scholarly journals Left ventricular systolic and diastolic function during orthostatic heat stress

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Michael D Nelson ◽  
Luis A Altamirano‐Diaz ◽  
Stewart R Petersen ◽  
Timothy P Just ◽  
Darren DeLorey ◽  
...  
Keyword(s):  
Heat Stress ◽  
Diastolic Function ◽  
Left Ventricular ◽  
Systolic And Diastolic Function

Left ventricular systolic and diastolic function during tilt-table positioning and passive heat stress in humans

2011 ◽  
Vol 301 (2) ◽  
pp. H599-H608 ◽  
Author(s):  
Michael D. Nelson ◽  
Luis A. Altamirano-Diaz ◽  
Stewart R. Petersen ◽  
Darren S. DeLorey ◽  
Michael K. Stickland ◽  
...  
Keyword(s):  
Heat Stress ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Diastolic Function ◽  
Venous Return ◽  
Systolic Function ◽  
Left Ventricular ◽  
Tilt Table ◽  
Head Up Tilt ◽  
Systolic And Diastolic Function

The ventricular response to passive heat stress has predominantly been studied in the supine position. It is presently unclear how acute changes in venous return influence ventricular function during heat stress. To address this question, left ventricular (LV) systolic and diastolic function were studied in 17 healthy men (24.3 ± 4.0 yr; mean ± SD), using two-dimensional transthoracic echocardiography with Doppler ultrasound, during tilt-table positioning (supine, 30° head-up tilt, and 30° head-down tilt), under normothermic and passive heat stress (core temperature 0.8 ± 0.1°C above baseline) conditions. The supine heat stress LV volumetric and functional response was consistent with previous reports. Combining head-up tilt with heat stress reduced end-diastolic (25.2 ± 4.1%) and end-systolic (65.4 ± 10.5%) volume from baseline, whereas heart rate (37.7 ± 2.0%), ejection fraction (9.4 ± 2.4%), and LV elastance (37.7 ± 3.6%) increased, and stroke volume (−28.6 ± 9.4%) and early diastolic inflow (−17.5 ± 6.5%) and annular tissue (−35.6 ± 7.0%) velocities were reduced. Combining head-down tilt with heat stress restored end-diastolic volume, whereas LV elastance (16.8 ± 3.2%), ejection fraction (7.2 ± 2.1%), and systolic annular tissue velocities (22.4 ± 5.0%) remained elevated above baseline, and end-systolic volume was reduced (−15.3 ± 3.9%). Stroke volume and the early and late diastolic inflow and annular tissue velocities were unchanged from baseline. This investigation extends previous work by demonstrating increased LV systolic function with heat stress, under varied levels of venous return, and highlights the preload dependency of early diastolic function during passive heat stress.

Abstract 402: Vitamin C Deficiency Impairs Cardiac Function and Post-infarction Survival in the Mouse

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Adolfo G Mauro ◽  
Donatas Kraskauskas ◽  
Bassem M Mohammed ◽  
Bernard J Fisher ◽  
Eleonora Mezzaroma ◽  
...  
Keyword(s):  
Vitamin C ◽  
Cardiac Function ◽  
Diastolic Function ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Additional Group ◽  
Gulonolactone Oxidase ◽  
Low Levels ◽  
Systolic And Diastolic Function

Introduction: L-gulonolactone oxidase (Gulo) is the rate limiting enzyme for Vitamin C (VitC) biosynthesis. Humans rely on dietary VitC for collagen synthesis, extracellular matrix formation, and tissue regeneration. VitC deficiency is an unrecognized condition and its role in cardiac homeostasis and post-acute myocardial infarction (AMI) remodeling is unknown. Hypothesis: Low levels of VitC impair cardiac function and tissue repair following AMI. Methods: Adult male Gulo -/- knockout mice (C57BL6 background, N=8) and control C57BL (N=8), which are able to synthesize VitC were used. VitC deficiency was maintained supplying low levels of VitC (30mg/l) to Gulo -/- mice in drinking water. Mice underwent M-mode and Doppler echocardiography to measure left ventricular (LV) diameters and wall thicknesses, fractional shortening (FS), E and A waves, E/A ratio, isovolumetric relaxation time (IRT) and myocardial performance index (MPI). Experimental AMI was induced by coronary artery ligation for 7 days. An additional group of Gulo -/- were mice supplemented with physiological levels of VitC (330 mg/l) and underwent AMI. Results: VitC deficient Gulo -/- mice exhibited significantly reduced LV wall thicknesses, reduced FS, and impaired diastolic function, measured as significantly reduced E/A ratio and longer IRT (Panel A, B & C). Following AMI, 100% (8/8) of deficient Gulo -/- mice died within 5 days. Supplementation with physiological levels of VitC significantly improved survival after AMI (Panel D). Conclusion: VitC deficiency impairs systolic and diastolic function. Moreover, VitC is critical for the post-AMI survival.

Abstract 18506: Relief of Myocardial Edema in Advanced Decompensated Heart Failure is Associated with Improved Left Ventricular Systolic and Diastolic Function

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Frederik H Verbrugge ◽  
Endry Willems ◽  
Philippe B Bertrand ◽  
Ellen Gielen ◽  
Wilfried Mullens ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Index ◽  
Diastolic Function ◽  
T2 Mapping ◽  
Myocardial Edema ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Volume Index ◽  
Systolic And Diastolic Function ◽  
Cmr Imaging

Introduction: Cardiac magnetic resonance (CMR) imaging with quantitative T2-mapping allows identi[[Unable to Display Character: &#64257;]]cation of myocardial edema, improving risk-stratification in acute coronary syndromes and myocarditis. Hypothesis: Global myocardial edema contributes to left ventricular (LV) dysfunction in advanced decompensated heart failure (ADHF). Methods: CMR with quantitative T2-mapping was performed in consecutive ADHF patients (n=17) undergoing right heart catheterization for worsening dyspnea and volume overload. Patients received vasodilators and diuretics to achieve pulmonary capillary wedge pressure (PCWP) ≤18 mmHg and central venous pressure (CVP) ≤10 mmHg, while maintaining mean arterial pressure ≥65 mmHg. After reaching hemodynamic targets, the pulmonary arterial catheter was removed and CMR imaging repeated. Changes in LV T2-values, hemodynamics, and CMR volumetric measurements were compared. Results: Study patients (64±11 years, male 88%, LV ejection fraction 23±8%, ischemic cardiomyopathy 50%) received decongestive treatment during 5±2 days. PCWP and CVP decreased from 25±7 to 17±4 mmHg and 13±6 to 7±3 mmHg, respectively (p<0.001 for both), while cardiac index increased from 2.14±0.60 to 2.58±0.49 L/min/m 2 (p=0.012). LV T2-values dropped consistently from 59.6±4.9 ms to 56.3±5.2 ms after decongestion (p=0.002; Figure). Decreasing LV T2-values correlated well to both decreasing PCWP (r=0.75; p=0.001) and increasing cardiac index (r=0.58; p=0.023). Although LV end-diastolic volume index (142±31 to 135±34 mL/m 2 ; p=0.033) and end-systolic volume index (110±29 to 99±33 mL/m 2 ; p=0.001) both decreased significantly, the extent of these changes were not correlated to changing T2-values (r=0 and 0.11, respectively; p=ns). Conclusions: Global LV myocardial edema is observed in ADHF and reversible with successful decongestive therapy. Relief of myocardial edema strongly correlates with improvements in systolic and diastolic function.

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