvement of TAPSE and PASP was the treatment with thrombolytic therapy (p<0.0001).
Greater values of AT, minor RV diameter, greater LV diameter and a lesser RV/LV ratio were associated with a short-term improvement of TAPSE−/PASP− values. Patients with evidence of RV dysfunction (TAPSE−/PASP+), may benefit from thrombolytic therapy to improve a short- term RV function. After 1 month, also a decreased DIVC predicted improved RV function.
PMCID: PMC3789917  PMID: 24106551
3.  Age-Associated Increases in Pulmonary Artery Systolic Pressure in the General Population 
Circulation  2009;119(20):2663-2670.
In contrast to the wealth of data on isolated systolic hypertension involving the systemic circulation in the elderly, much less is known about age-related change in pulmonary artery systolic pressure (PASP) and its prognostic impact in the general population. We sought to define the relationship between PASP and age, evaluate which factors influence PASP and determine if PASP is independently predictive of mortality in the community.
Methods and Results
A random sample of Olmsted County, MN general population (N=2042) underwent echocardiography and spirometry and was followed for a median of 9 years. PASP was measured from the tricuspid regurgitation velocity. Left ventricular diastolic pressure was estimated using Doppler echocardiography (E/e' ratio) and arterial stiffening was assessed using the brachial artery pulse pressure. Among 1413 (69%) subjects with measurable PASP (63±11y; 43% male), PASP (median, 25th-75th percentile) was 26 (24-30) mmHg and increased with age (r=0.31; p<0.001). Independent predictors of PASP were age, pulse pressure and mitral E/e' (all p≤0.003). Increasing PASP was associated with higher mortality (hazard ratio 2.73 per 10 mmHg; p<0.001). In subjects without cardiopulmonary disease (any heart failure, coronary artery disease, hypertension, diabetes mellitus or chronic obstructive lung disease), the age-adjusted hazard ratio was 2.74 per 10 mmHg (p=0.016).
We provide the first population-based evidence of age-related increase in pulmonary artery pressure, its association with increasing left heart diastolic pressures and systemic vascular stiffening, as well as its negative impact on survival. Pulmonary artery pressure may serve as a novel cardiovascular risk factor and potential therapeutic target.
PMCID: PMC2753443  PMID: 19433755
hypertension; pulmonary; population; aging; vasculature
4.  Right ventricular dyssynchrony in patients with pulmonary hypertension is associated with disease severity and functional class 
Abnormalities in right ventricular function are known to occur in patients with pulmonary arterial hypertension.
Test the hypothesis that chronic elevation in pulmonary artery systolic pressure delays mechanical activation of the right ventricle, termed dyssynchrony, and is associated with both symptoms and right ventricular dysfunction.
Fifty-two patients (mean age 46 ± 15 years, 24 patients with chronic pulmonary hypertension) were prospectively evaluated using several echocardiographic parameters to assess right ventricular size and function. In addition, tissue Doppler imaging was also obtained to assess longitudinal strain of the right ventricular wall, interventricular septum, and lateral wall of the left ventricle and examined with regards to right ventricular size and function as well as clinical variables.
In this study, patients with chronic pulmonary hypertension had statistically different right ventricular fractional area change (35 ± 13 percent), right ventricular end-systolic area (21 ± 10 cm2), right ventricular Myocardial Performance Index (0.72 ± 0.34), and Eccentricity Index (1.34 ± 0.37) than individuals without pulmonary hypertension (51 ± 5 percent, 9 ± 2 cm2, 0.27 ± 0.09, and 0.97 ± 0.06, p < 0.005, respectively). Furthermore, peak longitudinal right ventricular wall strain in chronic pulmonary hypertension was also different -20.8 ± 9.0 percent versus -28.0 ± 4.1 percent, p < 0.01). Right ventricular dyssynchrony correlated very well with right ventricular end-systolic area (r = 0.79, p < 0.001) and Eccentricity Index (r = 0.83, p < 0.001). Furthermore, right ventricular dyssynchrony correlates with pulmonary hypertension severity index (p < 0.0001), World Health Organization class (p < 0.0001), and number of hospitalizations (p < 0.0001).
Lower peak longitudinal right ventricular wall strain and significantly delayed time-to-peak strain values, consistent with right ventricular dyssynchrony, were found in a small heterogeneous group of patients with chronic pulmonary hypertension when compared to individuals without pulmonary hypertension. Furthermore, right ventricular dyssynchrony was associated with disease severity and compromised functional class.
