Interventricular Mechanical Asynchrony in Pulmonary Arterial Hypertension

Marcus, J. Tim; Gan, C. Tji-Joong; Zwanenburg, Jaco J.M.; Boonstra, Anco; Allaart, Cor; Götte, Marco J.W.; Vonk‐Noordegraaf, Anton

doi:10.1016/j.jacc.2007.10.041

Cited by 369 publications

(101 citation statements)

References 22 publications

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“…Late systolic ventricular septal flattening and abnormal RV outflow tract Doppler flow (short acceleration time and notching attributable to reflected pressure waves) are consistent with elevated pulmonary impedance causing prolonged RV contraction and elevated PVR, respectively (case, Figure 3A), and help to distinguish resistive from passive PH-CHD 11,12 ; there are also quantitative echocardiographic methods to estimate PVR. [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: 93%

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

Opotowsky

2015

Circulation

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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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Section: Diagnosis: Echocardiographymentioning

confidence: 93%

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

Opotowsky

2015

Circulation

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“…92 Of interest, in these cases, the RV will contract after closure of the pulmonary valve, resulting in a so-called postsystolic contraction period. 93 Ventricular interdependency should be clearly interpreted as a sign of RV failure and can be measured by MRI by assessing the RV septum configuration 94 and differences in contraction time 92 or by the impact of ventricular interdependency on LV volumes. …”

Section: Ventricular Interdependencymentioning

confidence: 99%

Noninvasive Imaging in the Assessment of the Cardiopulmonary Vascular Unit

et al. 2015

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899N oninvasive imaging plays a key role in both the diagnosis and management of patients with pulmonary hypertension (PH). In recent years, there have been 2 major changes in perspective of imaging in PH. The first was the realization that imaging should focus on the evaluation of not only the pulmonary pressures but also the cardiopulmonary unit ( Figure 1). 1,2The second was the emergence of multimodality imaging with a complementary role for echocardiography, magnetic resonance (MRI), computed tomography, and positron emission tomography (PET).2-7 These techniques not only help in the diagnosis of PH but also help identify factors that determine risk and prognosis and gauge therapeutic effects on right ventricular (RV) function in patients with pulmonary arterial hypertension (PAH). Although echocardiography is the mainstay in the assessment of hemodynamic and ventricular function in PH, MRI has emerged as the gold standard for quantifying volumes, function, and flow in the right side of the heart. 2-7 PET is also offering novel insights into perfusion and blood flow, metabolism, neurohormonal activation, and other molecular processes in the right side of the heart but is used mainly for research at this time. Catheterization of the right side of the heart remains the gold standard for defining PH and assessing hemodynamics both at rest and with exercise. Invasive assessment of cardiac output (CO) may, however, have limited accuracy when assumed instead of measured oxygen consumption is used to derive CO (eg, using the Fick method) or when thermodilution is used in the setting of a low-CO state. [8][9][10] This review covers RV imaging studies performed in the field of PH and discusses recent advances in echocardiography and cardiac MRI and PET imaging for detailed assessment of RV function. The review starts with a discussion of important physiological considerations and unmet needs in imaging research of the right side of the heart in PH. Computed tomography angiography, which plays an important role in evaluating chronic thromboembolic PH, is not discussed extensively in this review. Physiological ConsiderationsAlthough PH is a syndrome affecting the pulmonary vasculature, survival of patients with PH is closely related to RV function. 1,[11][12][13][14] The RV initially adapts to the increased afterload by increasing its wall thickness and contractility. These mechanisms are, however, often insufficient, and RV dysfunction eventually occurs. After the recent Fifth World Symposium on Pulmonary Hypertension, a definition of failure of the right side of the heart secondary to PH was adopted: "Right heart failure in the setting of PH can be defined as a complex clinical syndrome due to a suboptimal delivery of blood or elevated systemic venous pressure at rest or exercise as a consequence of elevated RV afterload."2 The proposed definition takes into account both the systolic and diastolic characteristics of function of the right side of the heart, as well as physiological demands such as exercise.In underst...

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“…Pulmonary artery (PA) systolic pressure (PASP) was calculated as (PASP (mmHg) = RVSp + 5mmHg). For RV end-systolic wall stress, Laplace's law was used to calculate according to the formula Pr/2h where P (pressure) was quantified as PASP, r (radius) was calculated using the formula r = 0.620(RVSa) 1 3 , assuming spherical geometry as previously described (Marcus et al 2008) and h was quantified as RV wall thickness. RVOT (RV outflow tract) peak velocity and velocity time integral (VTI) were obtained using pulsed wave (PW) Doppler and RV stroke volume (ml)…”

Section: Conventional Echocardiographymentioning

confidence: 99%

The right ventricle following ultra-endurance exercise: insights from novel echocardiography and 12-lead electrocardiography

et al. 2014

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Purpose: There is contradictory evidence related to the impact of ultra-marathon running on right ventricular (RV) structure and function. Consequently, the aims of this study were to; 1) comprehensively assess RV structure and function before and immediately following a 100 mile ultramarathon in highly trained runners, 2) determine the nature of RV recovery 6 hours post-race, and 3) document 12-lead electrocardiogram (ECG) changes post-exercise.Methods: Echocardiography and 12-lead ECG were assessed in 15 competitors in a repeated measures design before and immediately after completion of the 2013 Western States Endurance Race. A subset of 9 were reassessed 6 hours into recovery. Standard echocardiography was used to determine RV size, function and wall stress. Myocardial speckle tracking (MST) provided peak, time to peak and temporal indices for RV longitudinal strain and strain rates (ε and SR).Results: RV size was increased post-race (inflow tract 14 %, outflow tract 11 %, P = 0.004 and 0.002). RV wall stress was elevated by 11 % post-race. Peak RV ε was reduced by 10 % (P = 0.007) and significantly delayed post-race (P = 0.008). Most changes in RV function persisted at the 6 hour assessment. Post-race there was an increase in the prevalence of right-sided ECG changes. Conclusions:Completion of a 100 mile ultra-marathon resulted in acute changes in RV structure and function that persisted 6 hours into recovery and are consistent with sustained exposure to an elevated RV wall stress. These findings were supported by right sided changes to the 12-Lead ECG.

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Interventricular Mechanical Asynchrony in Pulmonary Arterial Hypertension

Abstract: In PAH, the L-R delay in myocardial peak shortening is caused by lengthening of the duration of RV shortening. This L-R delay is related to LVSB, decreased LV filling, and decreased stroke volume.

Cited by 369 publications

References 22 publications

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

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

Noninvasive Imaging in the Assessment of the Cardiopulmonary Vascular Unit

The right ventricle following ultra-endurance exercise: insights from novel echocardiography and 12-lead electrocardiography

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