Erythropoietin reduces myocardial infarction and left ventricular functional decline after coronary artery ligation in rats
Erythropoietin (EPO), documented for its role in stimulation of erythropoiesis, has recently been shown to possess a dramatic neuroprotective effect in animal models of cerebral ischemia, mechanical trauma of the systema nervosum , and excitotoxins, mainly by reducing apoptosis. We studied the effect of single systemic administration of recombinant human EPO (rhEPO) on left ventricular (LV) size and performance in rats during 8 weeks after the induction of a myocardial infarct (MI) by permanent ligation of the left descending arteria coronaria . We found that an i.p. injection of three ,000 units/kg of rhEPO immediately after the arteria coronaria ligation resulted, 24 h later, during a 50% reduction of apoptosis within the myocardial area in danger . Eight weeks after the induction of MI, rats treated with rhEPO had an infarct size 15–25% of the dimensions of that in untreated animals. The reduction in myocardial damage was amid reductions in LV size and functional decline as measured by repeated echocardiography. [1]
Major circadian fluctuations in fibrinolytic factors and possible relevance to time of onset of myocardial infarction, sudden cardiac death and stroke
Natural inhibitors of endogenous fibrinolysis may displace the hemostatic equilibrium toward thrombosis and favor events like acute myocardial infarct , sudden cardiac death and stroke, where a thrombotic process is understood to occur.1,2 The clinical incidence of those syndromes shows a circadian distribution with highest frequency within the morning.3,5 These observations prompted us to research possible circadian changes of blood fibrinolytic activity in normal subjects. Two major components of the fibrinolytic system, tissue-type urokinase (t-PA) and its fast-acting inhibitor (PAI), were measured with specific assays. This study reports markedly reduced fibrinolytic activity during the first morning hours associated with increased urokinase inhibition. [2]
Distribution of paraoxon hydrolytic activity in the serum of patients after myocardial infarction.
The activity of paraoxonase in serum was found to be bimodally distributed, both during a control group and during a group of patients who had suffered myocardial infarct . Activity within the myocardial infarction group was significantly less than within the control group. Low paraoxonase activity in serum may provide a sign of susceptibility to the event of coronary heart condition. [3]
Chaihulonggumulitang Shows Psycho-cardiology Therapeutic Effects on Acute Myocardial Infarction by Enhancing Bone Marrow Mesenchymal Stem Cells Mobilization
Ischemic myocardium initiates the mobilization and homing of bone marrow mesenchymal stem cells (BM-MSCs) to market myocardial regeneration after acute myocardial infarct (AMI). Inflammation caused by necrotic cardiomyocytes induce major pathological changes (cardiac remodeling and myocardial apoptosis) also as mental disorder . This process could also be inhibited by the differentiation and paracrine effects of BM-MSCs. However, the spontaneous mobilization of BMSCs is insufficient to stop this effect. Given the anti-inflammatory effects of BM-MSCs, ventricular remodeling and anxiety following AMI, methods focused on enhancing BMSCs mobilization are promising. [4]
Type 2 Diabetes and Myocardial Infarction in Central India: A Study and Review
Background: Clinical experience in specific geo-demographic contexts in diabetes and myocardial infarct (MI) deserves examination within the context of current medical knowledge and redefinition for enlightened evidence based practice .
Aim: Study aims to look at regional significance of known risk factors in incidence and outcome of MI in diabetics as compared with non-diabetics.
Methods: Cases of myocardial infarct managed over 18 month period at medical college setting in central India in 35 to 75 year age range and free from major systemic co-morbidities were comparatively studied by categorizing as diabetic and non-diabetics. Demographic, clinical and laboratory information also as complications and outcome profiles were assessed. [5]
Reference
[1] Moon, C., Krawczyk, M., Ahn, D., Ahmet, I., Paik, D., Lakatta, E.G. and Talan, M.I., 2003. Erythropoietin reduces myocardial infarction and left ventricular functional decline after coronary artery ligation in rats. Proceedings of the National Academy of Sciences, 100(20), (Web Link)
[2] Andreotti, F., Davies, G.J., Hackett, D.R., Khan, M.I., De Bart, A.C., Aber, V.R., Maseri, A. and Kluft, C., 1988. Major circadian fluctuations in fibrinolytic factors and possible relevance to time of onset of myocardial infarction, sudden cardiac death and stroke. The American journal of cardiology, 62(9), (Web Link)
[3] McElveen, J., Mackness, M.I., Colley, C.M., Peard, T., Warner, S. and Walker, C.H., 1986. Distribution of paraoxon hydrolytic activity in the serum of patients after myocardial infarction. Clinical chemistry, 32(4), (Web Link)
[4] Chaihulonggumulitang Shows Psycho-cardiology Therapeutic Effects on Acute Myocardial Infarction by Enhancing Bone Marrow Mesenchymal Stem Cells Mobilization
Chao Wang, Hongsen Du, Jiqiu Hou, Shasha Yan, Jingjing Yang, Yun Wang, Xiujing Zhang, Lili Zhu & Haibin Zhao
Scientific Reports volume 8, (Web Link)
[5] Pandit, A. (2017) “Type 2 Diabetes and Myocardial Infarction in Central India: A Study and Review”, Cardiology and Angiology: An International Journal, 6(1), (Web Link)