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. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: Psychosomatics. 2016 Dec 9;58(3):252–265. doi: 10.1016/j.psym.2016.12.003

Non-cardiac Chest Pain: A Review for the Consultation-Liaison Psychiatrist

Kirsti A Campbell 1, Elizabeth N Madva 1, Ana C Villegas 1, Eleanor E Beale 1, Scott R Beach 1, Jason H Wasfy 1, Ariana M Albanese 1, Jeff C Huffman 1
PMCID: PMC5526698  NIHMSID: NIHMS871192  PMID: 28196622

Abstract

Background

Patients presenting with chest pain to general practice or emergency providers represent a unique challenge, as the differential is broad and varies widely in acuity. Importantly, most cases of chest pain in both acute and general practice settings are ultimately found to be non-cardiac in origin, and a substantial proportion of patients experiencing non-cardiac chest pain (NCCP) suffer significant disability. In light of emerging evidence that mental health providers can serve a key role in the care of patients with NCCP, knowledge of the differential diagnosis, psychiatric co-morbidities, and therapeutic techniques for NCCP would be of great use to both consultation-liaison (C-L) psychiatrists and other mental health providers.

Methods

We reviewed prior published work on (1) the appropriate medical workup of the acute presentation of chest pain, (2) the relevant medical and psychiatric differential diagnosis for chest pain determined to be non-cardiac in origin, (3) the management of related conditions in psychosomatic medicine, and (4) management strategies for patients with NCCP.

Results

We identified key differential diagnostic and therapeutic considerations for psychosomatic medicine providers in 3 different clinical contexts: acute care in the emergency department, inpatient C-L psychiatry, and outpatient C-L psychiatry. We also identified several gaps in the literature surrounding the short-term and long-term management of NCCP in patients with psychiatric etiologies or co-morbid psychiatric conditions.

Conclusions

Though some approaches to the care of patients with NCCP have been developed, more work is needed to determine the most effective management techniques for this unique and high-morbidity population.

Keywords: non-cardiac chest pain, consultation psychiatry, psychosomatic medicine, cardiac, disease management

INTRODUCTION

Chest pain is the presenting complaint of more than 7 million emergency department (ED) visits1 and as many as 27 million office visits1,2 in the United States each year. The differential diagnosis of chest pain is broad, and the initial workup is focused on excluding acute, life-threatening etiologies such as acute coronary syndrome (ACS) or pneumothorax. Though the proportion of ED visits resulting in an ACS diagnosis has decreased by 45% over the past decade, chest pain is triaged as requiring urgent or emergent evaluation 2–3 times more frequently than other symptoms.3 Many patients in ED3 and primary care settings2,4 have a negative cardiac workup, but continue to have symptoms.

This recurring chest pain of non-cardiac origin, termed “non-cardiac chest pain” (NCCP), represents a significant burden to providers across clinical settings. More than 50% of all cases of chest pain presenting to the ED3 and more than 80% of cases in primary care settings5 appear to be secondary to NCCP. The lifetime prevalence of NCCP is estimated to be as high as 33%.6 Furthermore, the broad differential diagnosis for chest pain and the potentially fatal consequences of missing an acutely life-threatening medical condition add complexity to clinical decision-making. Though the total financial burden of NCCP is difficult to assess, the cost may be as much as or greater than the cost for patients with an ACS.7 There are 2 million hospital admissions annually for chest pain in the United States, costing up to $8 billion,810 and three-fourths of admissions with an initial diagnosis of myocardial ischemia are shown to be incorrect.11

Quality of life (QOL) in patients with NCCP is diminished when compared with healthy controls (e.g., as measured by the SF-36 Health-Related Quality of Life [HR-QoL] questionnaire) and, notably, is as low as in patients with coronary artery disease (CAD).12 Several factors contribute to this low QOL, including social withdrawal, avoidance of activities that can elicit or exacerbate symptomatology, and the presence of co-morbid psychiatric conditions such as anxiety and depression. Many patients with NCCP also seek further cardiac assessment, despite diagnostic reassurance.13 Work performance is commonly affected: patients with NCCP take substantial time away from work and often become unemployed.14 Though no studies specifically investigate the cost of evaluating NCCP in Quality-Adjusted-Life-years, we can perhaps extrapolate from studies evaluating the cost effectiveness of diagnostics for chest pain in general. As an example, a study evaluating the cost effectiveness of inpatient telemetry found that it is only “cost effective” when patients have a risk of ACS greater than 3%.15 Further work is needed to elucidate the costs of NCCP, including costs from direct health care spending and lost productivity.

