Abstract 15899: A Hybrid Artificial Intelligence-Intrinsic Frequency Method for Instantaneous Determination of Myocardial Infarct Size

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Rashid Alavi ◽  
Wangde Dai ◽  
Robert A Kloner ◽  
Niema M Pahlevan
Keyword(s):  
Artificial Intelligence ◽  
Left Ventricle ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Myocardial Infarct Size ◽  
Ann Model ◽  
Sprague Dawley ◽  
Intrinsic Frequency ◽  
Frequency Method ◽  
Tetrazolium Chloride

Introduction: Intrinsic Frequency (IF) method is a recently developed systems-based method that extracts dynamics information about left ventricle function (LV), arterial dynamics, and the LV-arterial coupling from arterial waveforms. We have recently shown (Alavi et al. Circulation, 140 (2019), A12573-A12573) that IF can detect occurrence of an acute myocardial infarction (MI) using a single carotid pressure waveform. Here, we propose that the myocardial infarct size (area of necrosis over total LV area) can be approximated using a hybrid IF-artificial neural network (ANN) method. Methods: The standard MI model was used in anesthetized Sprague Dawley rats (n=27). The proximal left coronary artery was occluded for 30 minutes to ensure necrosis followed by 3 hours of reperfusion. The left ventricle slices were incubated in triphenyl tetrazolium chloride (TTC) to distinguish the necrotic (white) and the non-necrotic (dark red) areas (Fig.1a), thereby obtaining the size of MI through histopathology. IF parameters were computed from random carotid pressure waveforms 2 hours after the reperfusion. A 3-layer ANN model (4 input, 5 hidden, and 1 output node) was applied on IFs from 22 rats to design the ANN (18 for training, 4 for validation). The model was then tested on 5 different rats with the same MI procedure described above. Results: The results showed a significant correlation (R=0.64, P<0.0005) between our IF-artificial intelligence (IF-AI) model and the infarct size. The correlation was especially strong (R=0.84, P<0.0001) without the two outliers shown in Fig.1b. Conclusions: Our results suggest that a hybrid IF-AI method can predict the anatomic infarct size from an arterial waveform without advanced imaging. This technique is clinically significant since infarct sizes are link to the survival and development of heart failure in MI patients, and IF parameters can be obtained noninvasively from carotid waveforms using arterial tonometry devices or an iPhone.

scholarly journals Mechanically Unloading the Left Ventricle Before Coronary Reperfusion Reduces Left Ventricular Wall Stress and Myocardial Infarct Size

Circulation ◽  
2013 ◽  
Vol 128 (4) ◽  
pp. 328-336 ◽  
Author(s):  
Navin K. Kapur ◽  
Vikram Paruchuri ◽  
Jose Angel Urbano-Morales ◽  
Emily E. Mackey ◽  
Gerard H. Daly ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Wall Stress ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Myocardial Infarct Size ◽  
Ventricular Wall ◽  
Coronary Reperfusion

Abstract 300: Topical Application of IcyHot Reduces Myocardial Infarct Size in Rodents by a TRPA1-dependent Mechanism

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Yun Wu ◽  
Yao Lu ◽  
Eric R Gross
Keyword(s):  
Infarct Size ◽  
Transient Receptor Potential ◽  
Ischemia Reperfusion Injury ◽  
Calcium Influx ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Myocardial Infarct Size ◽  
Sprague Dawley ◽  
Area At Risk ◽  
Reactive Aldehydes

