A Simple Echocardiographic Method to Estimate Pulmonary Vascular Resistance

Opotowsky, Alexander R.; Clair, Mathieu; Afilalo, Jonathan; Landzberg, Michael J.; Waxman, Aaron B.; Moko, Lilamarie; Maron, Bradley A.; Vaidya, Anjali; Forfia, Paul R.

doi:10.1016/j.amjcard.2013.05.016

Cited by 59 publications

(62 citation statements)

References 27 publications

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“…Interestingly, the Opotowsky method had a superior receiver-operating characteristic curve for discrimination of PVR >3 Wood units compared with the Abbas method. 41 Finally, Choi et al 42 showed that Definity dye transit time from peak opacification of right ventricle to first appearance in the left ventricle could be used to estimate PVR and cardiac output. In that study, the transit time for the contrast to travel from the right ventricle to the left ventricle was directly proportional to PVR and inversely proportional to cardiac output.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Pulse Wave Transit Time is Associated with Right Ventricular–Pulmonary Artery Coupling in Pulmonary Arterial Hypertension

et al. 2016

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Pulmonary pulse wave transit time (pPTT), defined as the time for the systolic pressure pulse wave to travel from the pulmonary valve to the pulmonary veins, has been reported to be reduced in pulmonary arterial hypertension (PAH); however, the underlying mechanism of reduced pPTT is unknown. Here, we investigate the hypothesis that abbreviated pPTT in PAH results from impaired right ventricular-pulmonary artery (RV-PA) coupling. We quantified pPTT using pulsed-wave Doppler ultrasound from 10 healthy age-and sexmatched controls and 36 patients with PAH. pPTT was reduced in patients with PAH compared with controls. Univariate analysis revealed the following significant predictors of reduced pPTT: age, right ventricular fractional area change (RV FAC), tricuspid annular plane excursion (TAPSE), pulmonary arterial pressures (PAP), diastolic pulmonary gradient, transpulmonary gradient, pulmonary vascular resistance, and RV-PA coupling (defined as RV FAC/mean PAP or TAPSE/mean PAP). Although the correlations between pPTT and invasive markers of pulmonary vascular disease were modest, RV FAC (r = 0.64, P < 0.0001), TAPSE (r = 0.67, P < 0.0001), and RV-PA coupling (RV FAC/mean PAP: r = 0.72, P < 0.0001; TAPSE/mean PAP: r = 0.74, P < 0.0001) had the strongest relationships with pPTT. On multivariable analysis, only RV FAC, TAPSE, and RV-PA coupling were independent predictors of pPTT. We conclude that shortening of pPTT in patients with PAH results from altered RV-PA coupling, probably occurring as a result of reduced pulmonary arterial compliance. Thus, pPTT allows noninvasive determination of the status of both the pulmonary vasculature and the response of the RV in patients with PAH, thereby allowing monitoring of disease progression and regression.Keywords: pulse wave velocity, right ventricular-pulmonary artery coupling, echocardiography. Pulmonary arterial hypertension (PAH) is a lethal disease, characterized by pathological pulmonary vascular remodeling, that leads to elevated pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR), decreased pulmonary arterial compliance, and eventual right ventricular failure and death.1,2 Growing evidence suggests that pulmonary arterial compliance plays a critical role in the pathogenesis of PAH and right ventricular failure. 3 Decreased pulmonary arterial compliance causes premature reflection of waves from the distal pulmonary vasculature, leading to increased pulsatile right ventricular afterload and altered right ventricular-pulmonary artery (RV-PA) coupling. 3-5 Both loss of pulmonary arterial compliance and impaired RV-PA coupling are clinically important, because they are associated with increased mortality in patients with pulmonary hypertension. 6-11Pulse wave velocity, defined as the velocity of pressure waves traveling through the arterial system, correlates inversely with arterial compliance in the systemic circulation.12 With decreasing compliance, pulse wave velocity increases, and the time taken by the pressure wave to travel between...

