Myocardia infarction

Magnetic resonance angiography (MRA) is a method of imaging blood vessels in the presence of certain diseases, such as angiogenesis, tumors, atherosclerosis, coronary arteries [100], myocardium infarction, vascular injury, and blood flow reduction. Blood pool CA enhanced MRA increases the vessel-to-background ratio [101]. Blood pool CAs can be classified into two types, namely, low molecular weight Gd-based CAs and macromolecular CAs. 

Sejersten M, Birnbaum Y, Ripa RS et al. Electrocadiographic identification of patients with ST elevation acute myocardium infarction benefiting most from primary angioplasty versus fibrinolysis results from the DANAMI-2 trial. Circulation 2004 110 III—409. 

Glass IB Antiarrhythmic Agents. Class IB antiarrhythmic agents produce less inhibition of the inward sodium current than Class lA agents. In normal myocardial tissue, phase 0 may be unaffected or minimally depressed. However, in ischemic or infarcted tissue, phase 0 is depressed. Myocardial tissue exposed to Class IB agents exhibits decreased automaticity, shortened action potential duration, ie, shortened repolarization, and shortened refractory period. Excitability of the myocardium is not affected and conduction velocity is increased or not modified. The refractory period is shortened less than its action potential duration, thus the ratio of refractory period to action potential duration is increased by these agents. The net effect is increased refractoriness. The PR and QT intervals of the ECG are shortened and the QRS interval is unchanged (1,2). 

The increased concentrations of K, Ca, Fe, Br, Se and Rb in infarction and scar areas are observed for patient with the recent infarction. For the patients with old infarction the levels of these elements are decreased in the same areas. This reflects the intensity of metabolic processes in the pathological area of myocardium. Additionally, the elevated levels of Se was find out in myocardium of right ventricle in both patients, that may be caused by the increasing the activity of the glutathione peroxidase enzyme. 

CR is distributed in various organs with highest concentrations in skeletal muscle, myocardium, and brain and lesser amounts in the gastrointestinal tract, uterus, urinary bladder, and kidney ( ). The CR content of liver and red blood cells is negligible so that diseases of these tissues are unlikely to increase the serum CR activity. The serum CR level begins to increase in 2-4 hours after myocardial infarction and reaches a peak in 24-36 hours and returns to normal in about 3 days. 

Ascher, E.K. Stauffer, J-C.E. and Gaasch, W.H. Coronary artery spasm, cardiac arrest, transient electrocardiographic Q waves and stunned myocardium in cocaine-associated acute myocardial infarction. 

Intravenous or oral doses of a P-blocker should be administered early in the care of a patient with STE ACS, and then oral agents should be continued indefinitely. Early administration of a P-blocker to patients lacking a contraindication within the first 24 hours of hospitalization is a quality care indicator.2,3 In ACS the benefit of P-blockers mainly results from the competitive blockade of P,-adrenergic receptors located on the myocardium. Pi-Blockade produces a reduction in heart rate, myocardial contractility, and blood pressure, decreasing myocardial oxygen demand. As a result of these effects, P-blockers reduce the risk for recurrent ischemia, increase in infarct size and risk of reinfarction, and occurrence of ventricular arrhythmias in the hours and days following MI.39... 

Non-ST-segment elevation A type of myocardial infarction (MI) that is limited to the subendocardial myocardium and is smaller and less extensive than an ST-segment MI. There is usually no pathologic Q-wave on the electrocardiogram in non-ST-segment elevation. 

Two forms of xanthine oxidoreductase namely XO and XDH are present in many human and animal cells and plasma, XDH and XO are the predominant species in cytoplasma and serum, respectively [39]. Damaging effects of XO-catalyzed superoxide production in post-ischemic tissues were demonstrated by many authors. For example, Chambers et al. [40] and Hearse et al. [41] have shown that the suppression of superoxide production by the administration of XO inhibitor allopurinol or SOD resulted in the reduction of infarct size in the dog and of the incidence of reperfusion-induced arrhythmia in the rat. Similarly, Charlat et al. [42] has also shown that allopurinol improved the recovery of the contractile function of reperfused myocardium in the dog. However, the use of allopurinol as the XO inhibitor has been questioned because this compound may affect oxygen radical formation not only as a XO inhibitor but as well as free radical scavenger [43]. Smith et al. [44] also showed that gastric mucosal injury depends on the oxygen radical production catalyzed by XO and iron. 

Myocardial infarction, 3 710-711 and blood coagulation, 4 81 Myocardial pacemaker cells, 5 81 Myocardium, 5 79—80 Myoglobin, properties of standard, 3 836t Myosin, role in heart excitation and contraction coupling, 5 81 Myrac aldehyde, 2 278 24 485 Myrascone, 24 571... 

Three proteolytic enzymes, streptokinase, urokinase and tissue plasminogen activator, hydrolyse peptide bonds in fibrin which loosens the stracture of the clot and can results in its dispersal. This can restore flow of blood to the part of the myocardium affected by the clot. These are known as clot-busting enzymes. One or more of these enzymes is introduced into the circulation, and provided that this is done very soon after an infarct, damage to that part of the myocardium can be minimised. 

