...There is a considerable body of evidence indicating that
specific hemodynamics can produce dilatation in all arteries,
including central, peripheral, and pulmonary, which is
not discussed in the practice guidelines.1 In 1954, Holman15
observed that even minor degrees of obstruction of a normal
peripheral artery could cause rough periodic turbulence and
that this, rather than the severity of the obstruction, produced
the subsequent dilatation by means of tissue fatigue.
Aortic regurgitation can produce the effect of mild stenosis
by increasing the systolic velocity as a compensation to
maintain forward cardiac output. Mild hemodynamic abnormalities
that cause vessel dilatation occur in the pulmonary
trunk16 with poststenotic dilatation, but dilatation of the
pulmonary artery is rarely associated with BAV or aortic
dilatation, although the aorta and the pulmonary artery develop
from the same tissue from the truncus arteriosus.
Dilatation of the pulmonary artery as well as the aorta is
characteristic of Marfan syndrome, with the affected tissue
influenced by the abnormal genetics of the vessel walls, but
not in patients with BAVs, countering the idea of an inherited
tissue weakness.
Bruns et al17 showed experimentally that a vibrator with
a frequency in the acoustic range (96 Hz) activating a thin
metal strip in the center of an elastic tube, without touching
the walls, could produce an ?aneurysm? of the tube at the
point downstream of maximal periodic vibration in a relatively
short time. They compared this with Holman?s15
results using blood vessels and with clinical situations of
mild stenosis of the aorta and pulmonary artery that were
accompanied by a thrill. They postulated that the aneurysm
represented structural fatigue due to the acoustic energy that
was ?much greater than one would expect from turbulence.?
17...
