The Psychosocial Context Impacts Medication Adherence After Acute Coronary Syndrome

Background Depression is associated with poor adherence to medications and worse prognosis in patients with acute coronary syndrome (ACS). Purpose To determine whether cognitive, behavioral, and/or psychosocial vulnerabilities for depression explain the association between depression and medication adherence among ACS patients. Methods One hundred sixty-nine ACS patients who agreed to have their aspirin adherence measured using an electronic pill bottle for 3 months were enrolled within 1 week of hospitalization. Linear regression was used to determine whether depression vulnerabilities predicted aspirin adherence after adjustment for depressive symptoms, demographics, and comorbidity. Results Of the depression vulnerabilities, only role transitions (beta = −3.32; P = 0.02) and interpersonal conflict (beta -3.78; P = 0.03) predicted poor adherence. Depression vulnerabilities did not mediate the association between depressive symptoms and medication adherence. Conclusions Key elements of the psychosocial context preceding the ACS including major role transitions and conflict with close contacts place ACS patients at increased risk for poor medication adherence independent of depressive symptoms

Association of acute coronary syndrome-induced posttraumatic stress disorder symptoms with self-reported sleep

Background Symptoms of posttraumatic stress disorder (PTSD) after acute coronary syndrome (ACS) are associated with recurrent ACS events and mortality. Poor sleep may be a mechanism, but the association between PTSD and sleep after ACS is unknown. Purpose This study aims to estimate the association between ACS-induced PTSD symptoms and self-reported sleep. Methods ACS-induced PTSD symptoms were assessed 1-month post-ACS in 188 adults using the Impact of Events Scale-Revised. Sleep was assessed using the Pittsburgh Sleep Quality Index. Linear and logistic regression models were used to determine whether PTSD symptoms were associated with self-reported sleep, independent of sociodemographic and clinical covariates. Results In adjusted models, ACS-induced PTSD symptoms were associated with worse overall sleep (β = 0.22, p = 0.003) and greater impairment in six of seven components of sleep (all p values <0.05). Conclusions ACS-induced PTSD symptoms may be associated with poor sleep, which may explain why PTSD confers increased cardiovascular risk after ACS

The Effect of Enhanced Depression Care on Anxiety Symptoms in Acute Coronary Syndrome Patients: Findings from the COPES Trial

Similar to depression, anxiety is common after acute coronary syndromes (ACS), and is an independent predictor of worse outcomes [1,2,3]. Yet, post-ACS psychological interventions have focused on treating depression. We previously reported that an enhanced depression care intervention involving patient preference for problem-solving therapy (PST), antidepressant medications, or both followed by stepped care according to treatment response was effective at reducing depressive symptoms after ACS with an effect size of 0.59 SD [4]. We report here the independent effect of this intervention on anxiety

Posttraumatic stress disorder and risk for coronary heart disease: A meta-analytic review

Objective The aim of this study was to estimate the association of posttraumatic stress disorder (PTSD) with risk for incident coronary heart disease (CHD). Design A systematic review and meta-analysis were used as study designs. Data Sources Articles were identified by searching Ovid MEDLINE, PsycINFO, Scopus, Cochrane Library, PILOTS database, and PubMed Related Articles and through a manual search of reference lists (1948-present). Study Selection All studies that assessed PTSD in participants initially free of CHD and subsequently assessed CHD/cardiac-specific mortality were included. Data Extraction Two investigators independently extracted estimates of the association of PTSD with CHD, as well as study characteristics. Odds ratios were converted to hazard ratios (HRs), and a random-effects model was used to pool results. A secondary analysis including only studies that reported estimates adjusted for depression was conducted. Results Six studies met our inclusion criteria (N = 402,274); 5 of these included depression as a covariate. The pooled HR for the magnitude of the relationship between PTSD and CHD was 1.55 (95% CI 1.34-1.79) before adjustment for depression. The pooled HR estimate for the 5 depression-adjusted estimates (N = 362,950) was 1.27 (95% CI 1.08-1.49). Conclusion Posttraumatic stress disorder is independently associated with increased risk for incident CHD, even after adjusting for depression and other covariates. It is common in both military veterans and civilian trauma survivors, and these results suggest that it may be a modifiable risk factor for CHD. Future research should identify the mechanisms of this association and determine whether PTSD treatment offsets CHD risk

