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The authors discuss transcranial magnetic stimulation as a possible treatment for patients with cardiovascular disease and treatment-resistant depression.

Aims Despite its demonstrated benefits, cardiac rehabilitation (CR) attendance, and completion is suboptimal, particularly in women. The aims of this study were (i) to develop and pilot test a women-only yoga-based CR programme (the Women’s Yoga CR Programme; WYCRP); (ii) to investigate programme acceptability; and (iii) to investigate attendance and completion of the WYCRP and continuation to Phase III community-based CR. Methods and results Women eligible for CR at a tertiary hospital in Melbourne, Australia were recruited. Over a 6-month period in 2019, they were offered the WYCRP or usual CR. The WYCRP involved attendance at a 1-h yoga session following the usual 1-h mixed-sex education session, over a 7-week period. Participants completed pre- and post-programme questionnaires and attended focus groups to assess programme acceptability. Rates of attendance, completion, and continuation for the WYCRP were recorded and compared to those for the standard CR programme offered in 2018. In total, 27 women were eligible for the study and attended the initial CR assessment. Of those, 22 (81%) attended the WYCRP, 1 (4%) attended usual CR, and 4 (15%) did not attend CR. Ratings of programme acceptability were consistently positive; qualitative comments highlighted both physical and emotional benefits. While attendance at the WYCRP was not significantly higher than for usual CR the previous year (81% vs. 76%; P = 0.40), CR completion, and continuation were (95% vs. 56%; P = 0.02, and 72% vs. 12%; P < 0.001, respectively). Conclusion This pilot study has demonstrated that women-only yoga-based CR is appealing to women and can improve women’s CR completion and continuation. These preliminary findings support further development of women-only and yoga-based CR options.

Unlike noradrenaline, the sympathetic neurotransmitter which overflows to the circulation, adrenaline (ADR) is a secreted hormone, with a low plasma concentration, and plasma concentration for biological action a log order lower than that of noradrenaline. The venous drainage of the left adrenal medulla into the left renal vein does expose this vein to uniquely high plasma ADR concentrations and possible risk of thrombosis at high rates of ADR secretion. There is typically a different timeframe for adrenal medullary and sympathetic nervous system responses: ADR release is short term in contrast with sympathetic activation persisting for years in heart failure and hypertension. The historic view of Walter Cannon, subject to recent review, that the sympathoadrenal system is a unified biological system, was deconstructed further with demonstration of frequent mismatching of adrenal medullary and sympathetic nervous responses. Under gravity stimulation with standing, there is prompt sympathetic activation without ADR release. In many diseases, notably obesity, hypertension, heart failure and depressive illness, an activated sympathetic nervous system and silent adrenal medulla coexist. The therapeutic corollary of this is that ADR blockade is much less commonly needed clinically than pharmacological antagonism of the sympathetic nervous system.

IntroductionDistress is experienced by the majority of cardiac patients, yet no cardiac-specific measure of distress exists. The aim of this project is to develop and validate the Cardiac Distress Inventory (CDI). Using the CDI, health professionals will be able to identify key clusters of psychological, emotional and social concern to address with patients, postcardiac event.Methods and analysisAn item pool will be generated through: identification of items by a multidisciplinary group of clinician researchers; review of generic and condition-specific distress measures; focus group testing with cardiac rehabilitation professionals; feedback from patients. The COSMIN (COnsensus-based Standards for the selection of health Measurement INstruments) criteria will be used to inform the development of the methodology for determining the CDI’s psychometric properties. The item pool will be tested with 400 cardiac patients and responses subjected to exploratory factor analysis, Rasch analysis, construct validity testing and latent class analysis. Receiver operating characteristic analysis will be used to identify the optimal CDI cut-off score for distinguishing whether a person experiences clinically significant distress.Ethics and disseminationApproved by the Monash Health Human Research Ethics Committee (approval number—RES-19-0000631L-559790). The CDI will be made available to clinicians and researchers without charge. The CDI will be translated for use internationally. Study findings will be shared with cardiac patient support groups; academic and medical communities via publications and presentations; in the training of cardiac secondary prevention professionals; and in reports to funders. Authorship for publications will follow the uniform requirements for manuscripts submitted to biomedical journals.

