Impact of Decreased Transmural Conduction Velocity on the Function of the Human Left Ventricle: A Simulation Study

. 2020 ; 2020 () : 2867865. [epub] 20200403

Jazyk angličtina Země Spojené státy americké Médium electronic-ecollection

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/pmid32337235

This study investigates the impact of reduced transmural conduction velocity (TCV) on output parameters of the human heart. In a healthy heart, the TCV contributes to synchronization of the onset of contraction in individual layers of the left ventricle (LV). However, it is unclear whether the clinically observed decrease of TCV contributes significantly to a reduction of LV contractility. The applied three-dimensional finite element model of isovolumic contraction of the human LV incorporates transmural gradients in electromechanical delay and myocyte shortening velocity and evaluates the impact of TCV reduction on pressure rise (namely, (dP/dt)max) and on isovolumic contraction duration (IVCD) in a healthy LV. The model outputs are further exploited in the lumped "Windkessel" model of the human cardiovascular system (based on electrohydrodynamic analogy of respective differential equations) to simulate the impact of changes of (dP/dt)max and IVCD on chosen systemic parameters (ejection fraction, LV power, cardiac output, and blood pressure). The simulations have shown that a 50% decrease in TCV prolongs substantially the isovolumic contraction, decelerates slightly the LV pressure rise, increases the LV energy consumption, and reduces the LV power. These negative effects increase progressively with further reduction of TCV. In conclusion, these results suggest that the pumping efficacy of the human LV decreases with lower TCV due to a higher energy consumption and lower LV power. Although the changes induced by the clinically relevant reduction of TCV are not critical for a healthy heart, they may represent an important factor limiting the heart function under disease conditions.

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Glukhov A. V., Fedorov V. V., Kalish P. W., et al. Conduction remodeling in human end-stage nonischemic left ventricular cardiomyopathy. Circulation. 2012;125(15):1835–1847. doi: 10.1161/CIRCULATIONAHA.111.047274. PubMed DOI PMC

Lou Q., Janks D. L., Holzem K. M., et al. Right ventricular arrhythmogenesis in failing human heart: the role of conduction and repolarization remodeling. American Journal of Physiology. Heart and Circulatory Physiology. 2012;303(12):H1426–H1434. doi: 10.1152/ajpheart.00457.2012. PubMed DOI PMC

Akar F. G., Nass R. D., Hahn S., et al. Dynamic changes in conduction velocity and gap junction properties during development of pacing-induced heart failure. American Journal of Physiology-Heart and Circulatory Physiology. 2007;293(2):H1223–H1230. doi: 10.1152/ajpheart.00079.2007. PubMed DOI

Taggart P., Sutton P. M., Opthof T., et al. Inhomogeneous transmural conduction during early ischaemia in patients with coronary artery disease. Journal of Molecular and Cellular Cardiology. 2000;32(4):621–630. doi: 10.1006/jmcc.2000.1105. PubMed DOI

King J. H., Huang C. L.-H., Fraser J. A. Determinants of myocardial conduction velocity: implications for arrhythmogenesis. Frontiers in Physiology. 2013;4:p. 154. doi: 10.3389/fphys.2013.00154. PubMed DOI PMC

Vaverka J., Burša J., Sumbera J., Pásek M. Effect of transmural differences in excitation-contraction delay and contraction velocity on left ventricle isovolumic contraction: a simulation study. BioMed Research International. 2018;2018:10. doi: 10.1155/2018/4798512.4798512 PubMed DOI PMC

Yuniarti A. R., Lim K. M. The effect of electrical conductivity of myocardium on cardiac pumping efficacy: a computational study. Biomedical Engineering Online. 2017;16(1):p. 11. doi: 10.1186/s12938-016-0295-6. PubMed DOI PMC

Cordeiro J. M., Greene L., Heilmann C., Antzelevitch D., Antzelevitch C. Transmural heterogeneity of calcium activity and mechanical function in the canine left ventricle. American Journal of Physiology. Heart and Circulatory Physiology. 2004;286(4):H1471–H1479. doi: 10.1152/ajpheart.00748.2003. PubMed DOI

Agger P., Ilkjær C., Laustsen C., et al. Changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilation. Journal of Cardiovascular Magnetic Resonance. 2017;19(1):p. 93. doi: 10.1186/s12968-017-0404-0. PubMed DOI PMC

Hlaváč M., Holčík J., Moudr J. Biosignal (Analysis of Biomedical Signals and Images) Brno: VUTIUM Press; 2002. Model of short and long-term control of cardiovascular system; pp. 427–429.

