Search

Background: Cardiovascular disease is often studied through patient self-report and administrative data. However, these 2 sources provide different information, and few studies have compared them., Methods and Results: We compared data from a longitudinal, nationally representative survey of older Americans with matched Medicare claims. Self-reported heart attack in the previous 2 years was compared with claims-identified acute myocardial infarction (AMI) and acute coronary syndrome. Among the 3.1% of respondents with self-reported heart attack, 32.8% had claims-identified AMI, 16.5% had non-AMI acute coronary syndrome, and 25.8% had other cardiac claims; 17.3% had no inpatient visits in the previous 2.5 years. Claims-identified AMIs were found in 1.4% of respondents; of these, 67.8% reported a heart attack. Self-reports were less likely among respondents >75 years of age (62.7% versus 74.6%; P=0.006), with less than high school education (61.6% versus 71.4%; P=0.015), with at least 1 limitation in activities of daily living (59.6% versus 74.7%; P=0.001), or below the 25th percentile of a word recall memory test (60.7% versus 71.3%; P=0.019). Both self-reported and claims-identified cardiac events were associated with increased mortality; the highest mortality was observed among those with claims-identified AMI who did not self-report (odds ratio, 2.8; 95% confidence interval, 1.5-5.1) and among those with self-reported heart attack and claims-identified AMI (odds ratio, 2.5; 95% confidence interval, 1.7-3.6) or non-AMI acute coronary syndrome (odds ratio, 2.7; 95% confidence interval, 1.8-4.1)., Conclusions: There is considerable disagreement between self-reported and claims-identified events. Although self-reported heart attack may be inaccurate, it indicates increased risk of death, regardless of whether the self-report is confirmed by Medicare claims., (© 2015 American Heart Association, Inc.)

Background: There is considerable evidence that depression and low social support are associated with increased morbidity and mortality for patients with coronary heart disease (CHD). However, there is a lack of consensus regarding the measurement of social support and its relation to depression., Purpose: The primary purpose of the present study was to identify key dimensions of existing social support and depression measures for patients with CHD using factor analysis., Method: Seven hundred-five patients with a recent acute myocardial infarction and either depression, low social support, or both, completed measures of several types of social support and depression. Exploratory and confirmatory factor analysis were used to examine the underlying dimensions of the existing social support and depression measures, and to compare theoretically plausible models specifying the relation between the social support and depression factors., Results: Confirmatory factor analysis indicated that an approach in which smaller facets of depression are measured (somatic, cognitive/affective, anxious) and social support (perceived emotional support from intimate relationships; perceived tangible support from peripheral contacts; and the number of children, relatives, and friends in a patient's support network), may be the most optimal way to measure social support and depression in this population RMSEA = 0.05; CFI = 0.81; TLI = 0.88)., Conclusion: Efforts to identify patients at increased psychosocial risk may be improved by screening for these subcomponents of social support and depression.

Objectives: To determine if: 1) depressed patients with a recent acute myocardial infarction (AMI) have higher nighttime heart rate (HR) than nondepressed patients, and 2) elevated nighttime HR is associated with decreased survival post AMI. Depression is a risk factor for mortality post AMI. It is also associated with sleep disturbances and with elevated HR, which may be more pronounced at night. Resting and 24-hour HR have been found to predict mortality in patient and community samples., Methods: Ambulatory electrocardiographic data were obtained from 333 depressed patients and 383 nondepressed patients with recent AMI. They were followed for up to 30 months (median = 24 months)., Results: Depressed patients had higher nighttime HR (70.7 +/- 0.7 versus 67.7 +/- 0.6 beats per minute (bpm); p = .001), and daytime HR (76.4 +/- 0.7 versus 74.2 +/- 0.6 bpm; p = .02) than nondepressed patients, even after adjusting for potential confounds. Depression (hazard ratio (Haz R) = 2.19; p = .02) and nighttime HR (Haz R = 1.03; p = .004), but not daytime HR, predicted survival after adjusting for other major predictors and for each other. The interaction between nighttime HR and depression on survival approached, but did not achieve, significance (p = .08)., Conclusions: Mean day and nighttime HR values are higher in depressed patients than in nondepressed patients post AMI. Depression and elevated nighttime HR, but not daytime HR, are independent predictors of survival in these patients. Although depressed patients have a higher nighttime HR than nondepressed patients, nighttime HR predicts mortality in both depressed and nondepressed patients.

