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Massachusetts Chapter of the American College of Surgeons Massachusetts Chapter of the American College of Surgeons Massachusetts Chapter of the American College of Surgeons Massachusetts Chapter of the American College of Surgeons Massachusetts Chapter of the American College of Surgeons
56th Annual Meeting Abstracts


Ventricular Restraint Therapy for Heart Failure: Is the Right Ventricle Different from the Left Ventricle?
Lawrence S. Lee, MD, Suyog A. Mokashi, MD, Jan D. Schmitto, MD, PhD, Otavio Coelho-Filho, R., MD, Morton Bolman III, MD, Frederick Y. Chen, MD, PhD
Brigham and Women’s Hospital, Boston, MA

PURPOSE OF STUDY

The effects of ventricular restraint on the left ventricle (LV) are well documented, but the effects on the right ventricle (RV) are not known.  We hypothesized that restraint has different effects on the RV compared to the LV.

METHODS USED

This study was performed in two parts:

Part I: Acute Studies. We studied the acute effects of restraint on LV and RV mechanics in normal sheep (n=14) by utilizing our previously described technique of adjustable and measurable restraint in which a fluid-filled balloon is placed around the heart. Transmural pressure (Ptm), indices of myocardial oxygen consumption (MvO2), diastolic compliance (Cd), and end-systolic elastance (Ees) were assessed over four restraint levels for both the LV and RV.

Part II: Chronic Studies. We studied the chronic effects of passive restraint therapy over four months in an ovine model of ischemic dilated cardiomyopathy. Heart failure was induced in sheep (n=6) by coronary artery ligation, and a polypropylene mesh was wrapped around the heart to simulate current clinical restraint therapy. All subjects were followed with serial cardiac magnetic resonance imaging to assess LV and RV end-diastolic volume (EDV) and ejection fraction (EF).

SUMMARY OF RESULTS

In acute studies, restraint decreased LV Ptm (p<0.05) and indices of MvO2 (p<0.05) but did not affect LV Cd (p=0.52) or LV Ees (0.72). Restraint had no effect on RV Ptm (p=0.82), indices of MvO2 (p=0.72), or RV Ees (0.43), but caused a reduction in RV Cd (p<0.05). In chronic studies, restraint led to a decrease in LV EDV (p<0.05) but did not have any effect on RV EDV (p=0.82).

CONCLUSIONS

Ventricular restraint affects the LV and RV differently. Restraint induces beneficial changes in the LV, but the benefit to RV function is unclear. Unlike the LV, the RV demonstrates evidence of impaired ventricular filling at low restraint levels. Thus, with current devices, the RV may limit overall therapy.



TABLES AND CHARTS


Figure 1. (Left) Ventricular transmural myocardial pressure (Ptm) as a function of restraint level. LV Ptm decreases (a beneficial change) as restraint is increased, but RV Ptm stays unchanged. (Right) Change in the ventricular diastolic compliance (Cd) as a function of restraint level. Increasing restraint level causes a significant reduction in RV Cd (an adverse effect) but does not affect LV Cd.  *p<0.05

 

 

MRI pdf.pdf


 

Text Box: Figure 2. (Left) Cardiac MRI of ovine model of heart failure. Short axis views with LV (red) and RV (yellow) endocardial borders delineated at end-diastole. (Middle) EDV and (Right) EF over the 4 month chronic study period of simulated clinical restraint therapy. LV EDV decreases significantly by 6%, consistent with results seen in human clinical trials of passive restraint devices. RV EDV does not change. LV EF shows a non-significant trend toward improvement, but RV EF remains unchanged.  *p<0.05


 

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