dP/dtmax: An underestimated prognostic factor in large animal infarction model

Rita Garamvölgyi , Dénes Kőrösi , Ottó Tátrai , Emőke Bodor , Dániel Fajtai , Kornélia Farkas , András Vorobcsuk

Animal Models and Experimental Medicine ›› 2025, Vol. 8 ›› Issue (1) : 171 -178.

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Animal Models and Experimental Medicine ›› 2025, Vol. 8 ›› Issue (1) : 171 -178. DOI: 10.1002/ame2.12502
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dP/dtmax: An underestimated prognostic factor in large animal infarction model

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Abstract

The present study aims to establish a reproducible large animal experimental unit using a minipig model to monitor cardiac function changes. A 90-min closed-chest balloon occlusion of the left anterior descending branch of the coronary artery was used to induce myocardial infarction in Pannon minipigs. To monitor the cardiac function, measurements were made by cardiac magnetic resonance imaging (cMRI), invasive pressure monitoring, and a Pulse index Continuous Cardiac Output (PiCCO) hemodynamic system at 0, 72, and 720 h during the follow-up period. End-diastolic and end-systolic volumes (EDV, ESV), left ventricular ejection fraction (LVEF) obtained by cMRI evaluation, global ejection fraction and aortic dP/dtmax obtained by the invasive method, were recorded and compared. The 72- and 720-h EDV data showed a significant increase (p=0.012, <0.001) compared to baseline, and the Day 30 data showed a significant increase compared to Day 3 (p=0.022). The ESV 72 h after the infarction showed a significant increase (p=0.001) compared to baseline, which did not change significantly by Day 30 (p=0.781) compared to Day 3. EDV and ESV were significantly negatively correlated with aortic dpmax, and ESV was significantly correlated with LVEF. For LVEF and dPmax, a significant (p<0.001 and p=0.002) worsening was demonstrated at Day 3 compared to baseline, which was no longer statistically detectable for LVEF at Day 30 (p=0.141), while the difference for dPmax was maintained (p=0.002). The complementary use of PiCCO hemodynamic measurements in large animal models makes the previously used methodologies more robust and reliable.

Keywords

dp/dtmax / hemodynamic measurements / infarction model / minipig / PiCCO

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Rita Garamvölgyi, Dénes Kőrösi, Ottó Tátrai, Emőke Bodor, Dániel Fajtai, Kornélia Farkas, András Vorobcsuk. dP/dtmax: An underestimated prognostic factor in large animal infarction model. Animal Models and Experimental Medicine, 2025, 8(1): 171-178 DOI:10.1002/ame2.12502

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References

[1]

Virani SS, Alonso A, Benjamin EJ, et al. Heart disease and stroke Statistics-2020 update: a report from the American Heart Association. Circulation. 2020;141(9):e139-e596.

[2]

Johansson S, Rosengren A, Young K, Jennings E. Mortality and morbidity trends after the first year in survivors of acute myocardial infarction: a systematic review. BMC Cardiovasc Disord. 2017;17(1):53.

[3]

Lelovas PP, Kostomitsopoulos NG, Xanthos TT. A comparative anatomic and physiologic overview of the porcine heart. JAALAS. 2014;53(5):432-438.

[4]

Nunoya T, Shibuya K, Saitoh T, et al. Use of miniature pig for biomedical research, with reference to toxicologic studies. J Toxicol Pathol. 2007;20(3):125-132.

[5]

Yongming P, Zhaowei C, Yichao M, et al. Involvement of peroxisome proliferator-activated receptors in cardiac and vascular remodeling in a novel minipig model of insulin resistance and atherosclerosis induced by consumption of a high-fat/cholesterol diet. Cardiovasc Diabetol. 2015;14:1-13.

[6]

Stricker-Krongrad A, Shoemake C, Brocksmith D, Liu J, Hamlin R, Bouchard G. Comparative cardiovascular physiology and pathology in selected lineages of minipigs: relation to drug safety evaluation. Toxicol Res Appl. 2017;1:1-8.

[7]

Arlock P, Mow T, Sjöberg T, Arner A, Steen S, Laursen M. Ion currents of cardiomyocytes in different regions of the Göttingen minipig heart. J Pharmacol Toxicol Methods. 2017;86:12-18.

[8]

Authier S, Gervais J, Fournier S, Gauvin D, Maghezzi S, Troncy E. Cardiovascular and respiratory safety pharmacology in Göttingen minipigs: pharmacological characterization. J Pharmacol Toxicol Methods. 2011;64(1):53-59.

[9]

Gauvin DV, Tilley LP, Smith FW Jr, Baird TJ. Spontaneous cardiac arrhythmias recorded in three experimentally-and drug-naive laboratory species (canine, primate, swine) during standard pre-study screening. J Pharmacol Toxicol Methods. 2009;59(2):57-61.

[10]

Broman I. Laboratory animal welfare approach in science. SEEMEDJ. 2020;4(1):102-105.

