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This Article Full Text Full Text (PDF) Supplemental Movies All Versions of this Article: 293/5/H2747    most recent 00592.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Lionetti, V. Articles by Recchia, F. A. Search for Related Content PubMed PubMed Citation Articles by Lionetti, V. Articles by Recchia, F. A.

Mismatch between uniform increase in cardiac glucose uptake and regional contractile dysfunction in pacing-induced heart failure

¹Sector of Medicine, Scuola Superiore Sant'Anna, Pisa; ²Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche, Pisa, Italy; and ³Department of Physiology, New York Medical College, Valhalla, New York

Submitted 20 May 2007 ; accepted in final form 14 August 2007

Increased glucose utilization and regional differences in contractile function are well-known alterations of the failing heart and play an important pathophysiological role. We tested whether, similar to functional derangement, changes in glucose uptake develop following a regional pattern. Heart failure was induced in 13 chronically instrumented minipigs by pacing the left ventricular (LV) free wall at 180 beats/min for 3 wk. Regional changes in contractile function and stress were assessed by magnetic resonance imaging, whereas regional flow and glucose uptake were measured by positron emission tomography utilizing, respectively, the radiotracers [¹³N]ammonia and ¹⁸F-deoxyglucose. In heart failure, LV end-diastolic pressure was 20 ± 4 mmHg, and ejection fraction was 35 ± 4% (all P < 0.05 vs. control). Sustained pacing-induced dyssynchronous LV activation caused a more pronounced decrease in LV systolic thickening (7.45 ± 3.42 vs. 30.62 ± 8.73%, P < 0.05) and circumferential shortening (–4.62 ± 1.0 vs. –7.33 ± 1.2%, P < 0.05) in the anterior/anterior-lateral region (pacing site) compared with the inferoseptal region (opposite site). Conversely, flow was reduced significantly by 32% compared with control and was lower in the opposite site region. Despite these nonhomogeneous alterations, regional end-systolic wall stress was uniformly increased by 60% in the failing LV. Similar to wall stress, glucose uptake markedly increased vs. control (0.24 ± 0.004 vs. 0.07 ± 0.01 µmol·min^–1·g^–1, P < 0.05), with no significant regional differences. In conclusion, high-frequency pacing of the LV free wall causes a dyssynchronous pattern of contraction that leads to progressive cardiac failure with a marked mismatch between increased glucose uptake and regional contractile dysfunction.

heart failure; pacing; mismatch; dyssynchrony; glucose uptake