Right Ventricular Inefficiency in Repaired Tetralogy of Fallot: Proof of Concept for Energy Calculations From Cardiac MRI Data

Repaired tetralogy of Fallot (rTOF) patients develop right ventricular (RV) dilatation and dysfunction. To prevent their demise, pulmonary valve replacement is necessary, though appropriate timing for it is challenged by a paucity of reliable diagnostic parameters. In this pilot study, we hypothesized that stroke work (SW) and energy calculations would delineate the inefficiency of RV performance in rTOF. RV SW was calculated for both an rTOF and a normal subject by utilizing RV pressure and volume measurements obtained during cardiac catheterization and MRI studies. Energy transfer rate and ratio were computed at the main pulmonary artery (PA). Compared to the normal RV, the rTOF RV had higher operating pressure, lower computed SW (0.078 J vs. 0.115 J for normal), and higher negative energy transfer at the PA (0.044 J vs. 0.002 J for normal). Furthermore, the energy transfer ratio was nearly twice as high for the normal RV (1.06) as for the rTOF RV (0.56). RV SW and energy transfer ratio delineate important operational efficiency differences in blood flow from the RV to the PA between rTOF and normal subjects. Our pilot data suggest that the rTOF RV is significantly less efficient than normal.     

Acute Pulmonary Embolism and Chronic Thromboembolic Pulmonary Hypertension: Clinical and Serial CT Pulmonary Angiographic Features

In acute pulmonary embolism (PE), circulatory failure and systemic hypotension are important clinically for predicting poor prognosis. While pulmonary artery (PA) clot loads can be an indicator of the severity of current episode of PE or treatment effectiveness, they may not be used directly as an indicator of right ventricular (RV) failure or patient death. In other words, pulmonary vascular resistance or patient prognosis may not be determined only with mechanical obstruction of PAs and their branches by intravascular clot loads on computed tomography pulmonary angiography (CTPA), but determined also with vasoactive amines, reflex PA vasoconstriction, and systemic arterial hypoxemia occurring during acute PE. Large RV diameter with RV/left ventricle (LV) ratio > 1.0 and/or the presence of occlusive clot and pulmonary infarction on initial CTPA, and clinically determined high baseline PA pressure and RV dysfunction are independent predictors of oncoming chronic thromboembolic pulmonary hypertension (CTEPH). In this pictorial review, authors aimed to demonstrate clinical and serial CTPA features in patients with acute massive and submassive PE and to disclose acute CTPA and clinical features that are related to the prediction of oncoming CTEPH.     

sPAP/PAAT Ratio as a New Index of Pulmonary Vascular Load: A Study in Normal Subjects and Ssc Patients with and without PH

In pulmonary hypertension (PH), the development of right ventricular (RV) dilatation and RV failure are signs of accelerated progression of the disease, resulting in an increased risk of cardiac death. Even the noninvasive assessment of systolic blood pressure in the pulmonary artery undertaken by echocardiography does not provide a measure of ventricle–pulmonary interaction. Some studies have shown the potential for echocardiography to indirectly evaluate pulmonary vascular resistance (PVR) and the acceleration time of pulmonary outflow (PAAT). We used systolic pulmonary artery pressure (sPAP) and pulmonary vascular resistance to develop an sPAP/PAAT ratio (strength/surface unit)/(time) for this study. From January 2017 to December 2018, 60 healthy subjects and 63 patients with systemic scleroderma (Ssc) (60 females, 3 males), 27 with PH and 36 without PH at two-dimensional echocardiographic/Doppler, were screened. In normal subjects, the mean sPAP/PAAT ratio was 0.26 ± 0.063, which indicated optimal pulmonary arterial ventricle coupling and biventricular function. The data derived from the analysis of the Ssc patients showed that those presenting pre-capillary PH at cardiac catheterization had an sPAP/PAAT ratio of 0.40 ± 0.05. There was a significant correlation between sPAP/PAAT with Walk Distance (WD) and PVR, but not with TAPSE. Interobserver variability was less than 5%. The sPAP/PAAT ratio is a new parameter that may indicate pulmonary vascular afterload and interaction, both in normal subjects and in patients with Ssc and PH.     

