Relation of Systemic Venous Return, Pulmonary Vascular Resistance, and Diastolic Dysfunction to Exercise Capacity in Patients With Single Ventricle Receiving Fontan Palliation

Goldstein, Bryan H.; Connor, Chad; Gooding, Lindsay; Rocchini, Albert P.

doi:10.1016/j.amjcard.2009.12.020

Cited by 84 publications

(49 citation statements)

References 29 publications

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“…[9][10][11] Peak power output was lower in Fontan patients than controls, and this was associated with a steep rise in SVP during exercise. In the two Fontan patients with greatest peak power output, the baseline and increase in SVP response was the least impaired and similar to controls (Figure 1).…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

“…A prior study showed diastolic dysfunction was present in 57% of Fontan patients assessed and was associated with a reduced peak VO 2 and peak power, and none showed the expected decrease in PVR on exercise. 9 NIRS derived StO 2 has been used as a marker of the adequacy of end-organ O 2 delivery relative to demand. 14 We demonstrated profound changes in StO 2 -C and StO 2 -R in Fontan patients at rest and during exercise.…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

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Exercise-Induced Systemic Venous Hypertension in the Fontan Circulation

Navaratnam

Fitzsimmons

Grocott

et al. 2016

The American Journal of Cardiology

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Increasingly end-organ injury is being demonstrated late after institution of the Fontan circulation, particularly liver fibrosis and cirrhosis. The exact mechanisms for these late phenomena remain largely elusive. Hypothesizing that exercise induces precipitous systemic venous hypertension and insufficient cardiac output for the exercise demand, i.e. a possible mechanism for end-organ injury, we sought to demonstrate the dynamic exercise responses in systemic venous (SVP) and concurrent end organ perfusion. Ten stable Fontan patients and 9 control subjects underwent incremental cycle ergometry based cardiopulmonary exercise testing. SVP was monitored in the right upper limb and regional tissue oxygen saturation was monitored in the brain and kidney using Near Infrared Spectroscopy. SVP rose profoundly in concert with workload in the Fontan group, described by the regression equation 15.97+0.073 Watts per mm Hg. In contrast SVP did not change in healthy controls. Regional renal (p<0.01) and cerebral tissue saturations (p<0.001) were significantly lower and fell more rapidly in Fontan patients. We conclude that in a stable group of adult patients with Fontan circulation high intensity exercise was associated with systemic venous hypertension and reduced systemic oxygen delivery. This physiologic substrate has the potential to contribute to endorgan injury.

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Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

Exercise-Induced Systemic Venous Hypertension in the Fontan Circulation

Navaratnam

Fitzsimmons

Grocott

et al. 2016

The American Journal of Cardiology

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“…Furthermore, although resting PAP and PVR may be normal in Fontan patients, exercise PVR response is demonstrably abnormal. 85 The application of pulmonary vasodilator therapy in these clinical scenarios is an area of active investigation. [86][87][88] Pulmonary vasodilator therapy may also have a role in the management of CHD patients with ventricular-arterial uncoupling despite an absence of pulmonary vascular disease or PH.…”

Section: Emerging Roles For Pulmonary Vasodilator Therapymentioning

confidence: 99%

Clinical Evaluation and Management of Pulmonary Hypertension in the Adult With Congenital Heart Disease

