Differential regulation of MMP-2, TIMP-2 and IL-6 in valve replacement versus CABG patients

Perfusion ◽  
2002 ◽  
Vol 17 (6) ◽  
pp. 435-439 ◽  
Author(s):  
Masazumi Watanabe ◽  
Satoru Hasegawa ◽  
Nagahisa Ohshima ◽  
Hiroyuki Tanaka ◽  
Tohru Sakamoto ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Matrix Metalloproteinase ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Arterial Blood ◽  
Aortic Replacement ◽  
Lv Mass ◽  
Lv Remodeling ◽  
Baseline Levels ◽  
Cabg Patients

Background: Extracellular matrix degradation may play an important role in left ventricular (LV) remodeling. It has been reported that matrix metalloproteinase-2 (MMP-2) is activated under mechanical stress conditions. Therefore, we examined the release of MMP-2, its inhibitor and interleukin-6 (IL-6), which affects MMPs, in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). Methods: Arterial blood samples were obtained from 20 patients undergoing cardiac surgery and six patients with descending aortic replacement (as noncardiac control) with CPB. Samples were assayed for plasma MMP-2, tissue inhibitors of matrix metalloproteinase-2 (TIMP-2) and IL-6 concentration. Results: Plasma MMP-2 concentrations in the valvular disease patients were greater than in other patients ( p < 0.05) and correlated with the LV mass (r= 0.810, p < 0.0001) prior to the operation. Plasma MMP-2 concentrations decreased during CPB and gradually recovered to the baseline levels after CPB. Plasma TIMP-2 concentrations increased significantly during and after CPB in a biphasic manner. Plasma IL-6 concentrations also increased significantly during CPB ( p < 0.05 versus baseline levels). Conclusion: Plasma MMP-2 concentrations reflect the state of the left ventricle, and changes in plasma MMP-2 and TIMP-2 concentrations during CPB may play an important role in LV remodeling after cardiac surgery.

Selective spatiotemporal induction of matrix metalloproteinase-2 and matrix metalloproteinase-9 transcription after myocardial infarction

2006 ◽  
Vol 291 (5) ◽  
pp. H2216-H2228 ◽  
Author(s):  
Rupak Mukherjee ◽  
Joseph T. Mingoia ◽  
James A. Bruce ◽  
Jeffrey S. Austin ◽  
Robert E. Stroud ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Matrix Metalloproteinase ◽  
Spatial Relation ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Dependent Manner ◽  
Gene Promoters ◽  
Promoter Activation ◽  
Reporter Mice ◽  
Lv Remodeling

Myocardial remodeling after myocardial infarction (MI) is associated with increased levels of the matrix metalloproteinases (MMPs). Levels of two MMP species, MMP-2 and MMP-9, are increased after MI, and transgenic deletion of these MMPs attenuates post-MI left ventricular (LV) remodeling. This study characterized the spatiotemporal patterns of gene promoter induction for MMP-2 and MMP-9 after MI. MI was induced in transgenic mice in which the MMP-2 or MMP-9 promoter sequence was fused to the β-galactosidase reporter, and reporter level was assayed up to 28 days after MI. Myocardial localization with respect to cellular sources of MMP-2 and MMP-9 promoter induction was examined. After MI, LV diameter increased by 70% ( P < 0.05), consistent with LV remodeling. β-Galactosidase staining in MMP-2 reporter mice was increased by 1 day after MI and increased further to 64 ± 6% of LV epicardial area by 7 days after MI ( P < 0.05). MMP-2 promoter activation occurred in fibroblasts and myofibroblasts in the MI region. In MMP-9 reporter mice, promoter induction was detected after 3 days and peaked at 7 days after MI (53 ± 6%, P < 0.05) and was colocalized with inflammatory cells at the peri-infarct region. Although MMP-2 promoter activation was similarly distributed in the MI and border regions, activation of the MMP-9 promoter was highest at the border between the MI and remote regions. These unique findings visually demonstrated that activation of the MMP-2 and MMP-9 gene promoters occurs in a distinct spatial relation with reference to the MI region and changes in a characteristic time-dependent manner after MI.

