Figuring out how to treat postinfarction left ventricular remodeling using delayed-enhancement cardiac MR is not so cut and dried as it seems. Bright signal may signify dead myocardial tissue during DE-MR viability studies, but bright and dark myocardium both have stories to tell when dealing with remodeling.
That is one of the strengths of CMR for ventricular remodeling, according to Dr. Raymond Kim, codirector of Duke University Cardiovascular Imaging Center. Speaking at the Society for Cardiovascular Magnetic Resonance annual meeting, Kim described his group's experience with a new way of measuring viability.
Typically, measurement involves quantifying only those areas that are alive. For a diseased region of the heart, viability is usually expressed as the amount that is alive in this region as a percentage of a separate, normal region on the opposite side of the heart. Kim suggested that using MRI allows the physician to quantify both the amount that is alive and the amount that is dead. This way, for a diseased region of the heart, viability could be expressed as the amount that is alive as a percentage of the total amount of tissue in this region.
This change integrates the influence of living and dead myocardium into the equation, Kim said. Standard drug therapy is still recommended for patients with severe wall thinning, even without evidence of scarring. But in other instances, this change can help the clinician identify patients warranting revascularization who were previously considered poor candidates for intervention.
Kim cited as an example a 38-year-old woman who developed increasingly serious shortness of breath over a 28-day period. CMR performed six months earlier was normal. Physical symptoms suggesting a small infarction were reinforced by CMR and echocardiography showing cavity dilation, anterior wall thinning, and a more spherical appearance than on previous imaging-all symptoms of ischemic ventricular remodeling. SPECT uncovered a large predominately fixed defect in the anterior wall and apex, and coronary angiography demonstrated a significant stenosis of the proximal left anterior descending artery with little collateral flow.
Such evidence of ventricular remodeling rules out intervention, but Kim recommended it, partially because of the lack of DE-MRI hyperenhancement.
"After lots of struggle and argument, this person got a single-vessel bypass of the LAD," he said. "After revascularization, we saw a significant improvement in that wall, a reduction in cavity size, and a thickening of the anterior wall."
Duke University is undertaking a systematic study of patients with similar clinical presentations that appear to have little viability by traditional diagnostic tests, Kim said.
Because of its superb spatial resolution, CMR aids assessments of ventricular remodeling in more conventional ways as well. Usually associated with infarction or cardiomyopathy, left ventricular remodeling involves progressive left ventricular dilation, mural hypertrophy, deterioration of ventricular function, distortion of cavity shape, and alterations of mitral valve geometry causing mitral valve regurgitation. About 550,000 new cases are reported annually. Resultant heart failure contributes to 45,000 deaths per year.
Echocardiography is the imaging modality of choice for diagnosing and assessing risk, according to Dr. Martin G. St. John Sutton, director of cardiovascular imaging at the University of Pennsylvania. Two-D echo simply and reproducibly measures ventricular volumes, cavity size, and murality-all key indicators of risks from ventricular modeling. Ultrasound Doppler is well suited for detecting mitral valve regurgitation.
Technical innovations, such as 3D echo, automated edge detection, and faster ventricular volume measurements will strenghten and improve its performance, Sutton said.
Although echo's role is secure, some clinicians are adopting CMR, said Dr. Gunnar Lund of the Roentgen Institute in Dusseldorf, Germany. Its high spatial resolution translates into accurate measures of infarct size and reproducible characterizations of ventricular wall dilation, wall thinning, and microvascular obstructions.
"You can perform quantitative 3D analysis to get precise numbers concerning volume, motion, and function," Lund said.
CMR shows potential for predicting the onset of remodeling following infarction, myocardiomyopathy, or other causes, Lund said. His study of 55 consecutive patients with myocardial infarction found that CMR measures of infarct size were 92% accurate in predicting which patients would develop ventricular remodeling.
Several CMR studies have shown correlations between the extent of microvascular obstructions and other measures affecting the severity of ventricular remodeling. Remodeling is linked to large infarctions and lower left ventricular ejection fractions that tend to regress over time. Dr. Katherine C. Wu, a cardiologist at Johns Hopkins University, found that microvascular obstruction helps estimate the risk for future cardiac events for MI patients.
"By using these parameters with CMR, you can risk-stratify patients and use this information for early assignment to medical therapy, at least to reduce the problem of left ventricular remodeling," Lund said.
High reproducibility is also making CMR an increasingly popular alternative to echocardiography for testing reverse remodeling therapies. Although CMR procedures are considerably more expensive than 2D echocardiography, statistically significant findings can be rendered using far fewer patients with CMR, said Dr. Dudley Pennell, director of cardiac imaging at Royal Brompton Hospital in London.
CMR is still not the first choice in most clinics for determining the presence and reversibility of remodeling, Kim said. Further published studies are needed in order to familiarize more practitioners about its clinical utility before it will move into routine mainstream use.