Toxic reactive aldehydes are formed during ischemia-reperfusion. The ion channel transient receptor potential ankryin 1 (TRPA1) is irreversibly modified by reactive aldehydes which can cause calcium influx and cell death. Here we tested whether topically applied creams containing a reversible TRPA1 agonist could reduce myocardial infarct size. Male Sprague-Dawley rats 8-10 weeks age were subjected to an in vivo myocardial ischemia-reperfusion model of 30 minutes of left anterior descending (LAD) coronary artery ischemia followed by 2 hours reperfusion. Prior to ischemia, rats were untreated or had 1g of cream applied to the abdomen. The creams tested were IcyHot, Bengay, Tiger Balm, or preparation H (Fig. 1A). Hearts were negatively stained for the area at risk and the infarct size was determined by using TTC staining (Fig. 1B). A subset of rodents prior to receiving IcyHot also received an intravenous bolus of the TRPA1 antagonist TCS-5861528 (1mg/kg) or AP-18 (1mg/kg). Interestingly, both IcyHot and Bengay reduced myocardial infarct size compared to untreated rodents (Fig. 1C and 1D IcyHot: 41±3%*, Bengay: 50±2%* versus control 62±1%, n=6/group, *P<0.001). Both preparation H and Tiger Balm failed to reduce myocardial infarct size (Tiger Balm: 63±2%, preparation H 59±2%). Giving a TRPA1 antagonist prior to IcyHot also blocked the reduction in infarct size. Our additional data also indicates the methyl salicylate (mint) in IcyHot and Bengay is the agent that limits myocardial infarct size. Since IcyHot and Bengay are safely used by humans, targeting TRPA1 by using products such as these could be quickly translatable and widely used to reduce ischemia-reperfusion injury.

Brief pressure overload of the left ventricle reduces myocardial infarct size via activation of protein kinase C

2015 ◽  
Vol 78 (9) ◽  
pp. 506-512
Author(s):  
Chia-Yu Tang ◽  
Chang-Chi Lai ◽  
Shu-Chiung Chiang ◽  
Kuo-Wei Tseng ◽  
Cheng-Hsiung Huang
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Left Ventricle ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Pressure Overload ◽  
Myocardial Infarct Size ◽  
Kinase C

scholarly journals Therapeutic Effect of Local Injection of VX765 Sodium Alginate Nanogel on Myocardial Infarction

2021 ◽  
Author(s):  
Qingxin Tian ◽  
Jianlong Liu ◽  
Qin Chen ◽  
Mingxiao Zhang
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Infarct Size ◽  
Sodium Alginate ◽  
Cardiac Fibrosis ◽  
Myocardial Infarct ◽  
Morphological Observation ◽  
Myocardial Infarct Size ◽  
Sprague Dawley

Abstract Objectives: To determine the effect of polyethyleneimine/sodium alginate composite nano-gel (AG/PEI-VX765NGs) coated with VX765 on cardiac function in rats with myocardial infarction (MI). Methods: VX765-polyethyleneimine nano-microspheres (PEI-VX765 NP) were encapsulated by sodium alginate (AG) nanogel (NGs) to construct AG/PEI-VX765 NGs. The morphological observation was performed under scanning electron microscope (SEM). The viability was evaluated by using CCK-8 assay in vitro. Then, 24 male SPF Sprague-Dawley rats were randomly divided into 4 groups: Sham, MI, PEI-VX765NP, and AG/PEI-VX765NGs. After 28 days, rats in each group were subjected to assessment of cardiac function by echocardiography. The myocardial infarct size was evaluated by TTC test, and the differences in cardiac fibrosis and cardiomyocyte apoptosis between groups were analyzed by histological methods. Results: The prepared NGs shows a porous structure, while PEI-VX765 NP is uniformly distributed in the AG NGs samples. AG/PEI-VX765 NGs with a concentration of VX765 (range: 0-1000 μM) displayed no significant toxicity to cells. Meanwhile, we observed a relatively more persistent release of VX765 from AG/PEI-VX765 NGs compared with PEI-VX765. LVIDs and LVIDd in both PEI-VX765 and AG/PEI-VX765NGs groups were significantly smaller than those in MI group, while ejection fraction (EF) and short-axis shortening rate (FS) were markedly increased in the above-mentioned two groups. Compared with MI group, PEI-VX765 and AG/PEI-VX765NGs groups exhibited a significant reduction in the infarct size, degree of fibrosis, and the rate of TUNEL positive cells. Conclusion: AG/PEI-VX765NGs can significantly improve the cardiac function of rats with MI.

