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For:	Tennant R, Wiggers CJ. THE EFFECT OF CORONARY OCCLUSION ON MYOCARDIAL CONTRACTION. ACTA ACUST UNITED AC 1935. [DOI: 10.1152/ajplegacy.1935.112.2.351] [Citation(s) in RCA: 883] [Impact Index Per Article: 9.8] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]

Number

Cited by Other Article(s)

Ambrose JA, Albayati A. Takotsubo - The great pretender. Int J Cardiol 2025;434:133369. [PMID: 40360067 DOI: 10.1016/j.ijcard.2025.133369] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/03/2025] [Accepted: 05/09/2025] [Indexed: 05/15/2025]

Tonet E, Boccadoro A, Berloni ML, Amantea V, Grazzi G, Mazzoni G, Zagnoni S, Raisi A, Canovi L, Vitali F, Pavasini R, Scala A, Matese C, Guidi Colombi G, De Pietri M, Chiaranda G, Campo G. Effect of physical activity on left ventricular dimensions and function after myocardial infarction: a systematic review. Minerva Cardiol Angiol 2025;73:238-244. [PMID: 37870422 DOI: 10.23736/s2724-5683.23.06356-1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/24/2023]

Tomić S, Veljković S, Šljivo A, Radoičić D, Lončar G, Bojić M. Differentiating Apical and Basal Left Ventricular Aneurysms Using Sphericity Index: A Clinical Study. MEDICINA (KAUNAS, LITHUANIA) 2025;61:68. [PMID: 39859050 PMCID: PMC11766783 DOI: 10.3390/medicina61010068] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 11/30/2024] [Revised: 12/20/2024] [Accepted: 12/27/2024] [Indexed: 01/27/2025]

Abstract

Background and Objectives: Left ventricular aneurysm (LVA) causes geometric changes, including reduced systolic function and a more spherical shape, which is quantified by the sphericity index (SI), the ratio of the short to long axis in the apical four-chamber view. This study aimed to assess SI's value in A-LVA and B-LVA, identify influencing factors, and evaluate its clinical relevance. Materials and Methods: This clinical study included 54 patients with post-infarction LVA and used echocardiography to determine LVA locations (A-LVA near the apex and B-LVA in the basal segments), with SI and other echocardiographic measures assessed in both systole and diastole for the entire cohort and stratified by A-LVA and B-LVA groups. Results: Among the 54 patients, 41 had A-LVA and 13 had B-LVA. The mean SI was 0.55 in diastole and 0.47 in systole for the cohort. Patients with A-LVA had a mean SI of 0.51 in diastole and 0.44 in systole, while B-LVA patients exhibited significantly higher SI values, with 0.65 in diastole and 0.57 in systole, due to lower long-axis (L) values in both phases. The mean left ventricular ejection fraction (EF) was 23.95% in A-LVA and 30.85% in B-LVA, with no significant difference. However, apical aneurysms were larger (greater LVAV and LVAA) and more significantly reduced functional myocardium. LVEDV, LVESV, LVEDA, and LVESA did not differ significantly between A-LVA and B-LVA. In cases of severe mitral regurgitation (MR), SI was notably higher (0.75 in diastole) due to a marked reduction in the L axis. Conclusions: SI is key in differentiating A-LVA and B-LVA on echocardiography. B-LVA has lower volume and area values, but similar aneurysm and left ventricular volumes and EF. Higher SI in B-LVA is due to a reduced L-axis, and is worsened by severe mitral regurgitation (MR). Surgical ventricular reconstruction (SVR) compensates for L-axis reduction, with preservation of the L axis critical for achieving a more physiological shape. SI thus serves as a marker for left ventricular geometry and surgical outcomes.

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Fan L, Wang H, Kassab GS, Lee LC. Review of cardiac-coronary interaction and insights from mathematical modeling. WIREs Mech Dis 2024;16:e1642. [PMID: 38316634 PMCID: PMC11081852 DOI: 10.1002/wsbm.1642] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/13/2023] [Revised: 12/10/2023] [Accepted: 01/08/2024] [Indexed: 02/07/2024]

Halvorsrød MI, Thorstensen A, Kiss G, Støylen A. Segmental myocardial viability by echocardiography at rest. SCAND CARDIOVASC J 2023;57:2181390. [PMID: 38095169 DOI: 10.1080/14017431.2023.2181390] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/21/2022] [Accepted: 02/12/2023] [Indexed: 02/24/2023]

Lazăr MA, Ionac I, Luca CT, Petrescu L, Vacarescu C, Crisan S, Gaiță D, Cozma D, Sosdean R, Arnăutu DA, Cozlac AR, Luca SA, Gurgu A, Totorean C, Mornos C. Reduced Left Ventricular Twist Early after Acute ST-Segment Elevation Myocardial Infarction as a Predictor of Left Ventricular Adverse Remodelling. Diagnostics (Basel) 2023;13:2896. [PMID: 37761263 PMCID: PMC10528752 DOI: 10.3390/diagnostics13182896] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/10/2023] [Revised: 09/04/2023] [Accepted: 09/07/2023] [Indexed: 09/29/2023] Open

