Pulmonary Artery Acceleration Time Provides an Accurate Estimate of Systolic Pulmonary Arterial Pressure during Transthoracic Echocardiography

Yared, Kibar; Noseworthy, Peter A.; Weyman, Arthur E.; McCabe, Elizabeth L.; Picard, Michael H.; Baggish, Aaron L.

doi:10.1016/j.echo.2011.03.008

Cited by 157 publications

(152 citation statements)

References 27 publications

(33 reference statements)

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“…PAAT increased over the 10-week normoxic recovery in both groups, and although SuHx mice had lower PAAT than VeHx mice after 10 weeks of recovery, this difference was not significant. PAAT is known to become shorter with higher RV and PA pressure in both humans and animals, [24][25][26][27][28][29][30][31][32] and it is a useful marker of PH in small animals that do not reliably develop quantifiable tricuspid regurgitation. PAAT has been hypothesized to be shorter in PH because of the reduced compliance and increased impedance of the pulmonary arterial system, 33 and it may provide additional information about these important parameters (compliance and impedance) when compared with invasively measured RV pressure.…”

Section: Discussionmentioning

confidence: 99%

The Sugen 5416/Hypoxia Mouse Model of Pulmonary Hypertension Revisited: Long‐Term Follow‐Up

et al. 2014

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a SHV and GH contributed equally to this work.Abstract: The combination of a vascular endothelial growth factor receptor antagonist, Sugen 5416 (SU5416), and chronic hypoxia is known to cause pronounced pulmonary hypertension (PH) with angioobliterative lesions in rats and leads to exaggerated PH in mice as well. We sought to determine whether weekly SU5416 injections during 3 weeks of hypoxia leads to long-term development of angioobliterative lesions and sustained or progressive PH in mice. Male C57BL/6J mice were injected with SU5416 (SuHx) or vehicle (VehHx) weekly during 3 weeks of exposure to 10% oxygen. Echocardiographic and invasive measures of hemodynamics and pulmonary vascular morphometry were performed after the 3-week hypoxic exposure and after 10 weeks of recovery in normoxia. SuHx led to higher right ventricular (RV) systolic pressure and RV hypertrophy than VehHx after 3 weeks of hypoxia. Ten weeks after hypoxic exposure, RV systolic pressure decreased but remained elevated in SuHx mice compared with VehHx or normoxic control mice, but RV hypertrophy had resolved. After 3 weeks of hypoxia and 10 weeks of followup in normoxia, tricuspid annular plane systolic excursion was significantly decreased, indicating decreased systolic RV function. Very few angioobliterative lesions were found at the 10-week follow-up time point in SuHx mouse lungs. In conclusion, SU5416 combined with 3 weeks of hypoxia causes a more profound PH phenotype in mice than hypoxia alone. PH persists over 10 weeks of normoxic follow-up in SuHx mice, but significant angioobliterative lesions do not occur, and neither PH nor RV dysfunction worsens. The SuHx mouse model is a useful adjunct to other PH models, but the search will continue for a mouse model that better recapitulates the human phenotype.

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Section: Discussionmentioning

confidence: 99%

The Sugen 5416/Hypoxia Mouse Model of Pulmonary Hypertension Revisited: Long‐Term Follow‐Up

et al. 2014

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“…31 The PAAT can also provide useful information that aids in the accuracy of PH diagnosis. Limitations of this method are that, in patients with left-to-right shunts, the PAAT should be interpreted carefully 35 and that absolute PAAT values are very much heart rate dependent; the ratio of PAAT to PA ejection time has therefore been proposed to correct for the shortening of ejection with higher heart rates.…”

Section: Pa Acceleration Timementioning

confidence: 99%

Section: Pa Acceleration Timementioning

confidence: 99%

“…31 The forward flow velocity profile, obtained in the PA just distal to the pulmonary valve, is used to obtain the PAAT. 31 In adults at risk for PAH, a PAAT of less than 100 ms indicates a high probability of increased PAP. 32 A PAAT > 100 ms suggests that there is no PAH, whereas a PAAT < 100 ms would increase the likelihood that PAH is present.…”

