Michael Jerosch-Herold

ACCF/ACR/AHA/NASCI/SCMR 2010 Expert Consensus Document on Cardiovascular Magnetic Resonance A Report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents

Robert A. Harrington, MD, FACC, FAHA, Chair Jeffrey L. Anderson, MD, FACC, FAHA[††][1] Eric R. Bates, MD, FACC Charles R. Bridges, MD, MPH, FACC, FAHA Mark J. Eisenberg, MD, MPH, FACC, FAHA Victor A. Ferrari, MD, FACC, FAHA Cindy L. Grines, MD, FACC[††][1] Mark A. Hlatky, MD, FACC,

Utility of Cardiac Magnetic Resonance Imaging in the Diagnosis of Hypertrophic Cardiomyopathy

Background—Two-dimensional echocardiography is currently the standard test for the clinical diagnosis of hypertrophic cardiomyopathy (HCM). The present study was undertaken to determine whether cardiac MRI (CMR) affords greater accuracy than echocardiography in establishing the diagnosis and assessing the magnitude of left ventricular (LV) hypertrophy in HCM. Methods and Results—Forty-eight patients (age 34±16 years) suspected of having HCM (or with a confirmed diagnosis) were imaged by both echocardiography and CMR to assess LV wall thickness in 8 anatomic segments (total n=384 segments) and compared in a blinded fashion. Maximum LV thickness was similar by echocardiography (21.7±9.1 mm) and CMR (22.5±9.6 mm; P=0.21). However, in 3 (6%) of the 48 patients, echocardiography did not demonstrate LV hypertrophy, and CMR identified otherwise undetected areas of wall thickening in the anterolateral LV free wall (17 to 20 mm), which resulted in a new diagnosis of HCM. In the overall study group, compared with CMR, echocardiography also underestimated the magnitude of hypertrophy in the basal anterolateral free wall (by 20±6%; P=0.001), as well as the presence of extreme LV wall thickness (≥30 mm) in 10% of patients (P<0.05). Conclusions—CMR is capable of identifying regions of LV hypertrophy not readily recognized by echocardiography and was solely responsible for diagnosis of the HCM phenotype in an important minority of patients. CMR enhances the assessment of LV hypertrophy, particularly in the anterolateral LV free wall, and represents a powerful supplemental imaging test with distinct diagnostic advantages for selected HCM patients.

Cardiovascular Function in Multi-Ethnic Study of Atherosclerosis: Normal Values by Age, Sex, and Ethnicity

OBJECTIVE MRI provides accurate and high-resolution measurements of cardiac anatomy and function. The purpose of this study was to describe the imaging protocol and normal values of left ventricular (LV) function and mass in the Multi-Ethnic Study of Atherosclerosis (MESA). SUBJECTS AND METHODS Eight hundred participants (400 men, 400 women) in four age strata (45-54, 55-64, 65-74, 75-84 years) were chosen at random. Participants with the following known cardiovascular risk factors were excluded: current smoker, systolic blood pressure > 140 mm Hg, diastolic blood pressure > 90 mm Hg, fasting glucose > 110 mg/dL, total cholesterol > 240 mg/dL, and high-density lipoprotein (HDL) cholesterol < 40 mg/dL. Cardiac MR images were analyzed using MASS software (version 4.2). Mean values, SDs, and correlation coefficients in relationship to patient age were calculated. RESULTS There were significant differences in LV volumes and mass between men and women. LV volumes were inversely associated with age (p < 0.05) for both sexes except for the LV end-systolic volume index. For men, LV mass was inversely associated with age (slope = -0.72 g/year, p = 0.0021), but LV mass index was not associated with age (slope = -0.179 g/m2/year, p = 0.075). For women, LV mass (slope = -0.15 g/year, p = 0.30) and LV mass index (slope = 0.0044 g/m2/year, p = 0.95) were not associated with age. LV mass was the largest in the African-American group (men, 181.6 +/- 35.8 [SD] g; women, 128.8 +/- 28.1 g) and was smallest in the Asian-American group (men, 129.1 +/- 20.0 g; women, 89.4 +/- 13.3 g). CONCLUSION The normal LV differs in volume and mass between sexes and among certain ethnic groups. When indexed by body surface area, LV mass was independent of age for both sexes. Studies that assess cardiovascular risk factors in relationship to cardiac function and structure need to account for these normal variations in the population.

