Late preconditioning enhances recovery of myocardial function after infarction in conscious rabbits

2000 ◽  
Vol 279 (5) ◽  
pp. H2372-H2381 ◽  
Author(s):  
Hitoshi Takano ◽  
Xian-Liang Tang ◽  
Eitaro Kodani ◽  
Roberto Bolli
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Left Ventricular ◽  
Nitric Oxide Donor ◽  
Lv Function ◽  
Wall Thickening ◽  
Triphenyltetrazolium Chloride ◽  
Independent Evidence ◽  
Late Preconditioning ◽  
Conscious Rabbits

It is unknown whether late preconditioning (PC) enhances the recovery of left ventricular (LV) function after a myocardial infarction. Thus 25 conscious rabbits were subjected to a 30-min coronary occlusion followed by 28 days of reperfusion after PC 24 h earlier with either ischemia or nitric oxide donor administration [ S-nitroso- N-acetylpenicillamine (SNAP)]. The recovery of wall thickening (WTh) after reperfusion was significantly improved in the ischemic PC and SNAP PC groups compared with controls, both at rest and during dobutamine stress. Interestingly, neither ischemia- nor SNAP-induced late PC attenuated myocardial stunning from day 1 through day 14. Infarct size was smaller in the ischemic PC and SNAP PC groups compared with controls. In all groups, WTh at 28 days was positively and linearly related to the percentage of viable tissue in the region underlying the ultrasonic crystal ( r = 0.90), indicating that the improvement in LV function after both ischemia-induced and NO donor-induced late PC can be fully explained by the reduction in infarct size; a separate effect of late PC on LV remodeling or LV contractility need not be invoked. In conclusion, in conscious rabbits late PC, induced either by ischemia or pharmacologically, not only limits infarct size but also enhances the recovery of LV function after myocardial infarction. This finding has important clinical implications and provides triphenyltetrazolium chloride-independent evidence that late PC limits myocellular death after sustained ischemia.

scholarly journals Acute myocardial infarction in mice: assessment of transmurality by strain rate imaging

2007 ◽  
Vol 293 (1) ◽  
pp. H496-H502 ◽  
Author(s):  
Hélène Thibault ◽  
Ludovic Gomez ◽  
Erwan Donal ◽  
Gerard Pontier ◽  
Marielle Scherrer-Crosbie ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Strain Rate ◽  
Murine Model ◽  
Left Ventricular ◽  
Lv Function ◽  
Blue Dye ◽  
Area At Risk ◽  
Triphenyltetrazolium Chloride ◽  
In Vivo Evaluation ◽  
Strain Rate Imaging

In vivo evaluation of the transmural extension of myocardial infarction (TEI) is crucial to prediction of viability and prognosis. With the rise of transgenic technology, murine myocardial infarction (MI) models are increasingly used. Our study aimed to evaluate systolic strain rate (SR), a new parameter of regional function, to quantify TEI in a murine model of acute MI induced by various durations of ischemia followed by 24 h of reperfusion. Global and regional left ventricular (LV) function were assessed by echocardiography (13 MHz, Vivid 7, GE) in 4 groups of wild-type mice (C57BL/6, 2 mo old): a sham-treated group ( n = 10) and three MI groups [30 ( n = 11), 60 ( n = 10), and 90 ( n = 9) min of left coronary artery occlusion]. Conventional LV dimensions, anterior wall (AW) thickening, and peak systolic SR were measured before and 24 h after reperfusion. Area at risk (AR) was measured by blue dye and infarct size (area of necrosis, AN) and TEI by triphenyltetrazolium chloride staining. AN increased with ischemia duration (25 ± 2%, 56 ± 5%, 71 ± 6% of AR for 30, 60, and 90 min, respectively; P < 0.05). LV end-diastolic volume significantly increased with ischemia duration (30 ± 5, 34 ± 5, 43 ± 5 μl; P < 0.05), whereas LV ejection fraction decreased (63 ± 5%, 58 ± 6%, 46 ± 5%; P < 0.05). AW thickening decrease was not influenced by ischemia duration. Conversely, systolic SR decreased with ischemia duration (13 ± 5, 4 ± 3, −2 ± 6 s−1; P < 0.05) and was significantly correlated with TEI ( r = 0.89, P < 0.01). Receiver operating characteristic (ROC) curves identified systolic SR as the most accurate parameter to predict TEI. In conclusion, in a murine model of MI, SR imaging is superior to conventional echocardiography to predict TEI early after MI.

scholarly journals Single-Point Cardiac Troponin T at Coronary Care Unit Discharge after Myocardial Infarction Correlates with Infarct Size and Ejection Fraction