In some cases, NCCP could be considered a functional cardiac or gastrointestinal illness, characterized by symptoms without clear physiologic underpinnings or enzymatic, imaging, stress test, or anatomic confirmation of pathophysiologic processes.16 Although the literature surrounding functional gastrointestinal disorders (FGID) has advanced in the past decade with improved diagnostic and therapeutic techniques,17 recommendations for patients with functional chest pain are often focused solely on excluding CAD. Integrated care with a biopsychosocial approach may provide a feasible, cost-effective method for treating patients with NCCP,1820 but specific recommendations for providers regarding best practices for evaluation, intervention, and referral are limited.

In this review, we focus on diagnostic and therapeutic considerations in patients with NCCP relevant to the consultation-liaison (C-L) psychiatrist, both in the outpatient and inpatient setting. We additionally discuss recommendations for appropriate care drawing from the current literature on NCCP, which draws from literature in both internal medicine and psychiatry, and on functional gastrointestinal and neurological disorders, which has primarily been published in the gastroenterology and neurology literature. Though most patients with NCCP will first present to a primary care provider or ED physician, it is increasingly clear that mental health providers are a necessary part of the treatment team for many NCCP etiologies.

OVERVIEW OF NCCP

Initial Evaluation of Chest Pain

Evaluation of the patient presenting with chest pain to the ED focuses primarily on hemodynamic stabilization and exclusion of an acute life-threatening process. Accordingly, any patient with unstable vital signs will immediately undergo assessment of airway, breathing, and circulatory function with diagnostic evaluation (e.g., electrocardiogram [ECG], chest x-ray, and bedside echocardiogram) guided by the patient’s clinical presentation (hemodynamic stability, shortness of breath, diaphoresis, and localization of pain) for identification of acute life-threatening conditions such as ACS, pneumothorax, cardiac tamponade, aortic dissection, acute heart failure, esophageal rupture, or pulmonary embolism. In hemodynamically stable patients, common workup in addition to a detailed history and examination includes a 12-lead-ECG, a complete blood count, and cardiac enzymes, along with chest x-ray if clinical suspicion dictates or other workup has been negative. Importantly, premature closure of the differential diagnosis may be particularly harmful in patients with an underlying psychiatric co-morbidity, as there is a well-known higher burden of serious medical problems, including cardiovascular disease in patients with mental illness.21

In the outpatient setting, a detailed history and physical examination are important for determining the need for further referral or diagnostic testing. Symptoms suggestive of a possible acute ischemic process (e.g., escalating chest pain, typical angina, and diaphoresis)22 or unstable vital signs warrant emergent referral. Otherwise, an ECG is typically reserved for new-onset or evolving chest pain without a more obvious cause (e.g., pneumonia and traumatic chest wall injury), with potential referral to more acute settings based on findings.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis for chest pain involves multiple organ systems and varies widely in severity. The Table displays the common basic differential diagnosis for patients presenting with chest pain, and clinical considerations for each organ system are detailed later.

TABLE.

Selected etiologies of chest pain

System Disease
Cardiac chest pain Cardiac Ischemic
 Acute coronary syndrome
 Stable angina
 Valvular dysfunction
 Vascular spasm
Vascular
 Aortic or coronary artery dissection
 Pericarditis
 Microvasular disease
Inflammatory/infiltrative
 Autoimmune
 Drug-induced (clozapine)
 Infectious (viral and bacterial myocarditis)
 Pericardial effusion/cardiac tamponade
 Structural heart disease (hypertrophic cardiomyopathy)
Acute heart failure
Non-cardiac chest pain Gastrointestinal Gastroesophageal reflux disease
Gastric or duodenal ulcer
Esophageal rupture
Esophageal dismotility or spasm
Esophageal hypersensitivity
Pancreatitis
Biliary colic
Cholelithiasis
Choledocholithiasis
Splenomegaly
Diaphragmatic irritation
Eosinophilic esophagitis
Pulmonary Pulmonary embolism
Pneumothorax
Pneumonia
Malignancy
Chronic obstructive pulmonary disease Pleural effusion or pleuritis
Pulmonary hypertension
Musculoskeletal Costochondritis
Traumatic injury
Thoracic overbreathing pattern
Cervical rib
Thoracic outlet syndrome
Psychiatric Generalized anxiety disorder
Panic disorder
Major depressive disorder
Illness anxiety disorder
 Cardiophobia
Somatic symptom disorder
Deception syndromes
Substance use disorders (cocaine, methamphetamines, and alcohol)