Magnetic resonance quantification of the myocardial perfusion reserve with a Fermi function model for constrained deconvolution

The myocardial perfusion reserve, defined as the ratio of hyperemic and basal myocardial blood flow, is a useful indicator of the functional significance of a coronary artery lesion. Rapid magnetic resonance (MR) imaging for the noninvasive detection of a bolus-injected contrast agent as a MR tracer is applied to the measurement of regional tissue perfusion during rest and hyperemia, in patients with microvascular dysfunction. A Fermi function model for the distribution of tracer residence times in the myocardium is used to fit the MR signal curves. The myocardial perfusion reserve is calculated from the impulse response amplitudes for rest and hyperemia. The assumptions of the model are tested with Monte Carlo simulations, using a multiple path, axially distributed mathematical model of blood tissue exchange, which allows for systematic variation of blood flow, vascular volume, and capillary permeability. For a contrast-to-noise ratio of 6:1, and over a range of flows from 0.5 to 4.0 ml/min per g of tissue, the ratio of the impulse response amplitudes for hyperemic and basal flows is linearly proportional to the ratio of model blood flows, if the mean transit time of the input function is shorter than approximately 9 s. The uncertainty in the blood flow reserve estimates grows both at low (< 1.0 ml/min/g) and high (> 3-4 ml/min/g) flows. The predictions of the Monte Carlo simulations agree with the results of MR first pass studies in patients without significant coronary artery lesions and microvascular dysfunction, where the perfusion reserve in the territory of the left anterior descending coronary artery (LAD) correlates linearly with the intracoronary Doppler ultrasound flow reserve in the LAD (r = 0.84), in agreement with previous PET studies.

Expert Consensus DocumentACCF/ACR/AHA/NASCI/SCMR 2010 Expert Consensus Document on Cardiovascular Magnetic Resonance: A Report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents

American College of Cardiology Foundation Representative; †North merican Society for Cardiovascular Imaging Representative; ‡Society or Cardiovascular Magnetic Resonance Representative; §American cademy of Pediatrics; American College of Radiology Representaive; ¶ACCF Task Force Liaison; #American Heart Association epresentative. **The findings and conclusions in this expert consensus ocument reflect ACCF policy and do not necessarily represent the iews of the Uniformed Services University of the Health Sciences, the .S. Department of Defense, or the U.S. Government, by whom Dr.

Evidence for Microvascular Dysfunction in Hypertrophic Cardiomyopathy: New Insights From Multiparametric Magnetic Resonance Imaging

Background— Microvascular dysfunction in hypertrophic cardiomyopathy (HCM) may create an ischemic substrate conducive to sudden death, but it remains unknown whether the extent of hypertrophy is associated with proportionally poorer perfusion reserve. Comparisons between magnitude of hypertrophy, impairment of perfusion reserve, and extent of fibrosis may offer new insights for future clinical risk stratification in HCM but require multiparametric imaging with high spatial and temporal resolution. Methods and Results— Degree of hypertrophy, myocardial blood flow at rest and during hyperemia (hMBF), and myocardial fibrosis were assessed with magnetic resonance imaging in 35 HCM patients (9 [26%] male/26 female) and 14 healthy controls (4 [29%] male/10 female), aged 18 to 78 years (mean±SD, 42±14 years) with the use of the American Heart Association left ventricular 16-segment model. Resting MBF was similar in HCM patients and controls. hMBF was lower in HCM patients (1.84±0.89 mL/min per gram) than in healthy controls (3.42±1.76 mL/min per gram, with a difference of −0.95±0.30 [SE] mL/min per gram; P<0.001) after adjustment for multiple variables, including end-diastolic segmental wall thickness (P<0.001). In HCM patients, hMBF decreased with increasing end-diastolic wall thickness (P<0.005) and preferentially in the endocardial layer. The frequency of endocardial hMBF falling below epicardial hMBF rose with wall thickness (P=0.045), as did the incidence of fibrosis (P<0.001). Conclusions— In HCM the vasodilator response is reduced, particularly in the endocardium, and in proportion to the magnitude of hypertrophy. Microvascular dysfunction and subsequent ischemia may be important components of the risk attributable to HCM.

Myocardial blood flow quantification with MRI by model-independent deconvolution

Magnetic resonance (MR) imaging during the first pass of an injected contrast agent has been used to assess myocardial perfusion, but the quantification of blood flow has been generally judged as too complex for its clinical application. This study demonstrates the feasibility of applying model-independent deconvolution to the measured tissue residue curves to quantify myocardial perfusion. Model-independent approaches only require minimal user interaction or expertise in modeling. Monte Carlo simulations were performed with contrast-to-noise ratios typical of MR myocardial perfusion studies to determine the accuracy of the resulting blood flow estimates. With a B-spline representation of the tissue impulse response and Tikhonov regularization, the bias of blood flow estimates obtained by model-independent deconvolution was less than 1% in all cases for peak contrast to noise ratios in the range from 15:1 to 20:1. The relative dispersion of blood flow estimates in Monte Carlo simulations was less than 7%. Comparison of MR blood flow estimates against measurements with radio-isotope labeled microspheres indicated excellent linear correlation (R2 = 0.995, slope: 0.96, intercept: 0.06). It can be concluded from these studies that the application of myocardial blood flow quantification with MRI can be performed with model-independent methods, and this should support a more widespread use of blood flow quantification in the clinical environment.

