scholarly journals Circulatory Response to Rapid Volume Expansion and Cardiorespiratory Fitness in Fontan Circulation

Author(s):  
Thomas Möller ◽  
Vibeke Klungerbo ◽  
Simone Diab ◽  
Henrik Holmstrøm ◽  
Elisabeth Edvardsen ◽  
...  

AbstractThe role of dysfunction of the single ventricle in Fontan failure is incompletely understood. We aimed to evaluate hemodynamic responses to preload increase in Fontan circulation, to determine whether circulatory limitations in different locations identified by experimental preload increase are associated with cardiorespiratory fitness (CRF), and to assess the impact of left versus right ventricular morphology. In 38 consecutive patients (median age = 16.6 years, 16 females), heart catheterization was supplemented with a rapid 5-mL/kg body weight volume expansion. Central venous pressure (CVP), ventricular end-diastolic pressure (VEDP), and peak systolic pressure were averaged for 15‒30 s, 45‒120 s, and 4‒6 min (steady state), respectively. CRF was assessed by peak oxygen consumption (VO2peak) and ventilatory threshold (VT). Median CVP increased from 13 mmHg at baseline to 14.5 mmHg (p < 0.001) at steady state. CVP increased by more than 20% in eight patients. Median VEDP increased from 10 mmHg at baseline to 11.5 mmHg (p < 0.001). Ten patients had elevated VEDP at steady state, and in 21, VEDP increased more than 20%. The transpulmonary pressure difference (CVP‒VEDP) and CVP were consistently higher in patients with right ventricular morphology across repeated measurements. CVP at any stage was associated with VO2peak and VT. VEDP after volume expansion was associated with VT. Preload challenge demonstrates the limitations beyond baseline measurements. Elevation of both CVP and VEDP are associated with impaired CRF. Transpulmonary flow limitation was more pronounced in right ventricular morphology. Ventricular dysfunction may contribute to functional impairment after Fontan operation in young adulthood.ClinicalTrials.govidentifier NCT02378857

2021 ◽  
Author(s):  
Thomas Möller ◽  
Vibeke Klungerbo ◽  
Simone Diab ◽  
Henrik Holmstrøm ◽  
Elisabeth Edvardsen ◽  
...  

Abstract BackgroundThe role of dysfunction of the single ventricle in Fontan failure is incompletely understood.ObjectivesWe aimed to evaluate haemodynamic responses to preload increase in Fontan circulation, to determine whether circulatory limitations in different locations identified by experimental preload increase are associated with cardiorespiratory fitness (CRF), and to assess the impact of left versus right ventricular morphology.MethodsIn 38 consecutive patients (median age=16.6 years, 16 females), heart catheterisation was supplemented with a rapid 5-mL/kg body weight volume expansion. Central venous pressure (CVP), ventricular end-diastolic pressure (VEDP), and peak systolic pressure were averaged for 15‒30 s, 45‒120 s, and 4‒6 min (steady state), respectively. CRF was assessed by peak oxygen consumption (VO2peak) and ventilatory threshold (VT).ResultsMedian CVP increased from 13 mmHg at baseline to 14.5 mmHg (p<0.001) at steady state. CVP increased by more than 20% in eight patients. Median VEDP increased from 10 mmHg at baseline to 11.5 mmHg (p<0.001). Ten patients had elevated VEDP at steady state, and in 21, VEDP increased more than 20%. The transpulmonary pressure difference (CVP‒VEDP) and CVP were consistently higher in patients with right ventricular morphology across repeated measurements. CVP at any stage was associated with VO2peak and VT. VEDP after volume expansion was associated with VT.ConclusionsPreload challenge demonstrates the limitations beyond baseline measurements. Elevation of both CVP and VEDP are associated with impaired CRF. Transpulmonary flow limitation was more pronounced in right ventricular morphology. Ventricular dysfunction may contribute to functional impairment after Fontan operation in young adulthood.ClinicalTrials.govidentifier: NCT02378857


2000 ◽  
Vol 278 (5) ◽  
pp. H1414-H1420 ◽  
Author(s):  
Clifford Greyson ◽  
Ya Xu ◽  
Li Lu ◽  
Gregory G. Schwartz