Affiliation(s)

Mihai-Andrei Lazăr Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.) Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania; Research Center of the Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania
Ioana Ionac Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania;
Constantin-Tudor Luca Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.) Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania; Research Center of the Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania
Lucian Petrescu Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.)
Cristina Vacarescu Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.) Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania; Research Center of the Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania
Simina Crisan Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.) Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania; Research Center of the Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania
Dan Gaiță Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.) Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania; Research Center of the Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania
Dragos Cozma Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.) Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania; Research Center of the Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania
Raluca Sosdean Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.) Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania; Research Center of the Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania
Diana-Aurora Arnăutu Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania;
Alina-Ramona Cozlac Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.)
Slivia-Ana Luca Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.) Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania; Research Center of the Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania
Andra Gurgu Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.)
Claudia Totorean Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.) Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania; Research Center of the Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania
Cristian Mornos Cardiology Department, “Victor Babes” University of Medicine and Pharmacy, 2 Eftimie Murgu Sq., 300041 Timisoara, Romania; (M.-A.L.); (L.P.); (C.V.); (S.C.); (D.G.); (D.C.); (R.S.); (A.-R.C.); (S.-A.L.); (A.G.); (C.T.); (C.M.) Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania; Research Center of the Institute of Cardiovascular Diseases Timisoara, 13A Gheorghe Adam Street, 300310 Timisoara, Romania

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Pearce DP, Nemcek MT, Witzenburg CM. Don't go breakin' my heart: cardioprotective alterations to the mechanical and structural properties of reperfused myocardium during post-infarction inflammation. Biophys Rev 2023;15:329-353. [PMID: 37396449 PMCID: PMC10310682 DOI: 10.1007/s12551-023-01068-3] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/01/2023] [Accepted: 05/21/2023] [Indexed: 07/04/2023] Open

Solhjoo S, Liu T, Sidor A, Lee DI, O'Rourke B, Steenbergen C. Oxidative stress in the mitochondrial matrix underlies ischemia/reperfusion-induced mitochondrial instability. J Biol Chem 2022;299:102780. [PMID: 36496071 PMCID: PMC9852550 DOI: 10.1016/j.jbc.2022.102780] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/26/2022] [Revised: 11/28/2022] [Accepted: 11/30/2022] [Indexed: 12/12/2022] Open

Zhang H, Yu H, Walcott GP, Rogers JM. Ectopic foci do not co-locate with ventricular epicardial stretch during early acute regional ischemia in isolated pig hearts. Physiol Rep 2022;10:e15492. [PMID: 36259098 PMCID: PMC9579492 DOI: 10.14814/phy2.15492] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/27/2022] [Revised: 09/16/2022] [Accepted: 09/27/2022] [Indexed: 11/07/2022] Open

Abstract

Ectopic activation during early acute regional ischemia may initiate fatal reentrant arrhythmias. However, the origin of this ectopy remains poorly understood. Studies suggest that systolic stretch arising from dyskinesia in ischemic tissue may cause ectopic depolarization due to cardiac mechanosensitivity. The aim of this study was to investigate the link between mechanical stretch and ectopic electrical activation during early acute regional ischemia. We used a recently developed optical mapping technique capable of simultaneous imaging of mechanical deformation and electrical activation in isolated hearts. Eight domestic swine hearts were prepared in left ventricular working mode (LVW), in which the left ventricle was loaded and contracting. In an additional eight non-working (NW) hearts, contraction was pharmacologically suppressed with blebbistatin and the left ventricle was not loaded. In both groups, the left anterior descending coronary artery was tied below the first diagonal branch. Positive mechanical stretch (bulging) during systole was observed in the ischemic zones of LVW, but not NW, hearts. During ischemia phase 1a (0-15 min post-occlusion), LVW hearts had more ectopic beats than NW hearts (median: 19, interquartile range: 10-28 vs. median: 2, interquartile range: 1-6; p = 0.02); but the difference during phase 1b (15-60 min post-occlusion) was not significant (median: 27, interquartile range: 22-42 vs. median: 16, interquartile range: 12-31; p = 0.37). Ectopic beats arose preferentially from the ischemic border zone in both groups (p < 0.01). In LVW hearts, local mechanical stretch was only occasionally co-located with ectopic foci (9 of 69 ectopic beats). Despite the higher rate of ectopy observed in LVW hearts during ischemia phase 1a, the ectopic beats generally did not arise by the hypothesized mechanism in which ectopic foci are generated by co-local epicardial mechanical stretch.

