High concordance between mental stress-induced and adenosine-induced myocardial ischemia assessed using SPECT in heart failure patients

Hemodynamic and biomarker correlates

A.J. Wawrzyniak, V. Dilsizian, D.S. Krantz, K.M. Harris, M.F. Smith, A. Shankovich, K.S. Whittaker, G.A. Rodriguez, J.S. Gottdiener, J. Li, W.J. Kop, S.S. Gottlieb

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Abstract

Mental stress can trigger myocardial ischemia, but the prevalence of mental stress–induced ischemia in congestive heart failure (CHF) patients is unknown. We characterized mental stress–induced 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 tomography
Original languageEnglish
Pages (from-to)1527-1533
JournalJournal of Nuclear Medicine
Volume56
Issue number10
DOIs
Publication statusPublished - 2015

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Perfusion
Brain Natriuretic Peptide
Metalloproteases
Endothelin-1
Left Ventricular Function
Interleukin-10
Dilatation
Interleukin-6
Tumor Necrosis Factor-alpha

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Wawrzyniak, A.J. ; Dilsizian, V. ; Krantz, D.S. ; Harris, K.M. ; Smith, M.F. ; Shankovich, A. ; Whittaker, K.S. ; Rodriguez, G.A. ; Gottdiener, J.S. ; Li, J. ; Kop, W.J. ; Gottlieb, S.S. / High concordance between mental stress-induced and adenosine-induced myocardial ischemia assessed using SPECT in heart failure patients : Hemodynamic and biomarker correlates. In: Journal of Nuclear Medicine. 2015 ; Vol. 56, No. 10. pp. 1527-1533.
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title = "High concordance between mental stress-induced and adenosine-induced myocardial ischemia assessed using SPECT in heart failure patients: Hemodynamic and biomarker correlates",
abstract = "Mental stress can trigger myocardial ischemia, but the prevalence of mental stress–induced ischemia in congestive heart failure (CHF) patients is unknown. We characterized mental stress–induced 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 tomography",
author = "A.J. Wawrzyniak and V. Dilsizian and D.S. Krantz and K.M. Harris and M.F. Smith and A. Shankovich and K.S. Whittaker and G.A. Rodriguez and J.S. Gottdiener and J. Li and W.J. Kop and S.S. Gottlieb",
year = "2015",
doi = "10.2967/jnumed.115.157990",
language = "English",
volume = "56",
pages = "1527--1533",
journal = "Journal of Nuclear Medicine",
issn = "0161-5505",
publisher = "Society of Nuclear Medicine Inc.",
number = "10",

}

Wawrzyniak, AJ, Dilsizian, V, Krantz, DS, Harris, KM, Smith, MF, Shankovich, A, Whittaker, KS, Rodriguez, GA, Gottdiener, JS, Li, J, Kop, WJ & Gottlieb, SS 2015, 'High concordance between mental stress-induced and adenosine-induced myocardial ischemia assessed using SPECT in heart failure patients: Hemodynamic and biomarker correlates', Journal of Nuclear Medicine, vol. 56, no. 10, pp. 1527-1533. https://doi.org/10.2967/jnumed.115.157990

High concordance between mental stress-induced and adenosine-induced myocardial ischemia assessed using SPECT in heart failure patients : Hemodynamic and biomarker correlates. / Wawrzyniak, A.J.; Dilsizian, V.; Krantz, D.S.; Harris, K.M.; Smith, M.F.; Shankovich, A.; Whittaker, K.S.; Rodriguez, G.A.; Gottdiener, J.S.; Li, J.; Kop, W.J.; Gottlieb, S.S.

In: Journal of Nuclear Medicine, Vol. 56, No. 10, 2015, p. 1527-1533.

Research output: Contribution to journalArticleScientificpeer-review

TY - JOUR

T1 - High concordance between mental stress-induced and adenosine-induced myocardial ischemia assessed using SPECT in heart failure patients

T2 - Hemodynamic and biomarker correlates

AU - Wawrzyniak, A.J.

AU - Dilsizian, V.

AU - Krantz, D.S.

AU - Harris, K.M.

AU - Smith, M.F.

AU - Shankovich, A.

AU - Whittaker, K.S.

AU - Rodriguez, G.A.

AU - Gottdiener, J.S.

AU - Li, J.

AU - Kop, W.J.

AU - Gottlieb, S.S.

PY - 2015

Y1 - 2015

N2 - Mental stress can trigger myocardial ischemia, but the prevalence of mental stress–induced ischemia in congestive heart failure (CHF) patients is unknown. We characterized mental stress–induced 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 tomography

AB - Mental stress can trigger myocardial ischemia, but the prevalence of mental stress–induced ischemia in congestive heart failure (CHF) patients is unknown. We characterized mental stress–induced 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 tomography

U2 - 10.2967/jnumed.115.157990

DO - 10.2967/jnumed.115.157990

M3 - Article

VL - 56

SP - 1527

EP - 1533

JO - Journal of Nuclear Medicine

JF - Journal of Nuclear Medicine

SN - 0161-5505

IS - 10

ER -