Volume expansion and inotropic stimulation are used clinically to augment cardiac output during acute right ventricular (RV) pressure overload. We previously showed that a brief period of RV pressure overload causes RV free wall dysfunction that persists after normal loading conditions have been restored. However, the impact of volume expansion and inotropic stimulation on the severity of RV dysfunction after acute pressure overload is unknown. We hypothesized that the severity of RV dysfunction after RV pressure overload would be related to the level of RV free wall systolic stress during RV pressure overload, rather than to the specific interventions used to augment RV function. Chloralose-anesthetized, open-chest pigs were subjected to 1 h of RV pressure overload caused by pulmonary artery constriction, followed by 1 h of recovery after release of pulmonary artery constriction. A wide range of RV free wall systolic stress during RV pressure overload was achieved by either closing or opening the pericardium (to simulate volume expansion) and by administering or not administering dobutamine. The severity of RV free wall dysfunction 1 h after RV pressure overload was strongly and directly correlated with the values of two hemodynamic variables during RV pressure overload: RV free wall area at peak RV systolic pressure (determined by sonomicrometry) and peak RV systolic pressure, two of the major determinants of peak RV free wall systolic stress. Opening or closing the pericardium, and using or not using dobutamine during RV pressure overload, had no independent effects on the severity of RV dysfunction. The findings suggest that the goal of therapeutic intervention during RV pressure overload should be to achieve the required augmentation of cardiac output with the smallest possible increase in RV free wall systolic stress.


2020 ◽  
Vol 90 (2) ◽  
Author(s):  
Gian Marco Rosa ◽  
Andreina D'Agostino ◽  
Stefano Giovinazzo ◽  
Giovanni La Malfa ◽  
Paolo Fontanive ◽  
...  

Echocardiography of right ventricular (RV)-arterial coupling obtained by the estimation of the ratio of the longitudinal annular systolic excursion of the tricuspid annular plane and pulmonary artery systolic pressure (TAPSE/PASP) has been found to be a remarkable prognostic indicator in patients with HF. Our aim was to evaluate the impact of TAPSE, PASP and their ratio in the prognostic stratification of outpatients with HF aged ≥70 years and reduced to mid-range ejection fraction (EF). A complete echocardiographic examination was performed in 400 outpatients with chronic HF and left ventricular (LV) EF ≤50% who averaged 77 years in age. During a median follow-up period of 25 months (interquartile range: 8-46), there were 135 cardiovascular deaths. Two different Cox regression models were evaluated, one including TAPSE and PASP, separately, and the other with TAPSE/PASP. In the first model, LV end-systolic volume index, age, no angiotensin converting enzyme (ACE) inhibitor use, TAPSE, PASP and gender were found to be independently associated with the outcome after adjustment for demographics, clinical, biochemical, echocardiographic data. In the second model, TAPSE/PASP resulted the most important independent predictor of outcome (hazard ratio [HR]:0.07, p<0.0001) followed by LV end-systolic volume index, no ACE inhibitor use, age and gender. The use of the variable TASPE/PASP improved the predictive value of the new multivariable model (area under the curve [AUC] of 0.74 vs AUC of 0.71; p<0.05). TASPE/PASP improved the net reclassification (NRI = 14.7%; p<0.01) and the integrated discrimination (IDI = 0.04; p<0.01). In conclusion, the study findings showed that assessment of RV-arterial coupling by TAPSE/PASP was of major importance to assess the prognosis of patients with chronic HF and LV EF ≤50% aged ≥70 years.


1999 ◽  
Vol 86 (3) ◽  
pp. 867-873 ◽  
Author(s):  
Kei Nagashima ◽  
Gary W. Mack ◽  
Andrew Haskell ◽  
Takeshi Nishiyasu ◽  
Ethan R. Nadel

To test the hypothesis that exercise-induced hypervolemia is a posture-dependent process, we measured plasma volume, plasma albumin content, and renal function in seven healthy subjects for 22 h after single upright (Up) or supine (Sup) intense (85% peak oxygen consumption rate) exercise. This posture was maintained for 5 h after exercise. Plasma volume decreased during exercise but returned to control levels by 5 h of recovery in both postures. By 22 h of recovery, plasma volume increased 2.4 ± 0.8 ml/kg in Up but decreased 2.1 ± 0.8 ml/kg in Sup. The plasma volume expansion in Up was accompanied by an increase in plasma albumin content (0.11 ± 0.04 g/kg; P < 0.05). Plasma albumin content was unchanged in Sup. Urine volume and sodium clearance were lower in Up than Sup ( P < 0.05) by 5 h of recovery. These data suggest that increased plasma albumin content contributes to the acute phase of exercise-induced hypervolemia. More importantly, the mechanism by which exercise influences the distribution of albumin between extra- and intravascular stores after exercise is altered by posture and is unknown. We speculate that factors associated with postural changes (e.g., central venous pressure) modify the increase in plasma albumin content and the plasma volume expansion after exercise.