Abstract 13498: Reperfusion Therapy With Rapamycin Prevents Myocardial Ischemic Injury, Through Activation of AKT and ERK

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Scott M Filippone ◽  
Sean K Roh ◽  
Fadi N Salloum ◽  
Rakesh C Kukreja ◽  
Anindita Das
Keyword(s):  
Infarct Size ◽  
Map Kinases ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Reperfusion Therapy ◽  
Tunel Staining ◽  
Coronary Artery Ligation ◽  
Myocardial Infarct Size ◽  
Artery Ligation ◽  
Tetrazolium Chloride

Background: The selective inhibitor of mammalian target of rapamycin (mTOR), rapamycin (RAPA), has been shown to exert preconditioning-like cardioprotective effects against ischemia/reperfusion (I/R) injury. Two distinct mTOR complexes (mTORC1 and mTORC2) differentially regulate cardiomyocyte apoptosis and tissue damage following myocardial infarction. We hypothesized that reperfusion therapy with RAPA would reduce myocardial infarct size through differential modulation of mTOR complexes and MAP kinases. Methods and Results: Adult C57BL mice were subjected to 30 min of ischemia via left anterior descending coronary artery ligation followed by reperfusion for 24 hr. RAPA (0.25 mg/kg) or 10% DMSO (volume-matched control) was administered via intra-cardiac injection at the onset of reperfusion. Post I/R survival (90%) and cardiac function (fractional shortening, FS: 26.9±2.6%) were improved in RAPA-treated mice compared to control (survival: 60%, FS:16.7±3.2%). Additionally, RAPA caused significant reduction in myocardial infarct size (Fig. 1A), measured by tetrazolium chloride staining, and apoptosis (Fig. 1B) in peri-infarct regions, assessed by TUNEL staining. Western blot analysis revealed that RAPA restored Akt473 phosphorylation (target of mTORC2), but reduced ribosomal protein S6 phosphorylation (target of mTORC1) following I/R injury (Fig. 1C). The protective effect of RAPA was associated with increased phosphorylation of ERK1/2 and decreased phosphorylation of P38 (Fig. 1D). RAPA also attenuated pro-apoptotic protein Bax, in concert with increased pro-survival Bcl2 to Bax ratio (Fig. 1E). Conclusion: Reperfusion therapy with RAPA protects hearts against I/R injury by selective activation of mTORC2 and ERK with concurrent inhibition of mTOC1 and P38. We propose that RAPA could be a novel treatment strategy to modulate mTOR complexes and MAP kinase signaling for attenuation of reperfusion injury in the heart.

Sex differences in myocardial infarct size are abolished by sarcolemmal KATP channel blockade in rat

2006 ◽  
Vol 290 (6) ◽  
pp. H2644-H2647 ◽  
Author(s):  
Micah S. Johnson ◽  
Russell L. Moore ◽  
David A. Brown
Keyword(s):  
At Risk ◽  
Sex Differences ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Female Rats ◽  
Male Rats ◽  
Myocardial Infarct Size ◽  
Sprague Dawley

This study was conducted to examine the relationship between myocardial ATP-sensitive potassium (KATP) channels and sex differences in myocardial infarct size after in vitro ischemia-reperfusion (I/R). Hearts from adult male and female Sprague-Dawley rats were excised and exposed to an I/R protocol (1 h of ischemia, followed by 2 h of reperfusion) on a modified Langendorff apparatus. Hearts from female rats showed significantly smaller infarct sizes than hearts from males (23 ± 4 vs. 40 ± 5% of the zone at risk, respectively; P < 0.05). Administration of HMR-1098, a sarcolemmal KATP channel blocker, abolished the sex difference in infarct size (42 ± 4 vs. 45 ± 5% of the zone at risk in hearts from female and male rats, respectively; P = not significant). Further experiments showed that blocking the KATP channels in ischemia, and not reperfusion, was sufficient to increase infarct size in female rats. These data demonstrate that sarcolemmal KATP channels are centrally involved in mechanisms that underlie sex differences in the susceptibility of the intact heart to I/R injury.

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