Smooth muscle role on pulmonary arterial function during acute pulmonary hypertension in sheep

AIM: We determined the wall mechanical response of the pulmonary artery (PA) to acute pulmonary hypertension induced pharmacologically and by an occlusion maneuver, to study the vascular response of the local segment and its influence in the whole pulmonary circulation. METHODS: Pulmonary pressure and diameter were measured in six anaesthetized sheep under steady-state conditions. Transient hypertension in the PA was induced by phenylephrine (PHE) and a high pressure (HP) mechanical occlusion aimed at producing the same pulse and mean pressure responses. A viscoelastic arterial wall model was applied and the elastic (E(pd)) and viscous (micro) indexes were obtained. The micro/E(pd) ratio was adopted to quantify the damping performance of the arterial wall segment. The diastolic time constant was used as an indicator of the whole pulmonary buffering function. The systemic pressure was always measured. RESULTS: The pulmonary mean, systolic and pulse pressure increases (P < 0.05) were similar during PHE and HP, with respect to control. PHE also induced a systemic pressure rise (P < 0.05). The E(pd) elastic index increased during HP (P < 0.05) and tended to increase during PHE with respect to control. The viscous index micro only increased with PHE (P < 0.05) with respect to control and occlusion. The diastolic time constant increased with PHE with respect to control (P < 0.05). CONCLUSIONS: A pressure rise in the PA, induced by an occlusion maneuver, increased local stiffness. Similar pressure rises with smooth muscle activation (PHE), produced both a stiffness and viscous index increase. In PHE resistance increases more than compliance decreases so that the global net effect is a longer decay time. Smooth-muscle activation enhances the local damping effect (micro/E(pd)), concomitant with the buffering function improvement.     

A heart transplant candidate with severe pulmonary hypertension and extremely high pulmonary vascular resistance

Fixed pulmonary hypertension (PH) is a contraindication for heart transplantation (HTx). Several studies showed that use of a left ventricular assist device (LVAD) in patients with fixed PH who were initially deemed ineligible for HTx effectively decreased pulmonary arterial pressure (PAP), thus permitting HTx. We recently encountered a candidate for HTx who had severe PH with extremely high pulmonary vascular resistance (PVR). A 27-year-old female who had been diagnosed with dilated-phase hypertrophic cardiomyopathy and who was approved for HTx at age 25 was referred to our institute because of severe fatigability with moderate dyspnea even at rest due to severe bilateral heart failure. Despite continuous inotrope infusion, the patient’s symptoms were not relieved. Right heart catheterization (RHC) disclosed a PAP of 62/40 mmHg with severely reduced cardiac output (1.8 l/min). A PVR of 15.9 Wood units suggested progressive worsening of left ventricular function with almost irreversible remodeling of the pulmonary vasculature, and the patient was thought to be contraindicated for HTx. Following 3 weeks of aggressive medical treatment, repeat RHC demonstrated PVR lowering to 8.16 Wood units. This suggested it was likely that PVR could be reversed, and the patient underwent LVAD implantation. RHC performed after LVAD implantation showed a fall in PVR from the initial, extremely high measurement of 15.9 Wood units to 3.4 Wood units at 2 months postoperatively, and to 2.2 Wood units at 1 year. The patient is currently awaiting HTx with favorable LVAD support.     

Estrogen Preserves Pulsatile Pulmonary Arterial Hemodynamics in Pulmonary Arterial Hypertension

Pulmonary arterial hypertension (PAH) is caused by extensive pulmonary vascular remodeling that increases right ventricular (RV) afterload and leads to RV failure. PAH predominantly affects women; paradoxically, female PAH patients have better outcomes than men. The roles of estrogen in PAH remain controversial, which is referred to as “the estrogen paradox”. Here, we sought to determine the role of estrogen in pulsatile pulmonary arterial hemodynamic changes and its impact on RV functional adaption to PAH. Female mice were ovariectomized and replenished with estrogen or placebo. PAH was induced with SU5416 and chronic hypoxia. In vivo hemodynamic measurements showed that (1) estrogen prevented loss of pulmonary vascular compliance with limited effects on the increase of pulmonary vascular resistance in PAH; (2) estrogen attenuated increases in wave reflections in PAH and limited its adverse effects on PA systolic and pulse pressures; and (3) estrogen maintained the total hydraulic power and preserved transpulmonary vascular efficiency in PAH. This study demonstrates that estrogen preserves pulmonary vascular compliance independent of pulmonary vascular resistance, which provides a mechanical mechanism for ability of estrogen to delay disease progression without preventing onset. The estrogenic protection of pulsatile pulmonary hemodynamics underscores the therapeutic potential of estrogen in PAH.     