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Section: Discussionmentioning

confidence: 99%

Pulmonary Pulse Wave Transit Time is Associated with Right Ventricular–Pulmonary Artery Coupling in Pulmonary Arterial Hypertension

et al. 2016

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“…Whenever TR or PR was detected the Doppler beam was aligned as parallel as possible with the regurgitant flow in order to determine peak velocities and calculate peak pressure gradient (PG) using the modified Bernoulli equation (P ¼ 4 Â V max 2 ) and estimate peak systolic and mean PAP, respectively. Estimated right atrial pressures were not added to the calculated TR gradient, but a fixed right atrial pressure was added for calculating PVR (see in the following) [27]. Pulmonary hypertension was defined as a peak TR >2.8 m/s (estimated systolic PAP >30 mmHg) and/or peak PR >2.2 m/s (estimated d Vivid 7, GE Medical Systems, Munich, Germany.…”

Section: Animals Materials and Methodsmentioning

confidence: 99%

“…In cases in which no regurgitant jet was present hemodynamically significant PH was defined by the presence of RV hypertrophy/ dilatation, septal flattening, dilated main pulmonary artery in the absence of pulmonic stenosis and decreased left ventricle (LV) chamber size [28]. Pulmonary vascular resistance was calculated from estimated systolic pulmonary arterial pressure (sPAP) using a constant right atrial pressure of 8 mmHg (sPAP ¼ 8 þ 4 Â TR2) and RV outflow tract time-velocity integral using the following formula: PVR ¼ sPAP/RV outflow tract timevelocity integral þ 3 if mid-systolic notch (type III) [27]. Pulsed wave tissue Doppler imaging was performed to evaluate RV longitudinal myocardial velocities at the tricuspid lateral annulus using a standard left apical four-chamber view.…”

Section: Animals Materials and Methodsmentioning

confidence: 99%

Intrapulmonary arteriovenous anastomoses in dogs with severe Angiostrongylus vasorum infection: clinical, radiographic, and echocardiographic evaluation

Matos

Malbon

Dennler

et al. 2016

Journal of Veterinary Cardiology

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“…[13][14][15] Left atrial size, tissue Doppler, and mitral inflow velocity patterns may identify elevated left atrial pressure (case, Figure 3B), although this does not preclude coexisting increases in PVR. …”

Section: Diagnosis: Echocardiographymentioning

confidence: 99%

Clinical Evaluation and Management of Pulmonary Hypertension in the Adult With Congenital Heart Disease

Opotowsky

2015

Circulation

Self Cite

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200P ulmonary hypertension (PH) refers to elevated pulmonary artery (PA) pressure (PAP), defined as mean PAP≥25 mm Hg. PH is not synonymous with pulmonary arterial hypertension (PAH), which specifies resistive PH characterized by elevated pulmonary vascular resistance (PVR) and normal pulmonary venous pressure. Approximately 5% to 10% of adults with congenital heart disease (CHD) have PH, and this subset of CHD patients is at higher risk of hospitalization and death. [1][2][3] Understanding the epidemiology of PH associated with CHD (PH-CHD) is not straightforward, however, because definitions of PH-CHD and diagnostic techniques vary. Appropriate diagnosis and the management of PH-CHD rest on identifying the cause of elevated PAP: high pulmonary venous pressure, high pulmonary vascular resistance, high pulmonary flow, or some combination of these factors, which are referred to throughout this review as passive, resistive, hyperkinetic, and polygenic PH, respectively (Table 1).Prognosis in PH-CHD depends on the underlying cause, pulmonary vascular pathophysiology, and the interaction between the right heart and pulmonary circulation. Adult CHD is heterogeneous, with myriad permutations of underlying defects, previous interventions, and associated comorbidities. Although comprehensive understanding of clinical context is a prerequisite, identifying the optimal therapy for a patient with PH-CHD depends more heavily on an understanding of pathophysiology than it does on the underlying diagnosis. Therefore, the goal of this review is to frame an understanding of PH-CHD in terms of fundamental cardiopulmonary hemodynamic pathophysiology and to emphasize the clinical assessment and management of situations commonly encountered by adult cardiologists caring for patients with PH-CHD. Classifications of PH and PH-CHDClassification schemes in PH represent clinical perspectives of underlying pathophysiology and tend to parallel fundamental hemodynamic relationships of the pulmonary circulation. PVR

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A Simple Echocardiographic Method to Estimate Pulmonary Vascular Resistance

Cited by 59 publications

References 27 publications

Pulmonary Pulse Wave Transit Time is Associated with Right Ventricular–Pulmonary Artery Coupling in Pulmonary Arterial Hypertension

Pulmonary Pulse Wave Transit Time is Associated with Right Ventricular–Pulmonary Artery Coupling in Pulmonary Arterial Hypertension

Intrapulmonary arteriovenous anastomoses in dogs with severe Angiostrongylus vasorum infection: clinical, radiographic, and echocardiographic evaluation

Clinical Evaluation and Management of Pulmonary Hypertension in the Adult With Congenital Heart Disease

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