Infarction acute phase

Ticlopidine inhibits the P2Yj2 platelet ADP receptor, thus inhibiting ADP-dependent activation of the GP Ilb/IIIa receptor. It has a slow onset of action and takes 3-7 days to reach its maximal antiplatelet effect. It is inactive in vitro and must undergo activation by the hepatic cytochrome p450 enzyme system. Secondary prevention trials have found that ticlopidine-treated patients have an estimated RRR of 33% for the composite endpoint of stroke, myocardial infarction, or vascular death after ischemic stroke. Significant adverse effects include bone marrow depression, rash, diarrhea, and thrombotic thrombocytopenic purpura. No clinical trials have studied ticlopidine for the treatment of stroke in the acute phase. 

Elevated blood pressure should remain untreated in the acute period (first 7 days) after ischemic stroke because of the risk of decreasing cerebral blood flow and worsening symptoms. The pressure should be lowered if it exceeds 220/120 mm Hg or there is evidence of aortic dissection, acute myocardial infarction, pulmonary edema, or hypertensive encephalopathy. If blood pressure is treated in the acute phase, short-acting parenteral agents (e.g., labetalol, nicardipine, nitroprusside) are preferred. 

Lp(a) can behave as an acute-phase protein whose levels increase after myocardial infarction or surgery (CIO, LI 1, M2, M4, S30) and in patients suffering from rheumatoid arthritis (R2). 

Lidocaine is the most widely used local anesthetic. Its excellent therapeutic activity is fast-acting and lasts sufficiently long to make it suitable for practically any clinical use. It stabilizes cell membranes, blocks sodium channels, facilitates the secretion of potassium ions out of the cell, and speeds up the repolarization process in the cell membrane. It is used for terminal infiltration, block, epidural, and spinal anesthesia during operational interventions in dentistry, otolaryngology, obstetrics, and gynecology. It is also used for premature ventricular extrasystole and tachycardia, especially in the acute phase of cardiac infarction. Synonyms for this drug are xylocaine, neflurane, and many others. 

Liver disease, severe thrombocytopenia, obstructive cardiomyopathy. Acute phase of myocardial infarction. 

Regional ischemia in the course of atherosclerotic coronary artery disease is one of the most important causes of arrhythmia in the Western industrial world. These arrhythmias start with or often degenerate into ventricular fibrillation and are the main cause of sudden cardiac death in these countries. However, in the course of ischemia and infarction the mechanisms by which arrhythmia is induced vary with the duration of ischemia. In the acute phase of ischemia, i.e. within the first 2 1 h ventricular arrhythmias often occur. 

The acute phase of ischemia is followed by 3-6 h of predominantly sinus rhythm. Thereafter, the number of ventricular ectopic beats increases. In the subacute phase of infarction (12-24 h) ventricular arrhythmias often occur. One of the mechanisms involved is reinfarction. If there is no acute reinfarction involved, these arrhythmias have been suggested to originate from surviving strands of Purkinje fibers in the subendocardium. The predominant mechanism has been postulated to be abnormal automaticity in these fibers. These fibers exhibit an increased sensitivity for catecholamines. In some cases a combination of focal activity and reentry in these fibers may be possible. 

Theroux B Waters D.Qiu S, et al. Aspirin versus heparin to preventmyocardial infarction during the acute phase of unstable angina. Circulation 1993 88 2045-2048. 

Many mediators of inflammation have been identified— cytokines IL-6, tumor necrosis factor alpha cell adhesion molecules intracellular adhesion molecule-1 (ICAM-I), P-selectin and acute phase reactants CR.R fibrinogen, serum amyloid A, and soluble CD40 (Fig. I) (3). Myeloperoxidase is an enzyme secreted from monocytes, neutrophils, and macrophages. A single measurement taken from patient with chest pain in the emergency department predicted the early risk of myocardial infarction and the risk of major cardiac of ends in the next 30 days to six months (15). 

