ACE Inhibition and Heart Failure

A primary rhythm in the central nervous system that entrains both heart rate, blood pressure, and ventilation 1 is suggested by profound effects on angina through consciously focusing on breathing and intervening pauses; adaptation to stress manifested by slower, deeper breathing, contributing to a 6.5-fold reduction in mortality; and the role of a slower rate of living in a lifespan increased 5-fold. 2 This hypothesis is supported by the association of the reduction of blood pressure with longer, less recurrent speech hesitation pauses 1 second or more in length, manifested by pauses averaging 1.18 seconds at 2 per minute and 1.93 seconds at 1 per minute, thus yielding a ratio of 0.611, approximating the golden section 0.618 (range, 0.534 to 0.833). It is also supported by the fact that even brief (1-5-second) spontaneous pauses in ongoing patterned behaviors are accompanied by an immediate reduction of 5-hydroxytryptamine neuronal activity to or below baseline levels, coordinating autonomic, motor, and sensory functions 3 and serotonergic modulation of dopamine 4 lateralized to the right hemisphere, thereby preventing disruption of brain stem cardiovascular control and lefthemisphere dominance associated with hazardous surges of sympathetic tone in abnormal awake respiratory patterns that are common in chronic heart failure manifested by cardiac dysrhythmia and vasoconstriction. 1,2