Introduction Patients who are anxious or depressed after an acute cardiac event are at increased risk of a subsequent event and premature death. It is therefore important to identify these patients early in order to initiate supportive or even preventive measures. In the present study, we report on the prevalence of anxiety and depression during the first 12 months after an acute cardiac event, and the patient characteristics predictive of increased anxiety and depression risk in early and late convalescence. Methods We recruited a sample of 911 patients with acute myocardial infarction (AMI), acute coronary syndrome (ACS) and/or unstable angina (UA), and/or undergoing coronary artery bypass graft surgery (CABGS) was recruited. Patients completed the Hospital Anxiety and Depression Scale (HADS) close to the time of their event, and again during early (2-4 months post-event) and late (6-12 months post-event) convalescence. Using HADS-A and HADS-D cut-offs of 8+, prevalence rates for anxiety, depression and comorbid anxiety and depression were determined for each timepoint. Chi-square tests and odds ratios were used to identify baseline patient characteristics associated with increased anxiety and depression risk over 12 months. Results Anxiety rates were 43%, 28% and 27% at the time of the event, early and late convalescence. Depression rates were 22%, 17% and 15% respectively. Factors consistently associated with increased anxiety and depression risk were history of depression, financial strain, poor self-rated health, low socioeconomic status, younger age (

Despite the 60-year history of attempting to understand the relationship between personality and cardiovascular disease (CVD), individual dispositions that affect the manner in which people think, feel and act are not typically considered in cardiac clinical settings. To identify how persistent negative emotional states and behavioural traits impacted cardiovascular health, early studies focused on the Type A personality (competitive, aggressive) and, later on, the Type D personality (‘distressed’). Recent evidence on other personality types or behaviours, such as borderline personality disorder, alexithymia and neuroticism, suggest that it may be the core elements of these, alongside hostility and proneness to anger, that lead to atherosclerosis, endothelial dysfunction, coronary artery calcification, and inflammation. The current paper, and part 2 of the Psychology in Cardiology series, explores the evidence supporting different interventions for people with health-compromising personality factors, to assist in planning lifestyle modification.

After cardiac events, rates of depression and anxiety of 20–30% have been reported, along with elevated rates of post-traumatic stress disorder and higher rates of suicide. As unresolved negative affect is associated with greater morbidity and mortality, attempts have been made to understand the complexity of emotional and psychological responses to cardiac events. Although many studies purport to measure ‘cardiac distress’, they are often limited by adopting a definition of distress as depression plus anxiety. Following the lead of the oncology and diabetes fields in the development of condition-specific distress measures, this article argues for a multidimensional approach to cardiac distress and its measurement; it builds on the concept of the ‘cardiac blues’, to show the importance of understanding and measuring how this transient phenomenon of adjustment can become a persistent negative state which challenges the ability to cope with living after a cardiac event.

Background: The relative risks and benefits of children attending kindergarten or pre-school remain uncertain and controversial. We used data from the Bavarian Pre-School Morbidity Survey (BPMS) to look at the prevalence of developmental impairments in pre-school children entering primary school and to assess if these were correlated with the duration of kindergarten attendance. Methods: We collected data from all school beginners in the district of Dingolfing, Bavaria from 2004 to 2007 (n = 4,005) and utilised a retrospective cross-sectional study design to review the information. The children were assessed for motor, cognitive, language and psychosocial impairments using a standardized medical assessment. Point prevalence of impairments of speech, cognition, motor functioning and psychosocial functioning were compared by χ2-test for the variable of time spent in kindergarten. Results: We detected a high incidence of impairments, with boys showing higher rates than girls in all the areas assessed. Longer length of time spent in kindergarten was associated with reduced rates of motor, cognitive and psychosocial impairments. There was no clear correlation between length of kindergarten attendance and speech disorders. Conclusions: Kindergarten attendance may have a positive effect on a number of domains of development including motor, cognitive and psychosocial development, but no significant effect on speech impairments. Implications for public health policies are discussed.

Quetiapine is an antipsychotic drug whose effect appears to be mediated through antagonist activity at the dopamine and serotonin receptors. While Quetiapine is not currently classified as a controlled substance, there have been a growing number of reports of the drug being abused both in American prisons and in general community settings. These accounts have included reports of both intranasal and intravenous uses. In this paper we report two cases of prisoners deliberately feigning psychotic symptoms for the purposes of obtaining quetiapine. In both cases there appears to be some evidence of psychological dependence and of a discontinuation syndrome when the medication was ceased. Our report adds support to the possibility that quetiapine has clinically relevant reinforcing properties with potential for producing both dependence and withdrawal symptoms and as such it should be re-evaluated as a drug with addictive potential and abuse risk.

