Both posttraumatic stress disorder (PTSD) and major depressive disorder (MDD) are related to an increased risk for cardiovascular disease (CVD), with links to ischemic heart disease, myocardial infarction, cardiac mortality, and other cardiac conditions. Given that these disorders are associated with increased medical costs, disability, and employer burden, research has investigated which factors increase the likelihood that one will develop CVD. While one hypothesis suggests that individuals who exhibit exaggerated responses to stress are at greater risk of developing CVD, individuals with PTSD/depression have been shown to exhibit both exaggerated and blunted stress responses. The purpose of the present study was to examine whether differing PTSD symptomatology, depressive presentation, dissociation, or cognitive appraisals of stressful events can predict the nature of one’s cardiovascular response to stress. It was hypothesized that: (1) PTSD arousal would be positively related to cardiac reactivity and PTSD avoidance negatively related to cardiac reactivity; (2) depressive activation would be positively related to cardiovascular reactivity and depressive withdrawal negatively related to cardiovascular reactivity; (3) dissociative symptoms would be negatively related to cardiovascular reactivity; and (4) challenge appraisals would be related to greater cardiac reactivity and threat appraisals to greater peripheral resistance. Female participants (N = 57) were administered the Clinician-Administered PTSD Scale (CAPS) and Structured Clinical Interview for DSM-IV Axis I Disorders (SCID) by graduate research assistants. Participants subsequently completed a demographic questionnaire and the Traumatic Life Events Questionnaire (TLEQ), Beck Depression Inventory-II (BDI-II), Dissociative Experiences Scale II (DES II), and Stress Appraisal Measure (SAM) to assess traumatic life events, depression, dissociation, and cognitive appraisals, respectively. Participants’ cardiovascular reactivity (HR, CO, SBP, DBP, and TPR) in response to two stress tasks‒mental arithmetic and public speaking‒were assessed via impedance cardiography and an automated blood pressure cuff. Multivariate regression revealed support for some hypotheses as significant relationships were found between reactivity and PTSD avoidance, PTSD arousal, and depressive withdrawal. No significant relationships were found between reactivity and dissociation, depressive activation, or threat appraisals. This study provides preliminary support for the idea that differing psychological presentations can predict the type of cardiovascular response one exhibits in response to stress.

The mere exposure effect, positive affect elicited by exposure to a previously unfamiliar stimulus, is considered one of the most well established findings in the psychological literature. Yet its mechanism remains unknown. In Experiments 1 - 5, memory encoding was examined to determine whether the mere exposure effect was a form of conceptual or perceptual implicit priming, and, if not either, whether cardiovascular psychophysiology could reveal its nature. Experiment 1 examined the effects of study phase level of processing on recognition, the mere exposure effect, and word identification implicit priming. Deep relative to shallow processing improved recognition, but did not influence the mere exposure effect or word identification implicit priming. Experiments 2 and 3 examined the effect of study-test changes in font and orientation, respectively, on the mere exposure effect and word identification implicit priming. Different study-test font and orientation reduced word identification implicit priming, but had no influence on the mere exposure effect. The combined results from Experiments 1-3 suggested that conceptual and perceptual processing do not drive the mere exposure effect. Experiments 4 and 5 developed and used, respectively, an innovative cardiovascular psychophysiological implicit priming paradigm to examine whether stimulus-specific cardiovascular reactivity at study predicted the mere exposure effect at test. At encoding, stimulus-specific peripheral vasodilatation had predictive value for the mere exposure effect, but not for word identification implicit priming. Experiments 6 and 7 examined whether sustained or transitory anxiety (i.e., trait or state, respectively) would influence the mere exposure effect. Greater trait and state anxiety reduced the mere exposure effect. Together, the findings from these experiments (N = 362) identify a novel affective mechanism of implicit priming that is influenced by cardiovascular psychophysiology and variations in trait and state anxiety.

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Racial microaggressions are a type of perceived discrimination entailing a brief pejorative message by a perpetrator, whether verbal or nonverbal, intentional or unintentional, about a target person that operates below the level of conscious awareness. Research supports a relationship between perceived discrimination and worse mental and physical health outcomes, with the literature centered mainly on non-Hispanic blacks. Less research exists on how perceived discrimination, specifically racial microaggressions, affects the mental and physical health of Hispanic/Latinos. This study examined how exposure to racial microaggressions, using an experimental design whereby a confederate delivers two types of racial microaggressions, influences affect and cardiovascular reactivity (CVR) among Hispanic/Latinos and non-Hispanic whites. Results revealed that the experience of racial microaggressions did not evoke larger and longer lasting emotional and physiological arousal among Hispanic/Latinos and non-Hispanic Whites. Future directions are discussed.

Exaggerated cardiovascular reactivity and impaired recovery to psychological stress is independently related to cardiovascular disease (CVD), and may play a causal role in its development. I examined autonomic reactivity and recovery in 136 black, white, and Hispanic women who were predisposed to CVD, as indicated by a positive family history (FH+). Pre-ejection period (PEP; sympathetic) and respiratory sinus arrhythmia (RSA; parasympathetic) were measured during public speaking, mental arithmetic, and cold pressor tasks. Overall, FH+ participants exhibited greater RSA reactivity, while black participants exhibited impaired RSA recovery. These findings suggest that a hereditary predisposition for CVD is related to altered autonomic reactivity before any differences in resting levels are observed. Further, black participants did not exhibit a RSA rebound after the stress tasks, a key component in buffering the damaging effects of exaggerated sympathetic reactivity. These findings demonstrate the importance of examining parasympathetic activity in addition to sympathetic reactivity measures.

