Hemodynamic evaluation before and after closure of fenestrated Fontan. An acute study of changes in oxygen delivery.

Hijazi, Ziyad M.; Fahey, John T.; Kleinman, Charles S.; Kopf, Gary S.; Hellenbrand, William E.

doi:10.1161/01.cir.86.1.196

Cited by 84 publications

(39 citation statements)

References 18 publications

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“…23,24 These patients are born with a ventricle that has been submitted to a fetal volume overload of Ϸ230% of normal, which is augmented shortly thereafter in many patients by a shunt procedure to Ϸ280%. 25 This chronic volume overload has a deleterious effect on the ventricle until the subsequent bidirectional cavopulmonary shunt and Fontan operation. 26 In a manner similar to post-atrial switch patients, the coronary arterial supply of HLHS hearts may be inadequate to meet the needs of an increased myocardial mass.…”

Section: Potential Underlying Mechanisms Of Tv Failurementioning

confidence: 99%

Real-Time 3-Dimensional Echocardiography Provides New Insight Into Mechanisms of Tricuspid Valve Regurgitation in Patients With Hypoplastic Left Heart Syndrome

et al. 2009

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Background-Tricuspid regurgitation in hypoplastic left heart syndrome has an impact on outcome, but its mechanisms remain unclear. Methods and Results-Real-time 3-dimensional echocardiography was performed in 35 patients with hypoplastic left heart syndrome (age, 1 month to 10 years; 10 after first-stage Norwood, 12 after superior cavopulmonary shunt, 13 after Fontan). From the 3-dimensional data set, we marked the annulus in systole and diastole. At mid systole, we marked the location of the papillary muscle tip and point of chordal attachment to the leaflet. We traced the surfaces of the tricuspid valve leaflets and measured the volume of leaflet prolapse, tethering, annular and septal leaflet areas, and papillary muscle position. Seventeen patients had moderate tricuspid regurgitation (prolapse, 7; tethered leaflets, 7) and 18 mild (prolapse, 0; tethered leaflets, 7). Multiple linear regression analysis revealed that moderate tricuspid regurgitation is associated with leaflet tethering and prolapse; that in hypoplastic left heart syndrome with tethered leaflets, the papillary muscle is displaced laterally and the tricuspid annulus is more planar; and that enlargement of the annulus at mid systole, small septal leaflet area, and age affect the degree of prolapse. Conclusion-In hypoplastic left heart syndrome, moderate tricuspid regurgitation may be associated with increasing age, geometrical changes of the annulus, leaflet prolapse, lateral papillary muscle displacement, and subsequent leaflet tethering, as well as a smaller septal leaflet.

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Section: Potential Underlying Mechanisms Of Tv Failurementioning

confidence: 99%

Real-Time 3-Dimensional Echocardiography Provides New Insight Into Mechanisms of Tricuspid Valve Regurgitation in Patients With Hypoplastic Left Heart Syndrome

et al. 2009

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“…Cerebral arterial and venous O2 contents (CaO 2 and CvO 2 , respectively) were calculated using standard equations used by Hijazi et al (21) and Stringer et al (58) as follows:…”

Section: Calculationsmentioning

confidence: 99%

Human cerebral arteriovenous vasoactive exchange during alterations in arterial blood gases