Depression has been shown to be a risk factor for mortality during the 12 months following an acute myocardial infarction (MI), but few studies have examined whether it is associated with increased risk over longer periods. Most of the existing studies utilized depression questionnaires rather than diagnostic interviews, the gold standard for clinical depression diagnosis. The purpose of this study was to determine whether interview-diagnosed clinical depression affects survival for at least 5 years after an acute MI. Vital status was determined for 163 patients with major depression, 195 with minor depression or dysthymia, and 408 nondepressed patients, during a median follow-up period of 60 months after an acute MI. Survival analysis was used to model time from the index MI to death. There were 106 deaths during the follow-up. After adjusting for other risk factors for mortality, patients with either major or minor depression (HR=1.76; 95% CI: 1.19 to 2.60), major depression alone (HR=1.87; 95% CI: 1.17 to 2.98), or minor depression alone (HR=1.67; 95% CI: 1.06 to 2.64) were at higher risk for all-cause mortality compared to the nondepressed patients. Depression is an independent risk factor for death 5 years after an acute MI. Even minor depression is associated with an increased risk. Although it is not known whether treating depression can improve survival, patients with depression should be recognized as being at increased risk long after their acute MI.

Objective: To compare the impact of network support and different types of perceived functional support on all-cause mortality or nonfatal reinfarction for patients with a recent acute myocardial infarction (AMI)., Design: Participants were recruited from the Enhancing Recovery in Coronary Heart Disease (ENRICHD) trial; 2,481 AMI patients with depression or low social support were randomized to a cognitive-behavioral intervention or to a usual care control group. Data collection for certain measures of social support was limited: 2,466 participants completed the ENRICHD Social Support Inventory; 2,457 completed the Perceived Social Support Scale; 1,296 completed the Social Network Questionnaire; and 707 completed the Interpersonal Support and Evaluation List, Tangible Support subscale. Patients also completed the Beck Depression Inventory and were followed for up to 4.5 years., Main Outcome Measure: Time to death or nonfatal reinfarction., Results: Over the follow-up period, 599 patients (24%) died or had a nonfatal AMI. Survival models controlling age, sex, race, socioeconomic status, smoking, antidepressant use, and a composite measure of increased risk revealed that higher levels of perceived social support were associated with improved outcome for patients without elevated depression but not for patients with high levels of depression. Neither perceived tangible support nor network support were associated with more frequent adverse events., Conclusion: AMI patients should be assessed for multiple dimensions of perceived functional support and depression to identify those at increased psychosocial risk who may benefit from treatment., (Copyright 2007 APA.)

Objective: Depression is a risk factor for mortality after acute myocardial infarction (AMI), possibly as a result of altered autonomic nervous system (ANS) modulation of heart rate (HR) and rhythm. The purposes of this study were to determine: a) whether depressed patients are more likely to have an abnormal HR response (i.e., abnormal turbulence) to premature ventricular contractions (VPCs), and b) whether abnormal HR turbulence accounts for the effect of depression on increased mortality after AMI., Methods: Ambulatory electrocardiographic data were obtained from 666 (316 depressed, 350 nondepressed) patients with a recent AMI; 498 had VPCs with measurable HR turbulence. Of these, 260 had normal, 152 had equivocal, and 86 had abnormal HR turbulence. Patients were followed for up to 30 (median = 24) months., Results: Depressed patients were more likely to have abnormal HR turbulence (risk factor adjusted odds ratio = 1.8; 95% confidence interval [CI] = 1.0-3.0; p = .03) and have worse survival (odds ratio = 2.4; 95% CI = 1.2-4.6; p = .02) than nondepressed patients. When HR turbulence was added to the model, the adjusted hazard ratio for depression decreased to 1.9 (95% CI = 0.9-3.8; p = .08), and to 1.6 (95% CI = 0.8-3.4; p = .18) when a measure of HR variability (LnVLF) was added. The hazard was found to differ over time with depression posing little risk for mortality in year 1 but greater risk in years 2 and 3 of the follow up., Conclusion: ANS dysregulation may partially mediate the increased risk for mortality in depressed patients with frequent VPCs after an AMI.

