CLINICAL TRIAL REPORT

Clinical Trial Report: Time is Resonant for RightVentricular Evaluation

Andre Schmidt & Benedito C. Maciel &J. Antonio Marin-Neto

Published online: 30 March 2011# Springer Science+Business Media, LLC 2011

Masci PG, Francone M, Desmet W, et al.: Right ventricularischemic injury in patients with acute ST-segmentelevation myocardial infarction: Characterization withcardiovascular magnetic resonance. Circulation 2010,122:1405–1412.

Rating: •Of pathophysiologic and clinical importance.

Introduction: Cardiac magnetic resonance (CMR) is rapidlybecoming a preferred noninvasive tool to assess ischemicheart disease. Besides its excellent anatomical definition, itprovides accurate functional and tissue characterization,especially the extension of left ventricular (LV) myocardialdamage. CMR sequences have been extensively applied toallow precise evaluation of the infarcted LV. Right ventric-ular (RV) involvement is a common finding in autopsystudies of acute myocardial infarction (AMI) patients, butthere is scanty clinical information about the occurrence andclinical impact of RV ischemic injury in survivors of AMI.

Aims: The authors sought to characterize the CMR patternof RV ischemic injury and its impact on RV function early(1 week) after infarction and at 4 months’ follow-up. Theyhypothesized that acute post-infarct RV dysfunction resultsfrom stunned but viable rather than irreversibly damagedmyocardium.

Methods: It was a multicenter (three sites) study, usingseveral vendor scanners. Inclusion criteria were classicalclinical and electrocardiographic ST-segment elevationAMI definition. Exclusion criteria included prior myocar-dial infarction or revascularization, atrial fibrillation andother clinical conditions known to affect RV function, suchas chronic obstructive and interstitial pulmonary disease,and preexisting congenital or valvular heart disease.

CMR examination was performed within a week of theevent and included short axis cine images and bothventricles were completely encompassed by a stack ofcontiguous slices. Ejection fraction, regional wall function,mass and volumes of both LV and RV were obtained fromthese images. Myocardial ischemic involvement wasevaluated by two sequences in short-axis orientation: T2-weighted, short inversion time, inversion recovery, fastspin-echo imaging and a breath-hold T1-weighted contrast-enhanced, inversion-recovery, segmented gradient-echosequence. This protocol provided two ways to detectmyocardial involvement: edema in the T2-w imaging andmyocardial necrosis/fibrosis by late gadolinium enhance-ment (LGE) in the T1-w sequence. At 4 months’ follow-upCMR examination without T2-w sequence was performedin all patients.

Results: A total of 242 patients (203 men, 59±10 years)had CMR imaging of good quality. All patients were treatedwith primary PCI. Fifty-one percent (123 patients) pre-sented RV edema in the first CMR performed. RV LGE wasconcomitant in 31% of the initial CMR, but at 4-monthfollow-up only 10% remained with LGE. LV edema wasdetected in all patients at the first CMR and 97% showedconcomitant LV LGE that also persisted at CMR follow-up.

A. Schmidt : B. C. Maciel : J. A. Marin-Neto (*)Division of Cardiology, Department of Internal Medicine, MedicalSchool of Ribeirão Preto, University of São Paulo,São Paulo, Brazile-mail: marin_neto@yahoo.com

Curr Cardiovasc Imaging Rep (2011) 4:177–179DOI 10.1007/s12410-011-9085-5

A main finding was that RV ischemic involvement wasalways contiguous with the jeopardized LV myocardium, butwith variable extension. In the LV inferior infarcts, RVedemaand RV LGE were observed in 75% and 54%, respectively, ofpatients in the initial CMR. In the LV anterior infarcts, RVedema and RV LGE were detected in 33% and 11% ofpatients, respectively. The extent of RV edema was signifi-cantly larger in inferior than in anterior wall infarcts. At thefirst CMR examination, RV regional wall motion wassignificantly more impaired when RV edema was detectedand was correlated with the number of RV segments showingedema. Also, RV volumes were larger and RV ejectionfraction was lower in patients with RVedema detected duringthe first CMR examination. At the 4-month CMR all thesefunctional variables showed significant improvement in thegroup of patients with RVedema.

In order to assess the impact of RV ischemic injury, asubanalysis was performed. Among the 123 patients withbaseline RV edema at the first CMR, three patterns wereidentified: RV edema without LGE (49 patients), RV edemaand RV LGE at the 1-week CMR but not at the 4-monthCMR (49 patients), and RV edema and LGE at both CMRexaminations (25 patients). In contrast to patients showingonly RV edema, persistent RV LGE was associated withlarger RV volumes and lower RV ejection fraction.Interestingly, those patients with persistent RV LGE alsohad a significant late augmentation in RV ejection fractionat follow-up, but with an associated increase in RV end-diastolic volume without increase in end-systolic volume,suggesting adverse RV remodeling. Univariate and multi-variate analyses were used to demonstrate that RV edemawas independently associated with late RV EF improve-ment, despite other confounders like RV EF and RV LGE atthe first CMR, right coronary artery occlusion, and changesin LV volumes and function over time.

