Diastolic suction is impaired by bed rest: MRI tagging studies of diastolic untwisting

2008 ◽  
Vol 104 (4) ◽  
pp. 1037-1044 ◽  
Author(s):  
Todd A. Dorfman ◽  
Boaz D. Rosen ◽  
Merja A. Perhonen ◽  
Tommy Tillery ◽  
Roddy McColl ◽  
...  

Bed rest deconditioning leads to physiological cardiac atrophy, which may compromise left ventricular (LV) filling during orthostatic stress by reducing diastolic untwisting and suction. To test this hypothesis, myocardial-tagged magnetic resonance imaging (MRI) was performed, and maximal untwisting rates of the endocardium, midwall, and epicardium were calculated by Harmonic Phase Analysis (HARP) before and after −6° head-down tilt bed rest for 18 days with ( n = 14) and without exercise training ( n = 10). LV mass and LV end-diastolic volume were measured using cine MRI. Exercise subjects cycled on a supine ergometer for 30 min, three times per day at 75% maximal heart rate (HR). After sedentary bed rest, there was a significant reduction in maximal untwisting rates of the midwall (−46.8 ± 14.3 to −35.4 ± 12.4 °/s; P = 0.04) where untwisting is most reliably measured, and to a lesser degree of certainty in the endocardium (−50.3 ± 13.8 to −40.1 ± 18.5 °/s; P = 0.09); the epicardium was unchanged. In contrast, when exercise was performed in bed, untwisting rates were enhanced at the endocardium (−48.4 ± 20.8 to −72.3 ± 22.3 °/ms; P = 0.05) and midwall (−39.2 ± 12.2 to −59.0 ± 19.6 °/s; P = 0.03). The differential response was significant between groups at the endocardium (interaction P = 0.02) and the midwall (interaction P = 0.004). LV mass decreased in the sedentary group (156.4 ± 30.3 to 149.5 ± 27.9 g; P = 0.07), but it increased slightly in the exercise-trained subjects (156.4 ± 34.3 to 162.3 ± 40.5 g; P = 0.16); (interaction P = 0.03). We conclude that diastolic untwisting is impaired following sedentary bed rest. However, exercise training in bed can prevent the physiological cardiac remodeling associated with bed rest and preserve or even enhance diastolic suction.

2001 ◽  
Vol 91 (2) ◽  
pp. 645-653 ◽  
Author(s):  
Merja A. Perhonen ◽  
Fatima Franco ◽  
Lynda D. Lane ◽  
Jay C. Buckey ◽  
C. Gunnar Blomqvist ◽  
...  

Cardiac muscle adapts well to changes in loading conditions. For example, left ventricular (LV) hypertrophy may be induced physiologically (via exercise training) or pathologically (via hypertension or valvular heart disease). If hypertension is treated, LV hypertrophy regresses, suggesting a sensitivity to LV work. However, whether physical inactivity in nonathletic populations causes adaptive changes in LV mass or even frank atrophy is not clear. We exposed previously sedentary men to 6 ( n = 5) and 12 ( n = 3) wk of horizontal bed rest. LV and right ventricular (RV) mass and end-diastolic volume were measured using cine magnetic resonance imaging (MRI) at 2, 6, and 12 wk of bed rest; five healthy men were also studied before and after at least 6 wk of routine daily activities as controls. In addition, four astronauts were exposed to the complete elimination of hydrostatic gradients during a spaceflight of 10 days. During bed rest, LV mass decreased by 8.0 ± 2.2% ( P = 0.005) after 6 wk with an additional atrophy of 7.6 ± 2.3% in the subjects who remained in bed for 12 wk; there was no change in LV mass for the control subjects (153.0 ± 12.2 vs. 153.4 ± 12.1 g, P = 0.81). Mean wall thickness decreased (4 ± 2.5%, P = 0.01) after 6 wk of bed rest associated with the decrease in LV mass, suggesting a physiological remodeling with respect to altered load. LV end-diastolic volume decreased by 14 ± 1.7% ( P = 0.002) after 2 wk of bed rest and changed minimally thereafter. After 6 wk of bed rest, RV free wall mass decreased by 10 ± 2.7% ( P = 0.06) and RV end-diastolic volume by 16 ± 7.9% ( P = 0.06). After spaceflight, LV mass decreased by 12 ± 6.9% ( P = 0.07). In conclusion, cardiac atrophy occurs during prolonged (6 wk) horizontal bed rest and may also occur after short-term spaceflight. We suggest that cardiac atrophy is due to a physiological adaptation to reduced myocardial load and work in real or simulated microgravity and demonstrates the plasticity of cardiac muscle under different loading conditions.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
R Egoriti ◽  
F Landreani ◽  
L Costantini ◽  
E Mulder ◽  
D Gerlach ◽  
...  