Targeted deletion of MMP-2 attenuates early LV rupture and late remodeling after experimental myocardial infarction

2003 ◽  
Vol 285 (3) ◽  
pp. H1229-H1235 ◽  
Author(s):  
Shunji Hayashidani ◽  
Hiroyuki Tsutsui ◽  
Masaki Ikeuchi ◽  
Tetsuya Shiomi ◽  
Hidenori Matsusaka ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Left Ventricular ◽  
Experimental Myocardial Infarction ◽  
Matrix Metalloproteinase 2 ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Targeted Deletion ◽  
Arterial Blood ◽  
Lv Remodeling

Matrix metalloproteinase-2 (MMP-2) is prominently overexpressed both after myocardial infarction (MI) and in heart failure. However, its pathophysiological significance in these conditions is still unclear. We thus examined the effects of targeted deletion of MMP-2 on post-MI left ventricular (LV) remodeling and failure. Anterior MI was produced in 10- to 12-wk-old male MMP-2 knockout (KO) and sibling wild-type (WT) mice by ligating the left coronary artery. By day 28, MI resulted in a significant increase in mortality in association with LV cavity dilatation and dysfunction. The MMP-2 KO mice had a significantly better survival rate than WT mice (56% vs. 85%, P < 0.05), despite a comparable infarct size (50 ± 3% vs. 51 ± 3%, P = not significant), heart rate, and arterial blood pressure. The KO mice had a significantly lower incidence of LV rupture (10% vs. 39%, P < 0.05), which occurred within 7 days of MI. The KO mice exerted less LV cavity dilatation and improved fractional shortening after MI by echocardiography. The LV zymographic MMP-2 level significantly increased in WT mice after coronary artery ligation; however, this was completely prevented in KO mice. In contrast, the increase in the LV zymographic MMP-9 level after MI was similar between KO and WT mice. MMP-2 activation is therefore considered to contribute to an early cardiac rupture as well as late LV remodeling after MI. The inhibition of MMP-2 activation may therefore be a potentially useful therapeutic strategy to manage post-MI hearts.

scholarly journals Association arterial stiffness reduction with improved left ventricular longitudinal and torsional deformation after 3 years of antihypertensive treatment

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Tzortzis ◽  
I Ikonomidis ◽  
H Triantafyllidi ◽  
J Thymis ◽  
A Frogoudaki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Ace Inhibitors ◽  
Antihypertensive Treatment ◽  
Left Ventricular ◽  
Torsional Deformation ◽  
Flow Reserve ◽  
Stiffness Reduction ◽  
Arterial Blood ◽  
Lv Mass

Abstract Background We investigated the effects of antihypertensive treatment on vascular function, longitudinal and torsional deformation in hypertensives. Methods In 200 untreated patients with arterial hypertension (age 52.5±11.6 years, 56% females), we measured at baseline and after a 3-year of antihypertensive treatment (160 received ACEi± diuretics and 40 CCBs± diuretics): a) 24h ambulatory blood pressure b) Carotid-femoral pulse wave velocity (PWV) b) Coronary flow reserve (CFR), LV mass index (LVMI), the global longitudinal strain (GLS) and diastolic (LongSRSE) strain rate, peak twisting (Tw-deg) and untwisting at mitral valve opening (UtwMVO), at peak E (UtwE) and at the end of the E wave (UtwendE) of the mitral inflow as well as twisting (TwVel-deg/sec) velocity using speckle tracking imaging. We calculated the % change of LV untwisting as difference between peakTw and UtwMVO, UtwpeakE and UtwendE. Results Compared to baseline, there was an improvement of GLS (−19.9±3.4 vs. −18.7±3.1%), LongSRS (−1.08±0.22 vs. −0.98±0.26 1/s), LongSRE (1.09±0.36 vs. 0.99±0.31 1/s), peak Tw (16.2±5.1 vs. 18.7±5.9 deg), Tw velocity, and the %LV untwisting (31.04±19.28 vs 26.02±15.69% at MVO, 60.04±19.78 vs 53.96±19.76% at peakE and 79.98±14.24 vs 75.90±17.01% at endE) post-treatment. In parallel, CFR (2.72±0.61 vs. 2.55±0.64), PWV (10.34±1.93 vs. 11.2±2.08 m/s) and LVMI were improved (p&lt;0.01 for all comparisons). By ANOVA, the interaction term between changes of all the above parameters and antihypertensive treatment (ACE inhibitors vs calcium channel blockers) was not significant (p&gt;0.05). By multivariate analysis, the reduction of 24h meanBP and PWV independently determined the respective improvement of GLS (b=0.478 and b=0.248 respectively), LongS (b=0.428 and b=0.201 respectively) as well as Twisting (b=0.449 and b=0.294 respectively) after adjusting for changes in LV mass, CFR and atherosclerotic risk factors (p&lt;0.05). Conclusions Long-term optimal blood pressure control with ACE inhibitors and CCBs improves LV longitudinal and torsional mechanics in hypertensives in parallel with arterial stiffness and blood pressure. This improvement in LV deformation and twisting was independently related to changes in arterial blood pressure and arterial stiffness. Funding Acknowledgement Type of funding source: None