Aboelkassem Y., Virag Z. A hybrid Windkessel-Womersley model for blood flow in arteries. Journal of Theoretical Biology. 2019;462:499–513. doi: 10.1016/j.jtbi.2018.12.005. PubMed DOI

Zhou S., Xu L., Hao L., et al. A review on low-dimensional physics-based models of systemic arteries: application to estimation of central aortic pressure. Biomedical Engineering Online. 2019;18(1):p. 41. doi: 10.1186/s12938-019-0660-3. PubMed DOI PMC

Westerhof N., Lankhaar J. W., Westerhof B. E. The arterial Windkessel. Medical & Biological Engineering & Computing. 2009;47(2):131–141. doi: 10.1007/s11517-008-0359-2. PubMed DOI

Greger R., Windhorst U. Comprehensive Human Physiology: From Cellular Mechanisms to Integration. Berlin Heidelberg: Springer; 2013.

Russell K., Eriksen M., Aaberge L., et al. A novel clinical method for quantification of regional left ventricular pressure-strain loop area: a non-invasive index of myocardial work. European Heart Journal. 2012;33(6):724–733. doi: 10.1093/eurheartj/ehs016. PubMed DOI PMC

Kou S., Caballero L., Dulgheru R., et al. Echocardiographic reference ranges for normal cardiac chamber size: results from the NORRE study. European Heart Journal Cardiovascular Imaging. 2014;15(6):680–690. doi: 10.1093/ehjci/jet284. PubMed DOI PMC

Channer K. S., Jones J. V. Atrial systole: its role in normal and diseased hearts. Clinical Science. 1988;75(1):1–4. doi: 10.1042/cs0750001. PubMed DOI

Manolas J. Invasive and noninvasive assessment of exercise-induced ischemic diastolic response using pressure transducers. Current Cardiology Reviews. 2015;11(1):90–99. doi: 10.2174/1573403x10666140704111537. PubMed DOI PMC

Curtiss E. I., Matthews R. G., Shaver J. A. Mechanism of normal splitting of the second heart sound. Circulation. 1975;51(1):157–164. doi: 10.1161/01.cir.51.1.157. PubMed DOI

Takimoto E., Kass D. A. Regulation of cardiac systolic function and contractility. In: Hill J. A., Olson E. N., editors. Muscle 2-Volume Set: Fundamental Biology and Mechanisms of Disease. 1st. Boston/Waltham: Academic Press; 2012. pp. 285–297.

Silbernagl S., Despopoulos A. Color Atlas of Physiology. 6th. Thieme; 2009. DOI

Sedmera D., Gourdie R. G. Why do we have Purkinje fibers deep in our heart? Physiological Research. 2014;63(Supplement 1):S9–18. PubMed

Zaklyazminskaya E., Dzemeshkevich S. The role of mutations in the SCN5A gene in cardiomyopathies. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 2016;1863(7):1799–1805. doi: 10.1016/j.bbamcr.2016.02.014. PubMed DOI

Katholi R. E., Couri D. M. Left ventricular hypertrophy: major risk factor in patients with hypertension: update and practical clinical applications. International Journal of Hypertension. 2011;2011:10. doi: 10.4061/2011/495349.495349 PubMed DOI PMC

Szymczyk E., Wierzbowska-Drabik K., Drozdz J., Krzeminska-Pakula M. Mitral valve regurgitation is a powerful factor of left ventricular hypertrophy. Polskie Archiwum Medycyny Wewnętrznej. 2008;118(9):478–483. PubMed