Abstract Aims Prolonged immobilization generates cardiac deconditioning, a risk factor for cardiovascular disease, and efficient countermeasures (CM) are needed to prevent it. Our aim was to assess by Cine-MRI the effects of long-term strict head-down (−6 degrees) bed-rest (BR) deconditioning, and the effectiveness of high-intensity jump training CM, on left ventricular (LV) function and mass. Methods 23 male participants (29±6 years, 181±6 cm, 77±7 kg) were enrolled. The experiment was conducted at: envihab (Koln, DLR, Germany) as part of the European Space Agency BR studies. Volunteers were randomly allocated to the jump training group (JUMP, n=12) or the control group (CTRL, n=11). A typical training session consisted of 4x10 countermovement jumps and 2x10 hops in a sledge jump system, with 5–6 sessions per week. Steady-state free precession cine-MRI images were obtained (25 frames/cardiac cycle, 8mm thickness, no gap, no overlap) as stack of short-axis images covering the whole LV from base to apex, before (PRE) and after 58-days (HDT58) of BR. Endocardial and epicardial semi-automated contouring was performed using custom software. Results In CTRL group, at HDT58 a reduction in LV mass (9%), end-diastolic (21%), end-systolic (8%) and stroke volume (23%) were observed, while ejection fraction did not change. In JUMP group, the reduction in LV end-diastolic volume was only by 9%, followed by a decrease in end-systolic (10%) and stroke volume (10%), with a preservation of LV mass. In both groups, ejection fraction did not change. Left ventricular changes after 58d BR EDV (ml) ESV (ml) SV (ml) EF (%) Mass (g) CTRL PRE 171 (163; 191) 60 (58; 65) 113 (102; 124) 64 (63; 67) 133 (121; 160) HDT58 143 (131; 149)* 56 (50; 58)* 86 (83; 92)* 62 (60; 63)* 127 (106; 138)* JUMP PRE 156 (140; 204) 70 (61; 84) 91 (78; 117) 58 (56; 60) 118 (104; 134) HDT58 141 (135; 175)* 63 (54; 69)* 90 (78; 92)* 58 (55; 60) 113 (105; 128) Results expressed as median (25th; 75th percentiles). *p<0.05 Wilcoxon non parametric paired test (PRE vs HDT58). CTRL: control group; JUMP: countermeasure group. Conclusions Cardiac adaptation to deconditioning due to immobilization induced by BR resulted in a reduction of cardiac volumes and function, together with a decrease in LV mass. Interestingly, the applied JUMP countermeasure appeared able to partially reverse these effects, in particular by reducing the decrease in end-diastolic volume and preserving LV mass. This information could be useful for better understanding physiologic changes in patients undergoing long periods of immobilization, as well as to apply the studied countermeasure during space flight to reduce cardiac deconditioning. Acknowledgement/Funding Italian Space Agency (contract 2018-7-U.0),CNES/DAR 48ehz747.01950965,BELSPO, via the European Space Agency PRODEX program (PEA 4000110826)


2006 ◽  
Vol 100 (3) ◽  
pp. 1090-1090 ◽  
Author(s):  
Marieta V. Pancheva ◽  
Vladimir S. Panchev ◽  
Adelina V. Suvandjieva

