Introduction: Coronary vascular dysfunction (CVaD) is associated with major adverse outcomes, recurrent chest pain, and can be triggered by mental stress. Hypothesis: We hypothesized that women with CVaD have heightened emotional response and attenuated recovery compared to reference control (RC) women. Methods: Women diagnosed with CVaD (cases, n=57, age: 57±1 years) by abnormal adenosine or acetylcholine response during invasive coronary function testing were enrolled in Cardiac Autonomic Nervous System Study and compared to age-matched, asymptomatic RCs women (n=25, age: 56±3 years), free of cardiac or risk factor history. All underwent two 4-minute standardized mental stress tests - anger recall and mental arithmetic - followed by 15 minutes of recovery. Emotional arousal (tension, anxious, depressed) and chest pain were assessed via self-reported Likert scale at baseline, after stress, and after recovery. The difference between post-stress or post-recovery and baseline scores was used to evaluate stress provocation and recovery. Increased differences indicate more provocation or recovery attenuation. We utilized multivariate models adjusted for anti-anginal medications, statins, and aspirin or traditional cardiovascular risk factors and chest pain to assess associations between CVaD and chest pain or emotional arousal, respectively. Results: The two groups did not differ in hemodynamic response to mental stress (p>0.05). In multivariate models, CVaD status was associated with more stress-provoked chest pain (β 1.24 [0.1, 2.4], p=0.03) and more attenuated chest pain recovery (β 1.5 [0.6, 2.3], p=0.001) than RC. Similarly, after adjustment, cases were associated with more stress-provoked anxiety (β 1.2 [0.2, 2.2], p=0.02) and tension (β 1.2 [0.001, 2.4], p=0.05) while having more attenuated recovery of anxiety (β 1.1 [0.1, 2.0], p=0.02) and tension (β 1.1 [0.2, 2.0], p=0.02) compared to RC. There were no differences in feelings of depression between the two groups. Conclusions: Response to mental stress is heightened with attenuated recovery in women with CVaD. An improved understanding of mechanisms in stress response and CVaD is needed for potential therapeutic targets that may improve angina and quality of life.