Cardiac Causes of Chest Pain

Cardiac causes of chest pain can include myocarditis, pericarditis, acute heart failure, aortic dissection, exertional angina, and ACS. Unfortunately, both the physical examination and detailed history are frequently insufficient to rule out an acute cardiac process, though are useful in suggesting specific etiologies, such as back pain of tearing quality raising concern for aortic dissection or chest pain improved by leaning forward suggesting pericarditis.

Integrating the patient’s history, physical examination, and diagnostic studies becomes critically important in identifying both the patients at highest risk of acute cardiac processes and those at risk of undergoing unnecessary repeated cardiac workups. Potential indications for need to avoid further cardiac diagnostic testing include residual pain after multiple negative investigations or reassuring recent coronary angiogram.23 Notably, there are no established guidelines for sufficient exoneration of cardiac causes of persistent chest pain, but periodic future investigations in patients who have had previously negative workups are warranted, as some may come to develop underlying cardiac disease.

Gastrointestinal Causes of Chest Pain

Gastrointestinal etiologies, particularly gastroesophageal reflux disease (GERD), account for a substantial proportion of NCCP, and often manifest with typical angina symptoms, including squeezing or burning substernal discomfort.24 A small number of cases can be caused by ulcerative disease or esophageal motility disorders. Esophageal hypersensitivity,25 which may be owing to abnormal visceral proprioception exacerbated by multiple factors including psychological stress, represents a potential functional etiology.24

Pulmonary Causes of Chest Pain

Several pulmonary pathologies, including those of vascular, parenchymal, and pleural origin, can present with chest pain. Both symptoms (e.g., subjectively reported dyspnea and cough) and physical signs (e.g., tachypnea, wheezing, localized crackles on examination, and low oxygen saturation) can be useful in suggesting a pulmonary etiology.

Musculoskeletal Causes

Musculoskeletal etiologies of chest pain, including costochondritis and traumatic injury, may account for nearly half of all non-emergent cases of chest pain.26 Physical examination findings, such as reproducibility on palpation, can be useful in suggesting a musculoskeletal cause. Plausible traumatic injury in the medical history is also suggestive of musculoskeletal pathology.

THE PSYCHIATRIC DIFFERENTIAL DIAGNOSIS

Appropriate recognition of underlying psychiatric disorders—either those directly causing the experience of chest pain or those contributing to distress in combination with other factors—can be of great value. Establishing the relative contribution of psychiatric pathology to NCCP cases is difficult, as psychiatric contributors are usually treated as diagnoses of exclusion. For example, a patient may develop a thoracic hyperventilatory breathing pattern precipitated or exacerbated by psychologic arousal, leading to musculoskeletal chest pain.27 A thorough psychiatric differential diagnosis should include panic disorder (PD), generalized anxiety disorder (GAD), post-traumatic stress disorder (PTSD), major depressive disorder (MDD), illness anxiety disorder (IAD), and somatic symptom disorder (SSD).

Anxiety Disorders

Although many patients with chest pain of any origin will experience anxiety during the episode, symptoms suggestive of a more chronic underlying anxiety disorder are present in most patients presenting with chest pain in primary care settings and in up to one-third of patients presenting to the ED.28 Importantly, there is likely a bidirectional relationship between chest pain and underlying anxiety disorders. For example, the discomfort and potential implications (e.g., an ACS) of an episode of chest pain may precipitate a panic attack, and the physical manifestations of persistent worry may be anginal in character.