Cardiac muscle adapts well to changes in loading conditions. For example, left ventricular (LV) hypertrophy may be induced physiologically (via exercise training) or pathologically (via hypertension or valvular heart disease). If hypertension is treated, LV hypertrophy regresses, suggesting a sensitivity to LV work. However, whether physical inactivity in nonathletic populations causes adaptive changes in LV mass or even frank atrophy is not clear. We exposed previously sedentary men to 6 ( n = 5) and 12 ( n = 3) wk of horizontal bed rest. LV and right ventricular (RV) mass and end-diastolic volume were measured using cine magnetic resonance imaging (MRI) at 2, 6, and 12 wk of bed rest; five healthy men were also studied before and after at least 6 wk of routine daily activities as controls. In addition, four astronauts were exposed to the complete elimination of hydrostatic gradients during a spaceflight of 10 days. During bed rest, LV mass decreased by 8.0 ± 2.2% ( P = 0.005) after 6 wk with an additional atrophy of 7.6 ± 2.3% in the subjects who remained in bed for 12 wk; there was no change in LV mass for the control subjects (153.0 ± 12.2 vs. 153.4 ± 12.1 g, P = 0.81). Mean wall thickness decreased (4 ± 2.5%, P = 0.01) after 6 wk of bed rest associated with the decrease in LV mass, suggesting a physiological remodeling with respect to altered load. LV end-diastolic volume decreased by 14 ± 1.7% ( P = 0.002) after 2 wk of bed rest and changed minimally thereafter. After 6 wk of bed rest, RV free wall mass decreased by 10 ± 2.7% ( P = 0.06) and RV end-diastolic volume by 16 ± 7.9% ( P = 0.06). After spaceflight, LV mass decreased by 12 ± 6.9% ( P = 0.07). In conclusion, cardiac atrophy occurs during prolonged (6 wk) horizontal bed rest and may also occur after short-term spaceflight. We suggest that cardiac atrophy is due to a physiological adaptation to reduced myocardial load and work in real or simulated microgravity and demonstrates the plasticity of cardiac muscle under different loading conditions.


2013 ◽  
Vol 114 (8) ◽  
pp. 1052-1057 ◽  
Author(s):  
Angela L. Spence ◽  
Louise H. Naylor ◽  
Howard H. Carter ◽  
Lawrence Dembo ◽  
Connor P. Murray ◽  
...  

Cardiac adaptation in response to exercise has historically been described using echocardiography. Cardiac magnetic resonance (CMR), however, has evolved as a preferred imaging methodology for cardiac morphological assessment. While direct imaging modality comparisons in athletes suggest that large absolute differences in cardiac dimensions exist, it is currently unknown whether changes in cardiac morphology in response to exercise training are comparable when using echocardiography and CMR. Twenty-two young men were randomly assigned to undertake a supervised and intensive endurance or resistance exercise-training program for 24 wk. Echocardiography and CMR assessment of left ventricular (LV) mass, LV end-diastolic volume, internal cavity dimensions, and wall thicknesses were completed before and after training. At baseline, pooled data for all cardiac parameters were significantly different between imaging methods, while LV mass ( r = 0.756, P < 0.001) and volumes (LV end-diastolic volume, r = 0.792, P < 0.001) were highly correlated across modalities. Changes in cardiac morphology data with exercise training were not significantly related when echocardiographic and CMR measures were compared. For example, posterior wall thickness increased by 8.3% ( P < 0.05) when assessed using echocardiography, but decreased by 2% when using CMR. In summary, echocardiography and CMR imaging modalities produce findings that differ with respect to changes in cardiac size and volume following exercise training.


2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Marie Schroeder ◽  
Angus Z Lau ◽  
Albert P Chen ◽  
Jennifer Barry ◽  
Damian J Tyler ◽  
...  