2002 ◽  
Vol 48 (9) ◽  
pp. 1432-1436 ◽  
Author(s):  
Mauro Panteghini ◽  
Claudio Cuccia ◽  
Graziella Bonetti ◽  
Raffaele Giubbini ◽  
Franca Pagani ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ejection Fraction ◽  
Infarct Size ◽  
Cardiac Troponin ◽  
Coronary Care Unit ◽  
Troponin T ◽  
Left Ventricular ◽  
Lv Function ◽  
Cardiac Troponin T ◽  
Coronary Care

Abstract Background: One of the major concerns in replacing creatine kinase MB (CK-MB) with cardiac troponins is the lack of evidence of the ability of troponins to estimate the size of acute myocardial infarction (AMI). We investigated the ability of a single measurement of cardiac troponin T (cTnT) at coronary care unit (CCU) discharge to estimate infarct size and assess left ventricular (LV) function in AMI patients. Methods: We studied 65 AMI patients in whom infarct size was estimated by CK-MB peak concentrations and gated single-photon emission computed tomography (SPECT) myocardial perfusion using technetium-99m sestamibi and LV function by SPECT imaging. Measurements of cTnT and SPECT were performed 72 h (median) after admission (range, 40–160 h). SPECT was also repeated 3 months later. Results: We found a significant correlation between cTnT and both the peak CK-MB concentrations (r = 0.76; P &lt;0.001) and the perfusion defect size at SPECT (r = 0.62; P &lt;0.001). cTnT was inversely related to LV ejection fraction (LVEF) assessed both early (r = −0.56; P &lt;0.001) and 3 months after AMI (r = −0.70; P &lt;0.001). cTnT &gt;2.98 μg/L predicted a LVEF &lt;40% at 3 months with a sensitivity of 86.7%, specificity of 81.4%, and a likelihood ratio for a positive test of 4.7 (95% confidence interval, 4.0–5.4). Conclusions: A single cTnT measurement at CCU discharge after AMI is useful as a noninvasive estimate of infarct size and for the assessment of LV function in routine clinical setting.

scholarly journals Elastin Stabilizes an Infarct and Preserves Ventricular Function

Circulation ◽  
2005 ◽  
Vol 112 (9_supplement) ◽  
Author(s):  
Tomohiro Mizuno ◽  
Terrence M. Yau ◽  
Richard D. Weisel ◽  
Chris G. Kiani ◽  
Ren-Ke Li
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Infarct Size ◽  
Left Ventricular ◽  
Myocardial Scar ◽  
Elastic Fibers ◽  
Control Group ◽  
Lv Function ◽  
Infarct Region ◽  
Lv Volume

Background— After a myocardial infarction, the injured region becomes fibrotic and the myocardial scar may expand if the ventricular wall lacks elasticity. Cardiac dilatation may precipitate the vicious cycle of progressive heart failure. The present study evaluated the functional benefits of increasing elastin within a myocardial scar using cell based gene therapy. Methods and Results— A myocardial infarction was generated by ligation of the left anterior descending artery in rats. Six days later, 2×10 6 syngeneic rat endothelial cells transfected with the rat elastin gene (elastin group, n=14) or an empty plasmid (control group, n=14) were transplanted into the infarct scar. Cardiac function, left ventricular (LV) volume, and infarct size were monitored over 3 months by echocardiography, Langendorff measurements, and planimetry. Elastin deposition was evaluated in the cells and in the infarct region by Western blot assay and by histological examination. Recombinant elastin was found in the scar in the elastin group but not the control group during the 3 months after cell transplantation. Histological assessment demonstrated organized elastic fibers within the infarct region. LV volume and infarct size were significantly smaller ( P <0.05) in the elastin group than in the control group. Cardiac function evaluated by echocardiography and during Langendorff perfusion was significantly better ( P <0.05) in the elastin group than in the control group. Conclusions— Expressing recombinant elastin within the myocardial scar reduced scar expansion and prevented LV enlargement after a myocardial infarction. Altering matrix remodeling after an infarct preserved the LV function for at least 3 months.