scholarly journals Cardiac Troponin T Concentrations, Reversible Myocardial Ischemia, and Indices of Left Ventricular Remodeling in Patients with Suspected Stable Angina Pectoris: a DOPPLER-CIP Substudy

2018 ◽  
Vol 64 (9) ◽  
pp. 1370-1379 ◽  
Author(s):  
Peder L Myhre ◽  
Torbjørn Omland ◽  
Sebastian I Sarvari ◽  
Heikki Ukkonen ◽  
Frank Rademakers ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Wall Motion ◽  
Troponin T ◽  
Left Ventricular ◽  
Reference Limit ◽  
Lv Mass ◽  
Lv Remodeling ◽  
Perfusion Defects ◽  
Stable Cad ◽  
Upper Reference Limit

Abstract BACKGROUND Cardiac troponin T concentrations measured with high-sensitivity assays (hs-cTnT) provide important prognostic information for patients with stable coronary artery disease (CAD). However, whether hs-cTnT concentrations mainly reflect left ventricular (LV) remodeling or recurrent myocardial ischemia in this population is not known. METHODS We measured hs-cTnT concentrations in 619 subjects with suspected stable CAD in a prospectively designed multicenter study. We identified associations with indices of LV remodeling, as assessed by cardiac MRI and echocardiography, and evidence of myocardial ischemia diagnosed by single positron emission computed tomography. RESULTS Median hs-cTnT concentration was 7.8 ng/L (interquartile range, 4.8–11.6 ng/L), and 111 patients (18%) had hs-cTnT concentrations above the upper reference limit (&gt;14 ng/L). Patients with hs-cTnT &gt;14 ng/L had increased LV mass (144 ± 40 g vs 116 ± 34 g; P &lt; 0.001) and volume (179 ± 80 mL vs 158 ± 44 mL; P = 0.006), lower LV ejection fraction (LVEF) (59 ± 14 vs 62 ± 11; P = 0.006) and global longitudinal strain (14.1 ± 3.4% vs 16.9 ± 3.2%; P &lt; 0.001), and more reversible perfusion defects (P = 0.001) and reversible wall motion abnormalities (P = 0.008). Age (P = 0.009), estimated glomerular filtration rate (P = 0.01), LV mass (P = 0.003), LVEF (P = 0.03), and evidence of reversible myocardial ischemia (P = 0.004 for perfusion defects and P = 0.02 for LV wall motion) were all associated with increasing hs-cTnT concentrations in multivariate analysis. We found analogous results when using the revised US upper reference limit of 19 ng/L. CONCLUSIONS hs-cTnT concentrations reflect both LV mass and reversible myocardial ischemia in patients with suspected stable CAD.

scholarly journals Hesperidin Prevents Nitric Oxide Deficiency-Induced Cardiovascular Remodeling in Rats via Suppressing TGF-β1 and MMPs Protein Expression

2018 ◽  
Author(s):  
Putcharawipa Maneesai ◽  
Sarawoot Bunbupha ◽  
Prapassorn Potue ◽  
Thewarid Berkban ◽  
Upa Kukongviriyapan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Wall Thickness ◽  
Tumor Necrosis ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Cardiovascular Remodeling ◽  
Necrosis Factor

