Psychological Distress and Arrhythmia: Risk Prediction and Potential Modifiers

The connection between the heart and the brain has long been anecdotally recognized but has systematically been studied only relatively recently. Cardiac arrhythmias, especially ventricular arrhythmias that can lead to sudden cardiac death, remain a major public health concern and there is mounting evidence that psychological distress plays a critical role both as a predictor of high-risk cardiac substrate and as an inciting trigger. The transient, unpredictable nature of emotions and cardiac arrhythmias has made their study challenging, but evolving technologies in monitoring and imaging along with larger epidemiological data sets have encouraged more sophisticated studies examining this relationship. Here we review the research on psychological distress including anger, depression and anxiety on cardiac arrhythmias, insights into proposed mechanisms, and potential avenues for future research

Antipsychotic medications and sudden cardiac arrest: More than meets the eye?

Sudden cardiac arrest (SCA) remains an important public health problem and is stubbornly difficult to predict or prevent. A growing literature has emerged studying psychiatric conditions, such as depression and schizophrenia, and risk of arrhythmia and SCA.1–3 This field is challenging from an epidemiologic perspective, partly because of the rarity of SCA events in the general population without known heart disease and the potential confounding factors that may influence findings.4 For instance, there is increased recognition that treatments for mental illness may themselves raise cardiac risk

Endemic invasive amoebiasis in northern Australia

In October 2000, a 10-year-old Aboriginal boy from the Darwin region of the Northern Territory was referred to hospital with a 24-hour history of abdominal pain, initially generalised, but then localising to the right iliac fossa. The pain was accompanied by occasional vomiting, but no fever or diarrhoea was noted. At laparotomy, a gangrenous, unruptured appendix was removed. Postoperatively, the patient made a good recovery. Neither he nor any family members had travelled outside the Northern Territory.Histological sections of the surgical specimen showed changes typical of acute suppurative appendicitis. Closer examination, however, revealed numerous round-to-oval structures resembling trophozoites (see Box). When the possibility of invasive amoebiasis was raised, staining of the section with Entamoeba histolytica-specific sera confirmed the diagnosis. E. histolytica serology was negative

Relationship between premature ventricular complexes and depressive symptoms in non-ST-elevation acute coronary syndrome

Aims: Depression is a recognized risk marker for mortality among acute coronary syndrome (ACS) patients. We hypothesized that ventricular arrhythmia detected by inpatient telemetry monitoring is more frequent among ACS patients with elevated depressive symptoms compared to those without depressive symptoms. Methods and results: We analysed data from patients enrolled in a prospective observational study of depression in ACS. Telemetry recordings during the index admission (average recording 21.3±3.0 hours) were analysed for frequent premature ventricular complexes (PVCs), defined as ≥10 per hour. The self-report Beck Depression Inventory (BDI) was used to assess depressive symptoms. Among 200 ACS patients, frequent PVCs were observed in 29% of patients with moderate depressive symptoms (BDI ≥10), 27% of those with mild symptoms (BDI 5–9), and only 11% of those with no/minimal symptoms (p=0.02). Log-transformed PVCs per hour were associated with depressive symptom category (p=0.008). In a multivariable logistic regression model that included age, gender, left ventricular ejection fraction, cardiovascular risk score, heart rate, and QT interval, mild symptoms (OR 3.02, 95% 0.97–9.43, p=0.058) and moderate-severe symptoms (OR 3.94, 95% CI 1.27–12.22, p=0.018) were associated with frequent PVCs. Conclusions: In this sample of ACS patients, depressive symptoms were independently associated with frequent PVCs during inpatient telemetry monitoring

Relations Between Depressive Symptoms, Anxiety, and T Wave Abnormalities in Subjects Without Clinically-Apparent Cardiovascular Disease (from the Multi-Ethnic Study of Atherosclerosis [MESA])

The aim of this study was to test the hypothesis that depression and anxiety are associated with electrocardiographic (ECG) repolarization abnormalities in the Multi-Ethnic Study of Atherosclerosis (MESA), a cohort free of symptomatic cardiovascular disease. Depressive symptoms were assessed by using the Center for Epidemiologic Studies Depression Scale and trait anxiety symptoms by using the Spielberger State-Trait Anxiety Inventory; both were categorized according to uppermost quartile. T-wave inversions in ECG leads other than V1 to V3 were obtained from electrocardiograms obtained at rest during the baseline examination. Participants with major intraventricular conduction abnormalities and those taking antiarrhythmics, antidepressants, and/or antipsychotics were excluded. Logistic regression models were estimated with multivariable adjustment for traditional cardiovascular disease risk factors. Among 5,906 participants, elevated depressive symptoms were associated with increased odds of T-wave inversion after multivariable adjustment (odds ratio 2.02, 95% confidence interval 1.33 to 3.06, p = 0.001), whereas greater trait anxiety was associated with reduced odds of T-wave inversion (odds ratio 0.47, 95% confidence interval 0.29 to 0.77, p = 0.003). The divergent associations of depressive symptoms and trait anxiety with ECG T-wave inversions were similar in men and women, and these associations were present across the racial and ethnic subgroups (non-Hispanic white, African-American, Hispanic, and Chinese). In conclusion, symptoms of depression and anxiety were independently yet oppositely associated with ECG T-wave inversions. Negative emotions may have a differential impact on cardiovascular mortality through unique relations with cardiac repolarization

Genomic islands from five strains of Burkholderia pseudomallei

<p>Abstract</p> <p>Background</p> <p><it>Burkholderia pseudomallei </it>is the etiologic agent of melioidosis, a significant cause of morbidity and mortality where this infection is endemic. Genomic differences among strains of <it>B. pseudomallei </it>are predicted to be one of the major causes of the diverse clinical manifestations observed among patients with melioidosis. The purpose of this study was to examine the role of genomic islands (GIs) as sources of genomic diversity in this species.</p> <p>Results</p> <p>We found that genomic islands (GIs) vary greatly among <it>B. pseudomallei </it>strains. We identified 71 distinct GIs from the genome sequences of five reference strains of <it>B. pseudomallei</it>: K96243, 1710b, 1106a, MSHR668, and MSHR305. The genomic positions of these GIs are not random, as many of them are associated with tRNA gene loci. In particular, the 3' end sequences of tRNA genes are predicted to be involved in the integration of GIs. We propose the term "tRNA-mediated site-specific recombination" (tRNA-SSR) for this mechanism. In addition, we provide a GI nomenclature that is based upon integration hotspots identified here or previously described.</p> <p>Conclusion</p> <p>Our data suggest that acquisition of GIs is one of the major sources of genomic diversity within <it>B. pseudomallei </it>and the molecular mechanisms that facilitate horizontally-acquired GIs are common across multiple strains of <it>B. pseudomallei</it>. The differential presence of the 71 GIs across multiple strains demonstrates the importance of these mobile elements for shaping the genetic composition of individual strains and populations within this bacterial species.</p