2232Circulating levels of ST2 are associated with myocardial injury, left ventricular function and future adverse clinical events in patients with ST-elevation myocardial infarction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Shetelig ◽  
T Ueland ◽  
S Limalanathan ◽  
P Hoffmann ◽  
P Aukrust ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Clinical Outcome ◽  
Infarct Size ◽  
Left Ventricular ◽  
St Elevation Myocardial Infarction ◽  
Lv Function ◽  
Clinical Events ◽  
Increased Risk ◽  
All Cause Mortality ◽  
St Elevation

Abstract Background Soluble ST2, a member of the IL-1 receptor family, seems to be associated with adverse outcome in acute myocardial infarction and heart failure (HF), and is suggested to be involved in left ventricular (LV) remodelling. Purpose To elucidate a possible role of ST2 in LV injury, remodelling and prognosis in ST-elevation myocardial infarction (STEMI) patients. The main objectives of the study were to investigate whether circulating ST2 levels were associated with infarct size, LV function, adverse remodeling and clinical outcome in a cohort of patients with STEMI. Methods 270 patients with clinically stable first-time STEMI treated with primary percutaneous coronary intervention (PCI) were included. Blood samples were drawn before and immediately after the PCI procedure, at day 1 (median 18.3 hours after PCI) and after 4 months. Cardiac magnetic resonance (CMR) was performed in the acute phase and after 4 months. Clinical events and all-cause mortality were registered during 12 months' and 70 months' follow-up, respectively. A composite endpoint was defined as death, MI, unscheduled revascularisation >3 months after the index infarction, rehospitalisation for HF or stroke. Associations between ST2 and CMR parameters and clinical events were evaluated with linear regression and logistic regression, respectively. Results There was a significant increase in ST2 levels from the PCI procedure to day 1 with a subsequent decline from day 1 to 4 months in the POSTEMI cohort. Patients with high ST2 levels (>median) at all sampling points during hospitalisation had significantly larger infarct size, lower myocardial salvage, lower LVEF, larger increase in EDV and higher frequency of MVO. After adjustment for relevant clinical variables, peak CRP and peak troponin T, ST2 measured at day 1 remained associated with infarct size (β 2.0 per SD of ST2, p<0.001) and LVEF (β −1.8 per SD of ST2, p=0.02) at 4 months. High levels of ST2 measured at day 1 (>75th percentile) were associated with increased risk of having an adverse clinical event during the first year and with long-term all-cause mortality (Figure). High levels of ST2 measured in a stable phase 4 months after STEMI were also associated with an increased risk of all-cause mortality (Figure). Figure 1 Conclusions High levels of ST2 in STEMI patients were associated with large infarct size, impaired recovery of LV function, and adverse clinical outcome in patients with STEMI. ST2 measured 4 months after STEMI remained associated with all-cause mortality.

Measurement of troponin I 48h after admission as a tool to rule out impaired left ventricular function in patients with a first myocardial infarction

2005 ◽  
Vol 43 (8) ◽  
Author(s):  
Mauro Panteghini ◽  
Graziella Bonetti ◽  
Franca Pagani ◽  
Francesca Stefini ◽  
Raffaele Giubbini ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Troponin I ◽  
Single Photon ◽  
Single Point ◽  
Photon Emission ◽  
Left Ventricular ◽  
Lv Function ◽  
Emission Computed Tomography ◽  
First Myocardial Infarction

AbstractFew studies have evaluated cardiac troponin I (cTnI) as a marker for infarct size and left ventricular (LV) dysfunction. Here we investigated the ability of a single-point cTnI, measured with a second-generation assay (Access AccuTnI), to estimate infarct size and assess LV function in patients with a first myocardial infarction (AMI). cTnI measurements were performed 12 and 48h after admission in 63 consecutive AMI patients. LV function was evaluated by gated single-photon emission computed tomography (SPECT) and infarct size was estimated by CK-MB peak and SPECT myocardial perfusion. LV function and infarct size were evaluated by SPECT before hospital discharge. SPECT was also repeated 3months later. Significant correlations (p<0.001) were found between cTnI at 12 and 48h and both the peak CK-MB (r=0.61 and r=0.82, respectively) and the perfusion defect size at SPECT (r=0.55 and r=0.61, respectively). cTnI at 12 and 48h were inversely related (p<0.001) to LV ejection fraction (LVEF) assessed both early (r=–0.45 and r=–0.57, respectively) and 3months after AMI (r=–0.51 and r=–0.69, respectively). cTnI >14.8 μg/L at 48h predicted an LVEF <40% at 3months with a sensitivity of 100% [95% confidence interval (CI) 73.5–100%], specificity of 65% (CI 49–79%), and a negative predictive value of 100%. Our findings demonstrate that a single cTnI measurement 48h after admission is useful for ruling out impaired LV function in a routine clinical setting.

scholarly journals Association Between Acute Inflammatory Response and Infarct Size in Stemi Patients Undergoing Primary PCI