Section: Pa Acceleration Timementioning

confidence: 99%

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Transthoracic Echocardiography in the Evaluation of Pediatric Pulmonary Hypertension and Ventricular Dysfunction

et al. 2016

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Transthoracic echocardiography (TTE) is the most accessible noninvasive diagnostic procedure for the initial assessment of pediatric pulmonary hypertension (PH). This review focuses on principles and use of TTE to determine morphologic and functional parameters that are also useful for follow-up investigations in pediatric PH patients. A basic echocardiographic study of a patient with PH commonly includes the hemodynamic calculation of the systolic pulmonary artery pressure (PAP), the mean and diastolic PAP, the pulmonary artery acceleration time, and the presence of a pericardial effusion. A more detailed TTE investigation of the right ventricle (RV) includes assessment of its size and function. RV function can be evaluated by RV longitudinal systolic performance (e.g., tricuspid annular plane systolic excursion), the tricuspid regurgitation velocity/right ventricular outflow tract velocity time integral ratio, the fractional area change, tissue Doppler imaging-derived parameters, strain measurements, the systolic-to-diastolic duration ratio, the myocardial performance (Tei) index, the RV/left ventricle (LV) diameter ratio, the LV eccentricity index, determination of an enlarged right atrium and RV size, and RV volume determination by 3-dimensional echocardiography. Here, we discuss the potential use and limitations of TTE techniques in children with PH and/or ventricular dysfunction. We suggest a protocol for TTE assessment of PH and myocardial function that helps to identify PH patients and their response to pharmacotherapy. The outlined protocol focuses on the detailed assessment of the hypertensive RV; RV-LV crosstalk must be analyzed separately in the evaluation of different pathologies that account for pediatric PH.

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“…Mean pulmonary arterial pressure (PAP) was figured out by the formula of 79-(0.45X pulmonary artery acceleration time) (13,14).…”

Section: Echocardiographymentioning

confidence: 99%

Effects of right ventricular dysfunction on exercise capacity and quality of life and associations with serum NT-proBNP levels in COPD: an observational study

Özdemirel¹,

Ulaşlı²,

Yetis³

et al. 2014

Anadolu Kardiyol Derg

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Objective: During the course of chronic obstructive pulmonary disease (COPD), pulmonary hypertension (PH) and right ventricular (RV) failure may develop due to elevated afterload of the RV. In those patients, exercise capacity is reduced due to pulmonary and cardiac limitations. We investigated relationships between serum N-terminal of proB-type natriuretic peptide (NT-proBNP) and RV functions with exercise capacity and quality of life in patients COPD.Methods: An observational case-control study was conducted. We enrolled 31 moderate and severe COPD patients, and 20 subjects without chronic diseases as control group. Parameters reflecting the right ventricular diastolic and systolic functions by echocardiography along with serum NT-proBNP levels were assessed. Cardiopulmonary exercise testing and Short Form-36 (SF-36) were applied. Results: Serum NT-proBNP levels were higher in COPD patients than control group (p=0.003). Serum NT-proBNP level was found to be related with pulmonary arterial pressure. Serum NT-proBNP levels were negatively correlated with anaerobic threshold oxygen uptake (AT VO 2 ) and peak oxygen uptake (PVO 2 ) values. Early ventricular filling velocity (Em) was lower in COPD patients. Em wave was significantly correlated with O 2 pulse. There was a positive relationship between tricuspid E/A ratio and VO 2 value at AT. SF-36 domains of physical functioning, general health and role limitation due to physical disorder were significantly correlated with AT VO 2 , PVO 2 and O 2 pulse. Conclusion: Exercise limitation may be predicted by assessment of right ventricule functions and NT-proBNP levels and exercise limitation impairs quality of life in COPD patients.

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Pulmonary Artery Acceleration Time Provides an Accurate Estimate of Systolic Pulmonary Arterial Pressure during Transthoracic Echocardiography

Cited by 157 publications

References 27 publications

The Sugen 5416/Hypoxia Mouse Model of Pulmonary Hypertension Revisited: Long‐Term Follow‐Up

The Sugen 5416/Hypoxia Mouse Model of Pulmonary Hypertension Revisited: Long‐Term Follow‐Up

Transthoracic Echocardiography in the Evaluation of Pediatric Pulmonary Hypertension and Ventricular Dysfunction

Effects of right ventricular dysfunction on exercise capacity and quality of life and associations with serum NT-proBNP levels in COPD: an observational study

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