• O Narayan, Q Li, P Mottram, I T Meredith, and J D Cameron.
• Monash Cardiovascular Research Centre, Monash Heart and School of Clinical Sciences at Monash Health, Monash University, Melbourne, AUSTRALIA.
• J. Hypertens. 2015 Jun 1; 33 Suppl 1: e61.

ObjectiveCardiac motion during systole has been shown to be closely associated with carotid pressure wave inflection point timing in young, healthy volunteers. In these individuals the inflection point occurred following the systolic pressure peak (Murgo Type C). The relationship between myocardial motion and the timing of inflection point in older patients with cardiovascular risk factors where the inflection point precedes peak systolic pressure remains unknown.Design And Method15 patients with cardiovascular risk factors were prospected enrolled and underwent simultaneous carotid tonometry and TDI tracking of medial mitral annular motion. Measurements were obtained in the resting state and following the administration of either intravenous dobutamine (10mcg/kg/min) or GTN (400mcg sub-lingual). The ECG R-wave was used as the fiducial marker to determine the timing of both peak systolic mitral annular motion (S') and the carotid pressure wave inlection point.Results30 paired measurements were obtained. Dobutamine increased SBP, HR and PP whereas GTN decreased these parameters. Augmentation index decreased following both agents. The left ventricular outflow tract velocity time integral (indicative of stroke volume) increased with dobutamine and decreased with GTN. Despite these changes, the timing of peak S' was significantly correlated with the timing of the carotid inflection point both at rest and with pharmacological intervention (R = 0.73, P = 0.002 and R = 0.89, P < 0.001 respectively).(Figure is included in full-text article.)Conclusions: Peak systolic mitral annular motion timing (representing the commencement of myocardial deceleration in systole) always precedes and remains coupled to carotid pressure wave inflection point timing in older patients with established cardiovascular risk factors. This data suggests that the morphology of the central blood pressure waveform may relate more strongly to local ventricular-vascular interactions, rather than wave reflections.

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