Hesperidin is a major flavonoid isolated from citrus fruits that exhibits several biological activities. This study aims to evaluate the effect of hesperidin on cardiovascular remodeling induced by N-nitro L-arginine methyl ester (L-NAME) in rats.&nbsp; Male Sprague-Dawley rats were treated with L-NAME (40 mg/kg); L-NAME plus hesperidin (15 mg/kg), or hesperidin (30 mg/kg), or captopril (2.5 mg/kg) for five weeks (n = 8/group). Hesperidin or captopril significantly prevented the development of hypertension in L-NAME rats.&nbsp; Moreover, hesperidin or captopril alleviated L-NAME-induced cardiac remodeling; increases in wall thickness, cross sectional area (CSA) and fibrosis of left ventricular (LV), and vascular remodeling; increases in wall thickness, CSA, vascular smooth muscle cells and collagen deposition in the aorta. These were associated with reduced oxidative stress markers, tumor necrosis factor-alpha (TNF-&alpha;), transforming growth factor-beta 1 (TGF-&beta;1) and enhancing plasma nitric oxide metabolite (NOx) in L-NAME treated groups. Furthermore, up-regulation of tumor necrosis factor receptor type 1 (TNF-R1) and TGF-&beta;1 protein expression and the over-expression of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) were suppressed in L-NAME rats treated with hesperidin or captopril. These data suggested that hesperidin had cardioprotective effects in L-NAME hypertensive rats. The possible mechanism may involve its antioxidant and anti-inflammatory effects.

scholarly journals Dissociation between cardiomyocyte function and remodeling with β-adrenergic receptor blockade in isolated canine mitral regurgitation

2008 ◽  
Vol 295 (6) ◽  
pp. H2321-H2327 ◽  
Author(s):  
Betty Pat ◽  
Cheryl Killingsworth ◽  
Thomas Denney ◽  
Junying Zheng ◽  
Pamela Powell ◽  
...  
Keyword(s):  
Mitral Regurgitation ◽  
Adrenergic Receptor ◽  
Volume Overload ◽  
Left Ventricular ◽  
Ultrastructural Changes ◽  
Receptor Blockade ◽  
Lv Mass ◽  
Lv Remodeling ◽  
Fractional Shortening ◽  
Adrenergic Receptor Blockade

The low-pressure volume overload of isolated mitral regurgitation (MR) is associated with increased adrenergic drive, left ventricular (LV) dilatation, and loss of interstitial collagen. We tested the hypothesis that β1-adrenergic receptor blockade (β1-RB) would attenuate LV remodeling after 4 mo of MR in the dog. β1-RB did not attenuate collagen loss or the increase in LV mass in MR dogs. Using MRI and three-dimensional (3-D) analysis, there was a 70% increase in the LV end-diastolic (LVED) volume-to-LV mass ratio, a 23% decrease in LVED midwall circumferential curvature, and a >50% increase in LVED 3-D radius/wall thickness in MR dogs that was not attenuated by β1-RB. However, β1-RB caused a significant increase in LVED length from the base to apex compared with untreated MR dogs. This was associated with an increase in isolated cardiomyocyte length (171 ± 5 μm, P < 0.05) compared with normal (156 ± 3 μm) and MR (165 ± 4 μm) dogs. Isolated cardiomyocyte fractional shortening was significantly depressed in MR dogs compared with normal dogs (3.73 ± 0.31 vs. 5.02 ± 0.26%, P < 0.05) and normalized with β1-RB (4.73 ± 0.48%). In addition, stimulation with the β-adrenergic receptor agonist isoproterenol (25 nM) increased cardiomyocyte fractional shortening by 215% ( P < 0.05) in β1-RB dogs compared with normal (56%) and MR (50%) dogs. In summary, β1-RB improved LV cardiomyocyte function and β-adrenergic receptor responsiveness despite further cell elongation. The failure to attenuate LV remodeling associated with MR could be due to a failure to improve ultrastructural changes in extracellular matrix organization.

scholarly journals Inhibition of class I histone deacetylase activity represses matrix metalloproteinase-2 and -9 expression and preserves LV function postmyocardial infarction

2015 ◽  
Vol 308 (11) ◽  
pp. H1391-H1401 ◽  
Author(s):  
Santhosh K. Mani ◽  
Christine B. Kern ◽  
Denise Kimbrough ◽  
Benjamin Addy ◽  
Harinath Kasiganesan ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Hdac Inhibitor ◽  
Histone Deacetylases ◽  
Left Ventricular ◽  
Class I ◽  
Matrix Metalloproteinase 2 ◽  
Lv Function ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Lv Remodeling