Widowhood and Mortality: A Meta-Analysis and Meta-Regression

The study of spousal bereavement and mortality has long been a major topic of interest for social scientists, but much remains unknown with respect to important moderating factors, such as age, follow-up duration, and geographic region. The present study examines these factors using meta-analysis. Keyword searches were conducted in multiple electronic databases, supplemented by extensive iterative hand searches. We extracted 1,377 mortality risk estimates from 123 publications, providing data on more than 500 million persons. Compared with married people, widowers had a mean hazard ratio (HR) of 1.23 (95% confidence interval (CI), 1.19–1.28) among HRs adjusted for age and additional covariates and a high subjective quality score. The mean HR was higher for men (HR, 1.27; 95% CI, 1.19–1.35) than for women (HR, 1.15; 95% CI, 1.08–1.22). A significant interaction effect was found between gender and mean age, with HRs decreasing more rapidly for men than for women as age increased. Other significant predictors of HR magnitude included sample size, geographic region, level of statistical adjustment, and study quality

Treating persistent depressive symptoms in post-ACS patients: The project COPES phase-I randomized controlled trial

Depression and sub-syndromal depressive symptoms are important predictors of morbidity and mortality after acute coronary syndrome (ACS). Prior trials of depression treatment in post-ACS patients have demonstrated no improvement for event-free survival, and only modest improvement in depression symptoms. These trials have raised a number of important issues regarding timing of depression intervention, acceptability of depression treatment to ACS patients, and safety for subsets of the treated population. This article describes Project COPES (Coronary Psychosocial Evaluation Studies), a multi-center Phase-I randomized clinical trial. Project COPES uses a patient preference depression treatment that has previously been found acceptable to medical patients, and a 3-month pre-randomization observation period to insure depression status. The study sample will include 200 post-ACS patients. The primary outcome is patient satisfaction with depression care. Secondary, exploratory aims include the acceptability of depression treatment, reduction in depressive symptoms, and the effects of treatment on two key pathways – medication adherence and inflammation – hypothesized to link depression to post-ACS prognosis. These analyses will provide important data to inform subsequent clinical trials with this population

Confluence of Depression and Acute Psychological Stress Among Patients With Stable Coronary Heart Disease: Effects on Myocardial Perfusion

Background: Depression is prevalent in coronary heart disease (CHD) patients and increases risk for acute coronary syndrome (ACS) recurrence and mortality despite optimal medical care. The pathways underlying this risk remain elusive. Psychological stress (PS) can provoke impairment in myocardial perfusion and trigger ACS. A confluence of acute PS with depression might reveal coronary vascular mechanisms of risk. We tested whether depression increased risk for impaired myocardial perfusion during acute PS among patients with stable CHD. Methods and Results: Patients (N=146) completed the Beck Depression Inventory‐I (BDI‐I), a measure of depression linked to recurrent ACS and post‐ACS mortality, and underwent single‐photon emission computed tomography myocardial perfusion imaging at rest and during acute PS. The likelihood of new/worsening impairment in myocardial perfusion from baseline to PS as a function of depression severity was tested. On the BDI‐I, 41 patients scored in the normal range, 48 in the high normal range, and 57 in the depressed range previously linked to CHD prognosis. A BDI‐I score in the depressed range was associated with a significantly greater likelihood of new/worsening impairment in myocardial perfusion from baseline to PS (odds ratio =2.89, 95% CI: 1.26 to 6.63, P=0.012). This remained significant in models controlling ACS recurrence/mortality risk factors and medications. There was no effect for selective serotonin reuptake inhibitor medications. Conclusions: Depressed patients with CHD are particularly susceptible to impairment in myocardial perfusion during PS. The confluence of PS with depression may contribute to a better understanding of the depression‐associated risk for ACS recurrence and mortality

Endothelial cell activation, reduced endothelial cell reparative capacity, and impaired endothelial-dependent vasodilation after anger provocation

