Right Ventricular Failure in Patients With Preserved Ejection Fraction and Diastolic Dysfunction: An Underrecognized Clinical Entity

Abstract Background Severe mitral regurgitation (MR) induces significant changes not only in the left, but also in the right ventricular (RV) morphology and function. Early treatment of MR is recommended, however, surgical procedure disrupts the native RV contractile pattern and predisposes the at-risk ventricle to develop postoperative RV failure (RVF) which is associated with poor outcomes. Purpose Accordingly, the PREPARE-MVR study (PRediction of Early PostoperAtive Right vEntricular failure in Mitral Valve Replacement/Repair patients) aims to explore the alterations of RV contraction pattern in patients undergoing MVR and to investigate the association of preoperative echocardiographic findings with early postoperative RVF. Methods We prospectively enrolled 70 patients (62±12 years, 67% males) undergoing open heart MVR. Thirty age and gender matched healthy volunteers served as control group. Transthoracic 3D echocardiography was performed preoperatively and at intensive care unit discharge. Furthermore, focused 2D echocardiogram was also obtained during the ICU stay. Forty-three patients also completed 6 months follow-up. 3D model of the RV was reconstructed and end-diastolic volume index (EDVi) along with RV ejection fraction (RVEF) were calculated. For in-depth analysis of RV mechanics, we decomposed the motion of the RV to compute longitudinal (LEF) and radial ejection fraction (REF). Right heart catheterization was performed to monitor RV stroke work index (RVSWi). Results RV morphology as assessed by EDVi was unaffected by surgery (preoperative vs postoperative; 73±17 vs 71±16 mL/m2, p=NS). RVEF was slightly decreased after MVR (52±6 vs 48±7%, p<0.05), whereas RV contraction pattern has changed notably. Before MVR, the longitudinal shortening was the main contributor to global systolic function (LEF/RVEF vs REF/RVEF; 0.53±0.10 vs 0.43±0.12; p<0.001), whereas in controls the longitudinal and radial shortening contributed equally to RVEF (0.47±0.07 vs 0.43±0.09; p=NS). Postoperatively, the radial motion became dominant (0.35±0.08 vs 0.47±0.09; p<0.001). However, this shift was only temporary as 6 months later the contraction pattern became similar to controls showing equal contribution of the two components (0.44±0.10 vs 0.42±0.11; p=NS). Postoperative RVF (defined as RVSWi <300 mmHg*mL/m2 or ICU TAPSE <10 mm) was detected in 14 [20%] patients. Preoperative LEF was associated with postoperative RVSWi (r=−0.61, p<0.001) and it was an independent predictor of postoperative RVF (OR=1.16 [1.03–1.35], p<0.05). Conclusion Severe MR induces a significant shift in the RV mechanical pattern which may influence the development of postoperative RV dysfunction and failure after MVR. Advanced indices of RV mechanics are associated with invasively measured parameters of RV contractility and may predict postoperative RVF.

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Multiscale structure-function relationships in right ventricular failure due to pressure overload

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00047.2018 ◽

2018 ◽

Vol 315 (3) ◽

pp. H699-H708 ◽

Cited By ~ 6

Author(s):

Tik-Chee Cheng ◽

Jennifer L. Philip ◽

Diana M. Tabima ◽

Timothy A. Hacker ◽

Naomi C. Chesler

Keyword(s):

Oxygen Consumption ◽

Right Ventricular ◽

Diastolic Dysfunction ◽

Pressure Overload ◽

Right Ventricular Failure ◽

Male Rats ◽

Ventricular Failure ◽

Functional Changes ◽

Organ Level ◽

The Impact

Right ventricular (RV) failure (RVF) is the major cause of death in pulmonary hypertension. Recent studies have characterized changes in RV structure in RVF, including hypertrophy, fibrosis, and abnormalities in mitochondria. Few, if any, studies have explored the relationships between these multiscale structural changes and functional changes in RVF. Pulmonary artery banding (PAB) was used to induce RVF due to pressure overload in male rats. Eight weeks postsurgery, terminal invasive measurements demonstrated RVF with decreased ejection fraction (70 ± 10 vs. 45 ± 15%, sham vs. PAB, P < 0.005) and cardiac output (126 ± 40 vs. 67 ± 32 ml/min, sham vs. PAB, P < 0.05). At the organ level, RV hypertrophy was directly correlated with increased contractility, which was insufficient to maintain ventricular-vascular coupling. At the tissue level, there was a 90% increase in fibrosis that had a direct correlation with diastolic dysfunction measured by reduced chamber compliance ( r2 = 0.43, P = 0.008). At the organelle level, transmission electron microscopy demonstrated an abundance of small-sized mitochondria. Increased mitochondria was associated with increased ventricular oxygen consumption and reduced mechanical efficiency ( P < 0.05). These results demonstrate an association between alterations in mitochondria and RV oxygen consumption and mechanical inefficiency in RVF and a link between fibrosis and in vivo diastolic dysfunction. Overall, this work provides key insights into multiscale RV remodeling in RVF due to pressure overload. NEW & NOTEWORTHY This study explores the functional impact of multiscale ventricular remodeling in right ventricular failure (RVF). It demonstrates correlations between hypertrophy and increased contractility as well as fibrosis and diastolic function. This work quantifies mitochondrial ultrastructural remodeling in RVF and demonstrates increased oxygen consumption and mechanical inefficiency as features of RVF. Direct correlation between mitochondrial changes and ventricular energetics provides insight into the impact of organelle remodeling on organ level function.

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