Evidence for Cardiovascular Autonomic Dysfunction in Neonates With Coarctation of the Aorta

Polson, Jaimie W.; McCallion, Naomi; Waki, Hidefumi; Thorne, Gareth C.; Tooley, Mark; Paton, Julian F. R.; Wolf, Andrew

doi:10.1161/circulationaha.105.602748

Cited by 67 publications

(51 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These factors include mechanical, 7,8 functional, 8,9 and structural 10 abnormalities in the systemic arterial bed, particularly of the precoarctation region and malfunctions of blood pressure (BP) regulatory systems, 10 -13 some of which appear to exist within the fetal or neonatal period before repair. 14,15 However, systolic BP is determined not only by the status of arteries, but also by the properties of the ventricles to which the blood vessels are coupled. Chronic cardiac ejection into stiff arteries may induce ventricular adaptation to confront the high systolic load by increasing ventricular systolic stiffness.…”

mentioning

confidence: 99%

Ventricular–Vascular Stiffening in Patients With Repaired Coarctation of Aorta

Senzaki¹,

Iwamoto²,

Ishido³

et al. 2008

Circulation

View full text Add to dashboard Cite

Background-Despite successful repair, patients with coarctation of the aorta (COA) often show persistent hypertension at rest and/or during exercise. Previous studies indicated that the hypertension is mainly due to abnormalities in the arterial bed and its regulatory systems. We hypothesized that ventricular systolic stiffness also contributes to the hypertensive state in these patients in addition to increased vascular stiffness. Methods and Results-The study involved 43 patients with successfully repaired COA and 45 age-matched control subjects. Ventricular systolic stiffness (end systolic elastance) and arterial stiffness (effective arterial elastance) were measured invasively by ventricular pressure-area relationship during varying preload before and after ␤-adrenergic stimulation. The mean systolic blood pressure was significantly higher with concomitant increases in both end systolic elastance and effective arterial elastance in patients with COA compared with control subjects (113.2Ϯ16.8 versus 91.0Ϯ9.1 mm Hg, 44.5Ϯ17.0 versus 19.2Ϯ6.7 mm Hg/mL/m 2 , and 27.8Ϯ11.4 versus 20.2Ϯ4.8 mm Hg/mL/m 2 , respectively; PϽ0.01 for each). End systolic elastance and effective arterial elastance of patients with COA showed exaggerated responses to ␤-adrenergic stimulation, further amplifying blood pressure elevation. Quantification analyses assuming that ventricular systolic stiffness of patients with COA is equal to that of the control revealed that ventricular systolic stiffness accounts for approximately 50% to 70% of the elevated blood pressure in patients with COA. Furthermore, combined ventricular-arterial stiffening amplified systolic pressure sensitivity to increased preload during abdominal compression and limited stroke volume gain/relaxation improvement induced by ␤-adrenergic stimulation. Conclusions-Increased ventricular systolic stiffness, coupled with increased arterial stiffness, plays important roles in hypertension in patients with repaired COA. Thus, ventricular systolic stiffness is a potentially suitable target for reduction of blood pressure and improvement of prognosis of patients with COA. (Circulation. 2008;118[suppl 1]:S191-S198.)

show abstract

mentioning

confidence: 99%

Ventricular–Vascular Stiffening in Patients With Repaired Coarctation of Aorta

Senzaki¹,

Iwamoto²,

Ishido³

et al. 2008

Circulation

View full text Add to dashboard Cite

show abstract

“…Although no meaningful statistical analyses of these data can be made, it is notable that the sBRS was markedly lower in the index case suggesting dampening of the baroreceptor reflex, as demonstrated previously in infants with CoA. 18 Time domain analyses of heart rate variability were higher in the control twin across all measurements (Figure 2), suggesting dominance of parasympathetic over sympathetic modulations in the control infant although wide variability may exist with these indices. Right arm pulse wave velocity values were repeatedly higher in the index case again suggesting large artery stiffness, implicated in systolic hypertension may be affected in the pre-CoA arterial bed, although it is unclear whether this is a consequence or a cause of high systolic blood pressure in this case.…”

Section: Early Change-a Case In Pointmentioning

confidence: 67%

“…Previously reported data have suggested increased aortic stiffness 17 and alteration in autonomic cardiac balance 18 in pre-operative neonates with CoA, suggesting an early maladaptive response to mechanisms responsible for longer term blood pressure control (discussed below). With this in mind, we measured non-invasive indices of autonomic balance, large artery stiffness and cardiac output in an 8-month-old male with native CoA and his monozygotic twin.…”