Patients with panic disorder provide a clinical model of stress. On a "good day," free from a panic attack, they show persistent stress-related changes in sympathetic nerve biology, including abnormal sympathetic nerve single-fiber firing ("salvos" of multiple firing within a cardiac cycle) and release of epinephrine as a cotransmitter. The coreleased epinephrine perhaps originates from in situ synthesis by phenylethanolamine N-methyltransferase (PNMT). In searching for biological evidence that essential hypertension is caused by mental stress—a disputed proposition—we note parallels with panic disorder, which provides an explicit clinical model of stress: (1) There is clinical comorbidity; panic disorder prevalence is increased threefold in essential hypertension. (2) For both, epinephrine cotransmission is present in sympathetic nerves. (3) In panic disorder and essential hypertension, but not in health, single-fiber sympathetic nerve firing salvos occur. (4) Tissue nerve growth factor is increased in both conditions (nerve growth factor is a stress reactant). (5) There is induction of PNMT in sympathetic nerves. Essential hypertension exhibits a further manifestation of mental stress: there is activation of noradrenergic brain stem neurons projecting to the hypothalamus and amygdala. These pathophysiological findings strongly support the view that chronic mental stress is important in the pathogenesis of essential hypertension. A hypothesis now under test is whether in both disorders, under prevailing conditions of ongoing stress, PNMT induced in sympathetic nerves acts as a DNA methylase, causing the norepinephrine transporter (NET) gene silencing that is present in both conditions. PNMT can have an intranuclear distribution, binding to DNA. We have demonstrated that the reduced neuronal noradrenaline reuptake present in both disorders does have an epigenetic mechanism, with demonstrable reduction in the abundance of the transporter protein, the NET gene silencing being associated with DNA binding by the methylation-related inhibitory transcription factor MeCP2.

Objective: The aim of this study was to investigate the prevalence of impairments of physical and psychosocial development in children commencing primary school and to analyse changes over 9 years in consecutive cohorts. Patients and method. We utilised a retrospective cross-sectional study design to assess the prevalence of impairments over nine consecutive cohorts of German children beginning school from 1997 to 2005. A total of 9,514 children were assessed for physical and psychosocial impairment using a manualised medical assessment. Results: There was a dramatic increase in the rates of motor and speech disorders detected among children tested over the 9-year period. We observed a seven-fold increase in motor impairments (OR 7.1; 95% CI 4.2–11.7) and almost a three-fold increase in speech disorders (OR 2.6; 95% CI 2.1–3.3) from 1997 to 2005. Males had higher rates of impairment in all domains of functioning as compared to females (26.0% vs 15.3%; p

It has always seemed plausible that short-term mental stress can act as a trigger for cardiac catastrophes, but the scientific evidence until recently was unconvincing. Panic disorder provides a special case, illustrating that mental stress responses can be a cause of triggered adverse heart events such as myocardial infarction and sudden death. In recent years systematic evidence has been gathered at times of disasters including war, missile attacks on civilians and earthquakes, which also strongly supports the proposition of an acute mental stress–heart attack link. Do these observations have a generality, applicable to the population at large? The answer is that no doubt they do, a finding reached by several national health bodies deliberating on this previously contested question. In individual personal life, ‘emotional earthquakes’ do occur. Heart attacks have been well documented to be triggered when very distressing news has been received involving family members, by armed robbery, assaults and even sporting teams or racehorses losing narrowly (or even winning) after a gripping struggle. The activation of the sympathetic nerves of the heart is of prime importance in such triggering of cardiac catastrophes by acute mental stress. It has always seemed plausible that short-term mental stress can act as a trigger for the development of abnormal heart rhythm and sudden death in patients with existing heart disease. For many years the existence of this relation of acute mental stress to heart attacks was largely based on individual anecdotes such as the celebrated case of the famous 18th-century English surgeon John Hunter, who wrote that he was at the mercy of any scoundrel who aggravated him, then subsequently proved the point by dying suddenly in the middle of a stormy meeting of the board of his hospital (Figure 1). Key to understanding the mechanisms by which triggering of heart attacks might occur is consideration of the ways in which the sympathetic nervous system and adrenal medulla are engaged in acute mental stress responses. Copyright © 2008 John Wiley & Sons, Ltd.

