High Concordance Between Mental Stress-Induced and @entity859 -Induced @entity741 Assessed Using SPECT in Heart Failure XXXX : Hemodynamic and Biomarker Correlates.

@entity1 @entity650 @entity1032 @entity859 @entity63 @entity310 @entity1356 @entity7 @entity3876 @entity2232 @entity384 @entity4155 @entity741 @entity1495 @entity453 @entity688
BACKGROUND: @entity1032 can trigger @entity741 , but the prevalence of @entity1032 -induced @entity63 in CHF @entity1 is unknown.. We characterized @entity1032 -induced and @entity859 -induced changes in myocardial perfusion and neurohormonal activation in CHF @entity1 with reduced LV function using single-photon emission computed tomography (SPECT) to precisely quantify segment-level myocardial perfusion. MATERIALS AND METHODS: 34 @entity453 ( @entity453 ) @entity1 (age 62  10 years) with CHF>3 months, ejection fraction<40% underwent both @entity859 and @entity1032 myocardial perfusion SPECT on consecutive days. @entity1032 consisted of anger recall (anger-provoking speech) followed by subtracting serial 7s). Presence and extent of @entity741 was quantified using the conventional 17 segment model. RESULTS: 68% of @entity1 had >= 1 @entity63 segment during @entity1032 ; 81% during @entity859 . On segment-by-segment analysis, perfusion to @entity1032 and @entity859 were highly correlated. No significant differences were found between any two time points for @entity3876 , @entity310 , @entity1356 , troponin, @entity7 , @entity4155 , @entity1495 , or CRP. However, @entity2232 and @entity650 increased, and @entity688 decreased, between the stressor and 30 minutes post-stress.Left ventricular end diastolic dimension was 179  65 ml at rest and increased to 217  71 after @entity1032 and 229  86 after @entity859 (p<0.01 for both). Resting end systolic volume was 129  60 ml at rest and increased to 158  66 after @entity1032 (p<0.05) and 171  87 after @entity859 (p0.07), with no significant differences between @entity859 and @entity1032 . Ejection fraction was 30  12 at baseline, 29  11 with @entity1032 , and 28  10 with @entity859 (P = NS). CONCLUSION: There was high concordance between @entity63 perfusion defects induced by @entity859 and @entity1032 , suggesting that @entity1032 is equivalent to pharmacologic stress in eliciting clinically significant \myocardial perfusion defects in CHF @entity1 . @entity384 suggests clinically important changes with both conditions. Psychosocial stressors during daily life may contribute to the @entity63 burden of CHF @entity1 with @entity453 .
