The Treatment of Myocardial Infarction in the Early Stage

2015 ◽  
pp. 134-147
Author(s):  
Kurt Berliner
Keyword(s):  
Myocardial Infarction ◽  
Early Stage

scholarly journals e0456 Relationship between hypokalaemia at the early stage of acute myocardial infarction and malignant ventricular arrhythmia

Heart ◽  
2010 ◽  
Vol 96 (Suppl 3) ◽  
pp. A142-A142
Author(s):  
F. Xianghua ◽  
Q. Peng ◽  
W. Yanbo ◽  
W. Xuechao ◽  
L. Shiqiang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Arrhythmia ◽  
Early Stage ◽  
Malignant Ventricular Arrhythmia

scholarly journals Echocardiographic global longitudinal strain is associated with infarct size assessed by cardiac magnetic resonance in acute myocardial infarction

2019 ◽  
Vol 6 (4) ◽  
pp. 81-89
Author(s):  
Gowsini Joseph ◽  
Tomas Zaremba ◽  
Martin Berg Johansen ◽  
Sarah Ekeloef ◽  
Einar Heiberg ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Magnetic Resonance ◽  
Longitudinal Strain ◽  
Early Stage ◽  
Global Longitudinal Strain ◽  
Apical Part ◽  
Left Ventricular ◽  
Percent Increase ◽  
Study Population

The aim of this study was to investigate if there was an association between infarct size (IS) measured by cardiac magnetic resonance (CMR) and echocardiographic global longitudinal strain (GLS) in the early stage of acute myocardial infarction in patients with preserved left ventricular ejection fraction (LVEF). Patients with ST-segment elevation myocardial infarction who underwent primary percutaneous coronary intervention were assessed with CMR and transthoracic echocardiogram within 1 week of hospital admission. Two-dimensional speckle tracking was performed using a semi-automatic algorithm (EchoPac, GE Healthcare). Longitudinal strain curves were generated in a 17-segment model covering the entire left ventricular myocardium. GLS was calculated automatically. LVEF was measured by auto-LVEF in EchoPac. IS was measured by late gadolinium enhancement CMR in short-axis views covering the left ventricle. The study population consisted of 49 patients (age 60.4 ± 9.7 years; 92% male). The study population had preserved echocardiographic LVEF with a mean of 45.8 ± 8.7%. For each percent increase of IS, we found an impairment in GLS by 1.59% (95% CI 0.57–2.61), P = 0.02, after adjustment for sex, age and LVEF. No significant association between IS and echocardiographic LVEF was found: −0.25 (95% CI: −0.61 to 0.11), P = 0.51. At the segmental level, the strongest association between IS and longitudinal strain was found in the apical part of the LV: impairment of 1.69% (95% CI: 1.14–2.23), P < 0.001, for each percent increase in IS. In conclusion, GLS was significantly associated with IS in the early stage of acute myocardial infarction in patients with preserved LVEF, and this association was strongest in the apical part of the LV. No association between IS and LVEF was found.

The Effect Of Fibrinolysis In The Early Stage Of Acute Myocardial Infarction

1981 ◽  
Author(s):  
K Genth ◽  
J Frank ◽  
J Schaefer ◽  
V Korten ◽  
D Heene
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Ventricular Function ◽  
Early Stage ◽  
Myocardial Infarct ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Time To Peak

The influence of streptokinase (SK) on myocardial infarct size and left ventricular function after acute myocardial infarction was investigated. 21 patients with myocardial infarction received SK (SK-group), 27 patients underwent conventional therapy (C-group). In both groups therapy started within 8 hours after onset of chest pain. In the SK-group initially 250 000 IU were administered intravenously, followed by a maintenance dose of 100 000 IU/h, lasting 15 hours. Blood samples at 8 hours intervals were collected for 3 days for serial CPK-analysis to calculate infarct size (I=∫f(t)×dt×K×bw). M-mode echocardiography was taken before start of t her a py and after 15, 24, 48 and 72 hours. AOP and heart rate were recorded continuously. Infarct size was 47±12g in the SK-group and 84±25g in the C-group (p<0.05). The average time to peak blood CPK-activity was 24 hours in the SK-group and 40 hours in the C-group. Peak CPK-level was significantly higher (p<0.5) in the SK-group (841±160U/l) than in the C-group (532±13 8 U / l ) . In 16 patients of the SK-group short periods of ventricular tachycardia were recorded during the period of fibrinolysis. Before therapy all patients showed abnormal motion of the posterior left ventricular wall and/or the interventricular septum, detected by echocardiography. 14 patients showed after fibrinolysis an improved or normalized motion.The results indicate that early fibrinolysis may reopen the occluded coronary artery. Reperfusion of the ischemic perfusion area may salvage jeo pardized myocardium, therefore infarct size was reduced and ventricular function improved.