Heme oxygenase-1 reduces murine monocrotaline-induced pulmonary inflammatory responses and resultant right ventricular overload

Monocrotaline (MT), a pyrrolizidine alkaloid, causes pulmonary hypertension (PH) in rats and is widely utilized to analyze the pathophysiology of PH. However, a murine PH model with which transgenic animals may be used has not been established. To establish a murine MT-induced PH model, we administered different amounts of MT and determined the extent of right ventricular (RV) overload and PH. We also examined the expression of heme oxygenase-1 (HO-1), a potential antistress protein in MT-treated animals, and evaluated the functional role of HO-1 by administering an HO-1 inhibitor. Significant pulmonary inflammation and RV hypertrophy were observed when mice were given 600 mg/kg weight of MT weekly for 8 weeks. In addition, elevated RV pressure and induction of HO-1 in lung and RV were observed with this dose of MT. Interestingly, inhibition of HO activity promoted inflammatory changes in the lung and the resultant RV hypertrophy. HO-1 may play defensive roles against murine MT-induced pulmonary inflammation and the resultant RV overload.     

Accuracy of Doppler echocardiography in the hemodynamic assessment of pulmonary circulation in patients with systemic sclerosis

PurposePulmonary hypertension (PH) is an ominous complication in systemic sclerosis patients (SSc) and echocardiography is a screening tool for its detection. The goal of this study was to assess the reliability of resting and exercise echo Doppler parameters with data obtained by right heart catheterization (RHC).Material and methodsWe included 91 patients (84 F, 53.3 ± 15.2 years) with SSc. Transthoracic echocardiography followed by exercise Doppler-echocardiography (EDE) were performed. A positive EDE was defined as a ≥20 mmHg increase in tricuspid regurgitation peak gradient (TRPG). RHC with exercise was performed in positive EDE patients and/or in subjects with resting TRPG > 31 mmHg.ResultsFinally, RHC was performed in 20 patients. The correlation for the echocardiography and invasive measurement of systolic (sPAP) and mean (mPAP) pulmonary artery pressure was r = 0.66 (p = 0.001) and r = 0.7 (p = 0.001), respectively. We also found significant correlation between echocardiography and invasive measurement of exercise sPAP r = 0.68 (p = 0.001) and exercise mPAP r = 0.67 (p = 0.002). There was a correlation between pulmonary vascular resistance (PVR) assessed by echocardiography and measured by RHC r = 0.49, p = 0.027. The equation derived within our population was: PVR by echocardiography = 9.6*TRV/TVI_RVOT+0.068. We also performed ROC analysis to predict PVR > 2 WU. Our results highlight that sPAP has the highest AUC (0.802, 95% CI 0.585–1).ConclusionDoppler resting and exercise echocardiography may provide a reliable, noninvasive method for determining resting and exercise sPAP, mPAP, and PVR in SSc patients, although it may underestimate or overestimate these values in some individuals. Doppler echocardiography does not replace RHC for definite hemodynamic assessment of suspected PH.     

肺动脉高压的肺动脉血管超声生物力学研究

目的采用超声成像技术与生物力学方法相结合的方法,对肺动脉高压(PH)进行了肺动脉(PA)的超声生物力学研究,试将PH患者肺动脉血管的生物力学性质参数用于临床评估PH。方法选择先天性心脏病室间隔缺损并肺动脉高压患者,同步记录肺动脉压力与肺动脉二维图像,从PA收缩加压与扩张开始点到PA达到压力或扩展最大程度时点,界定为10个测量时点、9个递增步骤,分别测量每个时点的PA内径值及收缩压数值及其递增量,然后使用血管生物力学数学模型分析其肺动脉应力-应变关系。结果随着PA压力的不断上升,PA血管内径的扩展性也逐渐受限,尤其是阻力型PH组的PA内径扩张明显受限制,阻力型PH组的肺动脉物质常数a值和b值的各个参数显著减小(P<0.001),表明肺动脉物质常数a值和b值在鉴别阻力型PH方面具有一定的预测作用。结论肺动脉超声生物力学方法在评估与选择先天性心脏病合并PH患者手术适应证方面具有一定的参考作用。     

