Helen T. Santiago

MENTAL STRESS AS A TRIGGER OF MYOCARDIAL ISCHEMIA AND INFARCTION

Recent research on the effects of behavioral activities on myocardial ischemia in coronary artery disease patients has provided a pathophysiologic model for understanding the mechanisms by which mental stress can trigger clinical cardiovascular events. This article reviews epidemiologic research implicating psychosocial stress as an acute trigger of myocardial infarction in patients with pre-existing coronary artery disease, and evidence for the pathophysiologic effects of acute mental stress in individuals with pre-existing coronary artery disease. Via its actions on the central and autonomic nervous systems, stress can produce a cascade of physiologic responses in vulnerable individuals that may lead to myocardial ischemia, ventricular fibrillation, plaque rupture, or coronary thrombosis. Also reviewed are field and laboratory studies that suggest important causal links between mental stress and myocardial ischemia, and evidence suggesting clinical significance for vulnerability to mental stress-induced ischemia.

Prognostic value of mental stress testing in coronary artery disease

This study assesses the prognostic value of mental stress-induced ischemic left ventricular wall motion abnormalities and hemodynamic responses in patients with stable coronary artery disease (CAD). Seventy-nine patients (76 men and 3 women) with prior positive exercise test results were exposed to mental arithmetic and a simulated public speech stress in 2 prior studies. Ischemic wall motion abnormalities were monitored using echocardiography or radionuclide ventriculography (RNV). During mental stress testing, new or worsened ischemic wall motion abnormalities to mental stress and exercise were ascertained, as were peak changes in blood pressure and heart rate to mental stress. The occurrence of subsequent cardiac events (including cardiac death, nonfatal myocardial infarction, or revascularization procedures) was ascertained. New cardiac events were observed in 28 of 79 patients (35%) after a median follow-up duration of 3.5 years (range 2.7 to 7.3). Survival analysis indicated that 20 of 45 patients with mental stress ischemia (44%) experienced new cardiac events more frequently than those without mental stress ischemia (8 of 34; 23%; p = 0.048). Type of cardiac event did not differ between mental stress-positive and stress-negative patients. After controlling for baseline blood pressure and study group status (echocardiography vs RNV), there was a significantly higher relative risk of subsequent events for patients with high versus low peak stress-induced diastolic blood pressure responses (RR = 2.4, confidence interval 1.1 to 5.2; p = 0.03). These results demonstrate that ischemic and hemodynamic measures obtained from mental stress testing may be useful in assessing prognosis in CAD patients with prior positive exercise test results.

Classification of panic attack subtypes in patients and normal controls in response to biological challenge: implications for assessment and treatment.

Panic attacks are symptomatically heterogeneous but efforts to describe such heterogeneity are relatively new. With regard to symptom presentation, at least three types of panic attack have been proposed based on the coupling or decoupling of verbal-cognitive and physiological symptoms: prototypic, cognitive, and nonfearful panic. The central aim of the present study was to address whether patients with panic disorder (PD) and nonclinical controls (NC) could be classified and discriminated (within and between groups) in terms of subtypes of panic attacks based on convergence and divergence of physiological and subjective arousal. Two samples of patients with PD (n = 94) and NC (n = 70) were exposed to single-breath vital capacity (VC) inhalations of 35% CO2/65% O2. Subjective anxiety and cardiovascular (heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DSP)) reactivity to the challenge were measured. For reactive participants, response patterns suggested the production of differentiated and stable panic attack subtypes described as: (1) prototypical (high subjective, high physiological), (2) cognitive (high subjective, low physiological), and (3) nonfearful (low subjective, high physiological). Subtype frequency differed between groups (prototypical: 33% PD, 8% NC; cognitive: 37% PD, 4% NC; nonfearful: 11% PD, 42% NC). A panic attack typology based on convergence and divergence of different response systems appears to reliably discriminate patients with panic disorder and may have relevance for predicting clinical characteristics, treatment modality, and prognosis.

Antidepressant discontinuation in the context of cognitive behavioral treatment for panic disorder

Cognitive behavioral treatment (CBT) has been shown to reduce risk for adverse reactions (e.g., rebound panic) following benzodiazepine taper for patients with panic disorder (PD). This study evaluated the effects of antidepressant discontinuation for patients with PD in the context of CBT. Patients with PD (n=21) on a stable dose of antidepressants completed a 12-week group CBT treatment and were randomly assigned to discontinue antidepressants during week 8 of the treatment. There were no statistically significant differences between groups at posttreatment or 6-month follow-up. Data indicate no apparent immediate or long-term adverse effects for antidepressant discontinuation for patients with PD receiving CBT.

