Revisiting the role of percutaneous revascularization versus medical therapy for later infarct-related artery occlusion (letter of comment on Ioannidis and Katritsis. Am Heart J. 2007;154:1065-71)

2008 ◽  
Vol 155 (4) ◽  
pp. e41 ◽  
Author(s):  
Darryn Appleton ◽  
Antonio Abbate ◽  
Giuseppe G.L. Biondi-Zoccai ◽  
Sara Delcré ◽  
Mario Bollati ◽  
...  
Keyword(s):  
Medical Therapy ◽  
Artery Occlusion ◽  
Infarct Related Artery ◽  
Percutaneous Revascularization

scholarly journals Role of electrocardiogram in identifying the infarct related artery in acute myocardial infarction and to correlate it with 2D echo and coronary angiogram

2020 ◽  
Vol 7 (3) ◽  
pp. 451
Author(s):  
Jacob Abraham Ruram ◽  
Rami Reddy Ganta ◽  
P. Arunachalam
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Artery Occlusion ◽  
Inferior Wall ◽  
St Segment Elevation ◽  
St Segment ◽  
Infarct Related Artery ◽  
St Elevation ◽  
Sensitivity Specificity

Background: The Electrocardiogram remains a crucial tool in the identification and management of acute myocardial infarction. A detailed analysis of patterns of ST segment elevation may influence decisions regarding the perfusion therapy. This study was undertaken to study the role of ECG in identifying the infarct related artery in acute ST elevation MI and to correlate its findings with 2 D ECHO and Coronary angiogram.Methods: A total of 100 patients who presented with acute ST elevation MI were randomly selected for the study. After admission all the patients underwent ECG, CPK, CK-MB levels, 2D ECHO and CAG. Patients with ST segment elevation from ECG was evaluated to identify culprit vessel and the ECG findings were then correlated with 2D ECHO and CAG to identify the Sensitivity, Specificity, Positive predictive value and Negative predictive value of ECG in identifying the infarct related artery.Results: Fifty-two (52%) patients had an Anterior wall MI, forty-two patients (42%) had an evidence of Inferior wall MI and Six patients (6%) were found to have Antero inferior wall MI in the study group. Thirty-eight (38%) had evidence of SVD, forty-six patients (46%) had DVD and Sixteen patients (16%) had TVD. Sensitivity, Specificity, PPV and NPV of the ECG in identifying the LAD artery occlusion were 60.5%, 100%, 100% and 44.4% respectively. Sensitivity, Specificity, PPV and NPV of ECG in identifying the RCA artery occlusion were 78.5%, 100%, 100% and 78.5% respectively. Sensitivity, Specificity, PPV and NPV of the ECG in identifying the LCx artery occlusion were 26%, 96%, 86% and 60% respectively.Conclusions: ECG was found to be a sensitive and specific tool in identifying the infarct related Coronary artery in acute ST elevation MI.

Heart failure in an elderly man: where is that coronary?

2021 ◽  
pp. 1-4
Author(s):  
Charlie J. Sang ◽  
Stephen A. Clarkson ◽  
Elizabeth A. Jackson ◽  
Firas Al Solaiman ◽  
Marc G. Cribbs
Keyword(s):  
Heart Failure ◽  
Coronary Artery ◽  
Pulmonary Artery ◽  
Medical Therapy ◽  
Coronary Arteries ◽  
Right Coronary Artery ◽  
Adult Population ◽  
Anomalous Coronary ◽  
Anomalous Coronary Arteries

Abstract Anomalous coronary arteries from the pulmonary artery are uncommon causes of heart failure in the adult population. This case demonstrates the unusual presentation in a patient with anomalous right coronary artery from the pulmonary artery and discusses the complex pathophysiology of this lesion and the role of guideline-directed medical therapy in the management of these patients.

Reduction of infarct size with d-myo-inositol trisphosphate: role of PI3-kinase and mitochondrial KATP channels

2006 ◽  
Vol 290 (2) ◽  
pp. H830-H836 ◽  
Author(s):  
Karin Przyklenk ◽  
Michelle Maynard ◽  
Peter Whittaker
Keyword(s):  
Infarct Size ◽  
Katp Channels ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Additional Treatment ◽  
Pi3 Kinase ◽  
Mitochondrial Katp Channels ◽  
Tetrazolium Staining ◽  
Sparing Effect

Prophylactic treatment with d- myo-inositol 1,4,5-trisphosphate hexasodium [d- myo-Ins(1,4,5)P3], the sodium salt of the endogenous second messenger Ins(1,4,5)P3, triggers a reduction of infarct size comparable in magnitude to that seen with ischemic preconditioning (PC). However, the mechanisms underlying d- myo-Ins(1,4,5)P3-induced protection are unknown. Accordingly, our aim was to investigate the role of four archetypal mediators implicated in PC and other cardioprotective strategies (i.e., PKC, PI3-kinase/Akt, and mitochondrial and/or sarcolemmal KATP channels) in the infarct-sparing effect of d- myo-Ins(1,4,5)P3. Fifteen groups of isolated buffer-perfused rabbit hearts [5 treated with d- myo-Ins(1,4,5)P3, 5 treated with PC, and 5 control cohorts] underwent 30 min of coronary artery occlusion and 2 h of reflow. One set of control, d- myo-Ins(1,4,5)P3, and PC groups received no additional treatment, whereas the remaining sets were infused with chelerythrine, LY-294002, 5-hydroxydecanoate (5-HD), or HMR-1098 [inhibitors of PKC, PI3-kinase, and mitochondrial and sarcolemmal ATP-sensitive K+ (KATP) channels, respectively]. Infarct size (delineated by tetrazolium staining) was, as expected, significantly reduced in both d- myo-Ins(1,4,5)P3- and PC-treated hearts versus controls. d- myo-Ins(1,4,5)P3-induced cardioprotection was blocked by 5-HD but not HMR-1098, thereby implicating the involvement of mitochondrial, but not sarcolemmal, KATP channels. Moreover, the benefits of d- myo-Ins(1,4,5)P3 were abrogated by LY-294002, whereas, in contrast, chelerythrine had no effect. These latter pharmacological data were corroborated by immunoblotting: d- myo-Ins(1,4,5)P3 evoked a significant increase in expression of phospho-Akt but had no effect on the activation/translocation of the cardioprotective ε-isoform of PKC. Thus PI3-kinase/Akt signaling and mitochondrial KATP channels participate in the reduction of infarct size afforded by prophylactic administration of d- myo-Ins(1,4,5)P3.

