Acute Aortic Disease.. - Index of

Acute Aortic Dissection 233
P t is usually simplified to the intravascular distending force, that is, the arterial
pressure. Indeed, arterial hypertension has been often associated with the propensity
to develop aortic dissection and aneurysms, and constitutes a common clinical
finding in acute aortic syndromes (3,37–39). An increment in systolic blood pressure
of 26 mmHg has been found equivalent to an increase in aortic diameter of
1 cm in terms of generated wall stress (16).
However, wall stress prediction is actually much more complex, particularly
in the presence of aneurismal dilatations where the assumption of a cylindrical
shape of Laplace’s law does not hold. Stress distribution in aneurysms is in fact
largely heterogeneous—depending on the shape of the dilatation, local differences
in the wall characteristics, or presence of mural thrombosis (17). Apart from
circumferential stress (perpendicular to the arterial wall), there is probably considerable
shear stress among lamellae, as there is slight motion of the different
layers of the media along the plane of the vessel wall. This shear stress also
increases significantly in the presence of aortic dilatation (31). As mentioned
earlier, uniformity in stress distribution is an important protective characteristic
of the arterial wall. Homogeneity of the media is lost in the presence of focal
fibrosis, calcification, islets of mucoid material, or intramural hemorrhage that can
occur with conditions associated with medial degeneration (13,31,40). This results
in nonuniform distribution of stress that can trigger dissection (31).
Although it is clear that wall stress is directly proportional to blood pressure,
observations made in the 1960s suggested that pressure itself is not the main
determinant of aortic disruption. Interestingly, both normal and diseased aortas were
found to be highly resistant to rupture from static forces, indicating the importance
of pulsatility as a contributor to wall rupture (41). This led to the hypothesis
that the morphology of the arterial pulse wave might have a stronger influence
than the actual pressure level (42,43).
In this regard, the contractile status of the myocardium plays an important
pathophysiological role. Impulse is defined as the product of force and time.
The term cardiac impulse has been employed to define the net force exerted by
the contracting myocardium during ejection. During systole, the maximum rate
of myocardial shortening occurs at the beginning of contraction, when load is
minimal, and the velocity of shortening decreases as load grows. This results in
maximal velocity of ejected blood early in systole, which coincides with the
maximal rate of pressure change within the ventricle (or dp/dt max). Information
regarding ventricular impulse and dp/dt max can be derived from the upslope of the
initial portion of the aortic pressure curve (Fig. 2) (44,45).
Sympathetic stimulation results in increases in cardiac impulse, whereas
reductions in sympathetic tone lead to diminished force of contraction and
decreased dp/dt max (44). The impact of dp/dt max and pulsatility is most prominent
in the ascending aorta and the aortic isthmus—areas where intimal tears often
develop (46). The maximal rate of pressure rise (dp/dt max) appears to be the most
important determinant of aortic rupture and the progression of dissection. It is
important to realize that regardless of the initial mechanism leading to wall