9 research outputs found
High concordance between mental stress-induced and adenosine-induced myocardial ischemia assessed using SPECT in heart failure patients:Hemodynamic and biomarker correlates
Mental stress can trigger myocardial ischemia, but the prevalence of mental stressâinduced ischemia in congestive heart failure (CHF) patients is unknown. We characterized mental stressâinduced and adenosine-induced changes in myocardial perfusion and neurohormonal activation in CHF patients with reduced left-ventricular function using SPECT to precisely quantify segment-level myocardial perfusion. Methods: Thirty-four coronary artery disease patients (mean age ± SD, 62 ± 10 y) with CHF longer than 3 mo and ejection fraction less than 40% underwent both adenosine and mental stress myocardial perfusion SPECT on consecutive days. Mental stress consisted of anger recall (anger-provoking speech) followed by subtraction of serial sevens. The presence and extent of myocardial ischemia was quantified using the conventional 17-segment model. Results: Sixty-eight percent of patients had 1 ischemic segment or more during mental stress and 81% during adenosine. On segment-by-segment analysis, perfusion with mental stress and adenosine were highly correlated. No significant differences were found between any 2 time points for B-type natriuretic peptide, tumor necrosis factor-α, IL-1b, troponin, vascular endothelin growth factor, IL-17a, matrix metallopeptidase-9, or C-reactive protein. However, endothelin-1 and IL-6 increased, and IL-10 decreased, between the stressor and 30 min after stress. Left-ventricular end diastolic dimension was 179 ± 65 mL at rest and increased to 217 ± 71 after mental stress and 229 ± 86 after adenosine (P < 0.01 for both). Resting end systolic volume was 129 ± 60 mL at rest and increased to 158 ± 66 after mental stress (P < 0.05) and 171 ± 87 after adenosine (P < 0.07), with no significant differences between adenosine and mental stress. Ejection fraction was 30 ± 12 at baseline, 29 ± 11 with mental stress, and 28 ± 10 with adenosine (P = not significant). Conclusion: There was high concordance between ischemic perfusion defects induced by adenosine and mental stress, suggesting that mental stress is equivalent to pharmacologic stress in eliciting clinically significant myocardial perfusion defects in CHF patients. Cardiac dilatation suggests clinically important changes with both conditions. Psychosocial stressors during daily life may contribute to the ischemic burden of CHF patients with coronary artery disease. Keywords: heart failure, mental stress, ischemia, myocardial perfusion, adenosine, single-photon emission computed tomograph
Nuclear magnetic resonance secondary shifts of a light-harvesting 2 complex reveal local backbone perturbations induced by its higher-order interactions
Solid state NMR/Biophysical Organic Chemistr
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Psychological stress and short-term hospitalisations or death in patients with heart failure
Objective Standard predictors do not fully explain variations in the frequency and timing of heart failure (HF) adverse events (AEs). Psychological stress can trigger acute cardiovascular (CV) events, but it is not known whether stress can precipitate AEs in patients with HF. We investigated prospective associations of psychological stress with AEs in patients with HF. Methods 144 patients with HF (77% male; 57.5±11.5, range 23â87â
years, left ventricular ejection fraction â€40%) were longitudinally evaluated for psychological stress (Perceived Stress Scale) and AEs (CV hospitalisations/death) at 2-week intervals for 3â
months and at 9-month follow-up. Results 42 patients (29.2%) had at least one CV hospitalisation and nine (6.3%) died. Patients reporting high average perceived stress across study measurements had a higher likelihood of AEs during the study period compared with those with lower stress (odds ratio=1.10, 95% confidence interval=1.04 to 1.17). In contrast to average levels, increases in stress did not predict AEs (p=0.96). Perceived stress was elevated after a CV hospitalisation (B=2.70, standard error (SE)=0.93, p=0.004) suggesting that CV hospitalisations increase stress. Subsequent analysis indicated that 24 of 38 (63%) patients showed a stress increase following hospitalisation. However, a prospective association between stress and AEs was present when accounting for prior hospitalisations (B=2.43, SE=1.23, p=0.05). Conclusions Sustained levels of perceived stress are associated with increased risk of AEs, and increased distress following hospitalisation occurs in many, but not all, patients with HF. Patients with chronically high stress may be an important target group for HF interventions aimed at reducing hospitalisations