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MYOCARDIAL TRIGLYCERIDE ACCUMULATION IS A POSSIBLE LINK BETWEEN LEFT VENTRICULAR DIASTOLIC...

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Stable Ischemic Heart Disease A1587 JACC April 1, 2014 Volume 63, Issue 12 MYOCARDIAL TRIGLYCERIDE ACCUMULATION IS A POSSIBLE LINK BETWEEN LEFT VENTRICULAR DIASTOLIC DYSFUNCTION AND CORONARY MICROVASCULAR DYSFUNCTION: A PILOT STUDY Poster Contributions Hall C Sunday, March 30, 2014, 9:45 a.m.-10:30 a.m. Session Title: Biomarkers, Predictors and Imaging in Stable Ischemic Heart Disease Abstract Category: 25. Stable Ischemic Heart Disease: Clinical Presentation Number: 1194-334 Authors: Janet Wei, Michael Nelson, Edward Szczepaniak, Louise Thomson, Daniel Berman, Debiao Li, C. Noel Bairey Merz, Lidia Szczepaniak, Cedars-Sinai Medical Center, Los Angeles, CA, USA Background: Women with coronary microvascular dysfunction (CMD), diagnosed by invasive coronary reactivity testing, are at increased risk for developing heart failure with preserved ejection fraction. Myocardial fat accumulation has been associated with diastolic dysfunction in other disease states. We propose that women with CMD have elevated myocardial triglyceride (TG) content with associated diastolic dysfunction. Methods: 3T cardiac proton magnetic resonance spectroscopy and myocardial tissue tagging were performed on 8 healthy women and 5 women with CMD and evidence of diastolic dysfunction (b-type natriuretic peptide>400 pg/mL or left ventricular end-diastolic pressure ≥12 mmHg). Myocardial TG content was expressed as a percentage fat-to-water ratio. Diastolic circumferential strain rate was measured in the midventricular short axis (Diagnosoft HARP). Results: Women with CMD had higher myocardial TG content and lower diastolic circumferential strain rate than normal controls (Figure). Myocardial TG content correlated inversely with diastolic circumferential strain rate (r= -0.779, p= 0.002). Conclusion: Myocardial TG accumulation is elevated in women with CMD compared to normal controls and significantly correlates with diastolic circumferential strain rate. Our results suggest that an “ischemia-triggered” shift in myocardial substrate utilization (from free fatty acids to glucose) leads to excessive myocardial fat accumulation and secondary diastolic dysfunction.
Transcript

Stable Ischemic Heart Disease

A1587JACC April 1, 2014

Volume 63, Issue 12

myocardial triglyceride accUmUlation is a PossiBle link BetWeen left ventricUlar diastolic dysfUnction and coronary microvascUlar dysfUnction: a Pilot stUdy

Poster ContributionsHall CSunday, March 30, 2014, 9:45 a.m.-10:30 a.m.

Session Title: Biomarkers, Predictors and Imaging in Stable Ischemic Heart DiseaseAbstract Category: 25. Stable Ischemic Heart Disease: ClinicalPresentation Number: 1194-334

Authors: Janet Wei, Michael Nelson, Edward Szczepaniak, Louise Thomson, Daniel Berman, Debiao Li, C. Noel Bairey Merz, Lidia Szczepaniak, Cedars-Sinai Medical Center, Los Angeles, CA, USA

Background: Women with coronary microvascular dysfunction (CMD), diagnosed by invasive coronary reactivity testing, are at increased risk for developing heart failure with preserved ejection fraction. Myocardial fat accumulation has been associated with diastolic dysfunction in other disease states. We propose that women with CMD have elevated myocardial triglyceride (TG) content with associated diastolic dysfunction.

methods: 3T cardiac proton magnetic resonance spectroscopy and myocardial tissue tagging were performed on 8 healthy women and 5 women with CMD and evidence of diastolic dysfunction (b-type natriuretic peptide>400 pg/mL or left ventricular end-diastolic pressure ≥12 mmHg). Myocardial TG content was expressed as a percentage fat-to-water ratio. Diastolic circumferential strain rate was measured in the midventricular short axis (Diagnosoft HARP).

results: Women with CMD had higher myocardial TG content and lower diastolic circumferential strain rate than normal controls (Figure). Myocardial TG content correlated inversely with diastolic circumferential strain rate (r= -0.779, p= 0.002).

conclusion: Myocardial TG accumulation is elevated in women with CMD compared to normal controls and significantly correlates with diastolic circumferential strain rate. Our results suggest that an “ischemia-triggered” shift in myocardial substrate utilization (from free fatty acids to glucose) leads to excessive myocardial fat accumulation and secondary diastolic dysfunction.

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