2005 ◽  
Vol 15 (S3) ◽  
pp. 35-38 ◽  
Author(s):  
Gábor Szabó ◽  
Susanne Bährle

During the past decades, different variants of the Fontan circulation have become the primary therapeutic option for physiological correction of congenital cardiac malformations in which restoration to biventricular circulations is impossible. Subsequent to creation of the Fontan circulation, the pulmonary and systemic circulations are in series, with only one pumping chamber. Thus, the functionally single ventricle must provide energy for flow of blood to the lungs, as well as to the body. Generally, patients who have undergone these procedures have a good prognosis, although they have subnormal cardiac output at rest, while their central venous pressure is significantly elevated. Despite an adequate haemodynamic situation at rest, exercise performance is usually reduced. Thus far, this reduction has been attributed to cardiac factors, such as the absence of the morphologically right ventricle, or impaired function of the morphologically left ventricle. Due to the mechanical coupling between the heart and the peripheral circulation, however, the inadequate response to exercise in terms of cardiac output might also be dependant on insufficient peripheral vascular adjustments. In this review, we assess the existing experimental and clinical studies which provide detailed analysis of ventriculo-arterial mechanics in the setting of the Fontan circulation.


2013 ◽  
Vol 2013 ◽  
pp. 1-5
Author(s):  
Richard M. Millis ◽  
Vernon Bond ◽  
M. Sadegh Asadi ◽  
Georges E. Haddad ◽  
Richard G. Adams

Body mass index (BMI) is negatively correlated with cardiorespiratory fitness, measured by maximal or peak oxygen consumption (VO2peak). VO2peak measurements require heavy aerobic exercise to near exhaustion which increases the potential for adverse cardiovascular events. This study tests the hypothesis that VO2 measured at a fixed submaximal workload of 30 W is a surrogate for VO2peak. We studied 42 normotensive African-American female university students, 18–25 years of age. We measured VO2peak, blood pressure, and VO2 at a 30 W exercise workload and computed BMI. We found significant negative correlations between BMI and VO2peak (r=−0.41, P<0.01) and between BMI and VO2 at 30 W (r=−0.53, P<0.001). Compared to VO2peak, VO2 at 30 W increased the significance of the negative correlation with BMI. The heart rate-systolic pressure product at 30 W was positively correlated with BMI (r=0.36, P<0.01) and negatively correlated with VO2peak (r=−0.38, P<0.001). The positive correlation between BMI and the heart rate-systolic pressure product and the greater negative correlation between VO2 and BMI at 30 W of exercise than that at exercise to fatigue suggest that normalized measurements of VO2 at the fixed exercise workload of 30 W could be useful surrogates for measurements of VO2peak.


2000 ◽  
Vol 10 (5) ◽  
pp. 447-457 ◽  
Author(s):  
Mitchell I. Cohen ◽  
David M. Bush ◽  
Robert J. Ferry ◽  
Thomas L. Spray ◽  
Thomas Moshang ◽  
...  