Panic Disorder

PD both contributes to and co-occurs with chest pain: up to 70% of panic attacks feature chest pain as a symptom,29,30 and between 25% and 60% of patients with chest pain referred for cardiac investigations have PD,31 including 31% of NCCP cases.32 Although PD is independently associated with higher incidence rates of coronary heart disease (CHD) and myocardial infarction, it is unclear whether this represents a bidirectional or causal relationship.33 A meta-analysis regarding the prevalence of PD among those seeking treatment for chest pain revealed that an atypical quality of chest pain, female sex, younger age, high levels of self-reported anxiety, and the absence of known CAD correlated with higher rates of PD.34 A study of 572 patients presenting to the ED with unexplained chest pain found that 42% of the cohort experienced panic attacks, and within that subset, 45% met criteria for PD.35

Generalized Anxiety Disorder

The prevalence of GAD in patients with NCCP ranges from as low as 5.7% to more than 30%.3638 GAD also frequently co-occurs with PD in patients with NCCP.39 Early studies of psychiatric illness found high rates of “anxiety neurosis,” which included both panic and GAD, in patients with normal coronary angiography.39,40 Interestingly, in a study supporting a high prevalence of GAD (more than 30%) in patients with normal angiography, every patient with GAD had concurrent PD.37

Post-traumatic Stress Disorder

Though the prevalence of PTSD in NCCP has not been formally studied, there appears to be a relatively robust relationship between CAD and PTSD. Some studies estimate that up to 16% of patients develop PTSD after (and related to) an ACS.4145 Furthermore, the relationship appears to be reciprocal: evidence also suggests that PTSD may be an independent risk factor for CAD, and there is some prospective evidence of an association between PTSD symptoms and risk of CHD development.43,46 The mechanism of this association has yet to be elucidated.

Regarding its possible contributions to the patient population with NCCP, PTSD can involve physical symptoms that mimic an ACS, including shortness of breath, chest tightness, and numbness that are ultimately non-cardiac in origin. This highlights the need for careful and thorough evaluation of patients with chest pain and concern for PTSD, as their chest pain may represent true CAD (indeed, ACS-induced PTSD may increase risk of ACS45) or NCCP related to underlying PTSD. A clue to the diagnosis of PTSD is the predictable occurrence of these symptoms in situations related to the precipitating trauma.

Other Psychiatric Disorders

Major Depressive Disorder

The associations between mood disorders and NCCP are likely complex and bidirectional. Some patients with MDD experience somatic symptoms, which may include subjective worsening of existing medical conditions or the development of new, unexplained physical symptoms such as pain. Additionally, stress caused by chronic chest pain may precipitate depressive episodes and detract from adaptive behaviors that promote psychologic well-being. A systematic review of psychologic outcomes in patients with NCCP presenting to the ED concluded that patients with NCCP had similar levels of depressive symptoms to those with a cardiac diagnosis, whereas patients with both cardiac and non-cardiac disease had higher levels of depressive symptoms than healthy controls. The prevalence of depressive symptoms in patients with NCCP in this review ranged from 9–40%.47

SSD and Related Disorders

SSD and related disorders encompass a group of illnesses that involve subjective physical symptoms for which there is no obvious medical explanation. Although some patients with SSD present with numerous physical complaints, whereas others may experience a single symptom, such as chest pain, that recurs over time. The hallmark of the disorder involves spending a disproportionate amount of time worrying about or attempting to mitigate physical symptoms. The estimated prevalence of SSD and related disorders in the general population is only 1–3%,48 though in certain medical population groups prevalence is estimated to be much higher. For example, in some neurological practices the prevalence is as high as 20–30%,48 and a large epidemiological study of chronic pain in the United States found a prevalence of 15%.49 Rates of SSD in NCCP have not been formally studied, but anecdotal evidence suggests that SSD accounts for a small but meaningful proportion of patients with NCCP.

Factitious disorder, which is now classified under somatic symptom and related disorders in the DSM-5 and refers to patients who feign symptoms for some primary (i.e., internally motivating) gain such as to achieve the sick role, can also be seen in patients with NCCP. Several extreme NCCP-related case reports exist, including a patient who feigned aortic dissection and underwent thoracotomy, and a patient who induced a recalcitrant supraventricular tachycardia with surreptitious albuterol misuse over several years.50,51 In a study of factitious disorder, nearly 5% of cases were referred from cardiology.52

Illness Anxiety Disorder

Although patients with SSD are preoccupied with chest pain as a symptom, patients with IAD are focused on the idea that their symptoms represent an ACS or other serious cardiac illness. Somatic symptoms may be a fairly minimal component of the presentation and are often overshadowed by ruminative worry about having an illness. Although many patients with IAD rotate through a variety of somatic preoccupations affecting multiple organ systems, some will focus on a particular symptom or organ system. At any particular point in their illness, a patient with IAD may be amenable to reassurance and dutiful clinical attention, though this reassurance often fades quickly, prompting repeated presentations. As with SSD, rates of IAD in NCCP are unknown.

