Elevated depression symptoms predict long-term cardiovascular mortality in patients with atrial fibrillation and heart failure.

BACKGROUND: Depression predicts prognosis in many cardiac conditions, including congestive heart failure (CHF). Despite heightened cardiac risk in patients with comorbid atrial fibrillation (AF) and CHF, depression has not been studied in this group. This substudy, from the AF-CHF Trial of rate- versus rhythm-control strategies, investigated whether depression predicts long-term cardiovascular mortality in patients with left ventricular ejection fraction or=14). Over a mean follow-up of 39 months, there were 246 cardiovascular deaths (111 presumed arrhythmic; 302 all-cause deaths). Cox proportional hazards models adjusted for other prognostic factors (including age, marital status, cause of CHF, creatinine level, left ventricular ejection fraction, paroxysmal AF, previous AF hospitalization, previous electrical conversion, and baseline medications) showed that elevated depression scores significantly predicted cardiovascular mortality (primary outcome), arrhythmic death, and all-cause mortality. The adjusted hazard ratios were 1.57 (95% confidence interval 1.20 to 2.07, P<0.001), 1.69 (95% confidence interval 1.13 to 2.53, P=0.01), and 1.38 (95% confidence interval 1.07 to 1.77, P=0.01), respectively. The risks associated with depression and marital status were additive, with the highest risk in depressed patients who were unmarried. CONCLUSIONS: Elevated depression symptoms are related to cardiovascular mortality even after adjustment for other prognostic indicators in patients with comorbid AF and CHF who receive optimized treatment. Unmarried patients are also at increased risk. Mechanisms and treatment options deserve additional study.

The importance of examining blood pressure reactivity and recovery in anger provocation research.

OBJECTIVE: We investigated the moderating relationship of hostility on emotional and physiological arousal due to acute anger provocation; stress reactivity and recovery were measured. METHOD: Forty-five participants completed a measure of trait hostility (CMHQ) and performed a mental arithmetic (serial 7s) task while receiving scripted comments at set intervals designed to provoke anger (harassment). The impact of trait hostility (high, medium or low) on arousal and recovery was examined. RESULTS: Participants low in self-reported hostility showed greater HR reactivity to the task but recovered quickly. Participants high in hostility showed noticeably slower recovery in SBP maintained after task completion. CONCLUSIONS: The findings underscore the importance of examining both reactivity and recovery data in anger provocation research because the apparent influence of trait hostility on cardiovascular functioning would have been missed if recovery had not been systematically studied.

Type D personality is related to cardiovascular and neuroendocrine reactivity to acute stress.

OBJECTIVE: The relationship between Type D personality (the joint tendency towards negative affectivity [NA] and social inhibition [SI]) and laboratory indices of cardiovascular health was examined. METHOD: 173 undergraduates (86 male) completed a stress protocol involving a mental arithmetic task with harassment. Blood pressure, heart rate (HR), and salivary cortisol were measured both prior to and during the task. RESULTS: The relationships between personality and both resting and reactivity levels were examined. Results indicated that socially inhibited men demonstrated heightened blood pressure reactivity. NA was related to dampened HR change during the stress task in men. Correlational analyses indicated that both Type D dimensions were associated with greater cortisol reactivity to stress; however, results no longer remained significant in more stringent regression analyses. CONCLUSION: Findings are consistent with the noted relationship between Type D and cardiovascular disease (CVD), and suggest a possible pathway to disease via an association with physiological hyperreactivity.

First episode of major depressive disorder and vascular factors in coronary artery disease patients: Baseline characteristics and response to antidepressant treatment in the CREATE trial.

OBJECTIVE: The CREATE trial reported that coronary artery disease (CAD) patients suffering from a first depression derived less benefit from citalopram relative to placebo than those with a recurrent depression. The present investigation sought to determine whether the differential benefit of citalopram between those with a first depression and those with recurrent depression could be explained by indicators of vascular depression and cardiac disease severity. METHODS: Secondary analyses of data from CREATE, a 12-week, randomized placebo-controlled trial of 284 patients with major depressive disorder and CAD were used. Recurrence subgroups were compared on baseline characteristics reflecting vascular depression and cardiac disease severity. Outcome measures were the mean change from baseline to 12 weeks on the 24-item Hamilton Depression Rating Scale administered centrally by telephone. ANCOVA was used to assess the potential interaction of each baseline variable with citalopram/placebo treatment in predicting outcomes. RESULTS: Few baseline differences differentiated patients with a first versus recurrent depression, and none accounted for the differential treatment efficacy in these subgroups. Patients with a cardiac event in the past 6 months (P=.02) and taking angiotensin-converting enzyme inhibitors (P=.03) experienced less change with citalopram relative to placebo. Older age, worse functional status, taking beta-blockers, presence of angina (all P<.05), and later age of first depression (P=.05) predicted smaller changes in depression, independent of treatment assignment. CONCLUSIONS: There was limited evidence that the lack of improvement with citalopram relative to placebo in CAD patients with a first depression can be attributed to vascular depression.

Influence of apologies and trait hostility on recovery from anger.

While there is growing evidence that quick recovery from stress is health-protective, relatively little is known about what factors affect recovery rates. We tested whether recovery from anger can be diffused with apologies. 184 participants performed a stress task involving verbal harassment and apologies. Participants were randomly assigned to one of four conditions: non-harassed control, good apology, pseudo-apology, or no apology. Measures of blood pressure and heart rate were taken at baseline, task and recovery periods. Participants scoring high in trait hostility displayed faster systolic blood pressure recovery when they received a genuine apology, but recovered more slowly when they received a pseudo-apology or no apology. Apologies did not influence subjective anger ratings. It was concluded that apologies may accelerate cardiovascular anger recovery among those with hostile personality predispositions.