Background: Depression is associated with an increased risk for mortality after acute myocardial infarction (MI). The purpose of this study was to determine whether low heart rate variability (HRV) mediates the effect of depression on mortality., Methods: Twenty-four-hour ambulatory electrocardiograms were obtained from 311 depressed patients with a recent acute MI who were enrolled in the Enhancing Recovery in Coronary Heart Disease (ENRICHD) clinical trial and from 367 nondepressed patients who met the ENRICHD medical inclusion criteria. Standard HRV indexes were extracted from the recordings., Results: The log of very low-frequency (LnVLF) power, an index of HRV derived from power spectral analysis of the electrocardiogram signal (0.0033-0.04 Hz [in milliseconds squared]), was lower in the depressed than in the nondepressed patients (P<.001). There were 47 deaths (6.1%) during a 30-month follow-up. After adjusting for potential confounders, the depressed patients remained at higher risk for all-cause mortality compared with the nondepressed patients (hazard ratio, 2.8; 95% confidence interval [CI], 1.4-5.4; P<.003). When LnVLF power was entered into the model, the hazard ratio for depression dropped to 2.1 (95% CI, 1.1-4.2; P = .03). The proportion of the risk for depression attributable to LnVLF power was 0.27 (95% CI, 0.23-0.31; P<.001)., Conclusions: Low HRV partially mediates the effect of depression on survival after acute MI. This finding helps to clarify the physiological mechanisms underlying depression's role as a risk factor for mortality in patients with coronary heart disease. It also raises the possibility that treatments that improve both depression and HRV might also improve survival in these patients.

Objective: Intervening in depression and/or low perceived social support within 28 days after myocardial infarction (MI) in the Enhancing Recovery in Coronary Heart Disease (ENRICHD) clinical trial did not increase event-free survival. The purpose of the present investigation was to conduct post hoc analyses on sex and ethnic minority subgroups to assess whether any treatment subgroup is at reduced or increased risk of greater morbidity/mortality., Methods: The 2481 patients with MI (973 white men, 424 minority men, 674 white women, 410 minority women) who had major or minor depression and/or low perceived social support were randomly allocated to usual medical care or cognitive behavior therapy. Total mortality or recurrent nonfatal MI (ENRICHD primary endpoint) and cardiac mortality or recurrent nonfatal MI (secondary endpoint) were analyzed as composite endpoints by group for time to first event using Cox proportional hazards regression., Results: There was a trend in the direction of treatment efficacy for white men for the primary endpoint (hazard ratio [HR], 0.80; 95% confidence interval, 0.61-1.05; p =.10) and a significant (p <.006, Bonferroni corrected) effect for the secondary endpoint (HR, 0.63; 95% CI, 0.46-0.87; p =.004). In contrast, the HRs for each of the other three subgroups were nonsignificant. The magnitude of differences in treatment effects between white men and the other subgroups remained significant for the secondary endpoint (p =.04) after adjustment for age, education, living alone, antidepressant use, comorbidity score, cardiac catheterization, ejection fraction, history of hypertension, and major depression., Conclusions: White men, but not other subgroups, may have benefited from the ENRICHD intervention, suggesting that future studies need to attend to issues of treatment design and delivery that may have prevented benefit among sex and ethnic subgroups other than white men.

The ENRICHD clinical trial, which compared an intervention for depression and social isolation to usual care, failed to decrease the rate of mortality and recurrent acute myocardial infarction (AMI) in post-AMI patients. One explanation for this is that depression was not associated with increased mortality in these patients. The purpose of this study was to determine if depression was associated with an increased risk of mortality in a subsample of the ENRICHD trial's depressed patients compared with a group of nondepressed patients recruited for an ancillary study. Three hundred fifty-eight depressed patients with an acute AMI from the ENRICHD clinical trial and 408 nondepressed patients who met the ENRICHD medical inclusion criteria were followed for up to 30 months. There were 47 deaths (6.1%) and 57 nonfatal AMIs (7.4%). After adjusting for other risk factors, depressed patients were at higher risk for all-cause mortality (hazard ratio 2.4, 95% confidence interval 1.2 to 4.7) but not for nonfatal recurrent infarction (hazard ratio 1.2, 95% confidence interval 0.7 to 2.0) compared with nondepressed patients. In conclusion, depression was an independent risk factor for death after AMI, but it did not have a significant effect on mortality until nearly 12 months after the acute event, nor did it predict nonfatal recurrent infarction.

