Noninvasive Detection of Fibrosis Applying Contrast-Enhanced Cardiac Magnetic Resonance in Different Forms of Left Ventricular Hypertrophy

Rudolph, André; Abdel-Aty, Hassan; Bohl, Steffen; Boyé, Philipp; Zagrosek, Anja; Dietz, Rainer; Schulz‐Menger, Jeanette

doi:10.1016/j.jacc.2008.08.064

Cited by 325 publications

(225 citation statements)

References 57 publications

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“…This, alongside the reduction in left atrial size seen in men but not women, may reflect a greater improvement in left ventricular cavity pressure, trans-mitral gradient and mitral valve tethering forces in men. 25,29 , however, these studies used different methods of MF quantification which most likely accounts for the increased values reported, rather than a true difference in absolute levels of MF.…”

Section: Discussionmentioning

confidence: 97%

Sex-related differences in left ventricular remodeling in severe aortic stenosis and reverse remodeling after aortic valve replacement: A cardiovascular magnetic resonance study

Dobson

Fairbairn

Musa

et al. 2016

American Heart Journal

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Section: Discussionmentioning

confidence: 97%

Sex-related differences in left ventricular remodeling in severe aortic stenosis and reverse remodeling after aortic valve replacement: A cardiovascular magnetic resonance study

Dobson

Fairbairn

Musa

et al. 2016

American Heart Journal

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“…47,77, 78 Approximately 70% of HCM patients have evidence of LGE on CMR. 79, 80 Olivotto et al found substantial amounts of LGE in a subset of patients with HCM and low-normal EF values (50-65%) in comparison with patients with higher EF, 81 but little or no association was found between EF and several standard clinical and demographic parameters, such as age, sex, LV cavity dimensions, wall thickness or LVM. Myocardial fibrosis was an independent predictor of adverse outcome in the study by O'Hanlon et al, which assessed the presence, amount and prognostic role of LGE in 217 patients with HCM followed for 3.1±1.7 years.…”

Section: Myocardial Fibrosis In Primary Lvhmentioning

confidence: 98%

From Left Ventricular Hypertrophy to Dysfunction and Failure

Lazzeroni

Rimoldi

Camici

2016

Circ J

119

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Left ventricular hypertrophy (LVH) is growth in left ventricular mass caused by increased cardiomyocyte size. LVH can be a physiological adaptation to strenuous physical exercise, as in athletes, or it can be a pathological condition, which is either genetic or secondary to LV overload. Physiological LVH is usually benign and regresses upon reduction/cessation of physical activity. Pathological LVH is a compensatory phenomenon, which eventually may become maladaptive and evolve towards progressive LV dysfunction and heart failure (HF). Both interstitial and replacement fibrosis play a major role in the progressive decompensation of the hypertrophied LV. Coronary microvascular dysfunction (CMD) and myocardial ischemia, which have been demonstrated in most forms of pathological LVH, have an important pathogenetic role in the formation of replacement fibrosis and both contribute to the evolution towards LV dysfunction and HF. Noninvasive imaging allows detection of myocardial fibrosis and CMD, thus providing unique information for the stratification of patients with LVH. DCM is generally caused by viral/bacterial myocarditis, exposure to cardiotoxic substances or is a manifestation of a systemic disease. Before cell death and fibrotic repair occur, multiple factors contribute to contractile dysfunction, including abnormalities in sarcolemmal integrity, energy production, calcium handling and force transmission. 10 Both systolic and diastolic dysfunction worsen with time and EF is progressively reduced, with symptoms and signs of HF. Secondary LVHCardiomyocyte hypertrophy is the primary mechanism by which the heart counteracts a protracted increase in stress (or load) on the ventricular wall. 11 According to Laplace's law, 12 wall stress is directly related to LV cavity size and intracavitary pressure and inversely related to wall thickness. Thus, wall thickening will counteract, at least in part, the increased stress and oxygen demand caused by pressure or volume overload, although, in the long run, this compensatory mechanism may become maladaptive. On the other hand, several other nonhemodynamic factors, including activation of the adrenergic and renin-angiotensin-aldosterone (RAAS) systems, release of growth factors and cytokines, contribute to the development of LVH. 13,14 Pressure Overload In most cases, pressure overload manifests as arterial hypertension (AH) or aortic stenosis (AS).Hypertensive Heart The most common condition associated with an increase in cardiac afterload and wall stress is AH. 15 Approximately 20-60% of patients with uncomplicated AH have evidence of increased LVM on echocardiography. 16 LVM can increase from wall thickening, chamber dilatation or both. Wall thickening occurs more commonly in response to pressure overload whereas chamber dilation occurs more commonly in response to volume overload. Although LV wall thickness is more closely related to systemic diastolic blood pressure (concentric hypertrophy), reflecting pure pressure load caused by increased systemic vascular resistance...

