Myocardial Tissue Characterization: Histological and Pathophysiological Correlation

Treibel, Thomas A.; White, Steven K; Moon, James

doi:10.1007/s12410-013-9254-9

Cited by 54 publications

(28 citation statements)

References 73 publications

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“…ECV increases in myocardial fibrosis, edema, and expansion of the extracellular space, with subsequent relative decrease in myocyte mass. 27 Conversely, an expanded cellular mass reduces ECV as the distribution volume for conventional extracellular contrast agents is reduced.…”

Section: Discussionmentioning

confidence: 99%

Athletic Cardiac Adaptation in Males Is a Consequence of Elevated Myocyte Mass

McDiarmid

Swoboda

Erhayiem

et al. 2016

Circ: Cardiovascular Imaging

100

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Background—Cardiac remodeling occurs in response to regular athletic training, and the degree of remodeling is associated with fitness. Understanding the myocardial structural changes in athlete’s heart is important to develop tools that differentiate athletic from cardiomyopathic change. We hypothesized that athletic left ventricular hypertrophy is a consequence of increased myocardial cellular rather than extracellular mass as measured by cardiovascular magnetic resonance.Methods and Results—Forty-five males (30 athletes and 15 sedentary age-matched healthy controls) underwent comprehensive cardiovascular magnetic resonance studies, including native and postcontrast T1 mapping for extracellular volume calculation. In addition, the 30 athletes performed a maximal exercise test to assess aerobic capacity and anaerobic threshold. Participants were grouped by athleticism: untrained, low performance, and high performance (O2max <60 or>60 mL/kg per min, respectively). In athletes, indexed cellular mass was greater in high- than low-performance athletes 60.7±7.5 versus 48.6±6.3 g/m2; P<0.001), whereas extracellular mass was constant (16.3±2.2 versus 15.3±2.2 g/m2; P=0.20). Indexed left ventricular end-diastolic volume and mass correlated with O2max (r=0.45, P=0.01; r=0.55, P=0.002) and differed significantly by group (P=0.01; P<0.001, respectively). Extracellular volume had an inverse correlation with O2max (r=−0.53, P=0.003 and left ventricular mass index (r=-0.44, P=0.02).Conclusions—Increasing left ventricular mass in athlete’s heart occurs because of an expansion of the cellular compartment while the extracellular volume becomes relatively smaller: a difference which becomes more marked as left ventricular mass increases. Athletic remodeling, both on a macroscopic and cellular level, is associated with the degree of an individual’s fitness. Cardiovascular magnetic resonance ECV quantification may have a future role in differentiating athlete’s heart from change secondary to cardiomyopathy.

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Section: Discussionmentioning

confidence: 99%

Athletic Cardiac Adaptation in Males Is a Consequence of Elevated Myocyte Mass

McDiarmid

Swoboda

Erhayiem

et al. 2016

Circ: Cardiovascular Imaging

100

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“…By labeling the extracellular myocardial space with gadoliniumbased contrast agent, measurement of native and post-contrast myocardial and blood T1 values allows estimation of the extent of the interstitial myocardial space via the calculation of the percentage or fraction of the myocardial extracellular volume (ECV) [3][4][5][6]. Intended as CMR-derived metrics for myocardial fibrosis [2,[7][8][9][10], ECV supplements native T1 mapping's potential to detect myocardial alterations.…”

Section: Introductionmentioning

confidence: 99%

Cardiac magnetic resonance T1 mapping. Part 1: Aspects of acquisition and evaluation

Reiter

Kräuter

et al. 2018

European Journal of Radiology

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While an enormous number of studies have documented pathological alterations of the myocardial native longitudinal relaxation time (T1) and the fraction of the extracellular myocardial volume (ECV), it has also become clear that continuously evolving T1 mapping sequence, acquisition and evaluation techniques have a substantial impact on quantitative results, making the translation of reported findings into routine clinical use particularly challenging. To provide a basis for the discussion of pathological myocardial T1 and ECV alterations, the present review aims to summarize the methodological aspects of myocardial T1 mapping along with technical and physiological factors influencing results and normal ranges of myocardial native T1 and ECV reported across studies. 2. Sequences and protocols Numerous techniques have been introduced for the generation of cardiac T1 maps [11-22], each of which possesses specific advantages and disadvantages with respect to acquisition time, spatial resolution, accuracy (systematic bias of estimated T1 compared to true T1), and

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“…Consequently, faster T2-mapping imaging is a feasible technique to quantitatively measure IMH in a rat model with myocardial infarction. However, IMH is merely one component of varying characteristics after myocardial infarction ( 20 ), and alternative components, such as inflammation and myocardial vascular obstruction ( 35 , 36 ), should be urgently explored by more investigations.…”

Section: Discussionmentioning

confidence: 99%

Quantitative assessment of salvaged myocardial zone and intramyocardial hemorrhage using non-contrast faster T2 mapping in a rat model by 7T MRI

Zhang

Wang

et al. 2017

Experimental and Therapeutic Medicine

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The aim of this study was to determine the myocardial area at risk (AAR), infarction-core size (IS) and the salvaged myocardial zone (SMZ), and to evaluate the imaging and histological characteristics of intramyocardial hemorrhage (IMH) after myocardial infarction using non-contrast T2 mapping on 7T magnetic resonance imaging (MRI). Twenty Sprague Dawley (SD) rats were randomly divided into the sham and model groups (n=10 in each). In the model group, myocardial infarction models were established by left anterior descending branch ligation. After 24 h, all animals were imaged on a 7.0 Tesla system with cine spiral imaging, T2 mapping with late gadolinium enhancement (LGE). The rats were then sacrificed for measurement of the IS and AAR using 2,3,5-triphenylterazolium chloride (TTC) and hematoxylin and eosin (H&E) staining. T2 mapping revealed that the AAR in the model group was significantly higher than that in the sham group. No remarkable T2 value was noted in the entire heart of the sham group. LGE and TTC staining demonstrated similar IS. T2 mapping and H&E staining revealed a similar AAR as well. T2 mapping characterized the IMH as a phenomenon resulting from the area of hypointensity in the hyperintensity involving the infarct-core zone and corresponding T2 value 928.6±1.52 msec with IMH vs. 35.8±2.61 msec without IMH; n=3 with 18 slices; P=0.032). In conclusion, non-contrast T2 mapping was a reliable approach to quantitatively evaluate the SMZ and IMH.

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Myocardial Tissue Characterization: Histological and Pathophysiological Correlation

Cited by 54 publications

References 73 publications

Athletic Cardiac Adaptation in Males Is a Consequence of Elevated Myocyte Mass

Athletic Cardiac Adaptation in Males Is a Consequence of Elevated Myocyte Mass

Cardiac magnetic resonance T1 mapping. Part 1: Aspects of acquisition and evaluation

Quantitative assessment of salvaged myocardial zone and intramyocardial hemorrhage using non-contrast faster T2 mapping in a rat model by 7T MRI

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