Integrating into the clinical practice of medicine the recent evidence that psychiatric illness and mental stress contributes to the development of cardiovascular disease has not been a seamless process. The evidence for such a link, in fact, had been slow in materializing. The importance of acute mental stress as a trigger for cardiac catastrophes (acute myocardial infarction, sudden death) and of depressive illness as a cause of coronary heart disease, however, is now firmly established. But the spectre of workplace litigation still does hang over the field, clouding the arguments and polarizing medical opinion. Now that a consensus finally seems to have been reached that mental stress, including in the workplace, is an important cause of coronary heart disease and hypertension, it is hoped that the primary outcome will be the implementation of preventive measures to reduce stress in the workplace, such as worker empowerment to end the very adverse high demand/low job control scenario, rather than a rash of lawsuits. Copyright © 2008 John Wiley & Sons, Ltd.

1. In searching for biological evidence that essential hypertension is caused by chronic mental stress, a disputed proposition, parallels are noted with panic disorder, which provides an explicit clinical model of recurring stress responses. 2. There is clinical comorbidity; panic disorder prevalence is increased threefold in essential hypertension. Plasma cortisol is elevated in both. 3. In panic disorder and essential hypertension, but not in health, single sympathetic nerve fibres commonly fire repeatedly within an individual cardiac cycle; this appears to be a signature of stress exposure. For both conditions, adrenaline cotransmission is present in sympathetic nerves. 4. Tissue nerve growth factor is increased in both (nerve growth factor is a stress reactant). There is induction of the adrenaline synthesizing enzyme, phenylethanolamine-N-methyltransferase, in sympathetic nerves, an explicit indicator of mental stress exposure. 5. The question of whether chronic mental stress causes high blood pressure, still hotly debated, has been reviewed by an Australian Government body, the Specialist Medical Review Council. Despite the challenging medicolegal implications, the Council determined that stress is one proven cause of hypertension, this ruling being published in the 27 March 2002 Australian Government Gazette. This judgement was reached after consideration of the epidemiological evidence, but in particular after review of the specific elements of the neural pathophysiology of essential hypertension, described above.

Objective: This study aimed to assess the lipid-lowering properties of omega-3 fatty acids (also known as n-3 polyunsaturated fatty acids) in a group of patients taking clozapine.Method: Twenty-eight persons suffering from schizophrenia or schizoaffective disorder and currently taking clozapine participated in an open-label single-arm trial. Participants received supplements of 10 g of fish oil (containing 1.8 g of eicosopentaenoic acid and 1.2 g of docosahexaenoic acid) for a period of 28 days. Plasma lipids were measured on days 0 and 28.Results: This study demonstrated high rates of lipid abnormalities in the participants. Participants taking omega-3 fatty acids demonstrated a statistically significant reduction in mean serum triglyceride levels of 22%. There was an associated increase in total cholesterol (6.6%) and low-density lipoprotein cholesterol (22%). Common side-effects included fishy burps or breath, but no serious side-effects or interactions where observed.Conclusion: Omega-3 fatty acids may be of value in patients taking clozapine and who have elevated serum triglyceride levels. Limitations of the study, practical implications and directions for future research are discussed.

Patients with panic disorder are at increased cardiac risk. While the mechanisms responsible remain unknown, activation of the sympathetic nervous system may be implicated. Using isotope dilution methodology, investigations of whole-body and regional sympathetic nervous activity have failed to show any differences between patients with panic disorder and healthy subjects. Using direct recording of single unit efferent sympathetic vasoconstrictor nerve activity by microneurography we examined sympathetic nervous function in patients with panic disorder more precisely than previously reported. The activity of multiunit and single unit vasoconstrictor sympathetic nerves was recorded at rest at the level of the peroneal nerve in 10 patients diagnosed with panic disorder and in nine matched healthy volunteers. Multiunit sympathetic activity was not different between the two groups (26 ± 3 bursts min−1 in patients with panic disorder and 28 ± 3 bursts min−1 in controls). The firing frequency of single unit vasoconstrictor neurones was also similar between the two groups (0.38 ± 0.09 versus 0.22 ± 0.03 Hz). However, the probability of firing during a sympathetic burst was higher in patients with panic disorder compared with healthy controls (45 ± 5%versus 32 ± 3%, P < 0.05). When only the neural bursts during which the vasoconstrictor neurone was active were considered, we found that in patients with panic disorder the neurones tended to fire more often in a ‘multiple spike’ pattern than in the controls (i.e. the probability of the neurone firing twice was 25 ± 3% in patients with panic disorder compared with 14 ± 3% in controls). Quantification from single vasoconstrictor unit recording provides evidence of a disturbed sympathetic firing pattern in patients with panic disorder.