肺动脉高压的肺动脉血管超声生物力学研究

目的采用超声成像技术与生物力学方法相结合的方法,对肺动脉高压(PH)进行了肺动脉(PA)的超声生物力学研究,试将PH患者肺动脉血管的生物力学性质参数用于临床评估PH。方法选择先天性心脏病室间隔缺损并肺动脉高压患者,同步记录肺动脉压力与肺动脉二维图像,从PA收缩加压与扩张开始点到PA达到压力或扩展最大程度时点,界定为10个测量时点、9个递增步骤,分别测量每个时点的PA内径值及收缩压数值及其递增量,然后使用血管生物力学数学模型分析其肺动脉应力-应变关系。结果随着PA压力的不断上升,PA血管内径的扩展性也逐渐受限,尤其是阻力型PH组的PA内径扩张明显受限制,阻力型PH组的肺动脉物质常数a值和b值的各个参数显著减小(P<0.001),表明肺动脉物质常数a值和b值在鉴别阻力型PH方面具有一定的预测作用。结论肺动脉超声生物力学方法在评估与选择先天性心脏病合并PH患者手术适应证方面具有一定的参考作用。     

Calpain inhibition preserves talin and attenuates right heart failure in acute pulmonary hypertension

Right heart failure from right ventricular (RV) pressure overload is a major cause of morbidity and mortality, but its mechanism is incompletely understood. We tested the hypothesis that right heart failure during 4 hours of RV pressure overload is associated with alterations of the focal adhesion protein talin, and that the inhibition of calpain attenuates RV dysfunction and preserves RV talin. Anesthetized open-chest pigs treated with the calpain inhibitor MDL-28170 (n = 20) or inactive vehicle (n = 23) underwent 4 hours of RV pressure overload by pulmonary artery constriction (initial RV systolic pressure, 64 ± 1 and 66 ± 1 mm Hg in MDL-28170 and vehicle-treated pigs, respectively). Progressive RV contractile dysfunction was attenuated by MDL-28170: after 4 hours of RV pressure overload, RV systolic pressure was 44 ± 4 mm Hg versus 49 ± 6 mm Hg (P = 0.011), and RV stroke work was 72 ± 5% of baseline versus 90 ± 5% of baseline, (P = 0.027), in vehicle-treated versus MDL-28170-treated pigs, respectively. MDL-28170 reduced the incidence of hemodynamic instability (death or systolic blood pressure of < 85 mm Hg) by 46% (P = 0.013). RV pressure overload disrupted talin organization. MDL-28170 preserved talin abundance in the RV free wall (P = 0.039), and talin abundance correlated with the maintenance of RV free wall stroke work (r = 0.58, P = 0.0039). α-actinin and vinculin showed similar changes according to immunohistology. Right heart failure from acute RV pressure overload is associated with reduced talin abundance and disrupted talin organization. Calpain inhibition preserves the abundance and organization of talin and RV function. Calpain inhibition may offer clinical utility in treating acute cor pulmonale.     

Influence of Vessel Distension and Myogenic Tone on Pulmonary Arterial Input Impedance. A Study using a Computer Model of Rabbit Lung

A computer model of the pulmonary arterial (PA) bed of rabbit lungs was designed in order to test experimental observations of changes in PA input impedance and pulsatile hydraulic power (cap.) during increased PA pressure. The computer model was based on a simple 3-component analog representation of single vessels (i.e. resistance, inertance and compliance). 16 generations of arterial vessels, from PA to 60 μm diameter, were combined to calculate PA input impedance. Input impedance was found to mimic closely that observed experimentally. Both venous pressure elevation and arteriolar constriction was found to reduce input impedance and Wp. By combining arteriolar constriction with increased myogenic tone of the larger arteries, Wp was found to show a minimum level at a certain PA pressure, dependent on the degree of arterial stiffening. Wp was found to follow changes in arterial volume and resistance during simulated vasoconstriction. Wp dissipation in arterial vessels was calculated to approx. 50% of total input Wp at physiological pressure conditions, and could be reduced by one half after PA pressure increase from 20 to 50 cm H₂O, despite a concurrent halving of arterial compliance. Arterial vessels smaller than 200 pm diameter were found to have negligible direct influence on PA input impedance.     