“Cardiophobia” is a subtype of IAD that specifically manifests in response to chest discomfort.53,54 It has been described as an unconscious negative interpretation of somatosensory and cardiopulmonary sensations that elicits anxious feelings and leads to avoidance of activities associated with chest discomfort.55,56 As with IAD, frequent visits to the doctor often develop as a mechanism of reassurance, and these patients can be reluctant to acknowledge that psychosocial factors might elicit autonomic physical sensations that coincide with their symptoms; such denial can play a major role in the maintenance of this condition.57

The Cardiac Anxiety Questionnaire58 was designed to evaluate cardiophobia and other heart-focused anxiety and has been used in several studies of patients with and without underlying CAD. In a study of 658 patients either self-referred or physician-referred for further evaluation of CAD, individuals without evidence of coronary artery calcification had higher mean scores on both attention to cardiac symptoms and fear of having these symptoms.59 This lends credence to the concept that the uncertainty prompted by not receiving a cardiac diagnosis can exacerbate worry about chest pain and possibly contribute to reductions in QOL.

Deception Syndromes

Though uncommon, deception syndromes, such as malingering, should be considered in patients presenting to physicians repeatedly with the same symptom. Patients may malinger chest pain to receive analgesics, such as opiates, to seek shelter, or to avoid other responsibilities, such as legal obligations. Although malingering can be difficult to confidently diagnose and is likely best considered as a diagnosis of exclusion, it should be considered whenever the symptoms seem incongruent to the patient’s presentation.60 It is important to consider deception syndromes in the differential diagnosis of NCCP because chest pain is an easily accessible and well-known medical complaint.

Contributions of Personality

Aspects of personality, including social inhibition and negative affectivity, have been studied as potential factors in cardiovascular well-being and persistent chest pain. In particular, there is some (albeit conflicting) evidence that the “type D” distressed personality type, defined in individuals who simultaneously experience negative emotions and inhibit self-expression, may be linked to NCCP, adverse cardiac outcomes, and impaired self-reported physical and mental health.6164 The TweeSteden Mild Stenosis (TWIST) observational study, as an example, demonstrated an association between type D personality and persistent chest pain.65

Evidence surrounding the contributions of the type A behavior pattern (TABP), characterized by a high competitive drive and ambition, as a risk factor for CHD is likewise inconclusive.66,67 Further study of possible associations between type A behavior pattern and persistent chest pain is warranted.

INTERVENTIONS TO TREAT NCCP

Several interventions for the treatment of NCCP have been evaluated. Small numbers of participants, short follow-up periods, inconsistency of study design, and few randomized controlled trials (RCTs) were noted as common limitations in a recent Cochrane review of 17 RCTs assessing psychologic interventions for NCCP symptom management.68 With so few studies, evaluating psychiatric care for patients with NCCP, more research is needed to determine the most effective methods of intervention.

Cognitive-Behavioral Therapy

The Cochrane review68 reported that cognitive-behavioral interventions were most successful in reducing chest pain severity and frequency. Cognitive-behavioral therapy (CBT) appears to be the most effective psychologic treatment for NCCP. By addressing maladaptive cognitions about physical symptoms, CBT can help patients with NCCP to reframe the etiology of their chest pain and to reduce the anxiety accompanying their symptoms. CBT can also be effective in targeting the misinterpretation of minor physical symptoms as a sign of more serious disease.

Several studies have evaluated the efficacy of CBT for NCCP. As an example, Mayou et al.69 used a multistage CBT intervention aimed at assessing patients’ baseline degree of limitation and beliefs about symptom causation; providing alternative non-cardiac explanations for symptoms; and identifying the role of hyperventilation, muscular tension, catastrophic thoughts, and patient-specific factors in causing or sustaining symptoms. Patients with persistent chest pain for 6 weeks after being reassured by a cardiologist that they had no cardiac disease were randomized into multistage CBT treatment (up to 12 sessions of individual therapy) or an “assessment only” control group (who underwent solely a baseline assessment). Both groups were provided with diaries to record symptoms and asked to follow-up at 3 and 6 months. At the 6-month follow-up, the CBT group showed significant improvement in symptom severity and all measures of social activity (e.g., functional limitation and level of social impairment) when compared with the control group. This study demonstrated that identifying maladaptive cognitions and providing appropriate alternative explanations for symptom causation, in addition to learning behavioral coping techniques, can lead to improvement of function.