Left ventricular (LV) remodeling, after myocardial infarction (MI), can result in LV dilation and LV pump dysfunction. Post-MI induction of matrix metalloproteinases (MMPs), particularly MMP-2 and MMP-9, have been implicated as causing deleterious effects on LV and extracellular matrix remodeling in the MI region and within the initially unaffected remote zone. Histone deacetylases (HDACs) are a class of enzymes that affect the transcriptional regulation of genes during pathological conditions. We assessed the efficacy of both class I/IIb- and class I-selective HDAC inhibitors on MMP-2 and MMP-9 abundance and determined if treatment resulted in the attenuation of adverse LV and extracellular matrix remodeling and improved LV pump function post-MI. MI was surgically induced in MMP-9 promoter reporter mice and randomized for treatment with a class I/IIb HDAC inhibitor for 7 days post-MI. After MI, LV dilation, LV pump dysfunction, and activation of the MMP-9 gene promoter were significantly attenuated in mice treated with either the class I/IIb HDAC inhibitor tichostatin A or suberanilohydroxamic acid (voronistat) compared with MI-only mice. Immunohistological staining and zymographic levels of MMP-2 and MMP-9 were reduced with either tichostatin A or suberanilohydroxamic acid treatment. Class I HDAC activity was dramatically increased post-MI. Treatment with the selective class I HDAC inhibitor PD-106 reduced post-MI levels of both MMP-2 and MMP-9 and attenuated LV dilation and LV pump dysfunction post-MI, similar to class I/IIb HDAC inhibition. Taken together, these unique findings demonstrate that selective inhibition of class I HDACs may provide a novel therapeutic means to attenuate adverse LV remodeling post-MI.

scholarly journals Left Ventricular Mass Index Is Associated With Cognitive Function in Middle-Age

2020 ◽  
Vol 13 (8) ◽  
Author(s):  
Alexander C. Razavi, ◽  
Camilo Fernandez ◽  
Jiang He ◽  
Tanika N. Kelly ◽  
Marie Krousel-Wood ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Cognitive Function ◽  
Systolic Blood Pressure ◽  
Middle Age ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Left Ventricular ◽  
Lv Mass ◽  
Lv Remodeling

Background: Elevated cardiovascular disease risk factor burden is a recognized contributor to poorer cognitive function; however, the physiological mechanisms underlying this association are not well understood. We sought to assess the potential mediation effect of left ventricular (LV) remodeling on the association between lifetime systolic blood pressure and cognitive function in a community-based cohort of middle-aged adults. Methods: Nine hundred sixty participants of the Bogalusa Heart Study (59.2% women, 33.8% black, aged 48.4±5.1 years) received 2-dimensional echocardiography to quantify relative wall thickness, LV mass, and diastolic and systolic LV function; and a standardized neurocognitive battery to assess memory, executive functioning, and language processing. Multivariable linear regression assessed the association of cardiac structure and function with a global composite cognitive function score, adjusting for traditional cardiovascular disease risk factors. Mediation analysis assessed the effect of LV mass index on the association between lifetime systolic blood pressure burden and cognitive function. Results: There were 233 (24.3%) and 136 (14.2%) individuals with concentric LV remodeling and concentric LV hypertrophy, respectively. Each g/m 2.7 increment in LV mass index was associated with a 0.03 standardized unit decrement in global cognitive function ( P =0.03). Individuals with concentric LV remodeling and isolated diastolic dysfunction had the poorest cognitive function, and a greater ratio between early mitral inflow velocity and early diastolic mitral annular velocity (E/e’) was associated with poorer cognitive function, even after adjustment for LV mass index (B=−0.12; P =0.03). A total of 18.8% of the association between lifetime systolic blood pressure burden and midlife cognitive function was accounted for by LV mass index. Conclusions: Cardiac remodeling partially mediates the association between lifespan systolic blood pressure burden and adult cognition in individuals without dementia or clinical cardiovascular disease. Slowing or reversing the progression of cardiac remodeling in middle-age may be a novel therapeutic approach to prevent cognitive decline.

