Perhaps the most plausible explanation for syncope during exercise in patients with aortic stenosis is left ventricular stretch baroreceptor or mechano-receptor stimulation with concomitant arterial hypotension, reduced venous return, and bradycardia. Ross and colleagues demonstrated that elevation of left atrial and left ventricular pressures in dogs caused a decrease in venous return, and a fell in systemic vascular resistance which was most prominent during extrasystoles. Johnson hypothesized that abrupt elevation of left ventricular systolic pressure without a corresponding rise in aortic pressure could allow left ventricular baroreceptors to produce “a violent depressor reflex.” This could lead to bradycardia, peripheral vasodilation, and hypotension, which would reduce coronary arterial flow and result in left ventricular dysfunction and arrhythmias. read
Mark et al further elucidated this mechanism in ten patients with AS, of whom six had a history of exertional syncope. They measured the forearm vascular response to supine leg exercise in the AS patients and five normal subjects. The forearm vascular response in normal subjects was appropriate vasoconstriction. In the patients with aortic stenosis, they noted forearm vasodilation and increased forearm blood flow. This was particularly marked in patients with a history of syncope. Forearm vasodilation reverted to vasoconstriction during exercise in three patients after aortic valve replacement. Activation of left ventricular baroreceptors could have resulted in reflex vasodilation with arterial hypotension and reduced coronary artery perfusion. This reflex plays a role in inhibition of sympathetic drive. Other investigators have demonstrated a reflex withdrawal of alpha adrenergic vasoconstrictor tone in the muscles as well as the skin of dogs in response to elevation of left ventricular pressures. These studies strongly support left ventricular baroreceptors as a major contributor to exertional syncope related to AS.