PMCID: PMC1215497  PMID: 16129028
Dyssynchrony; right ventricle; outcomes; pulmonary hypertension; strain imaging; tissue Doppler imaging
5.  Abnormal shortened diastolic time length at increasing heart rates in patients with abnormal exercise-induced increase in pulmonary artery pressure 
The degree of pulmonary hypertension is not independently related to the severity of left ventricular systolic dysfunction but is frequently associated with diastolic filling abnormalities. The aim of this study was to assess diastolic times at increasing heart rates in normal and in patients with and without abnormal exercise-induced increase in pulmonary artery pressure (PASP). Methods. We enrolled 109 patients (78 males, age 62 ± 13 years) referred for exercise stress echocardiography and 16 controls. The PASP was derived from the tricuspid Doppler tracing. A cut-off value of PASP ≥ 50 mmHg at peak stress was considered as indicative of abnormal increase in PASP. Diastolic times and the diastolic/systolic time ratio were recorded by a precordial cutaneous force sensor based on a linear accelerometer.
At baseline, PASP was 30 ± 5 mmHg in patients and 25 ± 4 in controls. At peak stress the PASP was normal in 95 patients (Group 1); 14 patients (Group 2) showed an abnormal increase in PASP (from 35 ± 4 to 62 ± 12 mmHg; P < 0.01). At 100 bpm, an abnormal (< 1) diastolic/systolic time ratio was found in 0/16 (0%) controls, in 12/93 (13%) Group 1 and 7/14 (50%) Group 2 patients (p < 0.05 between groups).
The first and second heart sound vibrations non-invasively monitored by a force sensor are useful for continuously assessing diastolic time during exercise. Exercise-induced abnormal PASP was associated with reduced diastolic time at heart rates beyond 100 beats per minute.
PMCID: PMC3268730  PMID: 22104611
Diastolic time; Pulmonary hypertension; Cutaneous heart sensor
6.  Echocardiographic Assessment of Pulmonary Artery Systolic Pressure and Outcomes in Ambulatory Heart Failure Patients 
Pulmonary hypertension (PH) in patients with heart failure (HF) is associated with worse outcomes and is rapidly being recognized as a therapeutic target. To facilitate pragmatic research efforts, data regarding the prognostic importance of noninvasively assessed pulmonary artery systolic pressure (PASP) in stable ambulatory patients with HF are needed.
Methods and Results
We examined the association between echocardiographic PASP and outcomes in 417 outpatients with HF (age, 54±13 years; 60.7% men; 50.4% whites; 24.9% with preserved ejection fraction). Median PASP was 36 mm Hg (interquartile range [IQR]: 29, 46). After a median follow‐up of 2.6 years (IQR: 1.7, 3.9) there were 72 major events (57 deaths; 9 urgent heart transplants; and 6 ventricular assist device implantations) and 431 hospitalizations for HF. In models adjusting for clinical risk factors and therapy, a 10‐mm Hg higher PASP was associated with 37% higher risk (95% CI: 18, 59; P<0.001) for major events, and 11% higher risk (95% CI: 1, 23; P=0.039) for major events or HF hospitalization. The threshold that maximized the likelihood ratio for both endpoints was 48 mm Hg; those with PASP ≥48 mm Hg (N=84; 20.1%) had an adjusted hazard ratio of 3.33 (95% CI: 1.96, 5.65; P<0.001) for major events and 1.47 (95% CI: 1.02, 2.11; P=0.037) for major events or HF hospitalization. Reduced right ventricular systolic function had independent prognostic utility over PASP for adverse outcomes. Right atrial pressure and transtricuspid gradient both contributed to risk.
Elevated PASP, determined by echocardiography, identifies ambulatory patients with HF at increased risk for adverse events.
PMCID: PMC3959670  PMID: 24492947
echocardiography; heart failure; mortality; outcomes; pulmonary hypertension
7.  Role of HIV and HHV-8 Infection in Pulmonary Arterial Hypertension 
AIDS (London, England)  2008;22(7):825-833.
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.
PMCID: PMC2711076  PMID: 18427200
pulmonary hypertension; AIDS; HIV infection; human herpesvirus 8 infection
8.  Pulmonary Pressures and Death in Heart Failure: A Community Study 
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.
PMCID: PMC3258551  PMID: 22240126
heart failure; pulmonary hypertension; mortality; community
9.  Pulmonary Hypertension in Heart Failure with Preserved Ejection Fraction: A Community-Based Study 
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.
PMCID: PMC2736110  PMID: 19324256
pulmonary hypertension; diastolic heart failure; heart failure with preserved ejection fraction
10.  The increase in pulmonary arterial pressure caused by hypoxia depends on iron status 
The Journal of Physiology  2008;586(Pt 24):5999-6005.