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Das SL, Sutherland BP, Lejeune E, Eyckmans J, Chen CS. Mechanical response of cardiac microtissues to acute localized injury. Am J Physiol Heart Circ Physiol 2022;323:H738-H748. [PMID: 36053751 DOI: 10.1152/ajpheart.00305.2022] [Citation(s) in RCA: 20] [Impact Index Per Article: 6.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]

Canty JM. Myocardial Injury, Troponin Release and Cardiomyocyte Death in Brief Ischemia, Failure and Ventricular Remodeling. Am J Physiol Heart Circ Physiol 2022;323:H1-H15. [PMID: 35559722 DOI: 10.1152/ajpheart.00093.2022] [Citation(s) in RCA: 24] [Impact Index Per Article: 8.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]

Limkakeng AT, Rowlette LL, Hatch A, Nixon AB, Ilkayeva O, Corcoran D, Modliszewski J, Griffin SM, Ginsburg GS, Voora D. A precision medicine approach to stress testing using metabolomics and microribonucleic acids. Per Med 2022;19:287-297. [DOI: 10.2217/pme-2021-0021] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/21/2022]

OUP accepted manuscript. Eur Heart J Cardiovasc Imaging 2022;23:496-497. [DOI: 10.1093/ehjci/jeac005] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/14/2022] Open

Wu D, Kampmann E, Qian G. Novel Insights Into the Role of Mitochondria-Derived Peptides in Myocardial Infarction. Front Physiol 2021;12:750177. [PMID: 34777013 PMCID: PMC8582487 DOI: 10.3389/fphys.2021.750177] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/30/2021] [Accepted: 09/28/2021] [Indexed: 01/02/2023] Open

Voigt JU. Shapes or numbers? Eur Heart J Cardiovasc Imaging 2021;22:866-867. [PMID: 34051080 DOI: 10.1093/ehjci/jeab093] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/13/2022] Open

Brainin P. Myocardial Postsystolic Shortening and Early Systolic Lengthening: Current Status and Future Directions. Diagnostics (Basel) 2021;11:diagnostics11081428. [PMID: 34441362 PMCID: PMC8393947 DOI: 10.3390/diagnostics11081428] [Citation(s) in RCA: 14] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/30/2021] [Revised: 07/26/2021] [Accepted: 08/04/2021] [Indexed: 11/21/2022] Open

Dwyer KD, Coulombe KL. Cardiac mechanostructure: Using mechanics and anisotropy as inspiration for developing epicardial therapies in treating myocardial infarction. Bioact Mater 2021;6:2198-2220. [PMID: 33553810 PMCID: PMC7822956 DOI: 10.1016/j.bioactmat.2020.12.015] [Citation(s) in RCA: 27] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/30/2020] [Revised: 12/18/2020] [Accepted: 12/18/2020] [Indexed: 12/14/2022] Open

Ostovaneh MR, Makkar RR, Ambale-Venkatesh B, Ascheim D, Chakravarty T, Henry TD, Kowalchuk G, Aguirre FV, Kereiakes DJ, Povsic TJ, Schatz R, Traverse JH, Pogoda J, Smith RD, Marbán L, Marbán E, Lima JAC. Effect of cardiosphere-derived cells on segmental myocardial function after myocardial infarction: ALLSTAR randomised clinical trial. Open Heart 2021;8:e001614. [PMID: 34233913 PMCID: PMC8264869 DOI: 10.1136/openhrt-2021-001614] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/04/2021] [Accepted: 06/01/2021] [Indexed: 02/07/2023] Open

Brainin P, Lindberg S, Olsen FJ, Pedersen S, Iversen A, Galatius S, Fritz-Hansen T, Gislason G, Søgaard P, Møgelvang R, Biering-Sørensen T. Early systolic lengthening by speckle tracking echocardiography predicts outcome after coronary artery bypass surgery. IJC HEART & VASCULATURE 2021;34:100799. [PMID: 34124339 PMCID: PMC8175274 DOI: 10.1016/j.ijcha.2021.100799] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/13/2021] [Accepted: 05/14/2021] [Indexed: 12/12/2022]

Zhang X, Shao C, Cheng S, Zhu Y, Liang B, Gu N. Effect of Guanxin V in animal model of acute myocardial infarction. BMC Complement Med Ther 2021;21:72. [PMID: 33618704 PMCID: PMC7898759 DOI: 10.1186/s12906-021-03211-7] [Citation(s) in RCA: 19] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/21/2020] [Accepted: 01/10/2021] [Indexed: 12/18/2022] Open

Ferraro E, Pozhidaeva L, Pitcher DS, Mansfield C, Koh JHB, Williamson C, Aslanidi O, Gorelik J, Ng FS. Prolonged ursodeoxycholic acid administration reduces acute ischaemia-induced arrhythmias in adult rat hearts. Sci Rep 2020;10:15284. [PMID: 32943714 PMCID: PMC7499428 DOI: 10.1038/s41598-020-72016-4] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/09/2020] [Accepted: 08/07/2020] [Indexed: 12/13/2022] Open

