Internet-based cognitive behavioral therapy reduces cardiac anxiety and chest pain frequency in non-cardiac chest pain patients
- Internet-based cognitive behavioral therapy (iCBT) reduced cardiac anxiety in people with noncardiac chest pain, but was not superior to psychoeducation.
- iCBT reduced the frequency of chest pain in people with non-cardiac chest pain.
Evidence evaluation level: 1 (great)
Chest pain is one of the most concerning symptoms in clinical practice. The differential diagnosis for chest pain includes life-threatening conditions of great concern, from pulmonary embolism to myocardial infarction. However, 50% of chest pain presentations to the emergency department are typically non-cardiac chest pain (NCCP). The association between chest pain and heart disease makes the symptoms extremely distressing for patients. This is called cardiac anxiety (CAx). CAx negatively impacts quality of life and leads to increased frequency of chest pain. Cognitive behavioral therapy (CBT) is the treatment of choice for CAx. The effectiveness of internet-delivered CBT (iCBT) in CAx has not been adequately investigated.
This non-randomized controlled trial investigated the effectiveness of nurse-led iCBT in the treatment of CAx compared to psychoeducation in Sweden. 109 of her NCCP patients were randomly assigned to her two treatment groups. There were 54 participants in the iCBT group and 55 participants in the psychoeducational group. Participants were included if they were Swedish-speaking, aged 18 years or older, had a complaint of NCCP within the past 6 months, had a diagnosis of CAx (cardiac anxiety questionnaire (CAQ) score >24), and had access to a computer. Participants who did not meet these criteria were excluded. Participants received either iCBT or psychoeducation for their 5 weeks, depending on treatment group. CAx was assessed post-study, 3, 6, and 12 months post-intervention. The primary outcome measured was her CAx using the CAQ. Secondary outcomes included fear of bodily sensations, depressive symptoms, and frequency of chest pain.
Regarding the primary outcome, iCBT showed success in reducing CAx, but was not superior to psychoeducation alone. Regarding secondary outcomes, iCBT was not shown to be superior to psychoeducation in reducing fear of bodily sensations or depressive symptoms. However, iCBT was statistically significant in reducing the frequency of chest pain. A limitation of this study is that the researchers did not take into account the possibility that participants would use further medical care to treat their chest pain. For example, if NCCP patients utilized further medical investigation to reassure them that their chest pain was not heart-related, they would likely feel less anxious than those who adhered only to the treatment arm utilized in the study. Nevertheless, the ability of iCBT to reduce her CAx and reduce the frequency of chest pain in general is a valuable finding. Increased frequency of chest pain further increases healthcare utilization by patients, impacting daily life and overall quality of life. This study shows that iCBT is a viable and convenient option for the treatment of her CAx.
Certain inflammatory cytokines may influence depression severity, suicidal thoughts, and behavior
- Interleukin-1β levels are significantly associated with depression severity but not suicidal thoughts or behavior
- Tumor necrosis factor alpha is strongly associated with suicidal ideation and behavior
Evidence evaluation level: 2 (good)
Depression affects approximately 8% of the total American adult population. The pathophysiology underlying this common mental health disorder is still under investigation. Previous research has shown that inflammation is associated with depression. However, further studies need to be conducted to uncover specific inflammatory markers associated with depression.
This cohort study conducted in China measured plasma cytokines in 82 participants. Participants were 18 years of age or older and had a confirmed DSM-V diagnosis of depression by a psychiatrist. People with other mental illnesses such as schizophrenia or bipolar disorder, people with a history of infection or antibiotic use within the past 3 months, people with autoimmune diseases, or immunosuppressive therapy. Those receiving this were excluded. Specifically, 14 plasma cytokines were measured at baseline by collecting venous blood samples in the morning after a fasting period the previous night. Participants’ depression severity was also collected at baseline using the Patient Health Questionnaire-9 (PHQ-9). Depression severity was followed up after 1, 2, and 3 months. The participants’ suicidal thoughts and behaviors were also assessed 3 months later using the Hamilton Depression Rating Scale (HDRS). Participants’ age, BMI, education, social support, and treatment for depression were also considered during data analysis and interpretation. The primary outcome measured depression severity.
As a result, interleukin-1β (IL-1β) levels were significantly associated with depression at all monthly follow-ups, even when adjusted for external factors (age, BMI, education, antidepressants, baseline PHQ-9). It was shown to be significantly associated with disease severity. . Tumor necrosis factor-α, but not IL-1β, was significantly associated with suicidal ideation and behavior. A limitation of this study is the lack of a healthy control group. Indeed, collecting data on inflammatory markers from healthy individuals would allow researchers to accurately compare differences and comment further on pathophysiological associations between specific cytokines and depression. . Nevertheless, this study provides deeper insight into the underlying physiology of depression and provides education about specific inflammatory markers that may be targeted in future treatments.
MMP-2 and TNF-α levels may be associated with the inflammatory process underlying schizophrenia
- Inflammatory markers MMP-2 and TNF-α were higher in the treatment-resistant (TRS) and chronic drug-treated schizophrenia (CMS) groups, respectively, compared to the healthy control group.
- MMP-2 and TNF-α showed no correlation with cognitive function in schizophrenia patients.
Evidence evaluation level: 2 (average)
The role of inflammation in the pathogenesis of many psychiatric disorders is an ongoing area of research. Schizophrenia is classified as a severe mental illness that affects approximately 0.5% of the American population. Understanding the physiological mechanisms underlying schizophrenia will help researchers develop targeted therapies for this life-altering disease. The specific inflammatory markers underlying the pathophysiology of schizophrenia should be further investigated.
This is a cross-sectional study with a case-control design comparing tumor necrosis factor-α (TNF-α) and matrix metalloproteinase-2 (MMP-2) levels in male patients with schizophrenia with those in healthy controls. was. group. Thirty-one patients with treatment-resistant schizophrenia (TRS), 49 patients with chronic drug-treated schizophrenia (CMS), and 53 healthy individuals were enrolled in the study. Han Chinese men aged 18 to 60 years with a confirmed diagnosis of schizophrenia according to DSM-IV criteria and who had not received treatment with anti-inflammatory drugs or antibiotics in the past 4 weeks were included in the study. Individuals with significant medical problems, endocrine disorders, degenerative brain diseases, or substance abuse disorders were excluded. TRS criteria required a poor response to his 6-month treatment with two antipsychotics and a Positive Negative Syndrome Scale (PANSS) score greater than 3 on each subscale. CMS was defined as patients with 6 months of effective treatment with one antipsychotic and a PANSS <3 on each subscale. Serum MMP-2 and TNF-α were measured from blood collected in the morning. Immediately thereafter, a clinical evaluation consisting of the PANSS to assess symptom severity and the Repeated Battery for Neuropsychological Status Assessment (RBANS) to assess cognitive function was performed by two psychiatrists. The primary outcome measured MMP-2 and TNF-α levels.
Results showed higher MMP-2 levels in the TRS group and higher TNF-α levels in the CMS group compared to the control group. The levels of both of these markers were not significantly different between the TRS and CMS groups. Interestingly, MMP-2 and TNF-α levels were not associated with cognitive function. A limitation of this study is that people with schizophrenia tend to take different medications. The researchers did their best to control for drug differences by converting the doses of these drugs into chlorpromazine equivalents. However, this does not allow us to control for the different mechanisms of action of these drugs, and thus how these drugs differentially affect her MMP-2 and TNF-α levels. Nevertheless, this is probably the first study of its kind to provide insight into the association between these specific inflammatory markers and schizophrenia, opening new avenues for research and future treatments. there is a possibility.
Image: P.D.
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