Mechanical dyssynchrony precedes QRS widening in ATP-sensitive K+ channel-deficient dilated cardiomyopathy.

Satsuki Yamada, D. Kent Arrell, Garvan M Kane, Timothy J Nelson, Carmen M Terzic, Atta Behfar, Saranya Purushothaman, Frits W. Prinzen, Angelo Auricchio, Andre Terzic

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Abstract

Contractile discordance exacerbates cardiac dysfunction, aggravating heart failure outcome. Dissecting the genesis of mechanical dyssynchrony would enable an early diagnosis before advanced disease. High-resolution speckle-tracking echocardiography was applied in a knockout murine surrogate of adult-onset human cardiomyopathy caused by mutations in cardioprotective ATP-sensitive K(+) (K(ATP)) channels. Preceding the established criteria of cardiac dyssynchrony, multiparametric speckle-based strain resolved nascent erosion of dysfunctional regions within cardiomyopathic ventricles of the K(ATP) channel-null mutant exposed to hemodynamic stress. Not observed in wild-type counterparts, intraventricular disparity in wall motion, validated by the degree, direction, and delay of myocardial speckle patterns, unmasked the disease substrate from asymptomatic to overt heart failure. Mechanical dyssynchrony preceded widening of the QRS complex and exercise intolerance and progressed into global myocardial discoordination and decompensated cardiac pump function, precipitating a low output syndrome. The present study, with the use of high-resolution imaging, prospectively resolved the origin and extent of intraventricular motion disparity in a K(ATP) channel-knockout model of dilated cardiomyopathy. Mechanical dyssynchrony established as an early marker of cardiomyopathic disease offers novel insight into the pathodynamics of dyssynchronous heart failure.

Original languageEnglish (US)
JournalJournal of the American Heart Association
Volume2
Issue number6
StatePublished - 2013

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Dilated Cardiomyopathy
Adenosine Triphosphate
Heart Failure
Asymptomatic Diseases
Cardiomyopathies
Echocardiography
Early Diagnosis
Hemodynamics
Mutation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Mechanical dyssynchrony precedes QRS widening in ATP-sensitive K+ channel-deficient dilated cardiomyopathy.",
abstract = "Contractile discordance exacerbates cardiac dysfunction, aggravating heart failure outcome. Dissecting the genesis of mechanical dyssynchrony would enable an early diagnosis before advanced disease. High-resolution speckle-tracking echocardiography was applied in a knockout murine surrogate of adult-onset human cardiomyopathy caused by mutations in cardioprotective ATP-sensitive K(+) (K(ATP)) channels. Preceding the established criteria of cardiac dyssynchrony, multiparametric speckle-based strain resolved nascent erosion of dysfunctional regions within cardiomyopathic ventricles of the K(ATP) channel-null mutant exposed to hemodynamic stress. Not observed in wild-type counterparts, intraventricular disparity in wall motion, validated by the degree, direction, and delay of myocardial speckle patterns, unmasked the disease substrate from asymptomatic to overt heart failure. Mechanical dyssynchrony preceded widening of the QRS complex and exercise intolerance and progressed into global myocardial discoordination and decompensated cardiac pump function, precipitating a low output syndrome. The present study, with the use of high-resolution imaging, prospectively resolved the origin and extent of intraventricular motion disparity in a K(ATP) channel-knockout model of dilated cardiomyopathy. Mechanical dyssynchrony established as an early marker of cardiomyopathic disease offers novel insight into the pathodynamics of dyssynchronous heart failure.",
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AU - Yamada, Satsuki

AU - Arrell, D. Kent

AU - Kane, Garvan M

AU - Nelson, Timothy J

AU - Terzic, Carmen M

AU - Behfar, Atta

AU - Purushothaman, Saranya

AU - Prinzen, Frits W.

AU - Auricchio, Angelo

AU - Terzic, Andre

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