Relation of Coronary Microvascular Dysfunction in Hypertrophic Cardiomyopathy to Contractile Dysfunction Independent from Myocardial Injury

SAJ Timmer, T Germans, MJW Gotte, IK Russel, M Lubberink, JM v.d. Berg, Folkert ten Cate, AA Lammertsma, P Knaapen, AC van Rossum

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Abstract

We studied the spatial relations among hyperemic myocardial blood flow (hMBF), contractile function, and morphologic tissue alterations in 19 patients with hypertrophic cardiomyopathy (HC). All patients were studied with oxygen-15 water positron emission tomography during rest and adenosine administration to assess myocardial perfusion. Cardiovascular magnetic resonance was performed to derive delayed contrast-enhanced images and to calculate contractile function (E(cc)) with tissue tagging. Eleven healthy subjects underwent similar positron emission tomographic and cardiovascular magnetic resonance scanning protocols and served as a control group. In the HC group, hMBF averaged 2.46 +/- 0.91 ml/min/g and mean E(cc) was -14.7 +/- 3.4%, which were decreased compared to the control group (3.97 +/- 1.48 ml/min/g and -17.7 +/- 3.2%, respectively, p <0.001 for the 2 comparisons). Delayed contrast enhancement (DCE) was present only in patients with HC, averaging 6.2 +/- 10.3% of left ventricular mass. In the HC group, E(cc) and DCE in the septum (-13.7 +/- 3.6% and 10.2 +/- 13.6%) significantly differed from the lateral wall (-16.0 +/- 2.8% and 2.4 +/- 5.9%, p <0.001 for the 2 comparisons). In general, hMBF and E(cc) were decreased in segments displaying DCE compared to nonenhanced segments (p <0.001 for the comparisons). In the HC group, univariate analysis revealed relations of hMBF to E(cc) (r = -0.45, p <0.001) and DCE (r = -0.31, p <0.001). Multivariate analysis revealed that E(cc) was independently related to hMBF (beta -0.37, p <0.001) and DCE (beta 0.28, p <0.001). In conclusion, in HC hMBF is impaired and related to contractile function independent from presence of DCE. When present, DCE reflected a progressed disease state as characterized by an increased perfusion deficit and contractile dysfunction. (C) 2011 Elsevier Inc. All rights reserved. (Am J Cardiol 2011;107:1522-1528)
Original languageUndefined/Unknown
Pages (from-to)1522-1528
Number of pages7
JournalAmerican Journal of Cardiology
Volume107
Issue number10
DOIs
Publication statusPublished - 2011

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