Abstract TMP25: Long Non-Coding RNA Mediates Stroke-Induced Neurogenesis

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Baoyan Fan ◽  
Wanlong Pan ◽  
Xinli Wang ◽  
Michael Chopp ◽  
Zheng Gang Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Regulation Of Gene Expression ◽  
Artery Occlusion ◽  
Loss Of Function ◽  
Bioinformatics Analyses ◽  
Guide Rna ◽  
Non Coding Rna ◽  
Cerebral Artery Occlusion ◽  
Long Non Coding Rna

Background and Purpose: Adult neurogenesis contributes to functional recovery after stroke. Long non-coding RNAs (lncRNAs) regulate stem cell self-renewal and differentiation. However, the role of lncRNAs in stroke-induced neurogenesis remains unknown. Methods and Results: Using lncRNA array and in situ hybridization, we analyzed lncRNA profiles of adult neural stem cells (NSCs) isolated from the subventricular zone neurogenic region in rats subjected to middle cerebral artery occlusion. We found that H19 was the most highly upregulated lncRNA (19 fold) in ischemic NSCs compared with non-ischemic NSCs. Reduction of endogenous H19 in NSCs by CRISPR-Cas9 genome editing significantly decreased the proliferation and increased the apoptosis of ischemic NSCs, as assayed by the number of BrdU + cells (56±5% vs 22±3%, p<0.01, n=3) and Caspase-3/7 activity compared to NSCs transfected with scrambled small guide RNA (sgRNA). Knockdown of H19 significantly decreased the number of Tuj1 + neuroblasts (8±2% vs 5±0.4%, p<0.01, n=3) and NG 2 + oliogodendrocyte progenitor cells (10±1% vs 5±0.3%, p<0.01, n=3), suggesting that deletion of H19 suppresses the proliferation and survival and blocks the differentiation of NSCs into neurons and oligodendrocytes. Additional RNA-sequencing and bioinformatics analyses revealed that genes deregulated by H19 knockdown were involved in transcription, apoptosis, proliferation, cell cycle and response to hypoxia. Western blot analysis validated that loss-of-function and gain-of-function of H19 significantly increased and reduced, respectively, the transcription of cell cycle-related genes including p27. Using ChIRP assay, we found that upregulated H19 in NSCs was physically associated with EZH2 which catalyzes the repressive H3K27me3 histone marker. Knockdown of H19 significantly reduced the enrichment of H3K27me3 at the promoter of p27, leading to the upregulation of p27 expression and consequently inhibition of NSC proliferation. Conclusions: H19 mediates stroke-induced neurogenesis by regulating genes involved in cell cycle and survival through the interaction with chromatin remodeling proteins. Our data provide novel insights into epigenetic regulation of gene expression by lncRNA in neurogenesis.

scholarly journals Bradykinin mediates cardiac preconditioning at a distance

2000 ◽  
Vol 278 (5) ◽  
pp. H1571-H1576 ◽  
Author(s):  
Regien G. Schoemaker ◽  
Caroline L. van Heijningen
Keyword(s):  
Sensory Nerve ◽  
Artery Occlusion ◽  
Area At Risk ◽  
Risk Area ◽  
Arterial Infusion ◽  
Remote Preconditioning ◽  
Male Wistar Rats ◽  
Hoe 140 ◽  
Cardiac Preconditioning

Preconditioning the heart by brief coronary (CAO) or mesenteric artery occlusion (MAO) can protect against damage during subsequent prolonged CAO and reperfusion. The role of bradykinin (BK) in remote cardiac preconditioning by MAO is investigated by antagonizing the BK B2 receptor [Hoechst 140 (HOE-140)] or simulating local BK release by mesenteric intra-arterial infusion. Anesthetized male Wistar rats ( n = 6–8) were treated with HOE-140 or saline before starting the preconditioning protocol, CAO, MAO, or non-preconditioned control. Infarct size related to risk area [ratio of infarct area to area at risk (IA/AR)] was determined after 3 h of reperfusion following a 60-min CAO. IA/AR was 62 ± 5% in controls and not affected by HOE-140 (58 ± 6%). CAO as well as MAO significantly protected the heart (IA/AR, 37 ± 3 and 35 ± 5%), which was prevented by HOE-140 (IA/AR, 71 ± 6 and 65 ± 7%, respectively). Brief intramesenteric BK infusion mimicked MAO (IA/AR, 26 ± 3%). Pretreatment with hexamethonium could abolish this protection (IA/AR, 67 ± 4%). These data indicate an important role for BK in remote preconditioning by MAO. Results support the hypothesis that remote preconditioning acts through sensory nerve stimulation in the ischemic organ.

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