scholarly journals In vivo quantification of myocardial stiffness in hypertensive porcine hearts using MR elastography

2016 ◽  
Vol 45 (3) ◽  
pp. 813-820 ◽  
Author(s):  
Ria Mazumder ◽  
Samuel Schroeder ◽  
Xiaokui Mo ◽  
Bradley D Clymer ◽  
Richard D White ◽  
...  
2011 ◽  
Vol 33 (5) ◽  
pp. 1224-1228 ◽  
Author(s):  
Arunark Kolipaka ◽  
Kiaran P. McGee ◽  
Armando Manduca ◽  
Nandan Anavekar ◽  
Richard L. Ehman ◽  
...  

2013 ◽  
Vol 305 (4) ◽  
pp. H575-H589 ◽  
Author(s):  
Katarzyna Kazmierczak ◽  
Ellena C. Paulino ◽  
Wenrui Huang ◽  
Priya Muthu ◽  
Jingsheng Liang ◽  
...  

The functional consequences of the familial hypertrophic cardiomyopathy A57G (alanine-to-glycine) mutation in the myosin ventricular essential light chain (ELC) were assessed in vitro and in vivo using previously generated transgenic (Tg) mice expressing A57G-ELC mutant vs. wild-type (WT) of human cardiac ELC and in recombinant A57G- or WT-protein-exchanged porcine cardiac muscle strips. Compared with the Tg-WT, there was a significant increase in the Ca2+ sensitivity of force (ΔpCa50 ≅ 0.1) and an ∼1.3-fold decrease in maximal force per cross section of muscle observed in the mutant preparations. In addition, a significant increase in passive tension in response to stretch was monitored in Tg-A57G vs. Tg-WT strips indicating a mutation-induced myocardial stiffness. Consistently, the hearts of Tg-A57G mice demonstrated a high level of fibrosis and hypertrophy manifested by increased heart weight-to-body weight ratios and a decreased number of nuclei indicating an increase in the two-dimensional size of Tg-A57G vs. Tg-WT myocytes. Echocardiography examination showed a phenotype of eccentric hypertrophy in Tg-A57G mice, enhanced left ventricular (LV) cavity dimension without changes in LV posterior/anterior wall thickness. Invasive hemodynamics data revealed significantly increased end-systolic elastance, defined by the slope of the pressure-volume relationship, indicating a mutation-induced increase in cardiac contractility. Our results suggest that the A57G allele causes disease by means of a discrete modulation of myofilament function, increased Ca2+ sensitivity, and decreased maximal tension followed by compensatory hypertrophy and enhanced contractility. These and other contributing factors such as increased myocardial stiffness and fibrosis most likely activate cardiomyopathic signaling pathways leading to pathologic cardiac remodeling.


2002 ◽  
Vol 17 (1) ◽  
pp. 72-85 ◽  
Author(s):  
Elijah E.W. Van Houten ◽  
Marvin M. Doyley ◽  
Francis E. Kennedy ◽  
John B. Weaver ◽  
Keith D. Paulsen

2017 ◽  
Vol 79 (2) ◽  
pp. 1043-1051 ◽  
Author(s):  
Arvin Arani ◽  
Hoon-Ki Min ◽  
Nikoo Fattahi ◽  
Nicholas M. Wetjen ◽  
Joshua D. Trzasko ◽  
...  

2007 ◽  
Vol 33 (11) ◽  
pp. 1706-1719 ◽  
Author(s):  
Stephen J. Hsu ◽  
Richard R. Bouchard ◽  
Douglas M. Dumont ◽  
Patrick D. Wolf ◽  
Gregg E. Trahey

1997 ◽  
Vol 272 (3) ◽  
pp. H1382-H1390 ◽  
Author(s):  
K. Todaka ◽  
J. Wang ◽  
G. H. Yi ◽  
M. Knecht ◽  
R. Stennett ◽  
...  

Exercise training improves functional class in patients with chronic heart failure (CHF) via effects on the periphery with no previously documented effect on intrinsic left ventricular (LV) properties. However, because methods used to evaluate in vivo LV function are limited, it is possible that some effects of exercise training on the failing heart have thus far eluded detection. Twelve dogs were instrumented for cardiac pacing and hemodynamic recordings. Hearts were paced rapidly for 4 wk. Six of the dogs received daily treadmill exercise (CHF(EX), 4.4 km/h, 2 h/day) concurrent with rapid pacing, while the other dogs remained sedentary (CHFs). Hemodynamic measurements taken in vivo at the end of 4 wk revealed relative preservation of maximum rate of pressure rise (2,540 +/- 440 vs. 1,720 +/- 300 mmHg/s, P < 0.05) and LV end-diastolic pressure (9 +/- 5 vs. 19 +/- 4 mmHg, P < 0.05) in CHF(EX) compared with CHFs. The hearts were then isolated and cross perfused for in vitro measurement of isovolumic pressure-volume relations; these results were compared with those of six normal dogs (N). Systolic function was similarly depressed in both groups of pacing animals [end-systolic elastance (Ees) values of 1.66 +/- 0.47 in CHFs, 1.77 +/- 0.38 in CHF(EX), and 3.05 +/- 0.81 mmHg/ml in N, with no changes in volume axis interceptors of the end-systolic pressure-volume relationship]. The diastolic myocardial stiffness constant, k, was elevated in CHFs and was normalized by exercise training (32 +/- 3 in CHFs, 21 +/- 3 in CHF(EX), 20 +/- 4 in N). Thus daily exercise training preserved in vivo hemodynamics during 4 wk of rapid cardiac pacing and was accompanied by a significant change in diastolic myocardial stiffness in vitro. These findings suggest that changes in heart function may contribute to the overall beneficial hemodynamic effects of exercise training in CHF by a significant effect on diastolic properties.


2018 ◽  
Vol 69 ◽  
pp. 10-18 ◽  
Author(s):  
Charlotte A. Guertler ◽  
Ruth J. Okamoto ◽  
John L. Schmidt ◽  
Andrew A. Badachhape ◽  
Curtis L. Johnson ◽  
...  

2007 ◽  
Vol 87 (6) ◽  
pp. 704-718 ◽  
Author(s):  
Richard L Segal

Physical therapists must be able to determine the activity and passive properties of the musculoskeletal system in order to accurately plan and evaluate therapeutic measures. Discussed in this article are imaging methods that not only allow for the measurement of muscle activity but also allow for the measurement of cellular processes and passive mechanical properties noninvasively and in vivo. The techniques reviewed are T1- and T2-weighted magnetic resonance (MR) imaging, MR spectroscopy, cine–phase-contrast MR imaging, MR elastography, and ultrasonography. At present, many of these approaches are expensive and not readily available in physical therapy clinics but can be found at medical centers. However, there are ways of using these techniques to provide important knowledge about muscle function. This article proposes creative ways in which to use these techniques as evaluative tools.


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