This study describes an internet-based intervention for people with panic disorder that consisted of a 5-module program. Participants accessed the program for 5-8 weeks and were then re-assessed 3 months later. Use of the program was associated with reductions in severity of panic disorder and in catastrophic misinterpretation of ambiguous panic body sensations in 9 people with this anxiety disorder. There were also non-significant trends for body vigilance to decrease over the course of the study. Further investigations of the efficacy of this medium for the treatment of panic disorder and the associated mechanisms of change are warranted.

Since the brain neurotransmitter changes characterising panic disorder remain uncertain, we quantified brain noradrenaline and serotonin turnover in patients with panic disorder, in the absence of a panic attack. Thirty-four untreated patients with panic disorder and 24 matched healthy volunteers were studied. A novel method utilising internal jugular venous sampling, with thermodilution measurement of jugular blood flow, was used to directly quantify brain monoamine turnover, by measuring the overflow of noradrenaline and serotonin metabolites from the brain. Radiographic depiction of brain venous sinuses allowed differential venous sampling from cortical and subcortical regions. The relation of brain serotonin turnover to serotonin transporter genotype and panic disorder severity were evaluated, and the influence of an SSRI drug, citalopram, on serotonin turnover investigated. Brain noradrenaline turnover in panic disorder patients was similar to that in healthy subjects. In contrast, brain serotonin turnover, estimated from jugular venous overflow of the metabolite, 5-hydroxyindole acetic acid, was increased approximately 4-fold in subcortical brain regions and in the cerebral cortex (P < 0.01). Serotonin turnover was highest in patients with the most severe disease, was unrelated to serotonin transporter genotype, and was reduced by citalopram (P < 0.01). Normal brain noradrenaline turnover in panic disorder patients argues against primary importance of the locus coeruleus in this condition. The marked increase in serotonin turnover, in the absence of a panic attack, possibly represents an important underlying neurotransmitter substrate for the disorder, although this point remains uncertain. Support for this interpretation comes from the direct relationship which existed between serotonin turnover and illness severity, and the finding that SSRI administration reduced serotonin turnover. Serotonin transporter genotyping suggested that increased whole brain serotonin turnover most likely derived not from impaired serotonin reuptake, but from increased firing in serotonergic midbrain raphe neurons projecting to both subcortical brain regions and the cerebral cortex.

Panic disorder can serve as a clinical model for testing whether mental stress can cause heart disease. Potential neural mechanisms of cardiac risk are the sympathetic activation during panic attacks, continuing release of adrenaline as a co-transmitter in the cardiac sympathetic nerves, and impairment of noradrenaline neuronal reuptake, augmenting sympathetic neural respnses. The phenotype of impaired neuronal reuptake of noradrenaline: an epigenetic mechanism? We suspect that this phenotype, in sensitizing people to heart symptom development, is a cause of panic disorder, and by magnifying the sympathetic neural signal in the heart, underlies increased cardiac risk. No loss of function mutations of the coding region of the norepinephrine transporter (NET) are evident, but we do detect hypermethylation of CpG islands in the NET gene promoter region. Chromatin immunoprecipitation methodology demonstrates binding of the inhibitory transcription factor, MeCP2, to promoter region DNA in panic disorder patients. Cardiovascular illnesses co-morbid with panic disorder. Panic disorder commonly coexists with essential hypertension and the postural tachycardia syndrome. In both of these cardiovascular disorders the impaired neuronal noradrenaline reuptake phenotype is also present and, as with panic disorder, is associated with NET gene promoter region DNA hypermethylation. An epigenetic ‘co-morbidity’ perhaps underlies the clinical concordance. Brain neurotransmitters. Using internal jugular venous sampling, in the absence of a panic attack we find normal norepinephrine turnover, but based on measurements of the overflow of the serotonin metabolite, 5HIAA, a marked increase (six to sevenfold) in brain serotonin turnover in patients with panic disorder. This appears to represent the underlying neurotransmitter substrate for the disorder. Whether this brain serotonergic activation is a prime mover, or consequential on other primary causes of panic disorder, including cardiac sensitization by faulty neuronal noradrenaline reuptake leading to cardiac symptoms and the enhanced vigilance which accompanies them, is unclear at present.