Peebles

Richards²,

Celi

et al. 2008

Journal of Applied Physiology

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Evidence from animal studies indicates that various vasoactive factors, including release of norepinephrine, endothelin, adrenomedullin, C-natriuretic peptide (CNP), and nitric oxide (NO), may play a role in arterial blood gas-induced alterations in CBF. For the first time, we directly quantified exchange of these vasoactive factors across the human brain. Using the Fick principle and transcranial Doppler ultrasonography, we measured CBF in 12 healthy humans at rest and during hypercapnia (4 and 8% CO 2), hypocapnia (voluntary hyperventilation), and hypoxia (12 and 10% O 2). At each level, blood was sampled simultaneously from the internal jugular vein and radial artery. With the exception of CNP and NO, the simultaneous quantification of norepinephrine, endothelin, or adrenomedullin showed no cerebral uptake or release during changes in arterial blood gases. Hypercapnia, but not hypocapnia, increased CBF and caused a net cerebral release of nitrite (a marker of NO), which was reflected by an increase in the venous-arterial difference for nitrite: 57 Ϯ 18 and 150 Ϯ 36 mol/l at 4% and 8% CO 2, respectively (both P Ͻ 0.05). Release of cerebral CNP was also observed during changes in CO 2 (hypercapnia vs. hypocapnia, P Ͻ 0.05). During hypoxia, there was a net cerebral uptake of nitrite, which was reflected by a decreased venous-arterial difference for nitrite: Ϫ96 Ϯ 14 mol/l at 10% O 2 (P Ͻ 0.05). These data indicate that there is a differential exchange of NO across the brain during hypercapnia and hypoxia and that CNP may play a complementary role in CO 2-induced CBF changes. cerebral circulation; nitric oxide; endothelium RESPIRATORY-INDUCED CHANGES in arterial PCO 2 (Pa CO 2 ) and, to a lesser extent, PO 2 (Pa O 2 ) play a major role in cerebral blood flow (CBF) regulation (9). Elevations in Pa CO 2 (hypercapnia) lead to vasodilation of cerebral arterioles in the downstream bed and a subsequent increase in CBF, whereas a reduction in Pa CO 2 (hypocapnia) leads to vasoconstriction and a subsequent decrease in CBF (28, 65). A fall in Pa O 2 (hypoxia) below a certain threshold (Ͻ40 Torr) also produces cerebral vasodilation (19). These arterial blood gas-induced changes in CBF are mediated through changes in cerebrovascular resistance via alterations in vascular smooth muscle diameter in response to changes in the level of intracellular calcium and/or calcium sensitivity (for review see Ref. 22). Cerebrovascular tone is influenced by several chemical substances, including nitric oxide (NO). NO, synthesized from the terminal guanidino nitrogen atom(s) of L-arginine in a two-step reaction that is catalyzed by the enzyme NO synthase (NOS) (48), is an important vasoactive factor that dilates the cerebral vasculature. Under normal conditions, two isoforms of NOS are expressed in the brain, endothelium-derived NOS (eNOS) and neuronal-derived NOS (nNOS) (61), although evidence for the role of eNOS vs. nNOS in the control of CBF is controversial (3). Vasodilation evoked by NO is initiated by an increase in cGMP (7).Pharmac...

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“…ic effects of test occlusion and selection of patients for transcatheter closure, 15,20 the methodology for transcatheter closure of fenestrations with the use of several different devices, 13,17,21,22 and the short-term follow-up of those patients. The present study, although significantly increasing the number of patients available for analysis, does not substantively alter the conclusions of those prior studies: generally, test occlusion modestly increases O 2 saturations, modestly increases right-sided pressures, and modestly reduces cardiac output.…”

Section: Previous Workmentioning

confidence: 99%

Clinical Outcome of Fenestrated Fontan Patients After Closure

et al. 2000

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Background —The late clinical status of Fontan patients after fenestration closure is unknown. Data are now available on all patients who underwent closure from 1989 to 1999. Methods and Results —All patients who underwent catheter closure of a Fontan fenestration were enrolled in either the Clamshell (1989 to 1994) or CardioSEAL (1996 to 1999) regulatory trials. Physiological values obtained at catheterization helped assess the hemodynamic effects of fenestration occlusion. In addition to survival, outcomes assessed included O 2 saturations, medication use, significant clinical findings (eg, heart failure, protein-losing enteropathy, or new arrhythmias), and somatic growth. Of 181 patients who underwent closure, 27 had additional significant leaks. The remaining 154 patients constituted the study group. Median time from closure to latest follow-up was 3.4 years (range 0.4 to 10.3 years). Fenestration closure increased O 2 saturation 9.4% on average ( P <0.001). The numbers of patients receiving digoxin or diuretics decreased at the most recent follow-up compared with baseline ( P <0.001), but use of antiarrhythmic agents increased marginally ( P =0.05). Height and weight percentiles rose (medians of 2 and 4, respectively; P <0.001). Clinical decompensation during follow-up of 154 patients was rare (4.5%), with 2 deaths, 3 Fontan revisions, and 1 patient each with protein-losing enteropathy and ascites. No other patient developed chronic congestive symptoms; 21 patients developed new arrhythmias, and 2 had a stroke or transient ischemic attack. Conclusions —Fenestration closure in Fontan patients was followed by improved oxygenation, reduced need for anticongestive medication, and improved somatic growth at latest follow-up. Death (1.3%) or chronic decompensation (3.2%) was rare.

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Hemodynamic evaluation before and after closure of fenestrated Fontan. An acute study of changes in oxygen delivery.

Cited by 84 publications

References 18 publications

Real-Time 3-Dimensional Echocardiography Provides New Insight Into Mechanisms of Tricuspid Valve Regurgitation in Patients With Hypoplastic Left Heart Syndrome

Real-Time 3-Dimensional Echocardiography Provides New Insight Into Mechanisms of Tricuspid Valve Regurgitation in Patients With Hypoplastic Left Heart Syndrome

Human cerebral arteriovenous vasoactive exchange during alterations in arterial blood gases

Clinical Outcome of Fenestrated Fontan Patients After Closure

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