State of the art: advanced imaging of the right ventricle and pulmonary circulation in humans (2013 Grover Conference series)

Abstract

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by remodeling and vasoconstriction of the pulmonary vasculature, ultimately leading to right ventricular (RV) failure and death. Recent developments in echocardiography, cardiovascular magnetic resonance imaging, computed tomography, and positron emission tomography allow advanced, noninvasive, in vivo assessment of the RV and have contributed to the identification of risk factors, prognostic factors, and monitoring of therapeutic responses in patients with PAH. Although far from reaching its future potential, these techniques have not only provided global RV assessment but also allowed evaluation of changes in cellular and molecular tissue processes, such as metabolism, oxygen balance and ischemia, angiogenesis, and apoptosis. Integrated application of these techniques could provide full insights into the different pathophysiological aspects of a failing RV in the setting of PAH. Recent advances in hybrid imaging have implemented simultaneous measurements of myocardial and vascular interactions and will be one of the most important potential future developments.

Keywords: cardiovascular magnetic resonance imaging; echocardiography; positron emission tomography; pulmonary arterial hypertension; right ventricle.

Figure 1

The presence of ventricular dyssynchrony illustrated in a patient with pulmonary arterial hypertension (PAH) measured by cardiac magnetic resonance imaging (CMR) strain analysis. Circumferential strain curves reflect myocardial shortening (negative strain) and stretching (positive stain) over time of the cardiac cycle for the right ventricular (RV) free wall (blue), left ventricular (LV) free wall (red), and interventricular septum (black). The LV, RV, and septum start simultaneously with shortening. However, RV peak shortening occurs later than LV peak shortening in the cardiac cycle. The aortic and pulmonary valves close (T_aortacl and T_pulmcl) at the time of LV peak shortening. The time of maximal leftward septal bowing (T_lvsb) occurs coincidently with septal stretching and with peak shortening of the RV. T_mitr-op and T_tric-op indicate the opening times of the mitral and tricuspid valves and indicate the onset of LV and RV filling.

Figure 2

Impaired right ventricular (RV) mechanical efficiency in patients with idiopathic pulmonary arterial hypertension (IPAH) is primarily determined by increased myocardial oxygen consumption (MVO₂). Dark bars = New York Heart Association (NYHA) functional class III patients; light gray bars = NYHA functional class II patients. Cardiac output (CO) measured by cardiovascular magnetic resonance imaging (CMR) is higher in NYHA II patients than NYHA III patients (A), and mean pulmonary artery pressure (PAP) was similar in both groups (B). RV myocardial blood flow measured by positron emission tomography (PET) with H₂¹⁵O tracers (C) and oxygen (O₂) extraction fraction estimated by PET using ¹⁵O₂ tracers (D) were not statistically higher in NYHA III patients compared with NYHA II patients. RV power output (i.e., product of CO and mean PAP) was comparable in both groups (E). There was a significantly higher MVO₂ per gram of myocardial tissue in NYHA III patients compared with NYHA II patients (F). A similar RV power output but higher MVO₂ led to a significant reduction in RV mechanical efficiency (i.e., ratio of RV power output and MVO₂) of ˜50% in NYHA III patients compared with NYHA II patients (G). Reprinted with permission from Wong et al.

Figure 3

Representative perfusion maps showing that biventricular perfusion reserve was diminished in patients with pulmonary arterial hypertension (PAH) compared with controls. Cardiovascular magnetic resonance imaging perfusion maps of the right ventricle (RV) and left ventricle (LV) were obtained under resting conditions and after adenosine induced stress. Perfusion scales are on the right. Myocardial perfusion at rest in a healthy control subject (A) is significantly increased during adenosine stress (B). C, Resting myocardial perfusion in the hypertrophic RV of a patient with PAH. D, After adenosine stress, myocardial perfusion does not increase in both the LV and RV, illustrating that the perfusion reserve is limited in patients with PAH compared with controls. Reprinted with permission from Vogel-Claussen et al.

Figure 4

In vivo molecular imaging of angiogenesis in a patient after acute myocardial infarction. Two weeks after acute myocardial infarction and percutaneous coronary intervention, a patient underwent cardiovascular magnetic resonance imaging (CMR) and positron emission tomography (PET)/computed tomography (CT). CMR gadolinium delayed contrast enhancement (DCE) was observed almost transmural in the anterior, anteriorseptal, anteriorlateral, and apical left ventricle wall (A, D). PET imaging with ¹³N-ammonia revealed impaired myocardial blood flow in correspondence with the regions of DCE (arrows; B, E). PET with the agent ¹⁸F arginine-glycine-aspartic acid peptide (¹⁸F-RGD), with affinity for the integrins, demonstrated focal signal areas in the infarcted area (C, F). This signal may reflect angiogenesis within the healing area (arrows). Polar maps of myocardial blood flow assessed by PET with ¹³N-ammonia (G, I) show severely reduced blood flow in the distal left anterior descending coronary artery perfusion region. Co-localized ¹⁸F-RGD signal corresponded to the regions of reduced blood flow (H, J), demonstrating the extent of the integrin expression in the infarcted area. Reprinted with permission from Makowski et al.