Background The risk of adverse clinical cardiac events is increased in patients with panic disorder (PD). We evaluated possible mechanistic links between PD and heart disease. We estimated cardiac vagal activity from heart rate variability (HRV) measurements and quantified sympathetic nervous system (SNS) activity using plasma noradrenaline tracer kinetics methodology. Methods Thirty-nine people with PD and 39 age- and gender-matched healthy volunteers were studied. In 19 participants with PD, both HRV and plasma noradrenaline kinetics were tested; in 20 with PD and 20 healthy volunteers, HRV measurements only were made, whereas in 19 healthy volunteers, noradrenaline kinetics only was tested. All panic disorder participants completed psychological measures of anxiety sensitivity and state and trait anxiety; healthy volunteers in whom HRV was measured also provided psychological measures. Results Sympathetic nervous tone in the heart, based on rates of cardiac noradrenaline spillover, was normal in PD. Noradrenaline and adrenaline plasma clearance and plasma tritiated noradrenaline and adrenaline extraction in transit through the heart, all dependent on the noradrenaline transporter (NET), were reduced in PD. Psychometric testing linked inhibition of anger to this deficit in NET functioning. Anxiety sensitivity was specifically associated with impaired cardiac NET. High- and low-frequency heart rate spectral power was unrelated to all plasma noradrenaline kinetics measurements. Conclusion Defective neuronal reuptake of noradrenaline, by augmenting the sympathetic neural signal in the heart, might have a dual effect, sensitizing the heart such as to lead to symptom development (and thus perhaps causing panic disorder) and, second, potentially contributing to adverse cardiac events in established PD.

Panic disorder serves as a clinical model for testing whether mental stress can cause heart disease. Our own cardiologic management of panic disorder provides case material of recurrent emergency room attendances with angina and electrocardiogram ischemia, triggered arrhythmias (atrial fibrillation, ventricular fibrillation), and documented coronary artery spasm, in some cases with coronary spasm being complicated by coronary thrombosis. Application of radiotracer catecholamine kinetics and clinical microneurography methodology suggests there is a genetic predisposition to panic disorder that involves faulty neuronal norepinephrine uptake, possibly sensitizing the heart to symptom generation. During panic attacks there are large sympathetic bursts, recorded by clinical microneurography in the muscle sympathetic nerve neurogram, and large increases in cardiac norepinephrine spillover, accompanied by surges of adrenal medullary epinephrine secretion. In other conditions such as heart failure and presumably here also, a high level of sympathetic nervous activation can mediate increased cardiac risk. The sympathetic nerve cotransmitter, neuropeptide Y (NPY), is released from the cardiac sympathetics during panic attacks, an intriguing finding given that NPY can cause coronary artery spasm. There is ongoing, continuous release of epinephrine from the heart in panic sufferers, perhaps attributable to epinephrine loading of cardiac sympathetic nerves by uptake from plasma during panic attacks, or possibly to in situ synthesis of epinephrine through the action of intracardiac phenylethanolamine-N-methytransferase (PNMT) activated by repeated cortisol responses. We have used internal jugular venous sampling and measurement of overflowing lipophilic brain monoamine metabolites to quantify brain norepinephrine and serotonin turnover in untreated patients with panic disorder. We find normal norepinephrine turnover but a marked increase in brain serotonin turnover in patients with panic disorder, in the absence of a panic attack, which presumably represents an underlying neurotransmitter substrate for the condition.

Publisher Summary There may be a precipitating cause of panic—such as being in a confining space (as in claustrophobia) or in public places (as in agoraphobia)—but in many cases, the occurrence of panic attacks is unexpected. Recurring attacks over a period of months or, in many cases, years, form the basis for the diagnosis of a panic disorder. This is a distressing and often very restricting condition, and it can lead to social avoidance behavior. Heart rate and blood pressure increase during a panic attack, primarily because of sympathetic nervous system (SNS) activation and adrenal medullary secretion of epinephrine (EPI). Affected individuals often fear that they have a heart disease because of the nature of their symptoms. Understanding autonomic nervous system (ANS) responses during a panic attack has been seen as relevant clinically because this might provide a rational basis for understanding the symptoms, and through this, for facilitating the treatment that can be based in part on patient self-knowledge as with cognitive behavior therapy. Clinical experience with the cardiologic management of patients with panic disorder has provided case material encompassing the range of cardiac complications that occur. A better understanding of the mechanism of coronary artery spasm in a panic disorder would facilitate therapeutic intervention.