Shorter CBT interventions have also been evaluated. Esler et al.70 assessed the efficacy of a single 1-hour CBT session in patients presenting to an ED with NCCP. Those in the CBT group had a significant decrease in chest pain frequency and levels of anxiety, but no change in symptom severity, QOL, or psychologic distress, at 1 and 3-month follow-ups compared with the control group who received only routine ED care. Beek et al.71 found that 6 CBT sessions in ED patients with NCCP and co-morbid PD or depression were effective in reducing symptoms of anxiety and depression.

Hypnosis

According to the Cochrane review of RCTs assessing psychologic interventions for NCCP, hypnotherapy may be an effective alternative to CBT, although only 1 RCT met inclusion criteria.68 Hypnosis focuses on relaxation and concentration as a basis for addressing NCCP symptoms and associated stress or anxiety. In a study of patients with angina-type chest pain and normal coronary angiography, a 17-week hypnosis treatment led to improvement in chest pain for 80% and improvement in QOL for 73% of the treatment group members—results that remained significant after adjustment for age and baseline levels of anxiety.72 A related 8-week, group-based, autosuggestive healing treatment also led to improvement in anxiety and QOL, with significant reduction of both symptom severity and frequency in women with NCCP.73 These results suggest that hypnosis and related treatments can be a useful tool for relieving the psychologic burden that accompanies the unexplained nature of NCCP, adding an element of control to the subjective experience of symptoms.

Breathing Training and Guided Physical Activity

A more basic application of relaxation and breathing training has also been shown to improve NCCP symptoms. A 6-week breathing retraining program in participants with hyperventilation and associated functional cardiac symptoms had a significant effect on CO2 levels, respiratory rate, and cardiac symptoms.74 These findings suggest that simple symptom-targeted interventions can help patients understand connections between behaviors (in this case hyperventilation) and chest pain, with beneficial effects.

Pharmacotherapy

Given the broad medical and psychiatric differential diagnosis for NCCP, the success of pharmacologic treatment depends on accurate identification of underlying conditions contributing to the chest pain. Trials of empiric proton pump inhibitors have been recommended for concurrent diagnosis and treatment of GERD in patients with chest pain inconsistent with cardiac disease,25,7578 as GERD is a significant contributor in many cases.78 From a psychopharma-cological standpoint, a recent meta-analysis of trials evaluating selective serotonin reuptake inhibitors (SSRIs) for the treatment of NCCP concluded that SSRIs were not superior to a placebo in improving symptoms of chest pain, suggesting that psychopharmacology alone is unlikely to be a sufficient management approach for NCCP.79 Notably, 3 of 4 studies included in the meta-analysis excluded patients with comorbid psychiatric disease; as a result, this meta-analysis does not speak to the efficacy of SSRIs in patients with NCCP who have comorbid SSRI-responsive psychiatric conditions (e.g., MDD). Although serotonin-norepinephrine reuptake inhibitors have been used for analgesia in pain syndromes such as diabetic peripheral neuropathy,80 fibromyalgia,81 and osteoarthritis,82 their application in patients with NCCP has not been thoroughly evaluated.

Care Management Approaches

Systematic and multidisciplinary team-based approach to evaluation and treatment have also been used for NCCP. In the United Kingdom, “rapid access chest pain clinics” were introduced in the early 2000s in an effort to integrate diagnostic care for patients with angina. Marks et al.83 called for exploration of a biopsychosocial treatment approach within the context of these clinics after demonstrating that patients with NCCP had panic-type beliefs and were less likely to understand and accept their illness than those with positive cardiac workups. They piloted a stepped-care biopsychosocial management program in which patients with NCCP were evaluated by both a cardiologist and clinical psychologist. Their management program, which involved a comprehensive evaluation for gastrointestinal, musculoskeletal, respiratory, and psychiatric symptoms, reassurance with a biopsychosocial formulation of the patient’s pain, and appropriate referral to CBT, when indicated, was effective in reducing frequency, severity, functional impact of and concern about symptoms, and frequency of visits to EDs, general practitioners, and cardiologists.18

