Gd-Enhanced CMR Risk-Stratifies in Ischemics, Nonischemics; Clinical Value Uncertain

March 08, 2013

CHICAGO — Two reports appearing this week added further insight to the literature on evaluation of cardiomyopathies with cardiac magnetic resonance (CMR) imaging, especially in associating scar burden by late gadolinium enhancement (LGE) and clinical outcomes.

One prospectively screened patients with nonischemic dilated cardiomyopathy using LGE-CMR and identified a subset with substantial left ventricular mid-wall fibrosis, which emerged as a significant predictor of mortality and serious ventricular arrhythmias even after researchers controlled for LVEF and other risk markers [1].

The other found that many patients with ischemic cardiomyopathy and left ventricular wall thinning that was not mostly scar could show, after coronary revascularization, significant functional and structural improvement in the thinned wall region[2].

Both studies are published in the March 6, 2013 issue of the Journal of the American Medical Association.

"Their common theme is scar and prognosis, and [both] are incremental in understanding gadolinium-enhancement [CMR]. These are both confirmatory studies," observed Dr Katherine C Wu (Johns Hopkins University School of Medicine, Baltimore, MD) for heartwire . "Yes, delayed-enhancement CMR does predict increased risk, but the problem is in applying that clinically." The risk increases were relative, but absolute risk was elevated in all of the patients screened, so in general they'd all be revascularized.

"The issue for clinical application is that you have to define a very low-risk group in which you wouldn't need therapy," said Wu, who isn't associated with either study. "That's CMR's challenge." In predicting such low risk, the risk marker couldn't be just scar or another single marker. "It will be in combination with other factors, [but] we don't know what they will be."

Mid-Wall Fibrosis as a Prognosticator

The prospective study from Dr Ankur Gulati (Royal Brompton Hospital, London, UK) and colleagues looked at 472 patients with nonischemic dilated cardiomyopathy, finding mid-wall fibrosis in 142 patients by LGE-CMR. The finding about tripled the risk of death from any cause and was associated with more than five times the risk of clinically important arrhythmic events over 5.3 years of follow-up.

Hazard Ratios (95%CI) for Clinical Outcomes Over 5.3 Years for 142 Patients With LGE-CMR Mid-Wall Fibrosis vs 330 Others in a Nonischemic Cardiomyopathy Cohort

Clinical outcome HR (95% CI) p
Death from any cause 2.96 (1.87–4.69) <0.001
SCD or aborted SCD (appropriate ICD shock, nonfatal VF, or sustained VT) 5.24 (3.15–8.72) <0.001
SCD=sudden cardiac death

The risks were only partially attenuated after LVEF and other standard predictors were controlled for, suggesting that the presence and scope of mid-wall fibrosis by LGE-CMR may be independently useful as a risk stratifier in such patients, according to the authors.

"Potentially Reversible" Myocardial Thinning

Also, a prospective study from three centers found that about 19% of 1055 CAD patients who underwent CMR viability testing showed regional left ventricular wall thinning that averaged about 34% of total LV surface area and was strongly associated with poor LV function and a history of MI. At delayed-enhancement CMR, wall thinning was predominantly from scarring in most of the patients, but 18% of patients had scarring involving <50% of the thinned wall, according to Dr Dipan J Shah (Duke University Medical Center, Durham, NC) and associates.

Moreover, in the 42 patients with both baseline and follow-up CMR of the thinning regions who had gone to coronary revascularization, the extent of scarring was inversely related to subsequent recovery of contractile function (p<0.001) and to end-diastolic wall thickening. Only those initially with <50% scar burden showed improved function, paired with a significant rise in systolic wall thickening (p<0.001).

"We believe the data indicate that myocardial thinning is potentially reversible and therefore should not be considered a permanent state. Our results suggest that common clinical characteristics will not be useful in predicting whether thinned regions have limited scar tissue," write Shah et al. "There were no differences in age, sex, cardiac risk factors, angina or heart-failure symptoms, or presence of Q waves between patients with extensive or limited scar burden."

The study's message is, "Don't equate [ventricular wall] thinning with lack of viability, and that's a good observation, a good message to pass on. But they looked at only 42 patients, and those patients were going to revascularization based on other clinical decisions," Wu said.

"Some people may equate thinning with lack of viability, and what [the authors] are showing is that those segments can recover. So you shouldn't use wall thinning [to] exclude from revascularization," she said. "The revascularization decision is much more complex than whether or not a particular wall is going to recover function."

Both Wu and an accompanying editorial questioned, for now, the usefulness of finding viability in such patients, noting that in the STICH viability substudy, it didn't seem to influence whether revascularization had a favorable effect on clinical outcomes.

In the editorial [3], Dr Deepak K Gupta (Brigham and Women's Hospital, Boston, MA) and associates noted that based on STICH, "conventional viability testing with single-photon-emission computed tomography or dobutamine echocardiography cannot help decide who should undergo revascularization or even identify who has improved survival."

As a result, based on the current study "in the context of the results from the STICH trial addressing the value of viability assessments in guiding revascularization decisions, the clinician is still left trying to decide what to do with a finding of viable myocardium."

Wu said she has no disclosures. The study from Gulati et al was supported by the National Institute for Health Research Cardiovascular Biomedical Research Unit at the Royal Brompton and Harefield NHS Foundation Trust and Imperial College, London, UK. Gulati reports receiving grant support from the National Institute for Health Research, CORDA, and Rosetrees Trust. Disclosures for the coauthors are listed in the paper. Shah reports serving as a consultant to Astellas; receiving grants pending from Siemens Medical Solutions, Astellas, and Methodist Hospital Research Institute; and receiving payment for lectures from AstraZeneca, Lantheus Medical Imaging, and Takeda. Disclosures for the coauthors are listed in the paper. Gupta et al had no disclosures.

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