Comparative effects of isosorbide dinitrate, prednisolone, indomethacin, and elastase on the development of monocrotaline-induced pulmonary hypertension

The pathogenesis of monocrotaline-induced pulmonary hypertension is not clear. Progressive pulmonary arteritis leading to vascular sclerosis, narrowing of the lumina, and thrombosis is the suspected sequence. To investigate this, we examined the effect of isosorbide dinitrate (ISDN), prednisolone, indomethacin, and elastase in 100 SD male rats, 4 weeks after the injection of monocrotaline (MCT) by cardiac catheterization, right ventricle-to-left ventricle plus septum weight ratio (RV/LV + S), histology, and electron microscopy. ISDN, a vasodilator, reduced the elevation of right ventricular (RV) pressure, RV/LV + S, and also pulmonary vascular remodeling; the characteristic histological feature was dilatation of small pulmonary arteries. Both prednisolone and indomethacin reduced RV pressure, RV/LV + S, and pulmonary vasculitis. Elastase, a protease which controls the metabolism of elastin in the arterial wall, likewise reduced RV pressure, RV/LV + S, and pulmonary vascular remodeling, with a significant decrease in elastosis of the small pulmonary arteries histologically. We concluded that all of the pathological processes resulting from arteritis are important in the development of MCT-induced pulmonary hypertension. In all experimental groups, decreased histopathologic changes correlated with decrease in the pressure. Elastase, which reduces pulmonary arterial sclerosis, is suggested as a new agent to treat pulmonary hypertension.     

Arterial compliance and stiffness following low-intensity resistance exercise

Purpose

Although acute high-intensity resistance exercise to exhaustion decreases arterial compliance and increases arterial stiffness, the effect of low-intensity resistance exercise (LRE) to exhaustion on arterial compliance and stiffness remains unknown. The present study investigated the acute effects of LRE on arterial compliance and stiffness.

Methods

Ten healthy individuals (age 26 ± 5 years) performed LRE (40 % of 1 repetition maximum) and control (CON: seated rest in the exercise room) trials on separate days in a randomized controlled crossover fashion. The LRE comprised three sets of bench presses to exhaustion with an inter-set rest period of 2 min. In the CON trial, LRE was not performed. Carotid arterial compliance, the β-stiffness index (via simultaneous B-mode ultrasound and applanation tonometry), carotid and brachial blood pressure and heart rate were measured before and at 30 and 60 min after both trials.

Results

Carotid arterial compliance and the β-stiffness index significantly increased and decreased, respectively (both P < 0.05), at 30 and 60 min after the LRE trials, but neither significantly differed after the CON trials. Carotid and brachial blood pressure and heart rate did not change at 30 and 60 min after both trials from baseline.

Conclusion

These results suggest that LRE acutely increases arterial compliance and decreases arterial stiffness.     

Left and right ventricular diastolic function during acute pericardial tamponade

The aim of the study was to determine the effect of acute pericardial tamponade on left (LV) and right ventricular (RV) intracavitary and transmural pressure-volume (P-V) relations and to assess the effect of changing blood volume during tamponade on LV and RV volumes. The experiments were done in 11 acutely instrumented anaesthetized dogs in which LV and RV volumes were determined by computed tomography (CT) (n = 5) and LV and RV diameters by sonomicrometry (n = 6). Pressures were measured in the pericardium (balloon transducer), in the aorta and in the ventricles. Incremental pericardial infusion (up to 180 ml) caused a progressive left and upward shift of the LV and the RV intracavitary P-V relationship. This shift was entirely due to increased pericardial pressure (PP). The induction of tamponade caused no change in the LV and RV transmural P-V relationship. During tamponade with ventricular filling pressures above 10-15 mmHg, blood volume expansion caused only minimal increase in LV and RV volumes. In conclusion, pericardial tamponade shifted the LV and the RV intracavitary diastolic P-V relation by increasing PP. However, there was no change in the transmural P-V relationship, indicating unchanged myocardial compliance. Volume loading caused only minimal increase in LV and RV volumes during tamponade.     

