Contrast-enhanced Cardiac MRI Research Articles

Early Onset and Progression of Left Ventricular Remodeling After Alcohol Septal Ablation in Hypertrophic Obstructive Cardiomyopathy

Alcohol septal ablation (ASA) reduces left ventricular outflow tract (LVOT) pressure gradient in patients with hypertrophic obstructive cardiomyopathy (HOCM), which leads to left ventricular remodeling. We sought to describe the early to midterm changes and modulating factors of the remodeling process using cardiac MRI (CMR). CMR was performed at baseline and 1 and 6 months after ASA in 29 patients with HOCM (age 52+/-16 years). Contrast-enhanced CMR showed no infarct-related hyperenhancement outside the target septal area. Septal mass decreased from 75+/-23 g at baseline to 68+/-22 and 58+/-19 g (P<0.001) at 1- and 6-month follow-up, respectively. Remote, nonseptal mass decreased from 141+/-41 to 132+/-40 and 111+/-27 g (P<0.001), respectively. Analysis of temporal trends revealed that septal mass reduction was positively associated with contrast-enhanced infarct size and transmural or left-sided septal infarct location at both 1 and 6 months. Remote mass reduction was associated with infarct location at 6 months but not with contrast-enhanced infarct size. By linear regression analysis, percentage remote mass reduction correlated significantly with LVOT gradient reduction at 6-month follow-up (P=0.03). Left ventricular remodeling after ASA occurs early and progresses on midterm follow-up, modulated by CMR infarct size and location. Remote mass reduction is associated with infarct location and correlates with reduction of the LVOT pressure gradient. Thus, myocardial hypertrophy in HOCM is, at least in part, afterload dependent and reversible and is not exclusively caused by the genetic disorder.

Myocardial Late Enhancement in Contrast-Enhanced Cardiac MRI: Distinction Between Infarction Scar and Non–Infarction-Related Disease

Our objective was to assess and compare the patterns of late enhancement (LE) in contrast-enhanced cardiac MRI caused by myocardial infarction and different myocardial diseases that are not related to ischemic infarction. A total of 811 consecutive contrast-enhanced cardiac MRI studies performed for different indications were reviewed for left ventricular myocardial LE after gadopentetate dimeglumine administration. MRI studies were performed on a 1.5-T scanner using an inversion recovery turbo FLASH sequence (TR/TE, 8/4 msec; flip angle, 25 degrees). The LE pattern of ischemic infarction scar was compared with that in nonischemic myocardial disease. LE was found in 421 (52%) patients. In all patients with myocardial infarction, LE included the subendocardial layer. Nineteen patients without history of myocardial infarction and angiographically excluded coronary artery disease showed different patterns of LE caused by myocarditis, sarcoidosis, arrhythmogenic right ventricular dysplasia, cardiomyopathy, endomyocardial fibrosis, and iatrogenic scars after biopsy, ablation of septal hypertrophy, and myocardial laser revascularization. LE in contrast-enhanced cardiac MRI is not specific for ischemic infarction. LE in ischemic infarction always involves the subendocardial layer, whereas it does not necessarily do so in other myocardial diseases. Therefore, if LE omit the subendocardial layer, different nonischemic myocardial diseases have to be considered. The pattern of LE might be helpful for the differential diagnosis of myocardial disease and in distinguishing it from ischemic disease.

Delayed contrast enhancement in a patient with perimyocarditis on contrast-enhanced cardiac MRI: case report

The findings of contrast-enhanced cardiac magnetic resonance imaging of a 19-year-old man with perimyocarditis in the subacute and chronic stage are presented. In perimyocarditis., it is useful to check the presence of delayed contrast enhancement to confirm the presence of the lesion and to evaluate the severity of inflammation in the acute stage as well as to determine the extent of fibrosis in the pericardium and myocardium in the chronic stage.

Visualization of Endomyocardial Fibrosis by Delayed-Enhancement Magnetic Resonance Imaging

An 18-year-old Venezuelan woman, with a history of idiopathic restrictive cardiomyopathy, presented at our hospital with ongoing dyspnea, palpitations, and lightheadedness. A medical evaluation revealed heart failure, pulmonary hypertension, and heparin-induced thrombocytopenia. Cardiac catheterization revealed normal coronary arteries. The left ventriculogram demonstrated late filling of the apex, which was almost obliterated by prominent trabeculations. Moderate mitral regurgitation with significant enlargement of the left atrium was observed. The ejection fraction was 44%, without regional wall motion abnormalities (Figure 1). Figure 1. End-systolic (A) and end-diastolic (B) frames of the left ventriculography show partial obliteration of the cavity …

Cardiac Sarcoidosis in a Patient With Hypertrophic Cardiomyopathy Demonstrated by Magnetic Resonance Imaging and Single Photon Emission Computed Tomography Dual-Isotope Scintigraphy

41-year-old man, who had been diagnosed with stage 2 pulmonary sarcoidosis 3 years earlier, was referred to the cardiac clinic complaining of palpitations, dyspnea, and atypical chest pain. Except for central obesity (body mass index of 37 kg/m 2 ) and hypertension, no abnormalities were found on physical examination. The 12-lead ECG demonstrated apical and inferolateral ST-segment elevation, whereas multiple polymorphic premature ventricular beats were found during exercise testing and 24-hour ambulatory ECG. Coronary angiography showed no abnormalities. Because of the man’s obesity, the image quality of the transthoracic echocardiography was suboptimal. Cardiac MRI revealed severe asymmetric hypertrophy of the left ventricle, a finding that points to hypertrophic cardiomyopathy. T2-weighted cardiac MRI revealed increased signal in the apical region (Figure 1), and contrast-enhanced cardiac MRI (0.1 mmol/kg gadolinium-diethylenetriamine pentaacetic acid [Gd-DTPA]) showed late enhancement of the same region (Figures 2 through 5). A dual-isotope 99m Tc-Hexamibi (Cardiolite, DuPont) and 111 In-pentetreotide (OctreoScan, Tyco Healthcare, Mallinckrodt Medical BV; dose 190 MBq) SPECT was performed during exercise (dose 280 MBq) and rest (dose 870 MBq), revealing a reversible apical perfusion defect and apical uptake of 111 Inpentetreotide (Figure 6). The presence of somatostatin receptors in the apical region suggests active apical cardiac sarcoidosis. The SPECT and cardiac MRI images were fused (Figures 7 and 8) by rigid-body transformations based on anatomic landmarks (apex and basal interventricular septum) and the geometric dimensions identified in the different types of images. The spatial image transformations were computed in the MatLab (MathWorks) programming environment. 111 Inpentetreotide binds to somatostatin receptors on macrophages and has been reported to be useful in the management of sarcoidosis. It is possible to differentiate between active inflammation and fibrosis with different cardiac MRI techniques (eg, T2-weighted versus contrast-enhanced T1weighted cardiac MRI). This case demonstrates the usefulness of matching different imaging techniques to visualize inflammation and the different stages of this process in the myocardium.