Discussion: This study presents a series of new informationconcerning the RV ischemic involvement following anAMI. First, it demonstrates that RV ischemic myocardialinjury as detected using CMR techniques is often present inST segment elevation AMI. Additionally, it shows that RVischemic abnormalities are contiguous to the LV myocar-dium affected and are not exclusive of inferior infarcts,since they were detected in 33% of anterior infarcts. Thepresence of RV edema and RV LGE 1 week after the AMIwas associated with regional and global RV dysfunction notrelated to any LV parameters. Of note, the extension of theRV ischemic injury as detected by CMR was significantlyreduced at 4-month follow-up, suggesting high RV recoverycapability after the ischemic insult. This was interpreted asplausibly resulting from more favorable RVoxygen demand/

supply due to lower stroke work, greater oxygen reserve,higher systolic/diastolic flow, and better protective anatomiccollaterals. On the other hand, despite functional parametersreturning to near normal values, a persistent ischemic injurydetected at 4 months was associated with adverse RVremodeling. Overall, the hypothesis borne out by the authors,that RV dysfunction after AMI is mostly caused by reversiblerather than irreversible ischemic changes, is fully supported bythe findings of this study.

Comments

It is noteworthy that two other recent investigations usingCMR and focusing on the ischemic involvement of the RVconvey diagnostic [1] and prognostic [2] information that isessentially superimposable to that provided in the paper byMasci and coworkers. This elegant study is one of the firstto use CMR as a tool to investigate the RV ischemicinvolvement following AMI. Despite the fact that roughly10% of the patients initially enrolled in the study failed toget an interpretable CMR examination, the results wouldseem to be applicable to most reperfused patients survivingan AMI after being treated with primary PCI. What remainsto be clarified is the pathophysiological meaning of thestriking reduction in LGE from the CMR examinationperformed during the first week after the AMI to the secondCMR test done at 4-month follow-up: only one third of thepatients initially showing LGE persisted with this abnor-mality. As discussed in the paper by Masci et al., a firstpossibility is that the actual volume of fresh myocardialnecrosis, as reflected by LGE at the first week after theAMI, shrinks to a fibrosis volume that in most patients fallsbelow the LGE detection threshold using the current CMRtechniques. If this is indeed the case, we must await forfurther refinement of the CMR protocol to augment itsspatial resolution when applied to the thinner RV wall.Some new sequences/refinements are currently beingtested. For instance, nulling the RV myocardium and LVmyocardium signal independently, and using thinner slices[2] or fat suppression together with LGE, seems to improveRV evaluation [3]. However, it is also possible that LGEearly after the AMI does not reflect exclusively thepresence of irreversible myocardial necrosis and may wellsignal the concomitant occurrence of severely stunned butstill viable myocardial tissue that will eventually recoverwithout replacement by fibrotic tissue.

The paper by Masci et al. is especially welcome,because, over the last decades RV evaluation has beenneglected both in clinical settings and for investigationalpurposes, mainly because of its complex anatomical andfunctional structure. In clinical practice, due to its avail-

178 Curr Cardiovasc Imaging Rep (2011) 4:177–179

ability and affordability echocardiography has been themainstay of evaluation of RV structure and function.However, there is limited ultrasound investigation reportingnormal reference values for RV dimensions, volumes, mass,and function. Moreover, only recently was a guidelinepublished to provide revised reference values for right-sided measures and to establish a standard uniform methodfor obtaining right heart images to assess RV size andfunction [4]. Although geometry-independent parametershave been developed, still the majority of the echocardio-graphic techniques used for assessment of RV function arebased on volumetric assumptions [4]. Such approach has aninherent limitation considering that the shape of the RV isless amenable to geometric simplification for the purpose ofvolume estimation than the LV. The issue of RV geometrymay possibly be overcome by 3D echocardiography usingreal-time 3D algorithms to accurately measure RV volumesand EF [5, 6]. Such methods are validated preferably usingCMR as the gold standard comparator [5].

In keeping with the work by Masci and collaborators,because CMR can provide a comprehensive anatomical andfunctional evaluation of the RV, it tends to become thepredominant diagnostic tool to evaluate this chamber in mostclinical settings outside the ischemic context. For instance,CMR is an accepted component of the diagnostic workup forthe differential diagnosis between arrhythmogenic RV cardio-myopathy/dysplasia and idiopathic RV tachycardia [7]. Also,CMR was recently employed to show that RV anatomicaland functional abnormalities associated with multiple ven-tricular ectopic beats of left bundle block morphologysignificantly impacted on the long-term prognosis of thepatients [8]. Finally, in the context of chronic Chagas heartdisease, ongoing studies using both CMR and the newstandard echocardiographic approaches focusing specificallyon the anatomical and functional assessment of the RV willpossibly yield results that could confirm and extend ourknowledge regarding the early striking damage seen in thisheart chamber during investigations employing radionuclideangiography methods [9, 10].

Disclosure

No potential conflicts of interest relevant to this article werereported.

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