The present study examined whether cardiovascular habituation to stress is affected by a change in the physical context in which a stressor is encountered. Twenty-five undergraduate students at the University of Central Florida, Palm Bay Campus, were exposed to 4 trials of a stressor consisting of mental arithmetic while under evaluative observation. It was hypothesized that if participants experienced a change in the physical context in which stress was experienced on the final trial, they would demonstrate impaired habituation to stress as indicated by measures of heart rate and blood pressure. Physical context was manipulated by either asking participants to move to another room upon the final exposure to the stressor or to remain in the same room in which they were initially exposed to the stressor for the final exposure. Participants were randomly assigned to one of 2 conditions, the Stable Room Condition (N = 10) or Novel Room condition (N = 15 ). Participants in the Stable Room Condition remained in the same physical context, or same room, throughout all trials and displayed habituation of systolic .blood pressure, diastolic blood pressure, and heart rate. Participants in the Novel Room condition were exposed to the same stressors, but were moved to a different physical context, or new room upon the final trial. The results demonstrated that participants in the novel room condition displayed significantly impaired habituation on measures on systolic blood pressure (p < .001) and diastolic blood pressure (p < .001). However, no significant difference in heart rate was observed between groups. These results indicate that a simple change in the physical context in which stress exposure occurs impairs cardiovascular habituation to stress. Implications and directions for future research are discussed.

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This thesis explored whether haemodynamic responses to psychological stress test predict future blood pressure (BP) levels: the Reactivity Hypothesis. The research included a systematic review and two prospective cohort studies in the UK and Thai samples. In addition, the Blunted Reactivity Hypothesis, which posits that cardiovascular reactivity is inversely related to symptoms of anxiety and depression, was examined in cross-sectional analyses. A systematic review with meta-analysis and meta-regression with 41 prospective cohort studies (from 1950 to 2012) examined whether cardiovascular responses to psychological stress tests predict future BP levels, hypertension status, preclinical coronary heart disease (CHD) and cardiac events. Three possible moderators were included in analyses: type of task (active versus passive coping), age group (children versus adults), and duration of follow-up (short versus long-term follow-up). The review found that systolic BP reactions to psychological stress tests predict future systolic BP levels and that there was better prediction in child samples with shorter follow-up periods. Similarly, diastolic BP reactions to psychological stress predicted future diastolic BP levels. Cardiovascular reactions to psychological stress tests did not predict hypertension, preclinical CHD, or cardiac events. Cross-sectional analysis of two studies conducted in the UK and Thailand provided some evidence that anxiety and depressive symptoms were negatively associated with cardiovascular reactivity: these findings supported the Blunted Cardiovascular Hypothesis. However, these relationships were observed in the UK sample, but not in the Thai sample. Further, Thai participants responded to psychological stress task with large cardiovascular reactions, of a similar magnitude to the UK participants and observed in previous studies of Europeans and North Americans. Finally, prospective analyses revealed that systolic BP responses to mental arithmetic predict future systolic BP levels after one year of follow-up in both UK and Thai individuals, after controlling for baseline cardiovascular activity and traditional risk factors. In contrast, haemodynamic responses did not predict future BP. These results provide support for the “Reactivity Hypothesis” although the effect sizes were relatively small. However, responses to only one of the three stressors, mental arithmetic, predicted future BP implicating beta-adrenergically mediated cardiovascular responses. However, there was no physiologic evidence (i.e., cardiac output responses) that suggested beta-adrenergic mechanisms. Accordingly, future studies should examine alternate mechanisms (e.g., platelet aggregation and endothelial function) and cardiovascular responses in larger samples with a longer follow-up to further clarify the predictive value of reactivity in the development of hypertension, along with potential mechanisms.

The consequences of early embryonic insults and how they affect subsequent life reflects the emerging concept of "fetal programming". The aim of this project is to study the effects of embryonic insults as they subsequently manifest themselves in adults, with emphasis on the heart and vasculature. My experiments establish that fetal programming operates on the bobwhite quail inducing similar changes as those observed in mammalians and other birds. The quail's fast development provides reliable data in a short period of time than other avian models (e.g. domestic chicken). Data on quail showed a correlation between egg mass and hatchling mass; where small eggs produce small hatchlings but a high mortality made it impractical as a stressor for this study. Hypoxia was used as a stressor during embryonic incubation, where it induced a low hatching weight in quail that was not observable in adult birds. Morphological measurements demonstrated an increased ventricular collagen content and reduced ventricular lumen in birds in adults incubated in hypoxia consistent with hypertension. The hematological analyzes showed few differences indicating organ remodeling instead of hematopoietic compensation. The assessment of vascular reactivity pointed out an impaired endothelium dependent relaxation commonly associated to hypertension in birds and mammals. Fetal programming could be a widespread response to an adverse prenatal environment in endotherms and the resulting data from this work contributes to our understanding of fetal programming in vertebrates and its long term consequences.