Introduction: Hypertrophic cardiomyopathy (HCM) is associated with myocardial scarring and ventricular tachycardia (VT). Contrast-enhanced cardiac magnetic resonance imaging (CE-CMR) can quantify myocardial scar, and scar imaging has been documented in patients with HCM. We investigated the assessment of myocardial scar in HCM patients using CE-CMR, and its correlation with proven VT.
Methods: Twenty-five patients (mean age 54 +/- 8) with HCM who underwent CE-CMR were identified, and clinical data obtained from chart review. Parameters of LV function were calculated from cine imaging, and myocardial scar was assessed using delayed enhancement imaging following gadolinium administration.
Results: Myocardial scar was detected in 16 (64%) patients with a mean mass 9 +/- 15 g. Scar was patchy, mid-myocardial and located in the basal anteroseptum, and RV insertion sites. Scar was seen in septal, apical and concentric variants of HCM. Scar mass correlated with both LV Mass (r2 = 0.74) and maximal LV wall thickness (r2 = 0.42). VT occurred in 32% of patients, and was associated with both increased scar mass and wall thickness compared to non-VT patients (21 +/- 22 g vs. 4 +/- 6 g, and 2.4 +/- 0.5 cm vs. 1.8 +/- 0.5 cm, p < 0.05). LV size and function were similar in patients with and without VT. A scar mass of >7 g predicted the presence of VT with a sensitivity of 75% and specificity 82%.
Conclusions: Myocardial scar imaged by CE-CMR is common in patients with HCM, and is predictive of VT. Scar is seen in all HCM variants, and is associated with maximal wall thickness. There may be a role for CE-CMR in improved risk stratification for individual patients with HCM.
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http://dx.doi.org/10.1016/j.hlc.2008.03.080 | DOI Listing |
Circ Res
December 2024
Department of Biomedical Engineering, School of Medicine and School of Engineering, University of Alabama at Birmingham. (Y.W., G.W., T.N., X.G., B.G., H.Z., A.G., M.R.-G., J.M.R., L.Y., J.Z.).
Background: When human induced pluripotent stem cells (hiPSCs) that CCND2-OE (overexpressed cyclin-D2) were differentiated into cardiomyocytes (hiPSC-CMs) and administered to the infarcted hearts of immunodeficient mice, the cells proliferated after administration and repopulated >50% of the scar. Here, we knocked out human leukocyte antigen class I and class II expression in hiPSC-CMs (hiPSC-CMs) to reduce the cells' immunogenicity and then assessed the therapeutic efficacy of hiPSC-CMs for the treatment of myocardial infarction.
Methods: hiPSC-CM and wild-type hiPSC-CM (hiPSC-CM) spheroids were differentiated in shaking flasks, purified, characterized, and intramyocardially injected into pigs after ischemia/reperfusion injury; control animals were injected with basal medium.
Front Cardiovasc Med
December 2024
National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Introduction: Cardiac fibrosis occurs in a wide range of cardiac diseases and is characterised by the transdifferentiation of cardiac fibroblasts into myofibroblasts these cells produce large quantities of extracellular matrix, resulting in myocardial scar. The profibrotic process is multi-factorial, meaning identification of effective treatments has been limited. The antifibrotic effect of the bile acid ursodeoxycholic acid (UDCA) is established in cases of liver fibrosis however its mechanism and role in cardiac fibrosis is less well understood.
View Article and Find Full Text PDFBiomater Sci
December 2024
Central Laboratory, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong 510910, China.
Myocardial infarction (MI) remains one of the most common and lethal cardiovascular diseases (CVDs), leading to the deterioration of cardiac function due to myocardial cell necrosis and fibrous scar tissue formation. Myocardial infarction (MI) remains one of the most common and lethal cardiovascular diseases (CVDs), leading to the deterioration of cardiac function due to myocardial cell necrosis and fibrous scar tissue formation. After MI, the anisotropic structural properties of myocardial tissue are destroyed, and its mechanical and electrical microenvironment also undergoes a series of pathological changes, such as ventricular wall stiffness, abnormal contraction, conduction network disruption, and irregular electrical signal propagation, which may further induce myocardial remodeling and even lead to heart failure.
View Article and Find Full Text PDFDiagn Interv Imaging
December 2024
IHU LIRYC, Heart Rhythm Disease Institute, Université de Bordeaux, INSERM U1045, 33604, Pessac, France; Department of Diagnostic and Interventional Radiology, Lausanne University Hospital and University of Lausanne, 1011 Lausanne, Switzerland; Department of Cardiovascular Imaging, Hôpital Cardiologique du Haut-Lévêque, CHU de Bordeaux, 33604 Pessac, France. Electronic address:
Purpose: The purpose of this study was to introduce and evaluate a novel two-dimensional wideband black-blood (BB) LGE sequence, incorporating wideband inversion recovery, wideband T2 preparation, and non-rigid motion correction (MOCO) reconstruction, to improve myocardial scar detection and address artifacts associated with implantable cardioverter defibrillators (ICDs).
Materials And Methods: The wideband MOCO free-breathing BB-LGE sequence was tested on a sheep with ischemic scar and in 22 patients with cardiac disease, including 15 with cardiac implants, at 1.5 T.
Cureus
November 2024
Cardiology, Henry Ford Health System, Detroit, USA.
Ventricular pseudoaneurysm (PSA) is a ventricular outpouching contained by adherent pericardium or myocardial scar tissue and represents a rare but potentially fatal complication of acute myocardial infarction (AMI). The vast majority of cases involve the left ventricular apex, in the area of infarct. It is extremely rare to see PSA formation within the interventricular septum (IVS).
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