This collaborative approach has been tested in other disorders. In FGID, collaboration with clinical psychologists for psychologic evaluation and patient-specific treatment, when initiated by the primary gastroenterologist, has reduced health care use.84 Importantly, this model is distinct from simple reflexive external referral to a mental health clinician; however, recommendations in both neurology85 and gastroenterology17 have emphasized the key role of the medical specialist (in this case, the cardiologist) in collaborating with the mental health provider to validate the patient’s symptoms and emphasizing the legitimacy and effectiveness of psychiatric interventions. Guidelines regarding patients with concurrent psychosocial risk factors and CHD have likewise suggested multimodal behavioral interventions.86

Clinical Recommendations

Diagnostic Delivery for the Clinician: Lessons Learned From Other Conditions

After a comprehensive assessment for medical and psychiatric causes of chest pain, if it appears that a patient has a psychosomatic disorder (e.g., SSD), it is vital for clinicians to address this with the patient. Such discussions can be challenging to navigate in the face of patients’ beliefs about (and likely investment in) the systemic medical etiology of their illness, but if done well, can lead to acceptance of effective treatment strategies.

Research on the management of functional disorders in gastroenterology and neurology has yielded useful lessons for the providers delivering a diagnosis of NCCP. Attentiveness to diagnostic labels can play a significant role in building a therapeutic relationship. In a study calculating the “number of patients needed to offend” associated with several diagnostic terms providers could apply to symptomatic weakness, researchers found that “medically unexplained weakness” was substantially more offensive to patients than “functional weakness,” despite frequent use of both terms by providers.87 A similar study in healthy adults indicated that the terms “persistent physical symptoms” and “functional symptoms” were preferred to “medically unexplained symptoms” or “complex physical symptoms.”88

Likewise, it is not just the wording of the diagnosis but also the overall approach that is important when discussing symptoms with patients with NCCP who appear to have somatic symptom and related disorders. Management guidelines for FGID note that empathic acknowledgment of patients’ concerns can reduce symptom severity89 and involving the patient in the therapeutic plan can improve adherence.17 In a similar manner, clinical guidelines for the management of functional neurologic symptoms have called for clearly validating the patient’s experience, explaining what disorders they do not have, and emphasizing self-help as a key part of getting better.85 Additionally, there is some evidence that illness representations, including the patient’s understanding of illness chronicity, personal control over symptoms, and possible risks of their condition, are associated with baseline psychologic distress and lower baseline QOL in patients with NCCP.90 Careful exploration of patients’ beliefs about their condition could yield clinically useful information regarding need for further psychiatric intervention.

Though these approaches have primarily been used in patients with somatic symptom and other related disorders, they can also be effective in patients with other psychiatric conditions, or those for whom an etiology is entirely unclear. Using well-accepted and non-pejorative terms, acknowledging worry and distress about the source of the symptoms, and clearly acknowledging that the patient’s experience is real, will all improve alliance, reduce resistance, and potentially allow greater acceptance of both pharmacologic and non-pharmacologic treatments.

Overall Approach to Treatment

When C-L psychiatrists are called to assist in the care of patients with NCCP, the first step, as described earlier, is establishing an empathic and therapeutic relationship, using appropriate diagnostic labels, and emphasizing the validity of the symptoms experienced, despite a negative cardiac work-up. Second, when NCCP is suspected, careful and broad psychiatric diagnostic assessment should be completed; however, if comorbid psychiatric conditions (such as MDD, PD, or GAD) are identified, the psychiatrist should clarify the extent to which the chest pain can be attributed to the psychiatric condition and provide suggestions for treatment to reduce distress and improve general function. Though many structured assessments of characteristics associated with underlying conditions that cause NCCP exist (such as the Toronto Alexithymia Scale or the Pain Catastrophizing Questionnaire), the use of these scales (outside of standard assessment tools for MDD, GAD, PD, and PTSD) is not diagnostic, and its utility in monitoring response to therapy in NCCP has not been shown. Targeted management of diagnosed primary psychiatric disorders is vital to improve overall outcomes and reduce their potential contribution to ongoing symptoms. This includes pharmacotherapy (e.g., SSRIs for MDD, PD, GAD, and PTSD), or the implementation of regularly scheduled visits with an identified medical practitioner, with careful assessment and physical examination (but no invasive testing unless objective abnormalities are identified) for patients with SSD or IAD.