ATP- and voltage-dependent electro-metabolic signaling regulates blood flow in heart. Proc Natl Acad Sci U S A 2020;117:7461-7470. [PMID: 32170008 DOI: 10.1073/pnas.1922095117] [Citation(s) in RCA: 40] [Impact Index Per Article: 8.0] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/20/2022] Open

Dehkordi P, Bauer EP, Tavakolian K, Zakeri V, Blaber AP, Khosrow-Khavar F. Identifying Patients With Coronary Artery Disease Using Rest and Exercise Seismocardiography. Front Physiol 2019;10:1211. [PMID: 31607951 PMCID: PMC6771305 DOI: 10.3389/fphys.2019.01211] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/16/2019] [Accepted: 09/05/2019] [Indexed: 11/26/2022] Open

Benz DC, Giannopoulos AA. Do we really need to look at volumetric measurements with ^99mTc single photon emission computed tomography (SPECT) myocardial perfusion imaging? J Nucl Cardiol 2019;26:1717-1719. [PMID: 29589207 DOI: 10.1007/s12350-018-1263-2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/19/2018] [Accepted: 03/19/2018] [Indexed: 10/17/2022]

Nemavhola F. Detailed structural assessment of healthy interventricular septum in the presence of remodeling infarct in the free wall - A finite element model. Heliyon 2019;5:e01841. [PMID: 31198871 PMCID: PMC6556880 DOI: 10.1016/j.heliyon.2019.e01841] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/10/2019] [Revised: 04/09/2019] [Accepted: 05/24/2019] [Indexed: 11/28/2022] Open

Limkakeng Jr AT, Leahy JC, Griffin SM, Lokhnygina Y, Jaffa E, Christenson RH, Newby LK. Provocative biomarker stress test: stress-delta N-terminal pro-B type natriuretic peptide. Open Heart 2018;5:e000847. [PMID: 30364466 PMCID: PMC6196976 DOI: 10.1136/openhrt-2018-000847] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/09/2018] [Revised: 07/30/2018] [Accepted: 08/31/2018] [Indexed: 11/04/2022] Open

Abstract

Objective

Stress testing is commonly performed in emergency department (ED) patients with suspected acute coronary syndrome (ACS). We hypothesised that changes in N-terminal pro-B type natriuretic peptide (NT-proBNP) concentrations from baseline to post-stress testing (stress-delta values) differentiate patients with ischaemic stress tests from controls.

Methods

We prospectively enrolled 320 adult patients with suspected ACS in an ED-based observation unit who were undergoing exercise stress echocardiography. We measured plasma NT-proBNP concentrations at baseline and at 2 and 4 hours post-stress and compared stress-delta NT-proBNP between patients with abnormal stress tests versus controls using non-parametric statistics (Wilcoxon test) due to skew. We calculated the diagnostic test characteristics of stress-delta NT-proBNP for myocardial ischaemia on imaging.

Results

Among 320 participants, the median age was 51 (IQR 44-59) years, 147 (45.9%) were men, and 122 (38.1%) were African-American. Twenty-six (8.1%) had myocardial ischaemia. Static and stress-deltas NT-proBNP differed at all time points between groups. The median stress-deltas at 2 hours were 10.4 (IQR 6.0-51.7) ng/L vs 1.7 (IQR -0.4 to 8.7) ng/L, and at 4 hours were 14.8 (IQR 5.0-22.3) ng/L vs 1.0 (-2.0 to 10.3) ng/L for patients with ischaemia versus those without. Areas under the receiver operating curves were 0.716 and 0.719 for 2-hour and 4-hour stress-deltas, respectively. After adjusting for baseline NT-proBNP levels, the 4-hour stress-delta NT-proBNP remained significantly different between the groups (p=0.009).

Conclusion

Among patients with ischaemic stress tests, static and 4-hour stress-delta NT-proBNP values were significantly higher. Further study is needed to determine if stress-delta NT-proBNP is a useful adjunct to stress testing.

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González-Montero J, Brito R, Gajardo AIJ, Rodrigo R. Myocardial reperfusion injury and oxidative stress: Therapeutic opportunities. World J Cardiol 2018;10:74-86. [PMID: 30344955 PMCID: PMC6189069 DOI: 10.4330/wjc.v10.i9.74] [Citation(s) in RCA: 116] [Impact Index Per Article: 16.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/27/2018] [Revised: 04/27/2018] [Accepted: 05/10/2018] [Indexed: 02/06/2023] Open

