Acute Aortic Disease.. - Index of

236 Sanz et al.
Hydralazin, a direct arterial vasodilator, increased the risk of aortic rupture due to
its inability to reduce dp/dt max and also probably because of direct toxic effects on
elastin ultrastructure (50,51). Drugs with sympathicomimetic activity also favored
rupture (52). On the other hand, propranolol, a nonselective β-1 and β-2 receptor
blocker, increased aortic tensile strength and reduced contractility and dp/dt max,
conferring the greatest protection (50,53). The cardioselective β-1 receptor antagonists
sotalol and practolol also lowered dp/dt max with little change in the aortic
tensile strength, resulting in partial protection from aortic rupture (50,53). Similar
partial protection was observed with reserpine, a drug that depletes catecholamine
stores and causes increases in aortic tensile strength, but increments in dp/dt max
(50,52). Interestingly, propranolol demonstrated protective actions at doses without
significant hemodynamic effects, suggesting direct effects on the arterial wall.
Subsequently, it was shown that propranolol enhances the formation and maturation
elastin crosslinks in the aorta, probably by stimulating of lysil-oxidase (54).
In one study, in patients with Marfan’s syndrome, intravenous propranolol failed
acutely to reduce dp/dt max, suggesting that it might be less effective in the presence
of a dilated aortic root (55).
Despite the important beneficial effects derived from decreasing dp/dt max,
the role of arterial pressure must not be underestimated. In a study involving dogs
with surgically produced dissection, progression in one hour was evaluated under
different pharmacological treatments. In agreement with prior considerations,
nitroprusside was effective in controlling arterial hypertension but not dissection
progression. However, the control of dp/dt max with propranolol alone was also
insufficient. The best results were reached with the combination of nitroprusside
and propranolol or with trimethaphan, an autonomic ganglion blocker with effects
in contractility and vascular resistance (56). Therefore, both aggressive reductions
in both blood pressure and dp/dt max constitute the basis for contemporary medical
therapy of acute aortic syndromes.
MEDICAL TREATMENT OF ACUTE AORTIC DISSECTION
General Considerations
An overview of the management of acute aortic dissection is shown in Figure 5.
Current recommendations, particularly with respect to medical treatment, are
largely based on noncontrolled experience and studies with limited numbers
of patients. As pointed out elsewhere, evidence-based medicine principles are
difficult to apply in a relatively uncommon and life-threatening condition (57).
Initial series suggested that medical therapy was a potential alternative to surgical
intervention in aortic dissection and that untreated patients fared worse than those
treated either medically or surgically (58–62).
In uncomplicated type B dissection, surgery does not improve survival
(63,64) and therefore these patients are managed medically in most instances.
Surgery (or percutaneous intervention) is usually reserved for those cases with