Section: Early Change-a Case In Pointmentioning

confidence: 92%

“…17,18 The genetic homogeneity in this case is interesting and provides a unique opportunity to assess variances in arterial compliance, BRS and cardiac autonomic balance between twin infants, and postulates on how this may affect longer term control of blood pressure.…”

Section: Potential Mechanisms Involved In the Hypertensive Responsementioning

confidence: 99%

“…Our group has previously demonstrated a reduction in baroreceptor gain and heart rate variability of approximately 40% in pre-operative neonates, with CoA compared with controls, suggesting early maladaptive autonomic control of blood pressure. 18 We postulated that failure of these control mechanisms to normalize in some patients could cause long-term impediments to normal blood pressure control, possibly leading to hypertension. Since then we have followed up this group of patients and found that the initial autonomic dysfunction between the two groups had normalized by 5 years of age.…”

Section: Multiple System Involvementmentioning

confidence: 99%

See 2 more Smart Citations

Hypertension and coarctation of the aorta: an inevitable consequence of developmental pathophysiology

et al. 2011

View full text Add to dashboard Cite

Patients with coarctation of the aorta develop early onset hypertension in spite of early effective repair. This is associated with significant morbidity and is arguably the single most important outcome variable in this patient group. We discuss the potential pathophysiological mechanisms involved in the development of hypertension with clinical reference to monozygotic twins, and review potential strategies for therapy and prevention in this setting.

show abstract

Anesthesia for Adult Congenital Aortic Surgery

Kussman

DiNardo²

2010

Anesthesia and Perioperative Care for Aortic Surgery

View full text Add to dashboard Cite

Congenital supravalvular aortic stenosis (SVAS) is a rare form of left ventricular outflow tract (LVOT) obstruction that often is associated with peripheral pulmonary artery stenoses (approximately 40% of patients). Congenital SVAS is an elastin arteriopathy and is most commonly associated with Williams-Beuren syndrome. Williams-Beuren syndrome, commonly referred to as Williams syndrome (WS), is characterized by the presence of SVAS and peripheral pulmonary artery stenoses in association with mental retardation and distinctive elfin facies. It is the result of a microdeletion in the q11.23 region of chromosome 7, which affects several genes, including the elastin gene.1 SVAS also occurs in a familial autosomal dominant form and in sporadic isolated incidences due to null alleles in the gene encoding for production of elastin; neither of these forms are associated with the extracardiac features of Williams-Beuren syndrome.Elastin is responsible for the distensibility of the aorta and large arteries during systole and subsequent recoil during diastole. This allows storage of hydrodynamic energy during systole and its release during diastole, an effect known as the windkessel effect. While loss of aortic distensibility alone is sufficient to elevate left ventricular (LV) afterload, the major impedance to LV ejection is the development of an obstructive aortic lesion. The reduced deposition of elastin in the arterial wall leads to increased proliferation of smooth muscle cells in the media of large arteries and subsequent development of obstructive hyperplastic intimal lesions.2 A characteristic hourglass narrowing of the aorta develops at the sinotubular junction. In approximately 30% of cases, there is diffuse tubular narrowing of the ascending aorta often extending to the arch and the origin of the brachiocephalic vessels.3,4 There may also be localized stenosis in the renal and mesenteric arteries. While peripheral pulmonary artery stenoses are characteristically associated with congenital SVAS, it is not uncommon for central pulmonary artery (pulmonary artery proximal to the hilum) stenoses to exist as well. The natural history of the pulmonary artery lesions is one in which there is a lessening in severity throughout childhood and adolescence. 5,6 Nonetheless, in approximately 40% of patients, severe pulmonary artery stenoses and right ventricular pressure overload exist in conjunction with SVAS and left ventricular pressure overload at the time surgical relief of

show abstract

Evidence for Cardiovascular Autonomic Dysfunction in Neonates With Coarctation of the Aorta

Cited by 67 publications

References 44 publications

Ventricular–Vascular Stiffening in Patients With Repaired Coarctation of Aorta

Ventricular–Vascular Stiffening in Patients With Repaired Coarctation of Aorta

Hypertension and coarctation of the aorta: an inevitable consequence of developmental pathophysiology

Anesthesia for Adult Congenital Aortic Surgery

Contact Info

Product

Resources

About