Abstract

Acute myocardial infarction (AMI) is the leading cause of death worldwide. Its associated mortality, morbidity and complications have significantly decreased with the development of interventional cardiology and percutaneous coronary angioplasty (PCA) treatment, which quickly and effectively restore the blood flow to the area previously subjected to ischemia. Paradoxically, the restoration of blood flow to the ischemic zone leads to a massive production of reactive oxygen species (ROS) which generate rapid and severe damage to biomolecules, generating a phenomenon called myocardial reperfusion injury (MRI). In the clinical setting, MRI is associated with multiple complications such as lethal reperfusion, no-reflow, myocardial stunning, and reperfusion arrhythmias. Despite significant advances in the understanding of the mechanisms accounting for the myocardial ischemia reperfusion injury, it remains an unsolved problem. Although promising results have been obtained in experimental studies (mainly in animal models), these benefits have not been translated into clinical settings. Thus, clinical trials have failed to find benefits from any therapy to prevent MRI. There is major evidence with respect to the contribution of oxidative stress to MRI in cardiovascular diseases. The lack of consistency between basic studies and clinical trials is not solely based on the diversity inherent in epidemiology but is also a result of the methodological weaknesses of some studies. It is quite possible that pharmacological issues, such as doses, active ingredients, bioavailability, routes of administration, co-therapies, startup time of the drug intervention, and its continuity may also have some responsibility for the lack of consistency between different studies. Furthermore, the administration of high ascorbate doses prior to reperfusion appears to be a safe and rational therapy against the development of oxidative damage associated with myocardial reperfusion. In addition, the association with N-acetylcysteine (a glutathione donor) and deferoxamine (an iron chelator) could improve the antioxidant cardioprotection by ascorbate, making it even more effective in preventing myocardial reperfusion damage associated with PCA following AMI.

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Lujan HL, Rivers JP, DiCarlo SE. A single electrical pulse within the protective zone of each cardiac cycle prevented reperfusion-induced ventricular tachycardia in conscious mice. Physiol Rep 2018;6. [PMID: 29380958 PMCID: PMC5789730 DOI: 10.14814/phy2.13578] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/10/2017] [Revised: 12/16/2017] [Accepted: 12/18/2017] [Indexed: 11/24/2022] Open

Abstract

Early pioneering investigators discovered, in anesthetized dogs, a protective period within the cardiac cycle. The protective period was a time within the cardiac cycle when a precisely timed stimulus prevented the initiation of ventricular fibrillation caused by an earlier stimulus. Thus, in addition to the susceptible period of repolarization discussed by Wiggers and Wegria (Am. J. Physiol. 131:296, 1940; Am. J. Physiol. 128:500, 1940), there is also a nearby protective period. This report describes a protective period within the cardiac cycle of conscious mice when a precisely timed stimulus prevented the initiation of ventricular tachycardia caused by an earlier stimulus. In addition, we tested the hypothesis that this precisely timed pulse within the protective period prevents reperfusion‐induced ventricular tachyarrhythmias in conscious mice. Mice (n = 6) were prepared to record arterial blood pressure and the electrocardiogram. In addition, a vascular occluder was placed around the left main coronary artery, and stimulating electrodes were secured onto the left ventricle. A single precisely timed electrical pulse (5 msec pulse width and 2.5 V) to the left ventricle arriving 13.9 ± 1.1 msec after the R‐wave, caused ventricular tachycardia occurring 24.9 ± 0.9 msec after the R‐wave. Importantly, a second precisely timed electrical pulse arriving 18.8 ± 0.5 msec after the first stimulus blocked the induction of ventricular tachycardia caused by the earlier stimulus. On an alternate day, the susceptibility to sustained ventricular tachycardia produced by 3.5 min of occlusion and reperfusion of the coronary artery was determined in conscious mice by use of the vascular occluder. Reperfusion resulted in ventricular tachycardia in all six mice. A precisely timed pulse within the protective period prevented ventricular tachycardia in all mice.

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Intervendor Differences in the Accuracy of Detecting Regional Functional Abnormalities. JACC Cardiovasc Imaging 2018;11:25-34. [DOI: 10.1016/j.jcmg.2017.02.014] [Citation(s) in RCA: 83] [Impact Index Per Article: 11.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/21/2016] [Revised: 01/24/2017] [Accepted: 02/17/2017] [Indexed: 11/19/2022]

Benz DC, Gaemperli O. The right timing for post-ischemic stunning. J Nucl Cardiol 2017;24:1302-1304. [PMID: 27048308 DOI: 10.1007/s12350-016-0473-8] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/08/2016] [Accepted: 03/08/2016] [Indexed: 12/20/2022]

Bhatt AS, Ambrosy AP, Velazquez EJ. Adverse Remodeling and Reverse Remodeling After Myocardial Infarction. Curr Cardiol Rep 2017;19:71. [DOI: 10.1007/s11886-017-0876-4] [Citation(s) in RCA: 97] [Impact Index Per Article: 12.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/24/2023]