Disordered metabolic substrate utilisation has been implicated in the pathogenesis of heart failure (HF). Hyperpolarised (HYP) 13C magnetic resonance, a technique in which the fate of 13C-labelled metabolites can be followed using MR imaging or spectroscopy, has enabled non-invasive assessment of metabolism. The aim of this study was to monitor carbohydrate metabolism alongside cardiac structure, function, and energetics, throughout HF progression. HF was induced in pigs (n=5) by right ventricular pacing at 188 bpm for 5 weeks. Pigs were examined at weekly time points: cine MRI assessed cardiac structure and function, HYP 13C2-pyruvate was administered intravenously and 13C MRS was used to assess 13C-glutamate production via Krebs cycle, 31P MRS assessed myocardial energetics, and HYP 13C1-pyruvate was administered to enable MRI of H13CO3- production from pyruvate dehydrogenase (PDH). At baseline, pigs had a normal left ventricular (LV) cardiac index (CI) and end diastolic volume (EDVi). The PCr/ATP was 2.3 ± 0.2. The 13C-glutamate/13C2-pyruvate was 4.3 ± 0.9%, and the H13CO3-/13C1-pyruvate ratio was 1.6 ± 0.2%. After 1–2 weeks of pacing, CI decreased to 3.3 ± 0.5 l/min/m2, PCr/ATP decreased to 1.7 ± 0.1, and 13C-glutamate/13C2-pyruvate decreased to 2.1 ± 0.6%. With the onset of HF, EDVi increased to 140.3 ± 14.1 ml/m2 and H13CO3-/13C1-pyruvate decreased to 0.5 ± 0.2%. In conclusion, we observed an early defect in Krebs' cycle that occurred alongside impaired cardiac energetics and function. Carbohydrate oxidation via PDH was maintained until the onset of HF. These results encourage use of metabolic therapies to delay/prevent the onset of heart failure in patients.


1998 ◽  
Vol 85 (4) ◽  
pp. 1368-1375 ◽  
Author(s):  
R. L. Stepien ◽  
K. W. Hinchcliff ◽  
P. D. Constable ◽  
J. Olson

The cardiac morphology of 77 conscious Alaskan sled dogs before and after 5 mo of endurance training (20 km/day team pulling a sled and musher) was studied using two-dimensional and M-mode echocardiography. Subgroups included dogs with at least one season of previous training (“veterans”) and dogs undergoing their first season of training (“rookies”). Training resulted in a significant ( P< 0.05) decrease in resting heart rate (−15%) and significant increases in interventricular septal thickness (systole, 15%; diastole, 13%), left ventricular (LV) internal dimension in diastole (LVIDd, 4%), LV free wall thickness in systole (9%) and diastole (LVWd, 9%), and left atrial diameter (5%) in all dogs, but the increase in LVWd was greater in rookies (16%) than in veterans (7%). Training increased end-diastolic volume index (8%), LV mass index (24%), and heart weight index (24%) and decreased the LVIDd-to-LVWd ratio (−6%) but did not alter cardiac index. We conclude that increased LV mass attributable to LV dilation and hypertrophy is associated with endurance training in Alaskan sled dogs. Disproportionate LV wall thickening accompanying LV dilation suggests that cardiac morphological changes are due to volume and pressure loading. These training-induced changes are similar to those documented in human athletes undergoing combined isometric and isotonic training and differ from studies of dogs trained on treadmills.


Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Michael P Bancks ◽  
Mercedes Carnethon ◽  
Lisa S Chow ◽  
David R Jacobs ◽  
Satoru Kishi ◽  
...  

Introduction: Whether trajectories in fasting glucose (FG) and insulin resistance (HOMA-IR) during young adulthood, before the onset of diabetes, are associated with cardiac function and structure in middle adulthood is unclear. Hypothesis: We tested the hypothesis that as compared to low-stable trajectory of FG and HOMA-IR, an increasing trajectory for each would be associated with worse cardiac structure and function in middle adulthood. Methods: We determined FG and HOMA-IR for 2,198 CARDIA participants, age 18-30 years, at baseline (1985-1986) and 7, 10, 15, 20, and 25 year follow-up exams who fasted for >8 hours and were not pregnant and were free from diabetes at all exams. At year 30 (2016), Doppler echocardiography and 2D-guided M-mode echocardiography was performed, measuring left atrial dimension, relative wall thickness, left ventricular (LV) mass, LV mass indexed to height, LV ejection fraction percentage, LV end-diastolic and systolic volume, and LV mass to volume ratio. Trajectories were determined using latent class analysis (SAS Proc Traj). We used multivariable linear regression to estimate adjusted means for echo measures according to FG and HOMA-IR trajectory group after adjustment for potential confounding factors. Results: For individuals free from diabetes in midlife, we identified three trajectory groups for both FG and HOMA-IR, low-stable to increasing, moderate-increasing, and high-increasing. Compared to low-stable trajectory for FG, increasing trajectory was associated with greater LV end-diastolic volume, whereas for HOMA-IR increasing trajectory was associated with lower LV end-diastolic volume ( Table ). Increasing FG trajectory was also associated with greater left atrial dimension, while HOMA-IR was not. Conclusion: Trajectory of both FG and HOMA-IR during young adulthood, in the absence of diabetes, was most prominently and differentially associated with LV end-diastolic volume. Future research should elaborate on differential associations of FG and HOMA-IR trajectory.


