New CMR-Identified Myocardial Injury Post-TAVR Linked With Decreased LV Function

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New ischemic myocardial injury, presumably of embolic origin, is common after transcatheter aortic valve replacement (TAVR) and is associated with a drop in left ventricular (LV) function, according to a study being published in the July 29, 2014, issue of the Journal of the American College of Cardiology.

Researchers led by Helge Mӧllmann, MD, of Kerckhoff Heart Center (Bad Nauheim, Germany), looked at 61 patients with severe aortic stenosis who underwent cardiac magnetic resonance (CMR) imaging (Sonata; Siemens Medical Solutions; Erlangen, Germany) at a median of 3 days before and 6 days after TAVR. All were treated between January 2011 and September 2013. Cardiac enzymes were measured at baseline and 1, 2, and 3 days after the procedure using the Elecsys Analyzer 2010 hs-cTnT assay (Roche Diagnostics; Mannheim, Germany).
TAVR was performed via the transfemoral route in 18 patients implanted with the Sapien XT valve (Edwards Lifesciences; Irvine, CA) and 17 treated with CoreValve (Medtronic; Minneapolis, MN). Twenty-six patients were also treated transapically with Sapien XT.

Before TAVR, 42 patients (68.8%) presented with ischemic-type myocardial late enhancement with an average mass of 10.9 g or 7.4% of total LV mass. Among these, 21.4% had no relevant CAD and 66.7% had no history of MI.

Eleven patients (18%) developed new myocardial injury affecting an average of 3.7 g or 1.8% of LV mass, primarily in the endocardial or intramural regions, and 4 patients (36.4%) had intramural lesions with a viable endocardial rim. No new infarcts were detected. Patients with and without new late enhancement had similar baseline characteristics, with the exception of more severe renal impairment in patients with new lesions. 

Patients with new myocardial late enhancement saw a decline in LVEF from 55.5 ± 14.1% before to 45.3 ± 14.9% after TAVR (P = .001). However, no differences were observed in patients without new late enhancement (53.9 ± 17.3% vs 54.6 ± 16.3%; P = NS).

Biomarkers Elevated Across the Board

Baseline high-sensitivity troponin T concentration was 24.9 ng/L and was above the 99th percentile (14 ng/L) in three-quarters of cases. All patients saw a rise in this biomarker above the 99th percentile after TAVR, with a 15-fold rise observed in 61 patients (55.7%), including 92.3% of those treated transapically and 28.5% of those treated transfemorally (P < .001). CK-MB concentration was 11 U/L at baseline, increasing to a maximum value of 21 U/L postprocedure, with a 5-fold rise in 26.2% of patients.

Neither baseline nor post-TAVR values of either biomarker were different between those with and without new late enhancement. However, in a subgroup analysis of transfemorally treated patients, those with new late enhancement had higher maximum concentrations of high-sensitivity troponin T compared with those without (242.9 vs 141.2 ng/l; P = .03). A similar trend was observed in the subgroup of patients treated transapically. CK-MB levels were similar between the cohorts in both subgroups.

Myocardial Injury Common

The findings suggest that “new ischemic-type hyperenhancement detected by CMR occurs in a notable proportion” of TAVR patients, according to Dr. Mӧllmann and colleagues. “The small size, subendocardial or intramural localization, and multifocal distribution of the lesions are findings that suggest an embolic origin. Furthermore, the prevalence of such lesions… argues in favor of an embolic cause and at the same time makes other potential causes, such as global or regional hypoperfusion, rather unlikely,” they write. 

Additionally, the results support the use of CMR as a “complementary method” of detecting ischemic lesions in future studies, the authors observe. 

The consistent biomarker elevations seen in all patients indicate that myocardial injury “commonly occurs to varying degrees,” they report. But myocardial injury after TAVR, which can stem from “multiple underlying mechanisms,” must be handled differently than that after PCI, which can “mostly be attributed to distal embolization,” the authors say. 

“Elevated cardiac biomarkers certainly indicate myocardial injury, but an explicit attribution to a definite cause is difficult,” they add. 

Potential Link Between TAVR-Related Damage, Outcomes

Although limited by a small, single-center population, Dr. Mӧllmann and colleagues write, the study shows that the “biomarker-based VARC II criteria fail to sufficiently discriminate patients with MI—especially in cases of the [transapical] approach,” they explain, adding that the revised criteria show 59% of patients had periprocedural myocardial injury when CMR showed “proof” in only 18%. 

Even with the study’s limitations, Javier Sanz, MD, and George Dangas, MD, both of Mount Sinai Medical Center (New York, NY), congratulated the investigators in an accompanying editorial. 

“It is most striking that the vast majority of these patients have low-grade, ongoing myocardial damage (by [late enhancement] and/or biomarkers), suggesting that such injury is chronic and directly related to the pathophysiology of severe aortic stenosis, even before any procedure,” they write. 

Additionally, the editorial authors point out that “enzyme elevation, regardless of [late enhancement] development, was consistently higher in the transapical access group. If we accept the prognostic importance of myocardial damage, then transapical TAVR should be reserved strictly for those patients who absolutely cannot undergo transarterial TAVR.”

But “most intriguing,” they say, is the “discrepancy between serum and imaging markers of myocardial damage.” The finding that most patients showed pre-TAVR damage and all had increased cardiac biomarkers while comparatively few developed new lesions on CMR “is not trivial because [LVEF] decreased exclusively in the new [late enhancement] group, a finding that can represent a link between TAVR-related myocardial damage and impaired outcomes.” 

Note: Dr. Dangas is a faculty member of the Cardiovascular Research Foundation, which owns and operates TCTMD.



1. Kim W-K, Rolf A, Liebetrau C, et al. Detection of myocardial injury by CMR after transcatheter aortic valve replacement. J Am Coll Cardiol. 2014;64:349-357.

2. Sanz J, Dangas G. Myocardial damage after TAVR assessed with CMR: a new piece in a puzzle [editorial]? J Am Coll Cardiol. 2014;64:358-360.

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  • Drs. Mӧllmann, Sanz, and Dangas report no relevant conflicts of interest.