Orthostatic and Exercise Effects in Children Years After Kawasaki Disease.

The long-term orthostatic and/or exercise hemodynamic effects in children years after Kawasaki disease (KD) were studied using clinical data from the treadmill exercise test (TMET). Heart rate (HR) and blood pressures (BPs) recorded in TMET were compared between two age, gender, and body scale-matched groups of patients with and without a history of KD. The KD group included 60 patients (9.8 ± 2.7 years old) 6.6 ± 2.6 years after KD without coronary arterial aneurysm. The non-KD group included 60 children (10.2 ± 2.7 years old) with other diagnoses. The exercise tolerance in TMET was not statistically different between the two groups. The KD group had a faster HR on standing than the non-KD group by 8.6% (101.5 ± 12.2 vs. 93.5 ± 15.9 bpm, respectively; P < 0.01), suggesting weaker and/or retarded orthostatic vasoconstriction. The pulse pressure was largely augmented above the 4th stage beyond 160 mmHg in 10.6 versus 0% (5 vs. 0) of the KD and non-KD groups (P < 0.05), respectively, while HR and BPs were not significantly different through exercise stages between the two groups. The KD group also showed a faster HR recovery five minutes after exercise than the non-KD group, by 5.7% (108.0 ± 11.6 vs. 102.2 ± 14.2 bpm, respectively; P < 0.05). Our results might indicate long-term subclinical impacts on the vascular tonus of children years after the disease that have not been recognized in previous studies.

Radius exponent in elastic and rigid arterial models optimized by the least energy principle.

It was analyzed in normal physiological arteries whether the least energy principle would suffice to account for the radius exponent x. The mammalian arterial system was modeled as two types, the elastic or the rigid, to which Bernoulli's and Hagen-Poiseuille's equations were applied, respectively. We minimized the total energy function E, which was defined as the sum of kinetic, pressure, metabolic and thermal energies, and loss of each per unit time in a single artery transporting viscous incompressible blood. Assuming a scaling exponent α between the vessel radius (r) and length (l) to be 1.0, x resulted in 2.33 in the elastic model. The rigid model provided a continuously changing x from 2.33 to 3.0, which corresponded to Uylings' and Murray's theories, respectively, through a function combining Reynolds number with a proportional coefficient of the l - r relationship. These results were expanded to an asymmetric arterial fractal tree with the blood flow preservation rule. While x in the optimal elastic model accounted for around 2.3 in proximal systemic (r >1 mm) and whole pulmonary arteries (r ≥0.004 mm), optimal x in the rigid model explained 2.7 in elastic-muscular (0.1 < r ≤1 mm) and 3.0 in peripheral resistive systemic arteries (0.004 ≤ r ≤0.1 mm), in agreement with data obtained from angiographic, cast-morphometric, and in vivo experimental studies in the literature. The least energy principle on the total energy basis provides an alternate concept of optimality relating to mammalian arterial fractal dimensions under α = 1.0.

Model combining hydrodynamics and fractal theory for analysis of in vivo peripheral pulmonary and systemic resistance of shunt cardiac defects.

The fractal state of the arterial vascular tree is considered to have a universal dimension related to the principle of minimum work rate, but can demonstrate the capacity to adapt to other dimensions in disease states such as congenital high-flow pulmonary hypertension (PH) by a process that is incompletely understood. To document and interpret fractal adaptation in patients with different degrees of PH, pulmonary and systemic vascular resistance was analyzed by a model that evaluated the fractal dimension, x, of the Poiseuille resistance contribution of the arterial vessel radius between 10 and 100µm, via the proportionality Q∝(R(peri)/BL)(-x/4), with Q, R(peri), and BL clinically observed variables representing total pulmonary or systemic blood flow, its peripheral arterial resistance, and body length, respectively. Identification of x in the pulmonary (P) and systemic (S) beds was evaluated from hemodynamic data of 213 patients, categorized into 7 groups by PH grade. In controls without PH, x(P)=2.2 while the dimension increased to 3.0, with the systemic dimension constant at x(S)=3.1. Our model predicts that severe grades of PH are associated with: a more elongated and hindered vessel in the periphery, and reductions in vessel numbers, as unit pulmonary resistive arterial trees (N(1)) and their component intra-acinar arteries (N(W)). These model network changes suggest a complex adaptive process of arterial network reorganization in the pulmonary circulation to minimize the work rate of high-flow congenital heart defects.

Clinical implication of main pulmonary artery Windkessel size after banding operation.

BACKGROUND: The Windkessel model, proposed in 1895 by O. Frank, successfully explained systemic and abnormal pulmonary hemodynamics of congenital cardiac defects. The model is essentially a functional one and describes only hemodynamics, not anatomical or geographic structures. Because pulmonary arterial banding (PAB) adds a substantial resistance proximal to arterioles, it provides an ideal anatomical structure of the Windkessel model, namely, an elastic reservoir of much dilated main pulmonary artery (mPA) followed by a substantial artificial resistance of banding. METHODS: The pulmonary artery (PA) Windkessel size (WS) of 10 patients, several months to years after PAB, were estimated both in peak systole (WSs) and minimum diastole (WSd), as the product of Windkessel compliance and proximal to distal pulmonary arterial pressure difference at each cardiac phase. They were compared to cineangiogram-determined corresponding volumes (Vs, Vd) of PA proximal to the band or mPA. RESULT: WSs and WSd correlated well with Vs and Vd, respectively, with the correlation coefficient of 0.91 and 0.62, indicating that the Windkessel in these patients corresponds to mPA. Among five patients whose resistance at the band comprised more than half of the whole PA resistance, the coefficients proved even better. CONCLUSION: Much bigger secondarily developed Windkessel, as placed proximal to the band on top of a substantial resistance at PAB, contributed much to alleviate the stress downstream at the periphery caused by greatly increased systolic stroke volume into mPA in these cardiac defects.

Clinical significance of reduced systemic Windkessel size in severe ventricular septal defect patients.

BACKGROUND: Large-shunt ventricular septal defect (VSD) infants manifest varied serious symptoms resulting from peripheral arterial constriction to compensate for increased pulmonary blood flow (Qp) and concomitantly decreased systemic blood flow (Qs). The aim of the present paper was therefore to estimate the whole arterial space proximal to arterioles as the systemic Windkessel size (WS) in these infants and compare it with aortic volume (AV) estimated angiographically. METHOD: Subjects were divided into three groups. Group 1a consisted of the so-called balanced-pressure VSD infants; group 1b consisted of those with normal or moderately increased pulmonary artery pressure (PAP) and highly augmented Qp; and group 2 consisted of those with a history of mucocutaneous lymph node syndrome as controls for Qp and pulmonary artery pressure. WS was computed from the Windkessel model, while the AV was calculated from the angiogram. Maximal systolic (WSs), mean (WSm), and minimum diastolic (WSd) WS were defined, computed, and compared. RESULT: All WS were significantly smaller in group 1a; those of group 1b were between group 1a and group 2, with Qs-dependent reduction of WS throughout all these three groups. WSs, WSm, and WSd had negative correlations with right ventricular systolic pressure/left ventricular systolic pressure in group 1a and group 1b. WSm, or the time averaged size, proved to be larger than the corresponding AV in all patients. The ratio of WSm/AV was significantly reduced in group 1a compared to group 1b and group 2, indicating that systemic arterial Windkessel space in severe VSD infants is significantly small, especially so in terms of space distal to aortic valve and proximal to arterioles. CONCLUSION: In severe VSD infants the whole systemic arterial space proximal to arterioles (WS) is reduced in size according to severity.