2018 ◽  
Vol 4 (3) ◽  
pp. 140-146 ◽  
Author(s):  
Mirabela Morariu ◽  
Emese Márton ◽  
András Mester ◽  
Mihaela Rațiu ◽  
Imre Benedek
Keyword(s):  
Myocardial Infarction ◽  
Inflammatory Response ◽  
Infarct Size ◽  
Acute Phase Proteins ◽  
Serum Levels ◽  
Scar Tissue ◽  
Left Ventricular ◽  
Lv Function ◽  
Hs Crp

ABSTRACT Background: The inflammatory response of the immune system plays a major role in the period following an acute myocardial infarction (MI), as it coordinates the formation of the fibrous scar tissue that replaces the infarcted myocardial cells and ultimately leads to healing and remodeling of the affected zone. Along with other pro- and anti-inflammatory cytokines and acute phase proteins, interleukin-6 (IL-6) and C-reactive protein (CRP) are associated with the extent of the infarct size (IS) and may serve as predictors for remodeling and adverse left ventricular (LV) function. Material and methods: A single-center, non-randomized, observational prospective study was conducted, which included 75 patients with primary revascularized ST-elevation myocardial infarction (STEMI). High-sensitivity CRP (hs-CRP) serum levels were determined on day 1 and day 5 following the acute event. IL-6 was also determined on day 1. All patients underwent cardiac magnetic resonance imaging (CMR) at 1-month follow-up with determination of LV function and quantification of the scar tissue using late gadolinium enhancement imaging. The patients were divided into 2 groups based on baseline hs-CRP values. Results: Patients with higher baseline hs-CRP levels presented significantly higher infarct size (p = 0.0003), higher transmural extent (p <0.0001), lower LV ejection fraction (p = 0.0024), end-systolic (p = 0.0021) and end-diastolic (p = 0.0065) volumes. Small IS (<10%) recorded the lowest levels of hs-CRP, while IS >20% presented the highest levels of hs-CRP, at baseline and day 5 (p = 0.4 and 0.001). IL-6 levels were also associated with the magnitude of infarct scar: 2.17 pg/mL for IS <10%, 15.52 pg/mL for IS between 10% and 20%, and 24.52 pg/mL for IS >20%, p = 0.002. Conclusion: hs-CRP and IL-6 serum levels following an MI are correlated with IS, transmurality extent of the scar tissue, as well as with altered systolic and diastolic LV function determined by CMR at 1-month follow-up.

Mechanism of sudden cardiac death in pigs with viable chronically dysfunctional myocardium and ischemic cardiomyopathy

2005 ◽  
Vol 289 (6) ◽  
pp. H2688-H2696 ◽  
Author(s):  
James A. Fallavollita ◽  
Brian J. Riegel ◽  
Gen Suzuki ◽  
Uma Valeti ◽  
John M. Canty
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Ischemic Cardiomyopathy ◽  
Left Ventricular ◽  
High Rate ◽  
Lv Function ◽  
Wall Thickening ◽  
Triphenyltetrazolium Chloride ◽  
Global Function ◽  
Lv Mass

Pigs with viable chronically dysfunctional myocardium and ischemic cardiomyopathy are at high risk of sudden cardiac death (SCD). We sought to identify the arrhythmic mechanism of SCD, the relation to changes in left ventricular (LV) function, and inducibility of malignant arrhythmias before SCD. Juvenile pigs ( n = 72) were instrumented with chronic stenoses on proximal left anterior descending and circumflex arteries. Survival was only 29% 3 mo after instrumentation, and all deaths were sudden and without prodromal symptoms of heart failure. Triphenyltetrazolium chloride staining demonstrated necrosis in only nine animals averaging 2.3 ± 0.9% of the LV, with no difference between SCD animals and survivors. Implantable loop recorders ( n = 13) documented both ventricular fibrillation ( n = 6) and bradyasystole ( n = 2) as the arrhythmic mechanism of death. Although regional and global function were depressed [anteroseptal wall thickening 1.8 ± 0.2 vs. 4.2 ± 0.2 mm in Sham animals ( P < 0.001); fractional shortening 21 ± 2 vs. 31 ± 1% in Sham animals ( P < 0.01)], there were no differences between SCD animals and survivors. LV mass increased in animals with ischemic cardiomyopathy and was greater in animals with SCD (4.0 ± 0.2 vs. 3.1 ± 0.1 g/kg in survivors; P < 0.001). Serial programmed ventricular stimulation failed to induce any sustained arrhythmias. We conclude that pigs with viable dysfunctional myocardium and globally reduced LV function have a high rate of SCD with a spectrum of arrhythmias similar to patients with ischemic cardiomyopathy. The risk is independent of necrosis but appears to increase with LV hypertrophy. Like patients with ischemic cardiomyopathy, programmed stimulation is insensitive to predict SCD when viable dysfunctional myocardium is the pathological substrate.