Opotowsky

2015

Circulation

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200P ulmonary hypertension (PH) refers to elevated pulmonary artery (PA) pressure (PAP), defined as mean PAP≥25 mm Hg. PH is not synonymous with pulmonary arterial hypertension (PAH), which specifies resistive PH characterized by elevated pulmonary vascular resistance (PVR) and normal pulmonary venous pressure. Approximately 5% to 10% of adults with congenital heart disease (CHD) have PH, and this subset of CHD patients is at higher risk of hospitalization and death. [1][2][3] Understanding the epidemiology of PH associated with CHD (PH-CHD) is not straightforward, however, because definitions of PH-CHD and diagnostic techniques vary. Appropriate diagnosis and the management of PH-CHD rest on identifying the cause of elevated PAP: high pulmonary venous pressure, high pulmonary vascular resistance, high pulmonary flow, or some combination of these factors, which are referred to throughout this review as passive, resistive, hyperkinetic, and polygenic PH, respectively (Table 1).Prognosis in PH-CHD depends on the underlying cause, pulmonary vascular pathophysiology, and the interaction between the right heart and pulmonary circulation. Adult CHD is heterogeneous, with myriad permutations of underlying defects, previous interventions, and associated comorbidities. Although comprehensive understanding of clinical context is a prerequisite, identifying the optimal therapy for a patient with PH-CHD depends more heavily on an understanding of pathophysiology than it does on the underlying diagnosis. Therefore, the goal of this review is to frame an understanding of PH-CHD in terms of fundamental cardiopulmonary hemodynamic pathophysiology and to emphasize the clinical assessment and management of situations commonly encountered by adult cardiologists caring for patients with PH-CHD. Classifications of PH and PH-CHDClassification schemes in PH represent clinical perspectives of underlying pathophysiology and tend to parallel fundamental hemodynamic relationships of the pulmonary circulation. PVR

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“…Thus, different investigators using distinct populations and/or clinical and sports settings have proposed that the O 2 pulse can indirectly reflect stroke volume, so that both the maximum value and the curve shape, which are a function of CPET duration, will be directly associated with cardiac inotropism and lusitropism (4)(5)(6)(7)(8)(9)(10). In this context, several studies have shown that relatively low maximum O 2 pulse values are associated with a lower survival rate among middle-aged individuals as well as patients with heart failure (11,12), most likely reflecting impaired inotropic and/or lusitropic capacity and then disturbing the stroke volume response to exercise.…”

mentioning

confidence: 99%

Stability of relative oxygen pulse curve during repeated maximal cardiopulmonary testing in professional soccer players

Perim¹,

Signorelli²,

Araújo³

2011

Braz J Med Biol Res

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During cardiopulmonary exercise testing (CPET), stroke volume can be indirectly assessed by O2 pulse profile. However, for a valid interpretation, the stability of this variable over time should be known. The objective was to analyze the stability of the O2 pulse curve relative to body mass in elite athletes. VO2, heart rate (HR), and relative O2 pulse were compared at every 10% of the running time in two maximal CPETs, from 2005 to 2010, of 49 soccer players. Maximal values of VO2 (63.4 ± 0.9 vs 63.5 ± 0.9 mL O2•kg-1•min-1), HR (190 ± 1 vs188 ± 1 bpm) and relative O2 pulse (32.9 ± 0.6 vs 32.6 ± 0.6 mL O2•beat-1•kg-1) were similar for the two CPETs (P > 0.05), while the final treadmill velocity increased from 18.5 ± 0.9 to 18.9 ± 1.0 km/h (P < 0.01). Relative O2 pulse increased linearly and similarly in both evaluations (r² = 0.64 and 0.63) up to 90% of the running time. Between 90 and 100% of the running time, the values were less stable, with up to 50% of the players showing a tendency to a plateau in the relative O2 pulse. In young healthy men in good to excellent aerobic condition, the morphology of the relative O2 pulse curve is consistent up to close to the peak effort for a CPET repeated within a 1-year period. No increase in relative O2pulse at peak effort could represent a physiologic stroke volume limitation in these athletes

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Relation of Systemic Venous Return, Pulmonary Vascular Resistance, and Diastolic Dysfunction to Exercise Capacity in Patients With Single Ventricle Receiving Fontan Palliation

Cited by 84 publications

References 29 publications

Exercise-Induced Systemic Venous Hypertension in the Fontan Circulation

Exercise-Induced Systemic Venous Hypertension in the Fontan Circulation

Clinical Evaluation and Management of Pulmonary Hypertension in the Adult With Congenital Heart Disease

Stability of relative oxygen pulse curve during repeated maximal cardiopulmonary testing in professional soccer players

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