scholarly journals Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction

2007 ◽  
Vol 292 (4) ◽  
pp. H1847-H1860 ◽  
Author(s):  
Marina R. Bergman ◽  
John R. Teerlink ◽  
Rajeev Mahimkar ◽  
Luyi Li ◽  
Bo-Qing Zhu ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Matrix Metalloproteinase ◽  
Ventricular Remodeling ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Membrane Type ◽  
Volume Relation

Although enhanced cardiac matrix metalloproteinase (MMP)-2 synthesis has been associated with ventricular remodeling and failure, whether MMP-2 expression is a direct mediator of this process is unknown. We generated transgenic mice expressing active MMP-2 driven by the α-myosin heavy chain promoter. At 4 mo MMP-2 transgenic hearts demonstrated expression of the MMP-2 transgene, myocyte hypertrophy, breakdown of Z-band registration, lysis of myofilaments, disruption of sarcomere and mitochondrial architecture, and cardiac fibroblast proliferation. Hearts from 8-mo-old transgenic mice displayed extensive myocyte disorganization and dropout with replacement fibrosis and perivascular fibrosis. Older transgenic mice also exhibited a massive increase in cardiac MMP-2 expression, representing recruitment of endogenous MMP-2 synthesis, with associated expression of MMP-9 and membrane type 1 MMP. Increases in diastolic [control (C) 33 ± 3 vs. MMP 51 ± 12 μl; P = 0.003] and systolic (C 7 ± 2 vs. MMP 28 ± 14 μl; P = 0.003) left ventricular (LV) volumes and relatively preserved stroke volume (C 26 ± 4 vs. MMP 23 ± 3 μl; P = 0.16) resulted in markedly decreased LV ejection fraction (C 78 ± 7% vs. MMP 48 ± 16%; P = 0.0006). Markedly impaired systolic function in the MMP transgenic mice was demonstrated in the reduced preload-adjusted maximal power (C 240 ± 84 vs. MMP 78 ± 49 mW/μl2; P = 0.0003) and decreased end-systolic pressure-volume relation (C 7.5 ± 1.5 vs. MMP 4.7 ± 2.0; P = 0.016). Expression of active MMP-2 is sufficient to induce severe ventricular remodeling and systolic dysfunction in the absence of superimposed injury.

Serial magnetic resonance imaging based assessment of the early effects of an ACE inhibitor on postinfarction left ventricular remodeling in rats

2005 ◽  
Vol 83 (12) ◽  
pp. 1109-1115 ◽  
Author(s):  
Fabrice Prunier ◽  
Laurent Marescaux ◽  
Florence Franconi ◽  
Alain Thia ◽  
Pierre Legras ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Experimental Studies ◽  
Left Ventricular ◽  
7 Tesla ◽  
Sham Operation ◽  
Resonance Imaging ◽  
Serial Magnetic Resonance Imaging ◽  
Lv Mass ◽  
Lv Remodeling

In vivo assessment of treatment efficacy on postinfarct left ventricular (LV) remodeling is crucial for experimental studies. We examined the technical feasibility of serial magnetic resonance imaging (MRI) for monitoring early postinfarct remodeling in rats. MRI studies were performed with a 7-Tesla unit, 1, 3, 8, 15, and 30 days after myocardial infarction (MI) or sham operation, to measure LV mass, volume, and the ejection fraction (EF). Three groups of animals were analyzed: sham-operated rats (n = 6), MI rats receiving lisinopril (n = 11), and MI rats receiving placebo (n = 8). LV dilation occurred on day 3 in both MI groups. LV end-systolic and end-diastolic volumes were significantly lower in lisinopril-treated rats than in placebo-treated rats at days 15 and 30. EF was lower in both MI groups than in the sham group at all time points, and did not differ between the MI groups during follow-up. Less LV hypertrophy was observed in rats receiving lisinopril than in rats receiving placebo at days 15 and 30. We found acceptable within- and between-observer agreement and an excellent correlation between MRI and ex vivo LV mass (r = 0.96; p < 0.001). We demonstrated the ability of MRI to detect the early beneficial impact of angiotensin-converting enzyme (ACE) inhibitors on LV remodeling. Accurate and noninvasive, MRI is the tool of choice to document response to treatment targeting postinfarction LV remodeling in rats.

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