Context: Depression and low perceived social support (LPSS) after myocardial infarction (MI) are associated with higher morbidity and mortality, but little is known about whether this excess risk can be reduced through treatment., Objective: To determine whether mortality and recurrent infarction are reduced by treatment of depression and LPSS with cognitive behavior therapy (CBT), supplemented with a selective serotonin reuptake inhibitor (SSRI) antidepressant when indicated, in patients enrolled within 28 days after MI., Design, Setting, and Patients: Randomized clinical trial conducted from October 1996 to April 2001 in 2481 MI patients (1084 women, 1397 men) enrolled from 8 clinical centers. Major or minor depression was diagnosed by modified Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria and severity by the 17-item Hamilton Rating Scale for Depression (HRSD); LPSS was determined by the Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) Social Support Instrument (ESSI). Random allocation was to usual medical care or CBT-based psychosocial intervention., Intervention: Cognitive behavior therapy was initiated at a median of 17 days after the index MI for a median of 11 individual sessions throughout 6 months, plus group therapy when feasible, with SSRIs for patients scoring higher than 24 on the HRSD or having a less than 50% reduction in Beck Depression Inventory scores after 5 weeks., Main Outcome Measures: Composite primary end point of death or recurrent MI; secondary outcomes included change in HRSD (for depression) or ESSI scores (for LPSS) at 6 months., Results: Improvement in psychosocial outcomes at 6 months favored treatment: mean (SD) change in HRSD score, -10.1 (7.8) in the depression and psychosocial intervention group vs -8.4 (7.7) in the depression and usual care group (P<.001); mean (SD) change in ESSI score, 5.1 (5.9) in the LPSS and psychosocial intervention group vs 3.4 (6.0) in the LPSS and usual care group (P<.001). After an average follow-up of 29 months, there was no significant difference in event-free survival between usual care (75.9%) and psychosocial intervention (75.8%). There were also no differences in survival between the psychosocial intervention and usual care arms in any of the 3 psychosocial risk groups (depression, LPSS, and depression and LPSS patients)., Conclusions: The intervention did not increase event-free survival. The intervention improved depression and social isolation, although the relative improvement in the psychosocial intervention group compared with the usual care group was less than expected due to substantial improvement in usual care patients.

Because of women's survival advantage, the impact of myocardial infarction (MI) on long-term mortality in women compared with men may be underestimated. The authors examined this issue in a community sample of 2,462 persons aged ≥65 years living in New Haven, Connecticut, who were free of MI at baseline and were followed for 10 years (1982–1992). By using proportional hazards models with MI hospitalizations and the sex-MI interaction as time-dependent covariables, survival for the MI cases from the date of MI was compared with survival of persons who, at the same follow-up time, were still alive and free of MI. Women survived longer than men mainly in the absence of MI. The multivariable-adjusted hazard ratios of death were 0.53 in the absence and 0.87 in the presence of MI, and MI was associated with a greater risk of death in women (adjusted hazard ratio = 5.9) than in men (adjusted hazard ratio = 3.6) (p = 0.01 for the sex-MI interaction). When out-of-hospital fatal infarctions were considered, the impact of MI on survival in women compared with men increased. In conclusion, in this elderly cohort, when viewed from a population perspective, MI had a greater impact on mortality in women and significantly narrowed women's typical survival advantage over men. Am J Epidemiol 2000;152:965–73. [ABSTRACT FROM PUBLISHER]

Presents a study which was done to determine whether functional disability is a predictor of clinical severity and mortality in elderly patients with myocardial infarction (MI). Whether functional disability before MI is associated with greater initial severity or higher mortality after MI; Findings of the study.

Presents information on a study which compared the survival and emotional support of elderly patients hospitalized for acute myocardial infarction. Methodology of the study; Results and discussion; Conclusions.

The author discusses the value of randomized controlled trial (RCT) methods aimed at examining social interventions. Topics mentioned include challenges posed by adherence to the standard biomedical models for RCTs to social experiments, the impact of maternity leave on women's mental health, and identification of the etiologic period, implementation and sustainability.