The decreased work capacity of the in-farcted myocardium leads to a reduction in stroke volume (SV) and hence cardiac output (CO). The fall in blood pressure (RR) triggers reflex activation of the sympathetic system. The resultant stimulation of cardiac 3-adreno-ceptors elicits an increase in both heart rate and force of systolic contraction, which, in conjunction with an a-adren-oceptor-mediated increase in peripheral resistance, leads to a compensatory rise in blood pressure. In ATP-depleted cells in the infarct border zone, resting membrane potential declines with a concomitant increase in excitability that may be further exacerbated by activation of p-adrenoceptors. Together, both processes promote the risk of fatal ventricular arrhythmias. As a consequence of local ischemia, extracellular concentrations of H+ and K+ rise in the affected region, leading to excitation of nociceptive nerve fibers. The resultant sensation of pain, typically experienced by the patient as annihilating, reinforces sympathetic activation. 

Mechanism of action - Disopyramide is a class lA antiarrhythmic agent that decreases the rate of diastolic depolarization (phase 4), decreases the upstroke velocity (phase 0), increases the action potential duration of normal cardiac cells, and prolongs the refractory period (phases 2 and 3). It also decreases the disparity in refractoriness between infarcted and adjacent normally perfused myocardium and does not affect alpha- or beta-adrenergic receptors. 

Myocardial infarction Minoxidil has not been used in patients who have had an Ml within the preceding month. A reduction in arterial pressure with the drug might further limit blood flow to the myocardium, although this might be compensated by decreased oxygen demand because of lower BP. 

Size and severity of ischemic areas correlate well with mortality in both stable CAD populations [70] and after myocardial infarction [71]. Moreover, the presence of ischemia in a dysfunctional segment of myocardium is a powerful predictor of functional recovery. Up to 83% of regions with reversible defects (ischemia) will improve with revascularization compared to only 33% for regions where no reversibility was demonstrated [72]. In patients with heart failure, viable poorly contracting myocardium correlates with recovery... 

In post myocardial infarction patients, LVEF is closely related to the infarct size by PET, as illustrated in Fig. 2.8 [79]. In such patients, the presence of viable myocardium is associated with good survival post revascularization, whereas the absence of viable... 

Fig. 2.9 Effect of revascularization on myocardial viability in post myocardial infarction (MI) patients. Almost half of all post MI patients will have completed necrosis without remaining areas of viable myocardium...

FDG PET and ° T1 SPECT may be particularly useful in the future for following replacement of infarcted myocardium using intracoronary injections of progenitor cells. In a small series of patients, this approach demonstrated a significant increase in myocardial viability and perfusion [116]. 

Lee KS, Marwick TH, Cook SA, Go RT, Fix JS, James KB et al. Prognosis of patients with left ventricular dysfunction, with and without viable myocardium after myocardial infarction. Relative efficacy of medical therapy and revascularization. Circulation 1994 90 2687-2694... 

In a proof-of-concept study in which Saito et al. [60] intravenously injected LacZ reporter gene-transfected MSCs into healthy rats, the MSCs preferentially engrafted in the bone marrow. When injected into rats subjected to repetitive periods of ischemia/reperfusion, however, the MSCs engrafted in the infarcted regions of the heart, where they participated in angiogenesis and expressed cardio-myocyte-specific proteins. When injected into rats 10 days after myocardial injury, MSCs preferentially homed to damaged myocardium. 

CD45 ABMMNCs in humans. These nonhemato-poietie ABMMNCs expressing eardiae preeursors are mobilized into the peripheral blood after a myoeardial infarction and home to the damaged myocardium in an SDF-1-CXCR4-, HGF-c-Met-, and LIF-LIF-R-dependent marmer [71]. 

Myocyte replication is the failing heart s attempt to compensate for a limited capacity for hypertrophy. When Urbanek et al. [37] used Ki-67 (a nuclear protein expressed during cell division) to assess the mitotic activity of myocytes, they observed significantly greater mitotic activity at infarct border zones than in distant myocardium or undiseased control hearts. The evidence that cardiac myocytes divide shortly after a myocardial infarction led investigators to search for the origin of the dividing myocytes [82]. This culminated in the description of resident CSCs [35-37]. 

Resident CSCs were first isolated in murine hearts. Characterization of these cells was based on the expression of the stem cell-related surface antigens c-Kit and Sea-1. In the first study, freshly isolated c-Kit /Lin cells were shown to be clono-genic and to differentiate into myocytes, smooth muscle cells, and endothelial lineage cells [35]. Those cells generated functional myocardium when injected into ischemic areas of the heart. The second study characterized CSCs as Sca-l/c-Kit. When treated in culture with 5-azacytidine, those cells differentiated into a myogenic lineage. Subsequently, intravenous injection of the cells in an ischemia/reperfusion model resulted in infarct healing with cardiomyocyte transdifferentiation... 

Transepicardial injection of stem cells has been performed during open surgical revascularization procedures to deliver the cells to infarct border zones or areas of infarcted or scarred myocardium. Because a sternotomy is required, this approach is highly invasive and associated with surgical complications. However, in the setting of a planned open... 

Another potential deleterious effect of bone marrow stem cell therapy is myocardial calcification. In a recent study, Yoon et al. [155] noted that direct transplantation of unselected bone marrow cells into acutely infarcted myocardium could induce significant intramyocardial calcification. In the same study, however, ABMMNCs did not. 

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