Key result
Tilt isoproterenol provocation, but not tilt alone, induced a significant reduction in cerebral blood flow velocity without remarkable hypotension in a heart transplant recipient.
Why the study?
Does isoproterenol provocation during upright tilt test induce cerebral hypoperfusion in a heart transplant recipient with a denervated heart?
Case Report (n=1)
Does isoproterenol provocation during upright tilt test induce cerebral hypoperfusion in a heart transplant recipient with a denervated heart?
Isoproterenol can induce cerebral hypoperfusion without remarkable hypotension in a denervated heart, suggesting vagal reflexes are not required for isoproterenol-induced cerebral hypoperfusion.
Isoproterenol tilt provocation may induce cerebral hypoperfusion without hypotension in denervated hearts; hypothesis-generating for syncope mechanisms.
To determine the effect of tilt isoproterenol provocation on cerebral perfusion in a patient with denervated heart, transcranial Doppler sonography was used to assess changes in cerebral blood flow velocity during upright tilt test. A 51-year-old man with history of syncopal spells after heart transplantation was evaluated by using upright tilt test with and without isoproterenol for 30 minutes, respectively, at 80 degrees inclined. Mean cerebral blood flow was measured in the main stem of the right middle cerebral artery. Blood pressure and heart rate were noninvasively monitored. Tilt isoproterenol provocation but not tilt alone induced a significant reduction in cerebral blood flow velocity, without remarkable hypotension. There was no change in respiratory activity. This may indicate that vagal reflexes are not implicated in the mechanism of isoproterenol to induce cerebral hypoperfusion and hence neurally mediated syncope.
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Philip C. Njemanze (1993) conducted a case report in Syncopal spells after heart transplantation (n=1). Tilt isoproterenol provocation vs. Tilt alone was evaluated on Cerebral blood flow velocity. Tilt isoproterenol provocation, but not tilt alone, induced a significant reduction in cerebral blood flow velocity without remarkable hypotension in a heart transplant recipient.
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