[11]

Spannbauer A, Traxler D, Zlabinger K, et al. Large animal models of heart failure with reduced ejection fraction (HFrEF). Front Cardiovasc. 2019;6:117.

[12]

Bertsch T, Janke C, Denz C, et al. Cardiac troponin I and cardiac troponin T increases in pigs during ischemia-reperfusion damage. Exper Toxicol Pathol. 2000;52:(2):157-159.

[13]

Pedrizzetti G, Claus P, Kilner PJ, Nagel E. Principles of cardiovascular magnetic resonance feature tracking and echocardiographic speckle tracking for informed clinical use. J Cardiovasc Magn Reson. 2016;18:51.

[14]

Voigt JU, Exner B, Schmiedehausen K, et al. Strain-rate imaging during dobutamine stress echocardiography provides objective evidence of inducible ischemia. Circulation. 2003;107:2120-2126.

[15]

Charles CJ, Rademaker MT, Scott NJA, Richards AM. Large animal models of heart failure: reduced vs. preserved ejection fraction. Animals. 2020;10(10):1906.

[16]

Shioura KM, Geenen DL, Goldspink PH. Assessment of cardiac function with the pressure-volume conductance system following myocardial infarction in mice. Am J Physiol Heart Circ Physiol. 2007;293(5):H2870-H2877.

[17]

Lindsey ML, Kassiri Z, Virag JAI, de tro Brás LE, Scherrer-Crosbie M. Guidelines for measuring cardiac physiology in mice. Am J Physiol Heart Circ Physiol. 2018;314(4):H733-H752.

[18]

Morimont P, Lambermont B, Desaive T, Janssen N, Chase G, D’Orio V. Aortic dP/dt max accurately reflects left ventricular contractility when effective preload independence is achieved. Crit Care. 2010;14:1-2.

[19]

Taylor SH, Snow HM, Linden RJ. Quantitation in morbid anatomy: relationship between left ventricular and aortic dP/dt (max). Proc R Soc Med. 1972;65(6):550-552.

[20]

Zhang YB, Zhang ZZ, Li JX, et al. Application of pulse index continuous cardiac output system in elderly patients with acute myocardial infarction complicated by cardiogenic shock: a prospective randomized study. World J Clin es. 2019;7(11):1291-1301.

[21]

Litton E, Morgan M. The PiCCO monitor: a review. Anaesth Intensive Care. 2012;40(3):393-409.

[22]

White HD, Norris RM, Brown MA, Brandt PW, Whitlock RM, Wild CJ. Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction. Circulation. 1987;76(1):44-51.

[23]

Heiberg E, Sjögren J, Ugander M, Carlsson M, Engblom H, Arheden H. Design and validation of segment—freely available software for cardiovascular image analysis. BMC Med Imaging. 2010;10:1.

[24]

Gödje O, Höke K, Lamm P, et al. Continuous, less invasive, hemodynamic monitoring in intensive care after cardiac surgery. Thorac Cardiovasc Surg. 1998;46(4):242-249.

[25]

Gödje O, Höke K, Goetz AE, et al. Reliability of a new algorithm for continuous cardiac output determination by pulse-contour analysis during hemodynamic instability. Crit Care Med. 2002;30(1):52-58.

[26]

The Jamovi Project. 2022. jamovi. (Version 2.3). https://www.jamovi.org

[27]

R Core Team R: A Language and environment for statistical computing. (R packages retrieved from MRAN snapshot 2022-01-01). 2021. https://cran.r-project.org

[28]

Gallucci M. GAMLj: General Analyses For Linear Models [jamovi module]. https://gamlj.github.io/ 2019.

[29]

Schuleri KH, Boyle AJ, Centola M, et al. The adult Göttingen minipig as a model for chronic heart failure after myocardial infarction: focus on cardiovascular imaging and regenerative therapies. Comp Med. 2008;58(6):568-579.

[30]

Dixon JA, Spinale FG. Large animal models of heart failure: a critical link in the translation of basic science to clinical practice. Circ Heart Fail. 2009;2(3):262-271.

[31]

Gaudron P, Eilles C, Kugler I, Ertl G. Progressive left ventricular dysfunction and remodeling after myocardial infarction. Potential mechanisms and early predictors. Circulation. 1993;87(3):755-763.

[32]

Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation. 1990;81(4):1161-1172.

[33]

Feng Y, Hemmeryckx B, Frederix L, et al. Monitoring reperfused myocardial infarction with delayed left ventricular systolic dysfunction in rabbits by longitudinal imaging. Quant Imaging Med Surg. 2018;8(8):754-769.

[34]

Angeli FS, Shapiro M, Amabile N, et al. Left ventricular remodeling after myocardial infarction: characterization of a swine model on beta-blocker therapy. Comp Med. 2009;59(3):272-279.

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2024 The Author(s). Animal Models and Experimental Medicine published by John Wiley & Sons Australia, Ltd on behalf of The Chinese Association for Laboratory Animal Sciences.

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