Pasipoularides A. Calcific aortic valve disease: part 2-morphomechanical abnormalities, gene reexpression, and gender effects on ventricular hypertrophy and its reversibility. Journal of Cardiovascular Translational Research. 2016;9(4):374–399. doi: 10.1007/s12265-016-9695-z. PubMed DOI PMC

Schneider D. J., Moore J. W. Patent ductus arteriosus. Circulation. 2006;114(17):1873–1882. doi: 10.1161/CIRCULATIONAHA.105.592063. PubMed DOI

Jashari H., Rydberg A., Ibrahimi P., Bajraktari G., Henein M. Y. Left ventricular response to pressure afterload in children: aortic stenosis and coarctation: a systematic review of the current evidence. International Journal of Cardiology. 2015;178:203–209. doi: 10.1016/j.ijcard.2014.10.089. PubMed DOI

Marian A. J., Braunwald E. Hypertrophic cardiomyopathy: genetics, pathogenesis, clinical manifestations, diagnosis, and therapy. Circulation Research. 2017;121(7):749–770. doi: 10.1161/CIRCRESAHA.117.311059. PubMed DOI PMC

van Veen A. A., van Rijen H. V., Opthof T. Cardiac gap junction channels: modulation of expression and channel properties. Cardiovascular Research. 2001;51(2):217–229. doi: 10.1016/s0008-6363(01)00324-8. PubMed DOI

Dasgupta C., Martinez A. M., Zuppan C. W., Shah M. M., Bailey L. L., Fletcher W. H. Identification of connexin43 (alpha1) gap junction gene mutations in patients with hypoplastic left heart syndrome by denaturing gradient gel electrophoresis (DGGE) Mutation Research. 2001;479(1–2):173–186. doi: 10.1016/s0027-5107(01)00160-9. PubMed DOI

Kashani A., Barold S. S. Significance of QRS complex duration in patients with heart failure. Journal of the American College of Cardiology. 2005;46(12):2183–2192. doi: 10.1016/j.jacc.2005.01.071. PubMed DOI

Dao D. T., Hollander S. A., Rosenthal D. N., Dubin A. M. QRS prolongation is strongly associated with life-threatening ventricular arrhythmias in children with dilated cardiomyopathy. The Journal of Heart and Lung Transplantation. 2013;32(10):1013–1019. doi: 10.1016/j.healun.2013.06.007. PubMed DOI

Ohkubo K., Watanabe I., Okumura Y., et al. Prolonged QRS duration in lead V2 and risk of life-threatening ventricular arrhythmia in patients with Brugada syndrome. International Heart Journal. 2011;52(2):98–102. doi: 10.1536/ihj.52.98. PubMed DOI

Jurak P., Halamek J., Meluzin J., et al. Ventricular dyssynchrony assessment using ultra-high frequency ECG technique. Journal of Interventional Cardiac Electrophysiology. 2017;49(3):245–254. doi: 10.1007/s10840-017-0268-0. PubMed DOI PMC

Cluitmans M., Brooks D. H., MacLeod R., et al. Validation and opportunities of electrocardiographic imaging: from technical achievements to clinical applications. Frontiers in Physiology. 2018;9, article 1305 doi: 10.3389/fphys.2018.01305. PubMed DOI PMC

Durrer D., van Dam R. T., Freud G. E., Janse M. J., Meijler F. L., Arzbaecher R. C. Total excitation of the isolated human heart. Circulation. 1970;41(6):899–912. doi: 10.1161/01.cir.41.6.899. PubMed DOI

Sommer G., Schriefl A. J., Andrä M., et al. Biomechanical properties and microstructure of human ventricular myocardium. Acta Biomaterialia. 2015;24:172–192. doi: 10.1016/j.actbio.2015.06.031. PubMed DOI

Holzapfel G. A., Ogden R. W. Constitutive modelling of passive myocardium: a structurally based framework for material characterization. Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences. 2009;367(1902):3445–3475. doi: 10.1098/rsta.2009.0091. PubMed DOI

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