Some Physical Properties of the Pulmonary Arterial Bed Deduced from Pulsatile Arterial Flow and Pressure

This study aimed to quantify changes of vascular compliance and resistance of the proximal and the peripheral pulmonary arterial vessels when vascular smooth muscle was stimulated. These above vascular characteristics were derived from registrations of pulsatile pressure and flow in the pulmonary artery (PA). An in situ cat lung preparation was used, with the right heart by-passed by a pulsatile blood pump. Vascular input impedance was derived from PA pulsatile pressure and flow recordings, and impedance characteristics were used for calculation of the variables of a simple lumped analog representation of the arterial bed. PA smooth muscle was stimulated by infusions of collagen suspension, by general hypoxia and by nor-adrenaline injections. Collagen caused 40% reduction of vascular compliance (C), no changes in proximal arterial resistance (Rl) and 18076 increase in peripheral vascular resistance (R2). Hypoxia caused 5096 reduced C, 20% increased R1 and 70% increased R2. Noradrenaline caused 20:6 reduced C and 30 % increased R1 and R2. These results, together with results derived from simulation of the observed impedance changes in a computer model of the lung arterial bed, indicated that collagen infusion elicited contraction of small and medium-sized arteries, with increased arterial volume as result of increased distending pressure. Hypoxia and noradrenaline, seemed both to cause contraction of the total arterial bed. This effect being most pronounced during hypoxia.     

Arterial haemodynamics on ventricular hypertrophy in rats with simulated aortic stiffness

Aortic stiffness (AS) exerts significant impact on the cardiovascular risks. We developed a new model to produce AS. The purposes were to evaluate the haemodynamic consequence and to correlate the haemodynamic parameters with the extent of ventricular hypertrophy (VH). We applied silicon gel for embedding of the abdominal and/or thoracic aorta. After 1–4 weeks of AS, the left ventricular weight (LVW), LVW to body weight (BW) ratio (LVW/BW), and the morphological changes in cardiomyotes were quantified for VH. We determined the aortic pressure (AP), stroke volume, cardiac output, total peripheral resistance (TPR), characteristic impedance (Zc), pulse wave reflection (P_b) and pulse wave velocity (PWV). Aortic embedding (AE) increased LVW, LVW/BW, systolic and pulse pressure (PP), Zc, P_b and PWV accompanied by decreases in diastolic pressure and arterial compliance. The magnitude of these haemodynamic and cardiac changes were in an order of combined, thoracic and abdominal AE. Correlation analysis revealed that the VH was well correlated with pulsatile haemodynamics such as Zc, PP, P_b and PWV, while less with steady components (Mean AP and TPR). Our results indicate that pulsatile haemodynamic parameters are significantly elevated after AS. The alterations in pulsatile haemodynamics are the major causes leading to VH.     

蛋白磷酸酶4显性负性突变体介导的活性抑制改善棕榈酸诱导的肝细胞脂性凋亡

目的 探讨抑制蛋白磷酸酶4(protein phosphatase 4,PP4)活性对肝细胞脂性凋亡的影响.方法 以400μmol/L的棕榈酸(palmitic acid,PA)处理HepG2细胞24 h建立肝细胞脂性凋亡模型;以西方饮食喂养C57BL/6J小鼠16w建立非酒精性脂肪肝炎(non-alcoholic s...     

In vivo hemodynamic responses to thoracic artificial lung attachment

A thoracic artificial lung (TAL) was attached to the pulmonary circulation in a porcine model. Proximal main pulmonary artery (PA) blood flow, in part or whole, was diverted to the TAL, and TAL outlet blood flow was split between the distal main PA and left atrium (LA). The right ventricle (RV) drove blood flow through the combined TAL/natural lung (NL) pulmonary system. Selective banding placed the TAL in parallel with the NLs, in series with the NLs, or in an intermediary hybrid configuration. Parallel TAL attachment lowered pulmonary system impedance, raised cardiac output (CO), and provided the greatest TAL blood flow rate, but reduced the NL blood flow rate which is important for pulmonary embolic clearance and metabolic blood processing. Hybrid or series TAL attachment raised pulmonary system impedance, lowered CO, increased RV oxygen consumption, and reduced RV oxygen supply. Redesign of the PA anastomoses, TAL inlet graft, and TAL entrance and exit would significantly improve hemodynamics and RV function with TAL attachment. Mean LA pressure increased throughout the experiment, which may indicate damage caused by graft attachment to the LA. Pulmonary resistance-flow rate curves may enable clinical prediction of tolerable TAL attachment configurations.     

Novel computed tomographic chest metrics to detect pulmonary hypertension

Background  

Early diagnosis of pulmonary hypertension (PH) can potentially improve survival and quality of life. Detecting PH using echocardiography is often insensitive in subjects with lung fibrosis or hyperinflation. Right heart catheterization (RHC) for the diagnosis of PH adds risk and expense due to its invasive nature. Pre-defined measurements utilizing computed tomography (CT) of the chest may be an alternative non-invasive method of detecting PH.