Editorial Comment

Decompressing the Left Atriumto Relieve the Right Ventricle

James Goldstein,* MD

Department of Cardiovascular Medicine, BeaumontHealth System, Royal Oak, Michigan

The benefits of ventricular assist devices (VAD) forhemodynamic stabilization of cardiogenic shock due toleft ventricular (LV) and/or right ventricular (RV) pumpfailure are well established [1]. VAD’s, both surgicallyimplanted and percutaneous, have been predominantlyused in patients with ventricular “contractile failure”resulting from acute myocardial infarction, refractorydecompensated congestive heart failure, and in variouspost-surgical settings. The present case report [2]describes the use of the percutaneous Tandem HeartLVAD in a patient with “acute-on-chronic” severe mitralregurgitation (MR), causing pulmonary edema, pulmo-nary arterial hypertension (PAHTN), RV failure (RVF),and ultimately cardiogenic shock. The magnitude ofRVF gave caution to mitral valve surgery, accordinglythe LVAD was placed both to reduce left atrial pressure(LAP) and unload the pulmonary circulation (therebyrelieving the RV) and concomitantly mechanicallyenhancing forward cardiac output (CO) and aortic pres-sure (AOP). The benefits were immediate and impres-sive: Reduction in LA, PA, and right heart pressures,with simultaneous increments in systemic CO and AOP.The hemodynamic relief provided allowed surgery tosubsequently proceed with a recovered RV and excellentclinical outcome. This innovative deployment of anLVAD stabilized this patient suffering from an incompe-tent mitral valve. Although the primary mechanism ofhemodynamic collapse differed from the usual “pumpfailure” indication for VAD, the ultimate hemodynamicgoals were similar: Unload the lungs and RV, whilerestoring systemic perfusion.

THE RV: VULNERABLE BUT RESILIENT

The dramatic response of this failing RV to relief ofexcess afterload is characteristic of this chamber. Inorder to appreciate the remarkable recovery of the RV,it is essential to consider the architecture and physiologyof the normal RV and its responses to acute and chronicpressure overload (as well as the benefits of therapeutic

interventions designed to relieve it). In contrast to theLV (a thick-walled “pressure pump” contracting into thehigh resistance systemic arterial circulation), the RV is athin-walled “volume pump” designed for ejection intothe low-resistance pulmonary circulation [3]. Under con-ditions of chronic increased afterload, the RV hascapacity for adaptive hypertrophy, which is usually suf-ficient to maintain compensation (depending on themagnitude and duration of afterload excess). In contrast,when faced with relatively acute elevation of pulmonaryvascular resistance (PVR), as exemplified by acute mas-sive pulmonary embolism (PE), the unprepared RV isunable to generate peak systolic pressures greater than50–60 mm Hg, with resultant RV dilation and failure,which may precipitate shock.

In the present case, the surgeons gave appropriatepause to operating under conditions of a profoundlyfailing RV. Long before cardiologists began to appreci-ate the importance of the RV, our surgical colleagueswere keenly aware of the miseries and disasters associ-ated with peri-operative RV dilation and failure. Theacutely dilating thin RV appears to move adverselydown the “descending” limb of the Frank–Starlingcurve, whereby recovery without decompression is dif-ficult. It also must be emphasized that the afterloadedfailing RV is exquisitely dependent on optimal AOP tomaintain RV myocardial perfusion. Under conditionsof severe PHTN, hypotension may precipitate abruptworsening of RV function and initiate a “death spiral.”

EFFECTS OF ELEVATED LA PRESSURE ON THERV: LESSONS FROM MITRAL STENOSIS

Increased PVR results from three basic mechanisms:(1) “Pre-capillary,” e.g. PE and primary PAHTN;(2) Intrinsic lung disease; and (3) “Post-capillary,” dueto increased LAP. In the present case, RVF developedfrom increased PVR attributable to elevated LAP

Conflict of interest: Nothing to report.

*Correspondence to: Dr. James Goldstein, 3601 W Thirteen Mile

Road, Royal Oak, MI 48073-6769. E-mail: jgoldstein@beaumont.edu

Received 26 November 2013; Revision accepted 27 November 2013

DOI: 10.1002/ccd.25314

Published online 17 January 2014 in Wiley Online Library

(wileyonlinelibrary.com)

VC 2014 Wiley Periodicals, Inc.

Catheterization and Cardiovascular Interventions 83:323–324 (2014)

resulting from “acute-on-chronic” severe MR. Classiclessons by Dr. Braunwald et al. on the responses of thepulmonary circulation and RV to chronic mitral steno-sis (and its surgical relief) offer insights applicable tothe present case [4]. In 1965, they observed thatchronic LAP elevation> 25 mm Hg induces PAHTNvia a tripartite response: (1) Passive backward trans-mission of LAP; (2) Pulmonary arteriolar vasoconstric-tion; and (3) Anatomic alterations in the pulmonaryarteriolar bed characterized by neo-intimal thickening,medial hypertrophy, and in some instances obliterativechanges. These responses, together with robust recruit-ment of lymphatic drainage, are protective to the lung(though at the price of lowered CO). Most importantand relevant to the present case, post-capillary severePHTN is largely reversible in response to interventionsthat reduce LAP: Mitral valve replacement typicallyresults in dramatic improvement in PAHTN and RVF[4]. However, the magnitude and temporal responsesare variable: Immediate decrements reflect relief ofpassive LA back-pressure and diminished vasoconstric-tion, with slower and less complete lowering of PVRlikely attributable to beneficial remodeling of the pul-monary arterial anatomic alterations (which to someextent may persist).

IMPORTANCE OF STABILIZING THE FAILING RV

These lessons pertain to the present case. Althoughthe clinical presentation was “sub-acute,” the fact that

RV and PA systolic pressures were markedly elevatedindicate that the RV had time to “prepare.” However,the dramatic near-complete immediate improvement ofRV function suggests that the pathophysiology of ele-vated PVR developed in a temporal “sweet-spot”:Long enough to allow the RV to adapt to generateforce sufficient to overcome very high PVR, but ofshort enough duration to minimize anatomic changeswhich might not have resolved so quickly. The authorsshould be congratulated for this inventive interventionfor severe life-threatening MR, demonstrating the bene-fits of a VAD to decompress the LA which therebyrelieved the RV (allowing it to “reascend”), while con-comitantly restoring systemic perfusion pressure whichfurther enhanced recovery of RV performance, andultimately more safely allowed successful definitivesurgical correction.

REFERENCES

1. Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart fail-

ure treated with continuous-flow left ventricular assist device.

N Engl J Med 2009;361:2241–2251.

2. Hira RS, Thamwiwat A, Kar B. TandemHeart placement for

cardiogenic shock in acute severe mitral regurgitation and right

ventricular failure. Catheter Cardiovasc Interv 2014;83:319–322.

3. Goldstein JA, Rich JD, editors. Faces of right ventricular failure.

Cardiol Clin 2012;30:303–310.

4. Braunwald E, Braunwald N, Ross J, Morrow AG. Effects of

mitral-valve replacement on the pulmonary vascular dynamics of

patients with pulmonary hypertension. N Engl J Med 1965;273:

509–514.

324 Goldstein

Catheterization and Cardiovascular Interventions DOI 10.1002/ccd.Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).