Quantification of myocardial perfusion using dynamic 64-detector computed tomography.

Objectives:The purpose of this study was to determine the ability of dynamic 64 slice multidetector computed tomography (d-MDCT) to provide an accurate measurement of myocardial blood flow (MBF) during first-pass d-MDCT using semiquantitative and quantitative analysis methods. Materials and Methods:Six dogs with a moderate to severe left-anterior descending artery stenosis underwent adenosine (0.14 mL · kg−1 · min−1) stress d-MDCT imaging according to the following imaging protocol: iopamidol 10 mL/s for 3 seconds, 8 mm × 4 collimation, 400 milliseconds gantry rotation time, 120 kV, and 60 mAs. Images were reconstructed at 1-second intervals. Regions of interest were drawn in the LAD and remote territories, and time-attenuation curves were constructed. Myocardial perfusion was analyzed using a model-based deconvolution method and 2 upslope methods and compared with the microsphere MBF measurements. Results:The myocardial upslope-to-LV-upslope and myocardial upslope-to-LV-max ratio strongly correlated with MBF (R2 = 0.92, P < 0.0001 and R2 = 0.87, P < 0.0001, respectively). Absolute MBF derived by model-based deconvolution analysis modestly overestimated MBF compared with microsphere MBF (3.0 ± 2.5 mL · g−1 · min−1 vs. 2.6 ± 2.7 mL · g−1 · min−1, respectively). Overall, MDCT-derived MBF strongly correlated with microspheres (R2 = 0.91, P < 0.0001, mean difference: 0.45 mL · g−1 · min−1, P = NS). Conclusions:d-MDCT MBF measurements using upslope and model-based deconvolution methods correlate well with microsphere MBF. These methods may become clinically applicable in conjunction with coronary angiography and next generation MDCT scanners with larger detector arrays and full cardiac coverage.

Quantification of Diffuse Myocardial Fibrosis and Its Association With Myocardial Dysfunction in Congenital Heart Disease

Background—The etiology of ventricular dysfunction in adult congenital heart disease (ACHD) is not well understood. Diffuse fibrosis is a likely common final pathway and is quantifiable using MRI. Methods and Results—Patients with ACHD (n=50) were studied with cardiac MRI to quantify systemic ventricular volume and function and diffuse fibrosis. The fibrosis index for a single midventricular plane of the systemic ventricle was quantified by measuring T1 values for blood pool and myocardium before and after administration of gadolinium (0.15 mmol/kg) and then adjusted for hematocrit. Results were compared to healthy volunteers (normal controls, n=14) and patients with acquired heart failure (positive controls, n=4). Patients studied (age, 37±12 years; female sex, 40%) included 11 with a systemic right ventricle (RV), 17 with tetralogy of Fallot, 10 with cyanosis, and 12 with other lesions. The fibrosis index was significantly elevated in patients with ACHD compared to normal controls (31.9±4.9% versus 24.8±2.0%; P=0.001). Values were highest in patients with a systemic RV (35.0±5.8%; P<0.001) and those who were cyanotic (33.7±5.6%; P<0.001). The fibrosis index correlated with end-diastolic volume index (r=0.60; P<0.001) and ventricular ejection fraction (r=−0.53; P<0.001) but not with age or oxygen saturation in patients who were cyanotic. Late gadolinium enhancement did not account for the differences seen. Conclusions—Patients with ACHD have evidence of diffuse, extracellular matrix remodeling similar to patients with acquired heart failure. The fibrosis index may facilitate studies on the mechanisms and treatment of myocardial fibrosis and heart failure in these patients.

Analysis of myocardial perfusion MRI

Rapid MR imaging (MRI) during the first pass of an injected tracer is used to assess myocardial perfusion with a spatial resolution of 2–3 mm, and to detect any regional impairments of myocardial blood flow (MBF) that may lead to ischemia. The spatial resolution is sufficient to detect flow reductions that are limited to the subendocardial layer. The capacity of the coronary system to increase MBF severalfold in response to vasodilation can be quantified by analysis of the myocardial contrast enhancement. The myocardial perfusion reserve (MPR) is a useful concept for quantifying the vasodilator response. The perfusion reserve can be estimated from the ratio of MBFs during vasodilation and at baseline, in units identical to those used for invasive measurements with labeled microspheres, or from dimensionless flow indices normalized by their value for autoregulated flow at rest. The perfusion reserve can be reduced as a result of a blunted hyperemic response and/or an abnormal resting blood flow. The absolute quantification of MBF removes uncertainties in the evaluation of the vasodilator response, and can be achieved without the use of complex tracer kinetic models; therefore, its application to clinical studies is feasible. J. Magn. Reson. Imaging 2004;19:758–770.