1978 ◽  
Vol 235 (6) ◽  
pp. H767-H775 ◽  
Author(s):  
G. A. Geffin ◽  
M. A. Vasu ◽  
D. D. O'Keefe ◽  
D. G. Pennington ◽  
A. J. Erdmann ◽  
...  

In dogs anesthetized with chloralose-urethan on right heart bypass, left ventricular (LV) performance was assessed at constant LV stroke work before and for up to 2.5 h after crystalloid hemodilution was established. Lowering the hematocrit from 43.3 +/- 1.3% to 13.6 +/- 1.7% (SE) did not significantly change LV end-diastolic pressure (LVEDP) initially. After 80 min LVEDP increased slightly by 1.7 +/- 0.6 cmH2O (P less than 0.05) at a stroke work of 17.3 +/- 2.3 g.m. The value of dP/dt did not change significantly throughout. When LV function curves were generated by increasing cardiac output, the stroke work attained at an LVEDP of 10 cmH2O decreased with hemodilution from 23.9 +/- 3.5 to 20.8 +/- 3.9 g.m (NS). LV wall water content increased with hemodilution, from which it could be calculated that there was an 18.6% increase in LV mass. Thus, despite an increase in LV external girth demonstrated by LV circumferential gauges, it is possible that increased wall thickness due to the water gain resulted in little change or an actual decrease in LV end-diastolic volume. Thus, profound hemodilution can be attained with only slight depression of LV performance.


Author(s):  
Laura Banks ◽  
Saif Al-Mousawy ◽  
Mustafa A Altaha ◽  
Kaja Koneiczny ◽  
Wesseem Osman ◽  
...  

Background: The relationship between structural and electrical remodeling in the heart, particularly after long-standing endurance training, remains unclear. Signal-averaged electrocardiogram (SAECG) may provide a more sensitive method to evaluate cardiac remodeling than a 12-lead electrocardiogram (ECG). Accurate measures of electrical function (SAECG filtered QRS duration (fQRSd) and late potentials (LP) and left-ventricular mass (cardiac magnetic resonance, CMR) can allow an assessment of structural and electrical remodeling. Methods: Endurance athletes (45-65 years old, >10 years of endurance sport), screened to exclude cardiac disease, had standardized 12-lead ECG, SAECG, resting echocardiogram (ECHO), and CMR performed. SAECG fQRSd was correlated with QRS duration on the 12-lead ECG, and ECHO and CMR-derived left ventricular (LV) mass. Results: Participants (n=82, 67% male, mean age: 54±6 years, mean VO2max: 50±7 ml/kg/min) had a CMR-derived LV mass of 118±28 g/m2 and a fQRSd of 112±8 ms (46% had abnormal fQRSd (>114 msec), and 51% met clinical threshold for abnormal SAECG). fQRSd was positively correlated with the 12-lead ECG QRS duration (r=0.83), ECHO-derived LV mass (r=0.60), CMR-derived LV mass (r=0.58) and LV end-diastolic volume (r=0.63, p<0.001 for all). fQRSd had higher correlations with ECHO and CMR-derived LV mass than 12-lead ECG (p<0.0008 and p<0.0005, respectively). Conclusion: In a healthy cohort of middle-aged endurance athletes, the SAECG is often abnormal by conventional criteria, and is correlated with structural remodeling, but CMR evaluation does not indicate pathologic structural remodeling. SAECG fQRSd is superior to the 12-lead ECG for the electrocardiographic evaluation of LV mass.


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