ABSTRACT
Introduction: Myriad disorders cause right ventricular (RV) dilation and lead to tricuspid regurgitation (TR). Because the thin-walled, flexible RV is mechanically coupled to the pulmonary circulation and the left ventricular septum, it distorts with any disturbance in the cardiopulmonary system. TR, therefore, can result from pulmonary hypertension, left heart failure, or intrinsic RV dysfunction; but once it occurs, TR initiates a cycle of worsening RV volume overload, potentially progressing to right heart failure. Characteristic three-dimensional RV shape-changes from this process, and changes particular to individual TR causes, have not been defined in detail. Methods: Cardiac MRI was obtained in 6 healthy volunteers, 41 patients with ≥ moderate TR, and 31 control patients with cardiac disease without TR. The mean shape of each group was constructed using a three-dimensional statistical shape model via the particle-based shape modeling approach. Changes in shape were examined across pulmonary hypertension and congestive heart failure subgroups using principal component analysis (PCA). A logistic regression approach based on these PCA modes identified patients with TR using RV shape alone. Results: Mean RV shape in patients with TR exhibited free wall bulging, narrowing of the base, and blunting of the RV apex compared to controls (p < 0.05). Using four primary PCA modes, a logistic regression algorithm identified patients with TR correctly with 82% recall and 87% precision. In patients with pulmonary hypertension without TR, RV shape was narrower and more streamlined than in healthy volunteers. However, in RVs with TR and pulmonary hypertension, overall RV shape continued to demonstrate the free wall bulging characteristic of TR. In the subgroup of patients with congestive heart failure without TR, this intermediate state of RV muscular hypertrophy was not present. Conclusion: The multiple causes of TR examined in this study changed RV shape in similar ways. Logistic regression classification based on these shape changes reliably identified patients with TR regardless of etiology. Furthermore, pulmonary hypertension without TR had unique shape features, described here as the "well compensated" RV. These results suggest shape modeling as a promising tool for defining severity of RV disease and risk of decompensation, particularly in patients with pulmonary hypertension.
ABSTRACT
Tricuspid regurgitation (TR) is a failure in right-sided AV valve function which, if left untreated, leads to marked cardiac shape changes and heart failure. However, the specific right ventricular shape changes resulting from TR are unknown. The goal of this study is to characterize the RV shape changes of patients with severe TR. RVs were segmented from CINE MRI images. Using particle-based shape modeling (PSM), a dense set of homologous landmarks were placed with geometric consistency on the endocardial surface of each RV, via an entropy-based optimization of the information content of the shape model. Principal component analysis (PCA) identified the significant modes of shape variation across the population. These modes were used to create a patient-prediction model. 32 patients and 6 healthy controls were studied. The mean RV shape of TR patients demonstrated increased sphericity relative to controls, with the three most dominant modes of variation showing significant widening of the short axis of the heart, narrowing of the base at the RV outflow tract (RVOT), and blunting of the RV apex. By PCA, shape changes based on the first three modes of variation correctly identified patient vs. control hearts 86.5% of the time. The shape variation may further illuminate the mechanics of TR-induced RV failure and recovery, providing potential targets for therapies including novel devices and surgical interventions.
ABSTRACT
BACKGROUND: Therapy for moderate ischemic mitral regurgitation remains unclear. Determination of myocardial viability, a necessary prerequisite for an improvement in regional contractility, is a likely key factor in determining response to revascularization alone. Myocardial strain has been proposed as a viability measure but has not been compared with late gadolinium enhancement (LGE) cardiac magnetic resonance imaging. We hypothesized that abnormal strain overestimates nonviable left ventricular (LV) segments measured with LGE and that ischemia and mechanical tethering by adjacent transmural myocardial infarction (TMI) also decreases strain in viable segments. METHODS: Sixteen patients with mild or greater ischemic mitral regurgitation and 7 healthy volunteers underwent cardiac magnetic resonance imaging with noninvasive tags (complementary spatial modulation of magnetization [CSPAMM]), LGE, and stress perfusion. CSPAMM images were post-processed with harmonic phase and circumferential and longitudinal strains were calculated. Viability was defined as the absence of TMI on LGE (hyperenhancement >50% of wall thickness). The borderzone was defined as any segment bordering TMI. Abnormal strain thresholds (±1 to 2.5 SDs from normal mean) were compared with TMI, ischemia, and borderzone. RESULTS: 7.4% of LV segments had TMI on LGE, and more than 14.5% of LV segments were nonviable by strain thresholds (p < 0.005). In viable segments, ischemia impaired longitudinal strain (least perfused one-third of LV segments: -0.18 ± 0.08 versus most perfused: -0.22 ± 0.1, p = 0.01) and circumferential strain (-0.12 ± 0.1 versus -0.16 ± 0.08, p < 0.05). In addition, infarct proximity impaired longitudinal strain (-0.16 ± 0.11 borderzone versus -0.18 ± 0.09 remote, p = 0.05). CONCLUSIONS: Impaired LV strain overestimates nonviable myocardium compared with TMI on LGE. Ischemia and infarct proximity also decrease strain in viable segments.
