The Relationship of Filling Rate and Stroke Volume as a Marker of Left Ventricular Early Filling Dysfunction

2005 ◽  
Vol 11 (6) ◽  
pp. S111
2010 ◽  
Vol 108 (5) ◽  
pp. 1259-1266 ◽  
Author(s):  
Ben T. Esch ◽  
Jessica M. Scott ◽  
Mark J. Haykowsky ◽  
Ian Paterson ◽  
Darren E. R. Warburton ◽  
...  

Endurance-trained individuals exhibit larger reductions in left ventricular (LV) end-diastolic volume in response to lower body negative pressure (LBNP) compared with normally active individuals. However, the relationship between LV torsion and untwisting and the LV volume response to LBNP in endurance athletes is unknown. Eight endurance-trained athletes [maximal oxygen consumption (V̇o2max): 66.4 ± 7.2 ml·kg−1·min−1] and eight normally active individuals (V̇o2max: 41.9 ± 9.0 ml·kg−1·min−1) (all men) underwent two cardiac magnetic resonance imaging (MRI) assessments, the first during supine rest and the second during −30 mmHg LBNP. Right ventricular (RV) and LV volumes were assessed, myocardial tagging was applied in order to quantify LV peak torsion and peak untwisting rate, and filling rates were measured with phase-contrast MRI. In response to LBNP, endurance-trained individuals had greater reductions in RV and LV end-diastolic volume and stroke volume ( P < 0.05). Endurance athletes had reduced untwisting rates (20.3 ± 8.7°/s), while normally active individuals had increased untwisting rates (−16.2 ± 32.1°/s) in response to LBNP ( P < 0.05). Changes in peak untwisting rate were significantly correlated with change in peak torsion ( R = −0.87, P < 0.05), with the change in early filling rate and V̇o2max, but not with changes in end-diastolic or end-systolic volume ( P > 0.05). We conclude that increased untwisting rates in normally active subjects may mitigate the drop in early filling rate with LBNP and thus may be a compensatory mechanism for the reduction in stroke volume with volume unloading. The opposite response in athletes, who showed a decreased untwisting rate, may contribute to their larger reductions in LV end-diastolic and stroke volumes with volume unloading and their orthostatic intolerance.


2014 ◽  
Vol 64 (19) ◽  
pp. 1971-1980 ◽  
Author(s):  
Filip Zemrak ◽  
Mark A. Ahlman ◽  
Gabriella Captur ◽  
Saidi A. Mohiddin ◽  
Nadine Kawel-Boehm ◽  
...  

Open Heart ◽  
2018 ◽  
Vol 5 (2) ◽  
pp. e000831 ◽  
Author(s):  
Melissa Suzanne Burroughs Peña ◽  
Katrina Swett ◽  
Robert C Kaplan ◽  
Krista Perreira ◽  
Martha Daviglus ◽  
...  

ObjectiveTo describe the relationship of household secondhand smoke (SHS) exposure and cardiac structure and function.MethodsParticipants (n=1069; 68 % female; age 45–74 years) without history of tobacco use, coronary artery disease or severe valvular disease were included. Past childhood (starting at age <13 years), adolescent/adult and current exposure to household SHS was assessed. Survey linear regression analyses were used to model the relationship of SHS exposure and echocardiographic measures of cardiac structure and function, adjusting for covariates (age, sex, study site, alcohol use, physical activity and education).ResultsSHS exposure in childhood only was associated with reduced E/A velocity ratio (β=−0.06 (SE 0.02), p=0.008). SHS exposure in adolescence/adult only was associated with increased left ventricular ejection fraction (LVEF) (1.2 (0.6), p=0.04), left atrial volume index (1.7 (0.8), p=0.04) and decreased isovolumic relaxation time (−0.003 (0.002), p=0.03). SHS exposure in childhood and adolescence/adult was associated with worse left ventricular global longitudinal strain (LVGLS) (two-chamber) (0.8 (0.4), p= 0.049). Compared with individuals who do not live with a tobacco smoker, individuals who currently live with at least one tobacco smoker had reduced LVEF (−1.4 (0.6), p=0.02), LVGLS (average) (0.9 (0.40), p=0.03), medial E′ velocity (−0.5 (0.2), p=0.01), E/A ratio (−0.09 (0.03), p=0.003) and right ventricular fractional area change (−0.02 (0.01), p=0.01) with increased isovolumic relaxation time (0.006 (0.003), p=0.04).ConclusionsPast and current household exposure to SHS was associated with abnormalities in cardiac systolic and diastolic function. Reducing household SHS exposure may be an opportunity for cardiac dysfunction prevention to reduce the risk of future clinical heart failure.


2006 ◽  
Vol 54 (2) ◽  
pp. S344.2-S344
Author(s):  
A. Maksoud ◽  
I. Porter ◽  
K. Schneider ◽  
R. Joseph ◽  
P. Lebourveau ◽  
...  

Cardiology ◽  
2001 ◽  
Vol 96 (1) ◽  
pp. 7-15 ◽  
Author(s):  
Takeshi Motoyama ◽  
Hiroaki Kawano ◽  
Nobutaka Hirai ◽  
Ryusuke Tsunoda ◽  
Yasushi Moriyama ◽  
...  

2020 ◽  
Vol 51 (3) ◽  
pp. 172-181 ◽  
Author(s):  
Carl P. Walther ◽  
Wolfgang C. Winkelmayer ◽  
Anita Deswal ◽  
Jingbo Niu ◽  
Sankar D. Navaneethan

Background: Acute kidney injury (AKI) frequently complicates hospitalizations for left ventricular assist device (LVAD) implantation. Little is known about the relationship of AKI with subsequent readmissions, and we investigated the relationship of AKI during LVAD implantation hospitalization with all-cause and cause-specific 30-day readmissions. Methods: We used a United States (US) nationwide all-payer administrative database, identifying patients who underwent implantable LVAD placement 2010–2015. Patients were classified into 3 mutually exclusive groups based on presence and severity of AKI during the LVAD placement hospitalization: no AKI, AKI, and AKI requiring dialysis (AKI-D). Outcomes were all-cause and cause-specific 30-day readmissions. Results: Within 30 days after discharge 25.4% of patients were readmitted. Of those without AKI, 23.9% were readmitted, compared to 25.5% of those with AKI and 42.2% of those with AKI-D. Compared to no AKI (adjusted for demographics, index hospitalization and chronic comorbidity factors, and year), odds of 30-day readmission were 2.18 (95% CI 1.37–3.49) times higher for those with AKI-D, whereas those with AKI not requiring dialysis had similar 30-day readmission risk (OR 1.03 [95% CI 0.89–1.20]). Those with AKI-D had higher risk of 30-day readmission for infection (OR 2.02 [95% CI 1.13–3.61]), gastrointestinal (GI) bleed (2.32 [95% CI 1.24–4.34]), and kidney disease (13.9 [95% CI 4.0–48]). There was no increased risk for stroke readmission with AKI or AKI-D. Conclusion: AKI-D was associated with highest ­30-day readmission risk, possibly related to negatively synergistic effects of LVAD, kidney dysfunction, and dialysis related factors on infection and GI bleeding risks. AKI alone was not associated with increased readmission risk.


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