Abstract

Severe aortic stenosis (AS) untreated by aortic valve replacement is a fatal disease with a 3-year mortality rate of 75% once the classic symptoms of the disease ensue.1–4 Approximately 15% of AS patients present with syncope, which is an ominous occurrence.2 Indeed, a master cardiologist and my former mentor, Dr Lewis Dexter, quipped that sudden death in AS was simply prolonged syncope. Although exercise-induced arrhythmia and/or a pressure-induced vasodepressor response have been invoked to explain syncope in AS, the most commonly held theory invokes Ohm's law. This well-known principle states that V=I×R, where V is voltage, I is current, and R is resistance. Applied to the circulation, the terms are substituted such that P=CO×R, where P is pressure, CO is cardiac output (L/min), and R is the vascular resistance in the area of interest. The Figure diagrams the circulation in the patient with AS as having 3 major resistors: R1, the total pulmonary resistance made up of left ventricular (LV) filling pressure plus pulmonary vascular resistance that governs LV filling; R2, the resistance offered by the aortic valve; and R3, the systemic vascular resistance (SVR). Pressure at these 3 points in the circulation is determined by the product of CO×R. If resistance drops without a concomitant increase in output, pressure must also fall. In severe AS, it has been assumed that R2 (valve resistance) exceeds R3 (SVR) substantially. As such, a fall in SVR caused by exercise or by administration of a vasodilator would cause a fall in systemic pressure because R2, the severely stenotic aortic valve, would block a compensatory increase in forward output causing systemic hypotension and syncope. Is this theory proven? Article see p 2353 Figure. Diagram of the circulation as an electric circuit. …

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