In another study of 45 patients with ACS, the relationship between plaque rupture, CRR and prognosis was investigated with intravascular ultrasound (21). These 45 patients had a first acute myocardial infarction with or without ST segment elevation. Intravascular ultrasound was performed in the patients before any percutaneous coronary intervention and within six hours of symptoms (21). The remaining coronary vasculature was examined within one month. Forty-five culprit arteries and 84 other coronary arteries were examined with intravascular ultrasound. They found that plaque ruptures in 47% of the arteries at the culprit site in the acute phase of the myocardial infarction. In addition, intravascular ultrasound revealed 17 occult plaque ruptures at remote sites in 24% of the patients (21), These findings suggest that some patients with acute myocardial infarctions have multiple plaque ruptures in other coronary arteries and the culprit artery. 

Ischemic infarction of the spinal cord is difficult to establish in the early phase, only 50% of the patients show early demarcation within 24 h. The role of MRI in the acute phase is to exclude hematomyelia, spinal vascular malformation (which requires spinal angiography in special cases) or a compressive lesion. 

Fig. 1. Relationship between size of infarction and body temperature during the acute phase of cardiogenic embolism. Analyzed using ANOVA, the difference in body temperature among the groups was statistically significant at any period during the first 3 d after of admission.

Stroke induces an acute stress response—i.e., over-activation of the sympathetic nervous system and increased corticosteroid levels (with resultant neutrophiha and lymphocytopenia). This in turn leads to depressed immunity and altered immune responses during the acute phase of stroke and may predispose patients to infections, particularly pneumonia, which is the commonest cause of mortality after the first few days of stroke (Meisel et al., 2005). In the clinical setting, increased total white cell counts and neutrophilia, which correlate with infarct size, are independently associated with worse outcome after stroke. Recently a massive and early activation of the systemic immnne system has been shown to occur also in experimental stroke (Offner et al., 2006). 

AAG is a protein known as an acute phase reactant. As a result of inflammation, injury during physiological trauma, and stress,an increase in the binding capacity of AAG is commonly observed in patients. For a drug that is highly bound, an increase in AAG plasma levels will result in a significant decrease in unbound plasma fraction. Examples include propranolol, lidocaine, and disopyra-mide after myocardial infarction and propranolol and chlorpromazine in Crohn s disease. 

Atropine is an anticholinergic drug that is mainly used today in premedication and occasionally to treat bradycardia in the acute phase of myocardial infarction. 

Grenadier E, Keidar S, Kahana L, Alpan G, Marmur A, Palant A. The roles of serum myoglobin, total CK, and CK-2 isoenzymes in the acute phase of myocardial infarction. Am Heart J 1983 10 408-16. 

The coronary angiography (Figure 1.1) is especially important in the acute phase for diagnosing the disease and correlating the place of occlusion with the ST-segment deviations. It is also useful in the chronic phase of the disease. However, in the chronic phase of Q-wave myocardial infarction (MI) the ECG does not usually predict the... 

The injury vector has approximately the same direction as that of the vector of ischaemia and infarction but opposite sense (see p. 35, 60 and 131 and Figures 3.6, 4.8 and 5.3). Therefore, most probably, in case of injury of the lateral wall, an ST-segment depression will be especially recorded in V1-V2, and in case of injury of the inferobasal wall, the ST-segment depression will be recorded especially in V2-V3. However, further perfusion studies, with imaging techniques in the acute phase have to be done to validate this hypothesis. 

Consequently, in order to better assess the prognosis and the extent of the ACSs, and infarcts in the chronic phase, it is very important in the acute phase to establish the correlation between the ST-segment deviations/T changes and the site of occlusion and the area at risk (p. 66), and in the chronic phase between leads with Q wave and number and location of left-ventricular segments infarcted (p. 139) (Figures 1.8 and 1.9). 

In acute phase, usually the ECG shows at the same time patterns of injury, ischaemia and even necrosis, and in chronic phase there are frequently Q waves and abnormal T waves. These different ECG patterns are not present exactly in the same leads, because although the areas of infarction, injury and ischaemia often coincide, they are not usually identical and especially the injury pattern (ST-segment deviations) in acute phase is present in more leads than is the necrosis pattern (Q wave or equivalent) in chronic phase. 

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