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.
PMCID: PMC2655431  PMID: 18955380
11.  The increase in pulmonary arterial pressure caused by hypoxia depends on iron status 
The Journal of Physiology  2008;586(24):5999-6005.
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.
PMCID: PMC2655431  PMID: 18955380
12.  Accuracy of Non-Invasively Determined Pulmonary Artery Systolic Pressure 
The American journal of cardiology  2010;105(8):1192-1197.
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.
PMCID: PMC2994808  PMID: 20381676
Non-invasive pulmonary artery systolic pressure; Echocardiographic pulmonary artery systolic pressure
13.  Prognostic effects of pulmonary hypertension in patients undergoing cardiac resynchronization therapy 
Journal of Thoracic Disease  2010;2(2):71-75.
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.
PMCID: PMC3256451  PMID: 22263022
heart failure; cardiac resynchronization therapy; pulmonary artery systolic pressure; prognosis
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.
PMCID: PMC4145826  PMID: 25170276
pulmonary artery systolic pressure; Thailand; 6-minute walk distance; leukocyte-poor packed red cells
Cardiovascular Journal of Africa  2010;21(5):252-256.
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.
PMCID: PMC3721898  PMID: 20972511
hypertension; right ventricular function; echocardiography; systolic dysfunction; diastolic dysfunction
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.
PMCID: PMC3136662  PMID: 22654300
Pulmonary arterial hypertension;  Sickle cell disease;  Uric acid;  Pulmonary hypertension; Hemoglobinopathy
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.
PMCID: PMC4316285  PMID: 25653979
Global systolic dysfunction; Hypertrophic cardiomyopathy; Left-ventricular torsion; Strain imaging
AIDS (London, England)  2012;26(6):731-740.
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.
PMCID: PMC3606053  PMID: 22210636
HIV; pulmonary hypertension; emphysema; COPD; inflammation
High Altitude Medicine & Biology  2013;14(2):162-167.
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.
PMCID: PMC3694514  PMID: 23795737
acetazolamide; gingko Biloba; pulmonary artery systolic pressure; acute mountain sickness; randomized controlled trial
Circulation. Heart failure  2010;3(5):588-595.
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.
PMCID: PMC3048586  PMID: 20543134
heart failure; exercise; hemodynamics; diastole; diagnosis
Pulmonary Circulation  2013;3(2):426-431.
Pulmonary artery pressure (PAP) is known to regress after successful balloon mitral valvotomy (BMV). Data of persistent pulmonary artery hypertension (PPAH) following BMV is scarce. We analyzed the clinical, echocardiographic, and hemodynamic data of 701 consecutive patients who have undergone successful BMV in our institute from 1997 to 2003. Data of 287 patients who had PPAH (defined by pulmonary artery systolic pressure [PASP] of ≥ 40 mmHg at one year following BMV) were compared to the data of 414 patients who did not have PPAH. Patients who had PPAH were older (39.9 ± 9.9 years vs. 29.4 ± 10.1; P < 0.001). They had higher prevalence of atrial fibrillation (AF; 21.9 vs. 12.1%, P < 0.05), moderate or severe pulmonary artery hypertension (PAH) defined as PASP more than 50 mmHg (43.5 vs. 33.8%, P = 0.00), anatomically advanced mitral valve disease as assessed by Wilkin's echocardiographic score > 8 (33.7 vs. 23.2%, P < 0.001), and coexistent aortic valve disease (45.6 vs. 37.9%, P < 0.001) at the baseline. Those patients with PPAH had comparatively lower immediate postprocedural mitral valve area (MVA). On follow-up of more than five years, the occurrence of restenosis (39.3 vs. 10.1%, P = 0.000), new onset heart failure (14% vs. 4%, P < 0.05) and need for reinterventions (9.5% vs. 2.8%, P < 0.05) were higher in the PPAH group. Patients with PPAH were older, sicker, and had advanced rheumatic mitral valve disease. They had higher incidence of restenosis, new onset heart failure, and need for reinterventions on long term follow-up. PPAH represents an advanced stage of rheumatic valve disease and indicates chronicity of the disease, which may be the reason for the poorer prognosis of these patients. Patients with PPAH requires intense and more frequent follow-up.
PMCID: PMC3757839  PMID: 24015345
rheumatic heart disease; balloon mitral valvotomy; pulmonary artery hypertension; regression
It remains incompletely understood whether patients with transfusion related cardiac iron overload without signs of heart failure exhibit already subclinical alterations of systolic left ventricular (LV) dysfunction. Therefore we performed a comprehensive evaluation of systolic and diastolic cardiac function in such patients using tagged and phase-contrast CMR.