The experience of anger increases the acute and long-term risks of incident cardiovascular disease (CVD) events [1] and [2]. The mechanism(s) whereby anger is associated with increased CVD risk remains to be fully characterized. One promising candidate mechanism is endothelial dysfunction. Endothelial dysfunction, as evidenced by impaired endothelial-dependent vasodilation, is an early pathogenic process underlying atherosclerosis development and CVD onset. More recent investigations have elucidated the cellular pathways underlying endothelial dysfunction. Endothelial cell (EC) injury can be assessed by measuring circulating levels of EC-derived microparticles (EMPs), which are phospholipid rich, submicron particles derived and released from the membranes of activated or apoptotic ECs [3]. In addition, the discovery of circulating, bone marrow-derived endothelial progenitor cells (EPCs) capable of EC repair and regeneration [4] suggests that endothelial function represents a balance between ongoing injury and repair. We previously reported that anger provocation acutely impairs arterial vasomotion in apparently healthy individuals [5]. We conducted a study to examine the acute effects of anger provocation not only on arterial vasodilation but also on levels of EMPs and bone marrow-derived EPCs. To our knowledge, this is the first report concerning the adverse effects of anger provocation on cellular pathways underlying EC health

Depressive Symptoms and All-Cause Mortality in Unstable Angina Pectoris (from the Coronary Psychosocial Evaluation Studies [COPES])

Although depression is clearly associated with increased mortality after acute myocardial infarction, there is a paucity of data examining the impact of depression on patients with unstable angina (UA). We analyzed the relation between depressive symptoms and all-cause mortality in patients with UA who were enrolled in a prospective multicenter study of depression and acute coronary syndrome (ACS). Depressive symptoms were measured with the Beck Depression Inventory (BDI) within 1 week of the ACS event, and patients were selected for a BDI score 0 to 4 or ≥10. Our sample included 209 patients with UA, with 104 (50%) having a BDI score ≥10. Proportional hazards analyses adjusted for variables including left ventricular ejection fraction, Global Registry of Acute Coronary Events risk score, and Charlson co-morbidity index. In multivariable analyses, a BDI score ≥10 was associated with increased risk of 42-month all-cause mortality (hazard ratio 2.04, 95% confidence interval 1.20 to 3.46, p = 0.008) compared to a BDI score 0 to 4. In conclusion, our results confirm and extend previous evidence linking depression to worse outcomes in UA and suggest that interventions that address depression may be worth examining across the spectrum of risk in ACS

The Misdiagnosis of Hypertension: The Role of Patient Anxiety

Background: The white coat effect (defined as the difference between blood pressure [BP] measurements taken at the physician's office and those taken outside the office) is an important determinant of misdiagnosis of hypertension, but little is known about the mechanisms underlying this phenomenon. We tested the hypothesis that the white coat effect may be a conditioned response as opposed to a manifestation of general anxiety. Methods: A total of 238 patients in a hypertension clinic wore ambulatory blood pressure monitors on 3 separate days 1 month apart. At each clinic visit, BP readings were manually triggered in the waiting area and the examination room (in the presence and absence of the physician) and were compared with the mercury sphygmomanometer readings taken by the physician in the examination room. Patients completed trait and state anxiety measures before and after each BP assessment. Results: A total of 35% of the sample was normotensive, and 9%, 37%, and 19% had white coat, sustained, and masked hypertension, respectively. The diagnostic category was associated with the state anxiety measure (F3,237 = 6.4, P < .001) but not with the trait anxiety measure. Patients with white coat hypertension had significantly higher state anxiety scores (t = 2.67, P < .01), with the greatest difference reported during the physician measurement. The same pattern was observed for BP changes, which generally paralleled the changes in state anxiety (t = 4.86, P < .002 for systolic BP; t = 3.51, P < .002 for diastolic BP). Conclusions: These findings support our hypothesis that the white coat effect is a conditioned response. The BP measurements taken by physicians appear to exacerbate the white coat effect more than other means. This problem could be addressed with uniform use of automated BP devices in office settings