Literature DB >> 21377644

Relation of coronary microvascular dysfunction in hypertrophic cardiomyopathy to contractile dysfunction independent from myocardial injury.

Stefan A J Timmer1, Tjeerd Germans, Marco J W Götte, Iris K Rüssel, Mark Lubberink, Jurrien M Ten Berg, Folkert J Ten Cate, Adriaan A Lammertsma, Paul Knaapen, Albert C van Rossum.   

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.
Copyright © 2011 Elsevier Inc. All rights reserved.

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Year:  2011        PMID: 21377644     DOI: 10.1016/j.amjcard.2011.01.029

Source DB:  PubMed          Journal:  Am J Cardiol        ISSN: 0002-9149            Impact factor:   2.778


  4 in total

Review 1.  Targets for therapy in sarcomeric cardiomyopathies.

Authors:  Jil C Tardiff; Lucie Carrier; Donald M Bers; Corrado Poggesi; Cecilia Ferrantini; Raffaele Coppini; Lars S Maier; Houman Ashrafian; Sabine Huke; Jolanda van der Velden
Journal:  Cardiovasc Res       Date:  2015-01-29       Impact factor: 10.787

2.  Differentiation of infiltrative cardiomyopathy from hypertrophic cardiomyopathy using high-sensitivity cardiac troponin T: a case-control study.

Authors:  Toru Kubo; Yuichi Baba; Takayoshi Hirota; Katsutoshi Tanioka; Naohito Yamasaki; Shigeo Yamanaka; Tatsuo Iiyama; Naoko Kumagai; Takashi Furuno; Tetsuro Sugiura; Hiroaki Kitaoka
Journal:  BMC Cardiovasc Disord       Date:  2015-06-16       Impact factor: 2.298

3.  In hypertrophic cardiomyopathy reduction of relative resting myocardial blood flow is related to late enhancement, T2-signal and LV wall thickness.

Authors:  Katja Hueper; Antonia Zapf; Jan Skrok; Aurelio Pinheiro; Thomas A Goldstein; Jie Zheng; Stefan L Zimmerman; Ihab R Kamel; Roselle Abraham; Frank Wacker; David A Bluemke; Theodore Abraham; Jens Vogel-Claussen
Journal:  PLoS One       Date:  2012-07-30       Impact factor: 3.240

Review 4.  Unraveling the Genotype-Phenotype Relationship in Hypertrophic Cardiomyopathy: Obesity-Related Cardiac Defects as a Major Disease Modifier.

Authors:  Edgar E Nollet; B Daan Westenbrink; Rudolf A de Boer; Diederik W D Kuster; Jolanda van der Velden
Journal:  J Am Heart Assoc       Date:  2020-11-11       Impact factor: 6.106

  4 in total

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