19 patients requiring regular blood transfusions for chronic anemia and 8 healthy volunteers were investigated using cine, tagged, and phase-contrast and T2* CMR. LV ejection fraction, peak filling rate, end-systolic global midventricular systolic Eulerian radial thickening and shortening strains as well as left ventricular rotation and twist, mitral E and A wave velocity, and tissue e' wave and E/e' wave velocity ratio, as well as isovolumic relaxation time and E wave deceleration time were computed and compared to cardiac T2*.
Patients without significant iron overload (T2* > 20 ms, n = 9) had similar parameters of systolic and diastolic function as normal controls, whereas patients with severe iron overload (T2* < 10 ms, n = 5), had significant reduction of LV ejection fraction (54 ± 2% vs. 62 ± 6% and 65 ± 6% respectively p < 0.05), of end-systolic radial thickening (+6 ± 4% vs. +11 ± 2 and +11 ± 4% respectively p < 0.05) and of rotational twist (1.6 ± 0.2 degrees vs. 3.0 ± 1.2 and 3.5 ± 0.7 degrees respectively, p < 0.05) than patients without iron overload (T2* > 20 ms) or normal controls. Patients with moderate iron overload (T2* 10-20 ms, n = 5), had preserved ejection fraction (59 ± 6%, p = NS vs. pts. with T2* > 20 ms and controls), but showed reduced maximal LV rotational twist (1.8 ± 0.4 degrees). The magnitude of reduction of LV twist (r = 0.64, p < 0.001), of LV ejection fraction (r = 0.44, p < 0.001), of peak radial thickening (r = 0.58, p < 0.001) and of systolic (r = 0.50, p < 0.05) and diastolic twist and untwist rate (r = -0.53, p < 0.001) in patients were directly correlated to the logarithm of cardiac T2*.
Multiple transfused patients with normal ejection fraction and without heart failure have subclinical alterations of systolic and diastolic LV function in direct relation to the severity of cardiac iron overload. Among all parameters, left ventricular twist is affected earliest, and has the highest correlation to log (T2*), suggesting that this parameter might be used to follow systolic left ventricular function in patients with iron overload.
PMCID: PMC3108924  PMID: 21518461
Diabetes mellitus is capable of impairing the myocardial function. Several studies have documented the influential impact of diabetes mellitus on the left ventricular function. The right ventricular function plays a significant role in the overall myocardial contractility; hence, this study was undertaken to evaluate the effect of diabetes mellitus type II on the right ventricular function.
Twenty-two diabetic patients without any coronary artery disease, hypertension, or left ventricular dysfunction were studied. The right ventricular end diastolic diameter, tricuspid plane systolic excursion, right ventricular inflow Doppler parameters, longitudinal myocardial velocities, and deformation indices from the basal and apical segments of the right ventricular free wall of the case group were measured. The control group consisted of 22 healthy individuals.
The tricuspid annular plane systolic excursion (TAPSE) and tricuspid peak early to peak late diastolic flow velocities ratio (E/A) in the diabetic patients were significantly lower than those of the control group patients (18.9 vs. 23.2, p value < 0.001 and 0.96 vs. 1.21, p value = 0.012), but there were no significant differences in the right ventricular end diastolic diameter and the right ventricular Tei index between the two groups (p value = 0.72). The right ventricular basal peak myocardial systolic velocity (SM) (12 cm/sec vs. 13.4 cm/sec; p value = 0.03), basal and apical right ventricular free wall systolic strain (−13.3% and −18.7% vs. −20.2% and −25.7%; p value = 0.001), and apical strain rate (−1.2 1/s vs. −1.6 1/s; p value = 0.008 ) were significantly lower in the study group. There was a weak correlation between the right ventricular function and HbA1c as well as the duration of diabetes mellitus and C-reactive protein.
Our results suggest that diabetes mellitus type II can influence the right ventricular function in the absence of coronary artery disease, diastolic dysfunction, and pulmonary hypertension.
PMCID: PMC3537202  PMID: 23323079
Echocardiography; Diabetes mellitus; Ventricular function, right
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.
PMCID: PMC4300024  PMID: 25551792
Canine; Left ventricular deformation; Hypercortisolism; Hypertension; Hypertrophic cardiomyopathy
Pulmonary Medicine  2012;2012:252345.
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.
PMCID: PMC3414060  PMID: 22900167

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