Building a bridge to recovery: the pathophysiology of LVAD-induced reverse modeling in heart failure

Miyagawa, Shigeru; Toda, Köichi; Nakamura, Teruya; Yoshikawa, Yasushi; Fukushima, Satsuki; Saito, Shunsuke; Yoshioka, Daisuke; Saito, Tetsuya; Sawa, Yoshiki

doi:10.1007/s00595-015-1149-8

Cited by 32 publications

(21 citation statements)

References 72 publications

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“…In particular, investigators have shown that implantation of an LV assist device (LVAD), which is used as a bridge to transplantation or as "destination therapy," often leads to reversal of LV remodeling in patients with end-stage nonischemic DCM. The mechanisms by which LVAD support induces reversal of pathologic remodeling of the LV are thus under investigation in the aim to discover a drug or device that efficiently induces reverse LV remodeling [4][5][6].…”

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confidence: 99%

Histone Modification Is Correlated With Reverse Left Ventricular Remodeling in Nonischemic Dilated Cardiomyopathy

Ito

Miyagawa

Fukushima

et al. 2017

The Annals of Thoracic Surgery

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confidence: 99%

Histone Modification Is Correlated With Reverse Left Ventricular Remodeling in Nonischemic Dilated Cardiomyopathy

Ito

Miyagawa

Fukushima

et al. 2017

The Annals of Thoracic Surgery

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“…These findings suggest that additional therapy to treat the diseased myocardium may be required to prevent LV re-dilatation after surgery. Heart failure, especially due to DCM, features disease pathologies such as fibrosis, myocyte apoptosis, and ischemia [13], and a treatment target for DCM should focus on the damaged myocardium in addition to the valvular disease. Several recent papers reported that myoblast sheets applied to ischemic cardiomyopathy tissue [4, 14] could heal old myocardial infarction (OMI) [15, 16] or DCM [17, 18] in large or small animal models through potent angiogenesis, anti-fibrotic effects, and stem cell recruitment induced by cytokine paracrine effects.…”

Section: Discussionmentioning

confidence: 99%

Long-term outcome of a dilated cardiomyopathy patient after mitral valve surgery combined with tissue-engineered myoblast sheets—report of a case

et al. 2018

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BackgroundDilated cardiomyopathy (DCM) is a life-threatening heart muscle disease characterized by progressive heart failure, which often requires left ventricular assist device (LVAD) implantation or heart transplantation (HTx). A tissue engineering strategy using cell sheets for end-stage heart failure has emerged in recent years.Case presentationHere, we describe a 50-year-old DCM patient with severe symptoms of heart failure with severe mitral regurgitation (MR) who was not a candidate for LVAD or HTx. The patient underwent mitral valve replacement followed by the transplantation of autologous myoblast sheets.ConclusionThe patient’s clinical symptoms improved with a preservation of cardiac performance, and he has survived for over 6 years since the combined surgery. This combined method was feasible and appeared to be effective, and thus represents a promising strategy for treating severe heart failure in end-stage DCM and as an alternative treatment for selected patients who are not candidates for LVAD or HTx.

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“…Therefore, heart transplantation cannot serve as a standard therapeutic modality for every patient with end-stage heart failure. Left ventricular assist device (LVAD) has been saving many lives as a bridge to recovery, transplantation, and decision ( 3 – 5 ). Klotz et al reported that, even in end-stage heart failure, LVAD could reverse ventricular remodeling.…”

Section: Introductionmentioning

confidence: 99%

The Partial Support of the Left Ventricular Assist Device Shifts the Systemic Cardiac Output Curve Upward in Proportion to the Effective Left Ventricular Ejection Fraction in Pressure-Volume Loop

Kakino

Saku

Nishikawa

et al. 2020

Front. Cardiovasc. Med.

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Left ventricular assist device (LVAD) has been saving many lives in patients with severe left ventricular (LV) failure. Recently, a minimally invasive transvascular LVAD such as Impella enables us to support unstable hemodynamics in severely ill patients. Although LVAD support increases total LV cardiac output (CO TLV ) at the expense of decreases in the native LV cardiac output (CO NLV ), the underlying mechanism determining CO TLV remains unestablished. This study aims to clarify the mechanism and develop a framework to predict CO TLV under known LVAD flow (CO LVAD ). We previously developed a generalized framework of circulatory equilibrium that consists of the integrated CO curve and the VR surface as common functions of right atrial pressure (P RA ) and left atrial pressure (P LA ). The intersection between the integrated CO curve and the VR surface defines circulatory equilibrium. Incorporating LVAD into this framework indicated that LVAD increases afterload, which in turn decreases CO NLV . The total LV cardiac output (CO TLV ) under LVAD support becomes CO TLV = CO NLV +EF e · CO LVAD , where EF e is effective ejection fraction, i.e., E es /(E es +E a ). E es and E a represent LV end-systolic elastance (E es ) and effective arterial elastance (E a ), respectively. In other words, LVAD shifts the total LV cardiac output curve upward by EF e · CO LVAD . In contrast, LVAD does not change the VR surface or the right ventricular CO curve. In six anesthetized dogs, we created LV failure by the coronary ligation of the left anterior descending artery and inserted LVAD by withdrawing blood from LV and pumping out to the femoral artery. We determined the parameters of the CO curve with a volume-change technique. We then changed the CO LVAD stepwise from 0 to 70–100 ml/kg/min and predicted hemodynamics by using the proposed circulatory equilibrium. Predicted CO TLV , P RA , and P LA for each step correlated well with those measured (SEE; 2.8 ml/kg/min 0.17 mmHg, and 0.65 mmHg, respectively, r 2 ; 0.993, 0.993, and 0.965, respectively). The proposed framework quantitatively predicted the upward-shift of the total CO curve resulting from the synergistic effect of LV systolic function and LVAD support. The proposed framework can contribute to the safe management of patients with LVAD.

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Building a bridge to recovery: the pathophysiology of LVAD-induced reverse modeling in heart failure

Cited by 32 publications

References 72 publications

Histone Modification Is Correlated With Reverse Left Ventricular Remodeling in Nonischemic Dilated Cardiomyopathy

Histone Modification Is Correlated With Reverse Left Ventricular Remodeling in Nonischemic Dilated Cardiomyopathy

Long-term outcome of a dilated cardiomyopathy patient after mitral valve surgery combined with tissue-engineered myoblast sheets—report of a case

The Partial Support of the Left Ventricular Assist Device Shifts the Systemic Cardiac Output Curve Upward in Proportion to the Effective Left Ventricular Ejection Fraction in Pressure-Volume Loop

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