Nitric oxide triggers late preconditioning against myocardial infarction in conscious rabbits

1997 ◽  
Vol 273 (6) ◽  
pp. H2931-H2936 ◽  
Author(s):  
Yumin Qiu ◽  
Ali Rizvi ◽  
Xian-Liang Tang ◽  
Srinivas Manchikalapudi ◽  
Hitoshi Takano ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Infarction ◽  
Cell Death ◽  
Infarct Size ◽  
Control Group ◽  
Group Iii ◽  
Late Preconditioning ◽  
Group I ◽  
Conscious Rabbits ◽  
Group Ii

We tested the hypothesis that late preconditioning (PC) against myocardial infarction is triggered by the formation of nitric oxide (NO). Conscious rabbits underwent a 30-min coronary occlusion followed by 3 days of reperfusion. In group I (control group, n = 10), rabbits were not preconditioned, whereas in group II( n = 10), they were preconditioned 24 h earlier with a sequence of six 4-min occlusion/4-min reperfusion cycles. Myocardial infarct size (tetrazolium staining) was reduced by 50% by PC (28.6 ± 3.2% of the risk region in group II vs. 56.9 ± 5.9% in controls, P < 0.05). This reduction in cell death was associated with improved recovery of myocardial function [systolic thickening fraction (by sonomicrometry) at 3 days: 2.0 ± 11.0% of baseline in group II vs. −20.0 ± 2.8% in group I, P < 0.05]. Group III rabbits ( n = 11) underwent the same protocol as group II except that the rabbits received the NO synthase inhibitor N ω-nitro-l-arginine (l-NNA, 13 mg/kg) before the PC ischemia. In these animals, infarct size did not differ significantly from that observed in control rabbits, indicating thatl-NNA completely blocked the development of late PC against myocardial infarction. In group IV( n = 9), rabbits receivedl-NNA as in group III, but without the six occlusion-reperfusion cycles, and were subjected to the 30-min occlusion 24 h later. In this group, infarct size did not differ from that observed in controls, demonstrating that pretreatment withl-NNA, in itself, did not affect the extent of cell death. Taken together, these results indicate that, in the conscious rabbit, the development of late PC against myocardial infarction is triggered by the generation of NO during the PC ischemia. It is proposed that NO plays a key role in the delayed myocardial adaptation to ischemic stress.

Abstract 15343: Increasing Left Ventricular Mass is Associated With Greater Microvascular Obstruction During ST-elevation Myocardial Infarction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Nicole L Bonfig ◽  
Chase R Soukup ◽  
Ross F Garberich ◽  
Sarah J Davidson ◽  
Rose M Peterson ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Cardiac Mri ◽  
Microvascular Obstruction ◽  
Myocardial Edema ◽  
Left Ventricular ◽  
St Elevation Myocardial Infarction ◽  
Lv Function ◽  
Lv Mass ◽  
St Elevation

Introduction: The development of microvascular obstruction (MVO) in the setting of ST-Elevation Myocardial Infarction (STEMI) is a powerful predictor of reduced left-ventricular (LV) function, adverse LV remodeling and increased mortality. Although MVO is associated with increasing infarct size and ischemic duration, additional causes of MVO have not been clearly identified. Although MVO may arise from intravascular obstruction from embolization of thrombus, it may also arise from compression of the microvasculature due to increased myocardial edema and extravascular compressive forces. Hypothesis: Because left-ventricular hypertrophy (LVH) is associated with increased extravascular compressive forces, we hypothesized that patients with greater LV mass may be more susceptible to the development of MVO during STEMI. Methods: We measured MVO in 385 patients (59.4 + 12.3 years; 77% male) admitted to our Institution with STEMI who underwent cardiac MRI for measurement of LV function and infarct size following successful primary PCI. A total of 219 patients (57%) had MVO on cardiac MRI measured 1-3 days following PCI of which 172 patients had paired measurements of LV mass. Results: Patients with MVO (13.7 + 13.9 grams) had significantly greater infarct size (54 vs. 31 g; p < 0.001) and LV mass (151 vs 140 g; p<0.01) but reduced LVEF (43.1 vs. 47.8%) despite having similar ischemic times. Among patients with MVO, there was a linear increase in MVO with increasing LV mass (Figure). Conclusions: MVO increases with increasing LV mass and may contribute to the known adverse effects of LVH in STEMI.

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