Thrombosis in Myocardial Infarction

Antman developed a thrombosis in myocardial infarction (TIMI) risk score based on a database of 15,078 patients with STEMI or new onset of complete left bundle branch block (8), The score was validated in the TIMI 9 data set. Ten characteristics of these patients accounted for 97% of the predictive capacity of their multivariate model. These are included in the risk score (Table I). Points were given for difference parameters as listed in Table I. The risk score had a strong association with 30-day mortality. There was a greater >40-fold increase in mortality from TIMI risk score 0 to >8 at 30 days (Table I) (8), The TIMI risk score is easy to apply and can be done at the bedside. 

Decreased reperfusion at the microvascular level might also contribute to the poorer prognosis of diabetic patients. Recent work in acute myocardial infarction (Ml) has suggested that despite achieving comparable rates of thrombosis in myocardial infarction (TIMI)-3 flow, diabetics have poorer post-PCI myocardial reperfusion than nondiabetics, as evidenced by reduced ST-segment resolution and myocardial blush grade (15). 

Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone.

It is believed that heparin acts by neutralizing a number of active blood coagulation factors, thus disrupting the transformation of prothrombin into thrombin. Heparin is used to prevent thrombo-formation in myocardial infarctions, thrombosis, and embolism, for maintaining liquid conditions in the blood in artificial blood drcnlation and hemodialysis. Synonyms of this drug are arteven, hepalen, leparan, Uquemin, panheprin, vetren, and many others. 

Most drug discovery efforts focus on thrombin inhibition as a means to prevent the serious consequences of thrombus formation in myocardial infarction and stroke. Thrombin inhibitors may also prevent clot formation in patients prone to deep vein thrombosis or repeat heart attack. In combination with thrombus dissolution therapies, thrombin inhibitors may decrease the incidence of reocclusion due, in part, to the release of active clot-bound thrombin. 

Aspirin decreases the incidence of transient ischemic attacks, unstable angina, coronary artery thrombosis with myocardial infarction, and thrombosis after coronary artery bypass grafting (see Chapter 34 Drugs Used in Disorders of Coagulation). 

Therapeutic uses Streptokinase is approved for use in acute pulmonary embolism, deep venous thrombosis, acute myocardial infarction, arterial thrombosis, and occluded access shunts. 

Patients in atrial fibrillation who have a TIA or stroke without other clear etiology should be given anticoagulation therapy if there are no contraindications (European Atrial Fibrillation Trial Study Group 1993, 1995). Recent studies have shown that warfarin is as safe as aspirin in elderly patients with atrial fibrillation (Rash et al. 2007 Mant et al. 2007). Patients with presumed cardioembolic TIA or stroke secondary to other causes should certainly receive antithrombotic therapy. Also they may benefit from anticoagulation in certain circumstances, such as intracardiac mural thrombosis after myocardial infarction, although there have been no randomized trials in situations other than non-valvular atrial fibrillation. 

INR 2.0-3.0 Treatment of deep vein thrombosis pulmonary embolism systemic embolism prevention of venous thromboembolism in myocardial infarction mitral stenosis with embolism transient ischaemic attacks atrial fibrillation. 

If epoetin is given preoperatively without autologous predonation, there is an increased risk of hypertension, an increased risk of graft thrombosis and myocardial infarction in cardiac surgery, and an increased risk of venous thromboembolism in orthopedic patients (71). 

High doses of vitamin K can cause relapses in patients with thrombosis and myocardial infarction treated with dicoumarol (33). 

Even though apparently sudden, a heart attack is the end result of a buildup of causes over years, particularly atherosclerosis in the coronary arteries. The immediate cause is a blood clot (thrombus) that, once having formed, blocks the narrowed lumen of a coronary artery. This denies the affected part of the myocardium blood and therefore oxygen. Technically, this may be referred to as a coronary thrombosis or myocardial infarction (Ml). Angina pectoris, which should also be mentioned, is characterized by severe pain and oppression above the heart, radiating to the shoulder and down the left arm. 

Warfarin (initially 10 to 15 mg p.o. for three days) is indicated as an anticoagnlant in pntmonary emboli, deep-vein thrombosis (DVT), myocardial infarction (Ml), rhenmatic heart disease with heart valve damage, and atrial arrhythmias. 

Thrombolytics include tissue plasminogen activator (tPA, recombinant) and streptokinase (bacterial). They are used intravenously for short-term emergency management of coronary thromboses in myocardial infarction (MI), deep venous thrombosis, pulmonary embolism, and ischemic stroke (tPA). 

Coronary artery spasm and/or thrombosis may result in myocardial infarction, even in patients with no coronary disease. Diffuse myocardial necrosis similar to catecholamine myocarditis and chronic cardiomyopathy have been described. 

Excessive factor VIII activity in vulnerable arterial beds, for example atherosclerotic vessels, could lead to thrombotic events, such as venous thrombosis or myocardial infarction. In patients with hemophilia A... 

Although streptokinase is antigenic and frequently pyrogenic, these effects have not been sufficiently deleterious to preclude clinical utility.Clinical experience with this agent has been gained now in most types of thromboembolic diseases,85 with generally favorable results in the treatment of deep vein thrombosis (within 96 hours of onset of symptoms) and pulmonary embolism.9,85,86 A major effort has been expended in recent years to Investigate the usefulness of streptokinase in myocardial infarction, but results in this area are still open to ques tion.13 > 85,87-90... 

Indications for treatment with streptokinase include acute occlusion of arteries, deep vein thrombosis, and pulmonary embolism. Streptokinase therapy in coronary thrombosis, which is the usual cause of myocardial infarction (54,71,72), has proved to be valuable. In this frequently fatal condition, the enzyme is adrninistered intravenously at a dose of 1.5 million units over 60 min, or given by intracoronary infusion at a 20,000- to 50,000-unit bolus dose followed by 2000 to 4000 units/min for 60 min therapy must be instituted as soon as practicable after the diagnosis of heart attack is made. For deep vein thrombosis, pulmonary embolism, or arterial occlusion, streptokinase is infused at a loading dose of 250,000 units given over 30 min, followed by a maintenance dose of 100,000 units over a 60-min period. 

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