Effects of heart-rate feedback on estimated cardiovascular fitness in patients with panic disorder.

Psychological parameters that are believed to affect estimations of cardiovascular fitness were examined in patients with panic disorder and nonclinical controls. Fifty‐four participants [panic disorder patients (n = 27) and age‐ and sex‐matched nonclinical controls (n = 27)] completed a cycle ergometer test and were compared on the basis of estimated VO2 max. Participants were randomly assigned to experimental conditions in which they received heart‐rate feedback or no feedback during the test. Patients with panic disorder exhibited lower VO2 max and decreased exercise tolerance (i.e., were more likely to discontinue the test) than nonclinical controls. Furthermore, individuals with high anxiety sensitivity (i.e., a fear of autonomic arousal), but not a panic disorder diagnosis per se, achieved significantly lower VO2 max when provided with heart‐rate feedback. Moreover, diagnostic status interacted with levels of anxiety sensitivity to predict VO2 max. Patients with panic disorder display poorer cardiovascular fitness after controlling for anxiety and other factors that underestimate performance during fitness testing. Depression and Anxiety 12:59–66, 2000.

Pain in patients with panic disorder: relation to symptoms, cognitive characteristics and treatment outcome.

OBJECTIVE Although there has been a link between certain types of pain, notably chest pain, and panic disorder, the relation between pain and panic disorder has not been systematically evaluated. In the present study, the relation between pain symptoms (headache, chest pain, stomach pain, joint pain) and the clinical presentation of patients with panic disorder was evaluated. HYPOTHESES Pain was generally hypothesized to be related to increased symptoms of anxiety, panic-relevant cognitive domains and treatment outcome. In terms of specific pain domains, headache and chest pain were expected to be more closely related to anxiety-related symptoms. PARTICIPANTS AND METHODS Patients (n=139) meeting the criteria of the Diagnostic and Statistical Manual of Mental Disorders - Fourth Edition for panic disorder completed a set of standardized clinician-rated and self-reported measures. Moderator analyses were used in a subset of these patients completing a treatment outcome study. RESULTS Approximately two-thirds of the participants endorsed at least one current pain symptom. The hypotheses were partially supported, with pain being associated with higher levels of anxiety and depression symptoms, as well as panic frequency. Pain was also related to several cognitive features, including anxiety sensitivity and panic appraisals. Headache and chest pain were more highly associated with anxiety symptoms than was joint pain. Cognitive measures did not mediate the relation between anxiety and pain, and pain did not significantly moderate outcome in response to cognitive-behavioural therapy. CONCLUSIONS Co-occurring pain symptoms appear to be more highly related to phenomenology than to treatment response in patients with panic disorder.

Effects of cognitive behavioral treatment on physical health status in patients with panic disorder

The relationship between panic disorder and nonpsychiatric medical illness is complex, but some evidence suggests that panic disorder increases risk for a variety of nonpsychiatric medical conditions. Given the demonstrated efficacy of cognitive behavioral therapy (CBT) for panic disorder, we were interested in evaluating the effects of CBT for panic disorder on nonpsychiatric medical symptoms among these patients. Patients were randomized to a 12-week group-administered CBT protocol (n = 22) or a delayed-treatment control (n = 24). Treated patients showed marked improvement in both anxiety symptoms and physical health symptom ratings that were evident at midtreatment and were maintained through a 6-month follow-up period. Despite comparable rates of change, changes in anxiety symptoms did not appear to mediate the relationship between treatment and improved physical health ratings. These findings indicate that CBT appears to have an immediate and long-term beneficial impact on physical health and that this effect is independent from its impact on anxiety symptoms.

Evaluating the Etiology of Anxiety Sensitivity: Relation to Cardiovascular Perception and Reactivity

A large body of research has suggested that anxiety sensitivity (AS) acts as a specific vulnerability factor in the development of anxiety pathology. More recently, attention has turned to the etiology of AS per se. The present study tested several related etiological hypotheses derived from Expectancy theory. S. Reiss and R. J. McNally (1985) originally proposed that greater physiological reactivity would increase risk for developing heightened AS. Reactive individuals are believed to have greater opportunity to perceive unpleasant bodily perturbations, thereby increasing the likelihood that concerns and fears could be attached to the sensations. Nonclinical participants (N = 86) completed physical (e.g., orthostatic) and biological (e.g., 35% CO2) challenges and a heart beat perception task. AS was not related to heart beat perception but was related to greater tonic heart rate and greater diastolic blood pressure (DBP) reactivity to both the challenges. Higher DBP and higher heart beat accuracy interacted to predict higher AS.