AbstractOur study was designed to characterize the patterns of growth, in the medium term, of children with functionally univentricular hearts managed with a hemi-Fontan procedure in infancy, followed by a modified Fontan operation in early childhood. Failure of growth is common in patients with congenital cardiac malformations, and may be related to congestive heart failure and hypoxia. Repair of simple lesions appears to reverse the retardation in growth. Palliation of the functionally single ventricular physiology with a staged Fontan operation reduces the adverse effects of hypoxemia and prolonged ventricular volume overload. The impact of this approach on somatic growth is unknown. Retrospectively, we reviewed the parameters of growth of all children with functionally univentricular hearts followed primarily at our institution who had completed a staged construction of the Fontan circulation between January 1990 and December 1995. Measurements were available on all children prior to surgery, and annually for three years following the Fontan operation. Data was obtained on siblings and parents for comparative purposes. The criterions of eligibility for inclusion were satisfied by 65 patients. The mean Z score for weight was-1·5± 1·2 at the time of the hemi-Fontan operation. Weight improved by the time of completion of the Fontan circulation (−0·91 ±0·99), and for the first two years following the Fontan operation, but never normalized. The mean Z scores for height at the hemi-Fontan and Fontan operations were −0·67 ±1·1 and −0·89±1·2 respectively. At most recent follow-up, with a mean age of 6·1 ± 1·3 years, and a mean time from the Fontan operation of 4·4±1·4 years, the mean Z score for height was −1·15 ±1·2, and was significantly less than comparable Z scores for parents and siblings. In our experience, children with functionally univentricular hearts who have been palliated with a Fontan operation are significantly underweight and shorter than the general population and their siblings


2018 ◽  
Vol 9 (1) ◽  
pp. 204589401881774 ◽  
Author(s):  
Evan L. Brittain ◽  
Megha Talati ◽  
Niki Fortune ◽  
Vineet Agrawal ◽  
David F. Meoli ◽  
...  

Little is known about the impact of metabolic syndrome (MS) on right ventricular (RV) structure and function. We hypothesized that mice fed a Western diet (WD) would develop RV lipid accumulation and impaired RV function, which would be ameliorated with metformin. Male C57/Bl6 mice were fed a WD or standard rodent diet (SD) for eight weeks. A subset of mice underwent pulmonary artery banding (PAB). Treated mice were given 2.5 g/kg metformin mixed in food. Invasive hemodynamics, histology, Western, and quantitative polymerase chain reaction (qPCR) were performed using standard techniques. Lipid content was detected by Oil Red O staining. Mice fed a WD developed insulin resistance, RV hypertrophy, and higher RV systolic pressure compared with SD controls. Myocardial lipid accumulation was greater in the WD group and disproportionately affected the RV. These structural changes were associated with impaired RV diastolic function in WD mice. PAB-WD mice had greater RV hypertrophy, increased lipid deposition, and lower RV ejection fraction compared with PAB SD controls. Compared to untreated mice, metformin lowered HOMA-IR and prevented weight gain in mice fed a WD. Metformin reduced RV systolic pressure, prevented RV hypertrophy, and reduced RV lipid accumulation in both unstressed stressed conditions. RV diastolic function improved in WD mice treated with metformin. WD in mice leads to an elevation in pulmonary pressure, RV diastolic dysfunction, and disproportionate RV steatosis, which are exacerbated by PAB. Metformin prevents the deleterious effects of WD on RV function and myocardial steatosis in this model of the metabolic syndrome.


2021 ◽  
Vol 11 (2) ◽  
pp. 109-118
Author(s):  
Megan S. Joseph ◽  
Francis Tinney ◽  
Abhijit Naik ◽  
Raviprasenna Parasuraman ◽  
Milagros Samaniego-Picota ◽  
...  

<b><i>Introduction:</i></b> Pulmonary hypertension is common among patients with end-stage renal disease, although data regarding the impact of right ventricular (RV) failure on postoperative outcomes remain limited. We hypothesized that echocardiographic findings of RV dilation and dysfunction are associated with adverse clinical outcomes after renal transplant. <b><i>Methods:</i></b> A retrospective review of adult renal transplant recipients at a single institution from January 2008 to June 2010 was conducted. Patients with transthoracic echocardiograms (TTEs) within 1 year leading up to transplant were included. The primary end point was a composite of delayed graft function, graft failure, and all-cause mortality. <b><i>Results:</i></b> Eighty patients were included. Mean follow-up time was 9.4 ± 0.8 years. Eight patients (100%) with qualitative RV dysfunction met the primary end point, while 39/65 patients (60.0%) without RV dysfunction met the end point (<i>p</i> = 0.026). Qualitative RV dilation was associated with a significantly shorter time to all-cause graft failure (<i>p</i> = 0.03) and death (<i>p</i> = 0.048). RV systolic pressure was not measurable in 45/80 patients (56%) and was not associated with outcomes in the remaining patients. <b><i>Conclusion:</i></b> RV dilation and dysfunction are associated with adverse outcomes after renal transplant. TTE assessment of RV size and function should be a standard part of the pre-kidney transplant cardiovascular risk assessment.


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