Anavekar NS, Chareonthaitawee P, Narula J, Gersh BJ. Revascularization in Patients With Severe Left Ventricular Dysfunction: Is the Assessment of Viability Still Viable? J Am Coll Cardiol 2017;67:2874-87. [PMID: 27311527 DOI: 10.1016/j.jacc.2016.03.571] [Citation(s) in RCA: 38] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/23/2015] [Revised: 02/18/2016] [Accepted: 03/18/2016] [Indexed: 11/17/2022]

Ermis P. Stress echocardiography: An overview for use in pediatric and congenital cardiology. CONGENIT HEART DIS 2017;12:624-626. [PMID: 28580760 DOI: 10.1111/chd.12495] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/11/2017] [Accepted: 05/20/2017] [Indexed: 11/30/2022]

Barrabés JA, Inserte J, Rodríguez-Sinovas A, Ruiz-Meana M, Garcia-Dorado D. Early regional wall distension is strongly associated with vulnerability to ventricular fibrillation but not arrhythmia triggers following coronary occlusion in vivo. PROGRESS IN BIOPHYSICS AND MOLECULAR BIOLOGY 2017;130:387-393. [PMID: 28579517 DOI: 10.1016/j.pbiomolbio.2017.05.012] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Received: 01/30/2017] [Revised: 05/28/2017] [Accepted: 05/29/2017] [Indexed: 10/19/2022]

Ohanyan V, Yin L, Bardakjian R, Kolz C, Enrick M, Hakobyan T, Luli J, Graham K, Khayata M, Logan S, Kmetz J, Chilian WM. Kv1.3 channels facilitate the connection between metabolism and blood flow in the heart. Microcirculation 2017;24:10.1111/micc.12334. [PMID: 28504408 PMCID: PMC5433265 DOI: 10.1111/micc.12334] [Citation(s) in RCA: 17] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/20/2016] [Revised: 10/23/2016] [Accepted: 11/01/2016] [Indexed: 12/17/2022]

Krogh MR, Nghiem GM, Halvorsen PS, Elle OJ, Grymyr OJ, Hoff L, Remme EW. Gravity Compensation Method for Combined Accelerometer and Gyro Sensors Used in Cardiac Motion Measurements. Ann Biomed Eng 2017;45:1292-1304. [DOI: 10.1007/s10439-017-1798-4] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/16/2016] [Accepted: 01/12/2017] [Indexed: 10/20/2022]

Ieva R, Casavecchia G, Gravina M, Totaro A, Ferraretti A, Macarini L, Di Biase M, Brunetti ND. Prolonged QT and myocardium recovery after primary PCI: a cMRI study. Eur J Clin Invest 2016;46:873-9. [PMID: 27566477 DOI: 10.1111/eci.12670] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/24/2016] [Accepted: 08/25/2016] [Indexed: 01/04/2023]

Shanewise JS. How to Reliably Detect Ischemia in the Intensive Care Unit and Operating Room. Semin Cardiothorac Vasc Anesth 2016;10:101-9. [PMID: 16703242 DOI: 10.1177/108925320601000117] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022]

Long-Term Preservation of Left Ventricular Systolic Function in Patients With Refractory Angina Pectoris and Inducible Myocardial Ischemia on Optimal Medical Therapy. Am J Cardiol 2016;117:1558-1561. [PMID: 27055755 DOI: 10.1016/j.amjcard.2016.02.028] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/21/2015] [Revised: 02/23/2016] [Accepted: 02/23/2016] [Indexed: 11/22/2022]

Zheng J, Gropler RJ. Myocardial Hypoxia in Dilated Cardiomyopathy: Is it Just a Matter of Supply and Demand? Circ Heart Fail 2016;8:1011-3. [PMID: 26578667 DOI: 10.1161/circheartfailure.115.002677] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/16/2022]

Clarke SA, Richardson WJ, Holmes JW. Modifying the mechanics of healing infarcts: Is better the enemy of good? J Mol Cell Cardiol 2015;93:115-24. [PMID: 26631496 DOI: 10.1016/j.yjmcc.2015.11.028] [Citation(s) in RCA: 52] [Impact Index Per Article: 5.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/16/2015] [Revised: 11/09/2015] [Accepted: 11/26/2015] [Indexed: 02/06/2023]