Third, regardless of the presence of comorbid psychiatric illness, CBT has established efficacy in reducing the severity and frequency of chest pain in NCCP, and can be considered if a referral source is available; moreover, hypnosis and structured breathing exercises may also be considered. Finally, as suggested by the literature in both functional neurologic and gastrointestinal disorders, as well as early studies within the field of NCCP, ongoing interspecialty collaboration can improve patient care. No matter the modality of treatment outlined earlier, any approach that facilitates longitudinal collaboration among providers (e.g., colocation of psychiatric and medical providers for a given NCCP patient, or collaborative care-type models91) is likely to have the greatest success.

Future Directions

A substantial challenge in the evaluation and treatment of patients with NCCP is the lack of clear diagnostic criteria. At present, NCCP has been defined, with some variation, as “recurrent chest pain that is indistinguishable from ischemic heart pain after a reasonable workup has excluded a cardiac cause.”24 Although questionnaires92,93 aimed at differentiating subtypes of chest pain have been developed, the current definition of NCCP leaves open to interpretation what constitutes a reasonable workup and appropriate diagnostic criteria for NCCP for the definition of FGID. The ROME criteria conceptualize FGID as disorders of “gut-brain interaction” and use a destigmatizing biopsychosocial perspective to divide functional gastrointestinal symptoms into 8 categories (e.g., esophageal and gastroduodenal) with definitions based on the presence, rather than absence, of symptoms, much such as the DSM-5.94 Since their introduction in the 1980s, they have fostered more widespread recognition of and research into the pathophysiology and treatment of functional gastrointestinal conditions.17 The development of specific criteria for NCCP would likewise further advance understanding of NCCP and our ability to accurately diagnose and treat it Appendix 1.

Finally, regarding the optimal management of NCCP from a population health standpoint, an integrated care model may be best suited to coordinate the complex diagnostic and therapeutic management of NCCP. It is clear that cardiologists and primary care providers must play a key role by assessing physical complaints in an ongoing manner, validating symptoms, and communicating the success of psychiatric therapies for the treatment of NCCP, whereas practitioners of psychosomatic medicine and other mental health providers can provide accurate psychiatric assessment and treatment. A model similar to that of Chambers et al.,18 involving a shared assessment by a cardiologist and C-L psychiatrist and delivery of a biopsychosocial formulation, is one such approach. Given that existing effective approaches for NCCP and promising future collaborative care models all involve integration of cardiac and psychiatric expertise, psychosomatic medicine providers are uniquely positioned to be leaders in the development of improved care for this high-utilizing, high-morbidity population.

Acknowledgments

FUNDING

This work was supported by the National Institutes of Health, United States—National Heart, Lung, and Blood Institute (Grant no. R01HL113272).

APPENDIX 1

Psychotherapeutic interventions Major principles Goals in NCCP
Cognitive behavioral therapy Thoughts, feelings, and behaviors are inter-related. Automatic thoughts and cognitive distortions can result in maladaptive behaviors. Identify and correct misperceptions, misattributions, and cognitive distortions related to chest pain to improve function and modify maladaptive behaviors (e.g., recurrent ED visits).6971
Mindfulness-based therapy
 Mindfulness-based stress reduction (MBSR)
 Meditation
 Relaxation response
 Relaxation therapy
By maintaining full attention to and awareness of the moment, one can disengage from beliefs, thoughts, and emotions, and develop a greater sense of emotional stability and well-being. Maintain full attention to and awareness of the moment to disengage oneself from all beliefs, thoughts, and emotions, including those related to chest pain.95,96*
Hypnosis Inducing a state of deep relaxation or trance provides access to an open state of mind amenable to the therapist’s suggestions. Change beliefs about chest pain and behaviors related to those beliefs by offering suggestions for change during a state of deep relaxation or
Psychodynamic therapy Awareness of the unconscious interpretation, achieved through examination of past experiences and relationships, can affect current thoughts and behaviors. Identify how the unconscious interpretation is driving current thoughts about and behaviors related to chest pain to improve function.97*
Group therapy Sharing thoughts, feelings, and experiences in a group setting can facilitate improved insight and associated change through normalization and shared empathy. Share and learn from peers with similar experiences of chest pain to improve insight about symptoms and mobilize change.98,99*
*

Tested in patients with medically unexplained symptoms, somatic symptom, and related disorders, or chronic pain, not specifically in NCCP.

Footnotes

Disclosure

The authors disclosed no proprietary or commercial interest in any product mentioned or concept discussed in this article.

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