Abstract 11582: Vascular, Hemodynamic and Hormonal Response to Mental Stress and Risk of Mental Stress Induced Myocardial Ischemia
Introduction: Mental stress-induced myocardial ischemia (MSIMI) has been linked to adverse cardiovascular outcomes in patients with stable CAD. However, the underlying mechanisms are not well understood. We aimed to study vasomotor, hemodynamic and hormonal responses to mental stress (MS) and their relationships with MSIMI.
Methods: 660 patients with stable CAD underwent 99mTc sestamibi myocardial perfusion imaging before, and during a public speaking stressor. Hemodynamic parameters (heart rate, BP, rate-pressure product [RPP]), circulating catecholamines, and peripheral arterial tonometry (PAT, Itamar Inc.) were measured at rest, during, and after MS. MSIMI was defined as myocardial perfusion impairment with MS.
Results: Participant age was 63±9; 72% male. Overall, 102 (16.1%) patients developed MSIMI. During MS, there was a significant increase in heart rate, BP, RPP and epinephrine, but not norepinephrine levels. The mean PAT ratio, measured as a ratio of the lowest pulse wave amplitude during the speaking task to the final three minutes of pulse wave amplitude during rest, was 0.7 ± 0.3 indicating vasoconstriction with MS. Patients with MSIMI had a greater hemodynamic response (Figure) and a lower PAT ratio (0.6±0.3 vs 0.7±0.3, p=0.008), in comparison to those with no ischemia. After adjustment for age, CAD risk factors and beta blocker use, both higher hemodynamic response (change in RPP≥median) and more vasoconstriction (PAT ratio<median), but not catecholamine response, were independent predictors of MSIMI [OR(95%CI) of 1.8 (1.1-2.9) and 2 (1.2-3.3), p=0.02 and p=0.01, respectively]. A greater hemodynamic response and a lower PAT ratio had an incremental effect on incidence of MSIMI (Figure).
Conclusion: A greater hemodynamic response and peripheral vasoconstriction are associated with MSIMI, indicating that both increased myocardial demand and potentially coronary vasoconstriction contribute to this phenomenon.
Author Disclosures: M. Hammadah: None. A. Alkhoder: None. N. Isakadze: None. Z. Almuwaqqat: None. M. Obideen: None. N. Abdelhadi: None. M. Moureiden: None. M. Gafeer: None. I. Al Mheid: None. K. Wilmot: None. R. Ramadan: None. H. Mohamed Kelli: None. K. Hosny: None. A. Shah: None. P. Pimple: None. Y. Sun: None. E. Garcia: None. P. Raggi: None. B. Pearce: None. F. Esteves: None. D. Sheps: None. J. Bremner: None. V. Vaccarino: None. A. Quyyumi: None.
- © 2016 by American Heart Association, Inc.