Abstract

Myocardial infarction (MI) is a major source of morbidity and mortality worldwide, with over 7 million people suffering infarctions each year. Heart muscle damaged during MI is replaced by a collagenous scar over a period of several weeks, and the mechanical properties of that scar tissue are a key determinant of serious post-MI complications such as infarct rupture, depression of heart function, and progression to heart failure. Thus, there is increasing interest in developing therapies that modify the structure and mechanics of healing infarct scar. Yet most prior attempts at therapeutic scar modification have failed, some catastrophically. This article reviews available information about the mechanics of healing infarct scar and the functional impact of scar mechanical properties, and attempts to infer principles that can better guide future attempts to modify scar. One important conclusion is that collagen structure, mechanics, and remodeling of healing infarct scar vary so widely among experimental models that any novel therapy should be tested across a range of species, infarct locations, and reperfusion protocols. Another lesson from past work is that the biology and mechanics of healing infarcts are sufficiently complex that the effects of interventions are often counterintuitive; for example, increasing infarct stiffness has little effect on heart function, and inhibition of matrix metalloproteases (MMPs) has little effect on scar collagen content. Computational models can help explain such counterintuitive results, and are becoming an increasingly important tool for integrating known information to better identify promising therapies and design experiments to test them. Moving forward, potentially exciting new opportunities for therapeutic modification of infarct mechanics include modulating anisotropy and promoting scar compaction.

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Holmes JW, Laksman Z, Gepstein L. Making better scar: Emerging approaches for modifying mechanical and electrical properties following infarction and ablation. PROGRESS IN BIOPHYSICS AND MOLECULAR BIOLOGY 2015;120:134-48. [PMID: 26615948 DOI: 10.1016/j.pbiomolbio.2015.11.002] [Citation(s) in RCA: 23] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Received: 09/22/2015] [Revised: 11/13/2015] [Accepted: 11/20/2015] [Indexed: 12/31/2022]

Abstract

Following myocardial infarction (MI), damaged myocytes are replaced by collagenous scar tissue, which serves an important mechanical function - maintaining integrity of the heart wall against enormous mechanical forces - but also disrupts electrical function as structural and electrical remodeling in the infarct and borderzone predispose to re-entry and ventricular tachycardia. Novel emerging regenerative approaches aim to replace this scar tissue with viable myocytes. Yet an alternative strategy of therapeutically modifying selected scar properties may also prove important, and in some cases may offer similar benefits with lower risk or regulatory complexity. Here, we review potential goals for such modifications as well as recent proof-of-concept studies employing specific modifications, including gene therapy to locally increase conduction velocity or prolong the refractory period in and around the infarct scar, and modification of scar anisotropy to improve regional mechanics and pump function. Another advantage of scar modification techniques is that they have applications well beyond MI. In particular, ablation treats electrical abnormalities of the heart by intentionally generating scar to block aberrant conduction pathways. Yet in diseases such as atrial fibrillation (AF) where ablation can be extensive, treating the electrical disorder can significantly impair mechanical function. Creating smaller, denser scars that more effectively block conduction, and choosing the location of those lesions by balancing their electrical and mechanical impacts, could significantly improve outcomes for AF patients. We review some recent advances in this area, including the use of computational models to predict the mechanical effects of specific lesion sets and gene therapy for functional ablation. Overall, emerging techniques for modifying scar properties represents a potentially important set of tools for improving patient outcomes across a range of heart diseases, whether used in place of or as an adjunct to regenerative approaches.

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Ohanyan V, Yin L, Bardakjian R, Kolz C, Enrick M, Hakobyan T, Kmetz J, Bratz I, Luli J, Nagane M, Khan N, Hou H, Kuppusamy P, Graham J, Fu FK, Janota D, Oyewumi MO, Logan S, Lindner JR, Chilian WM. Requisite Role of Kv1.5 Channels in Coronary Metabolic Dilation. Circ Res 2015. [PMID: 26224794 DOI: 10.1161/circresaha.115.306642] [Citation(s) in RCA: 73] [Impact Index Per Article: 7.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/10/2023]

Dor V. Remodelado ventricular postinfarto de miocardio. Interés de la resonancia magnética cardíaca para destacar su fisiopatología y la eficacia de la reconstrucción ventricular. CIRUGIA CARDIOVASCULAR 2015. [DOI: 10.1016/j.circv.2014.06.002] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022] Open

Diakos NA, Pozios I, Katsaros L, Vakrou S, Sventzouri S, Michelinakis N, Tseliou E, Bonios M, Malliaras K, Papalois A, Anastasiou-Nana M, Terrovitis JV. Afterload-induced left ventricular diastolic dysfunction during myocardial ischaemia and reperfusion. Exp Physiol 2015;100:288-301. [DOI: 10.1113/expphysiol.2014.082131] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/22/2014] [Accepted: 12/12/2014] [Indexed: 11/08/2022]

Durak I, Kudaiberdieva G, Gorenek B. Prognostic implications of arrhythmias during primary percutaneous coronary interventions for ST-elevation myocardial infraction. Expert Rev Cardiovasc Ther 2014;13:85-94. [DOI: 10.1586/14779072.2015.987127] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/08/2022]

Effects of FX06 in vitro on platelet, coagulation, and fibrinolytic biomarkers in volunteers and patients with documented coronary artery disease. Am J Ther 2014;21:91-8. [PMID: 19770797 DOI: 10.1097/mjt.0b013e3181b0a6ff] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]