scholarly journals Excessive Neutrophil Extracellular Trap Formation Aggravates Acute Myocardial Infarction Injury in Apolipoprotein E Deficiency Mice via the ROS-Dependent Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Zheliang Zhou ◽  
Shuning Zhang ◽  
Suling Ding ◽  
Mieradilijiang Abudupataer ◽  
Zhiwei Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Apolipoprotein E ◽  
Myocardial Injury ◽  
Early Stage ◽  
Critical Role ◽  
Neutrophil Extracellular Trap ◽  
Coronary Artery Ligation ◽  
Infarct Zone ◽  
Dependent Pathway

Genetically human apolipoprotein E (APOE) ε32 is associated with a decreased risk of ischemic heart disease. ApoE deficiency in mice impairs infarct healing after myocardial infarction (MI). After the ischemic injury, a large number of neutrophils are firstly recruited into the infarct zone and then degrade dead material and promote reparative phase transformation. The role of ApoE in inflammation response in the early stage of MI remains largely unclear. In this study, we investigated the effect of ApoE deficiency on neutrophils’ function and myocardial injury after myocardial infarction. By left coronary artery ligation in ApoE-/- and wild-type (WT) mice, we observed increased infarct size and neutrophil infiltration in ApoE-/- mice. Within the infarct zone, more neutrophil extracellular traps (NETs) were observed in ApoE-/- mice, while increased ex vivo NET formation was detected in ApoE-/- mouse-derived neutrophils through the NADPH oxidase-ROS-dependent pathway. Suppressing overproduced NETs reduced myocardial injury in ApoE-/- mice after ligation. In general, our findings reveal a critical role of apolipoprotein E in regulating Ly6G+ neutrophil activation and NET formation, resulting in limiting myocardial injury after myocardial infarction. In such a process, apolipoprotein E regulates NET formation via the ROS-MAPK-MSK1 pathway.

Cytokine signaling during myocardial infarction: sequential appearance of IL-1 beta and IL-6

1995 ◽  
Vol 269 (2) ◽  
pp. R229-R235 ◽  
Author(s):  
I. Guillen ◽  
M. Blanes ◽  
M. J. Gomez-Lechon ◽  
J. V. Castell
Keyword(s):  
Myocardial Infarction ◽  
Endothelial Cells ◽  
Protein Synthesis ◽  
Proinflammatory Cytokines ◽  
Early Stage ◽  
Myocardial Infarct ◽  
Cytokine Signaling ◽  
Target Cells ◽  
Necrosis Factor Alpha

The purpose of this study was to investigate the significance of the sequential changes in proinflammatory cytokines observed in the plasma of patients early after myocardial infarct: a rise in interleukin (IL)-1 beta (308 +/- 126 vs. 141 +/- 78 pg/ml, P < 0.01) between 0 and 2 h followed by an IL-6 peak (49 +/- 24 vs. 14.5 +/- 13 pg/ml, P < 0.01) 4-9 h later. No significant changes in tumor necrosis factor-alpha (TNF-alpha) were observed at this early stage. The linkage between IL-1 beta and IL-6 secretions is supported by 1) the ability of patient's plasma drawn early after myocardial infarction to induce IL-6 mRNA and protein synthesis in cells that may be potential targets in vivo (fibroblasts and endothelial cells), 2) suppression of this activity by antibodies against IL-1 beta, and 3) a delay between IL-1 beta and IL-6 peaks in vivo (4-9 h), which is similar to the time required for maximal IL-6 production in IL-1 beta stimulated target cells in vitro (6 h). This sequential signaling might serve as the basis for an amplification mechanism of proinflammatory cytokines. In fact, a much greater synthesis of C-reactive protein was observed in hepatocytes when stimulated with conditioned medium of fibroblasts or endothelial cells that had previously been incubated with plasma of patients. The results of our work strongly suggest that, by inducing IL-6 in potential target cells, IL-1 beta could act as the primary, but indirect, signal that stimulates acute-phase protein synthesis after myocardial injury.

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