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“…Ischemic areas are known to be localized in the subendocardial area and definitely conform to one of the particular coronary territories. Previous studies reported that the extent of nonviable tissue in a myocardial segment can be used to predict recovery of function after revascularization (28). It is generally unlikely that myocardial scar or fibrosis in which more than 50% of myocardial wall thickness is involved at cardiac MR imaging will resume contractile function in the wake of coronary revascularization (2).…”

Section: Discussionmentioning

confidence: 99%

Quantitative evaluation of ischemic myocardial scar tissue by unenhanced T1 mapping using 3.0 Tesla MR scanner

Okur

Kantarcı

Kizrak³

et al. 2014

Diagn Interv Radiol

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Original Article PURPOSE We aimed to use a noninvasive method for quantifying T1 values of chronic myocardial infarction scar by cardiac magnetic resonance imaging (MRI), and determine its diagnostic performance. MATERIALS AND METHODSWe performed cardiac MRI on 29 consecutive patients with known coronary artery disease (CAD) on 3.0 Tesla MRI scanner. An unenhanced T1 mapping technique was used to calculate T1 relaxation time of myocardial scar tissue, and its diagnostic performance was evaluated. Chronic scar tissue was identified by delayed contrast-enhancement (DE) MRI and T2-weighted images. Sensitivity, specificity, and accuracy values were calculated for T1 mapping using DE images as the gold standard. RESULTSFour hundred and forty-two segments were analyzed in 26 patients. While myocardial chronic scar was demonstrated in 45 segments on DE images, T1 mapping MRI showed a chronic scar area in 54 segments. T1 relaxation time was higher in chronic scar tissue, compared with remote areas (1314±98 ms vs. 1099±90 ms, P < 0.001). Therefore, increased T1 values were shown in areas of myocardium colocalized with areas of DE and normal signal on T2-weighted images. There was a significant correlation between T1 mapping and DE images in evaluation of myocardial wall injury extent (P < 0.05). We calculated sensitivity, specificity, and accuracy as 95.5%, 97%, and 96%, respectively. CONCLUSIONThe results of the present study reveal that T1 mapping MRI combined with T2-weighted images might be a feasible imaging modality for detecting chronic myocardial infarction scar tissue.

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Noninvasive Detection of Fibrosis Applying Contrast-Enhanced Cardiac Magnetic Resonance in Different Forms of Left Ventricular Hypertrophy

Cited by 325 publications

References 57 publications

Sex-related differences in left ventricular remodeling in severe aortic stenosis and reverse remodeling after aortic valve replacement: A cardiovascular magnetic resonance study

Sex-related differences in left ventricular remodeling in severe aortic stenosis and reverse remodeling after aortic valve replacement: A cardiovascular magnetic resonance study

From Left Ventricular Hypertrophy to Dysfunction and Failure

Quantitative evaluation of ischemic myocardial scar tissue by unenhanced T1 mapping using 3.0 Tesla MR scanner

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