Solhjoo S, O'Rourke B. Mitochondrial instability during regional ischemia-reperfusion underlies arrhythmias in monolayers of cardiomyocytes. J Mol Cell Cardiol 2014;78:90-9. [PMID: 25268650 DOI: 10.1016/j.yjmcc.2014.09.024] [Citation(s) in RCA: 27] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/07/2014] [Revised: 09/16/2014] [Accepted: 09/19/2014] [Indexed: 01/05/2023]

Abstract

Regional depolarization of the mitochondrial network can alter cellular electrical excitability and increase the propensity for reentry, in part, through the opening of sarcolemmal KATP channels. Mitochondrial inner membrane potential (ΔΨm) instability or oscillation can be induced in myocytes by exposure to reactive oxygen species (ROS), laser excitation, or glutathione depletion, and is thought to be a major factor in arrhythmogenesis during ischemia-reperfusion. Nevertheless, the correlation between ΔΨm recovery kinetics and reperfusion-induced arrhythmias has been difficult to demonstrate experimentally. Here, we investigate the relationship between subcellular changes in ΔΨm, cellular glutathione redox potential, electrical excitability, and wave propagation during coverslip-induced ischemia-reperfusion (IR) in neonatal rat ventricular myocyte (NRVM) monolayers. Ischemia led to decreased action potential amplitude and duration followed by electrical inexcitability after ~15min of ischemia. ΔΨm depolarization occurred in two phases during ischemia: in phase 1 (<30min ischemia), mitochondrial clusters within individual NRVMs depolarized, while phase 2 ΔΨm depolarization (30-60min) was characterized by global functional collapse of the mitochondrial network across the whole ischemic region of the monolayer, typically involving a propagating metabolic wave. Oxidation of the glutathione (GSSG:GSH) redox potential occurred during ischemia, followed by recovery upon reperfusion (i.e., lifting the coverslip). ΔΨm recovered in the mitochondria of individual myocytes quite rapidly upon reperfusion (<5min), but was highly unstable, characterized by subcellular oscillations or flickering of clusters of mitochondria in NRVMs across the reperfused region. Electrical excitability also recovered in a heterogeneous manner, providing an arrhythmogenic substrate which led to formation of sustained reentry. Treatment with 4'-chlorodiazepam, a peripheral benzodiazepine receptor ligand, prevented ΔΨm oscillation, improved GSH recovery rate, and prevented reentry during reperfusion, indicating that stabilization of mitochondrial network dynamics is important for preventing post-ischemic arrhythmias. This article is part of a Special Issue entitled "Mitochondria: From Basic Mitochondrial Biology to Cardiovascular Disease".

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Tune JD. Coronary Circulation. ACTA ACUST UNITED AC 2014. [DOI: 10.4199/c00111ed1v01y201406isp054] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/23/2022]

Lujan HL, DiCarlo SE. Reperfusion-induced sustained ventricular tachycardia, leading to ventricular fibrillation, in chronically instrumented, intact, conscious mice. Physiol Rep 2014;2:2/6/e12057. [PMID: 24973331 PMCID: PMC4208649 DOI: 10.14814/phy2.12057] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/24/2022] Open

Abstract

Reperfusion‐induced lethal ventricular arrhythmias are observed during relief of coronary artery spasm, with unstable angina, exercise‐induced ischemia, and silent ischemia. Accordingly, significant efforts are underway to understand the mechanisms responsible for reperfusion‐induced lethal arrhythmias and mice have become increasingly important in these efforts. However, although reperfusion‐induced sustained ventricular tachycardia leading to ventricular fibrillation (VF) has been recorded in many models, reports in mice are sparse and of limited success. Importantly, none of these studies were conducted in intact, conscious mice. Accordingly, a chronically instrumented, intact, conscious murine model of reperfusion‐induced lethal arrhythmias has the potential to be of major importance for advancing the concepts and methods that drive cardiovascular therapies. Therefore, we describe, for the first time, the use of an intact, conscious, murine model of reperfusion‐induced lethal arrhythmias. Male mice (n = 9) were instrumented to record cardiac output and the electrocardiogram. In addition, a snare was placed around the left main coronary artery. Following recovery, the susceptibility to sustained ventricular tachycardia produced by 3 min of occlusion and reperfusion of the left main coronary artery was determined in conscious mice by pulling on the snare. Reperfusion culminated in sustained ventricular tachycardia, leading to VF, in all nine conscious mice. The procedures conducted in conscious C57BL/6J mice, a strain commonly used in transgenic studies, can be utilized in genetically modified models to enhance our understanding of single gene defects on reperfusion‐induced lethal ventricular arrhythmias in intact, conscious, and complex animals.

We describe, for the first time, the use of an intact, conscious, murine model of reperfusion‐induced lethal arrhythmias. This model has the potential to be of major importance for advancing the concepts and methods that drive antiarrhythmic therapies.

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