Acute myocardial infarction. See

Alteplase (6 to 10 mg IV bolus over the first 1 to 2 minutes, then 20 mg/hour for an additional 2 hours) is indicated for lysis of thrombi obstructing coronary arteries in management of acute myocardial infarction (see Eigure 44). 

Aspirin, by covalently acetylating the active site of cyclooxygenase, blocks the production of TXAj from its major precursor, arachidonic acid. By causing this mild hemostatic defect, low-dose aspirin has been shown to be effective in prevention of acute myocardial infarction (see Clinical Comments). For Ivan Applebod (who has symptoms of coronary heart disease), aspirin is used to prevent a first heart attack (primary prevention). For Ann Jeina and Cora Nari (who already have had heart attacks), aspirin is used to prevent a second heart attack (secondary prevention). 

Alteplase has proven effective in the early treatment of patients with acute myocardial infarction (i.e. those treated within 12 h after the first symptoms occur). Significantly increased rates of patient survival (as measured 1 day and 30 days after the initial event) are noted when tPA is administered in favour of streptokinase, a standard therapy (see later). tPA has thus established itself as a first-line option in the management of acute myocardial infarction. A therapeutic dose of 90-100 mg (often administered by infusion over 90 min) results in a steady-state alteplase concentration of 3-4 mg l 1 during that period. However, the product is cleared rapidly by the liver, displaying a serum half-life of approximately 3 min. As is the case for most thrombolytic agents, the most significant risk associated with tPA administration is the possible induction of severe haemorrhage. 

Retavase (Reteplase, rtPA see Ecokinase) Boehringer- Mannheim/ Centocor Acute myocardial infarction 1996 (USA)... 

Procainamide INa (primary) and IKr (secondary) blockade Slows conduction velocity and pacemaker rate prolongs action potential duration and dissociates from INa channel with intermediate kinetics direct depressant effects on sinoatrial (SA) and atrioventricular (AV) nodes Most atrial and ventricular arrhythmias drug of second choice for most sustained ventricular arrhythmias associated with acute myocardial infarction Oral, IV, IM eliminated by hepatic metabolism to /V-acetylprocainamide (NAPA see text) and renal elimination NAPA implicated in torsade de pointes in patients with renal failure Toxicity Hypotension long-term therapy produces reversible lupus-related symptoms... 

Thrombolytic therapy in the management of acute myocardial infarction requires careful patient selection, the use of a specific thrombolytic agent, and the benefit of adjuvant therapy. Considerable controversy surrounds the question of greater safety or efficacy of t-PA compared with the other thrombolytic agents (see Thrombolytic Drugs for Acute Myocardial Infarction). 

Observations from our laboratory show that post-infarcted myocardium is more tolerant to ischemia and reperfusion injury. Increased postischemic recovery of function and decreased LDH release were found in perfused rat hearts after 8 weeks of an acute myocardial infarction. This response was associated with downregulation of TRal and TRpi thyroid hormone nuclear receptors. Thus, it is likely that tissue hypothyroidism (at the receptor level) might account for the increased tolerance of those hearts to ischemia and reperfusion injury.215 See also chapter 2. 

Figure 8.16 (A) The ECG of a patient with an acute myocardial infarction due to LAD occlusion proximal to D1 and S1 (ST-segment elevation from V1 to V4 and in VR, and ST-segment depression in II, III, VF (II > III), V4 and V5-V6). The injury vector is slightly directed to the right (see Figures 4.18 and 4.19) and this explains the isoelectric ST in...

Figure 8.31 (A) A patient with an acute myocardial infarction with evident ST-segment elevation and frequent, polymorphic, repetitive, PVC that triggers VF (asterisk) that was resolved with cardioversion. (B) Primary ventricular fibrillation in a patient with acute Ml. VF appears suddenly, without previous PVC and without evident ST-segment elevation. However, the underlying sinus rhythm is fast, which can often be present in cases of primary ventricular fibrillation and express the sympathetic overdrive that is usually present in acute phase of Ml (see p. 252). The electric cardioversion resolved the problem.

Finally, high intraluminal shear forces develop in these thinning or eroded areas of the plaque s fibrous cap, inducing macrophages to secrete additional metalloproteinases that further degrade the arterial-fibrous cap matrix. This contributes further to plaque rupture and thrombus formation (see Fig. 34.22). The consequence is a macrovascular ischemic event such as an acute myocardial infarction (AMI) or an acnte cerebrovascular accident (CVA). 

Since her admission to the hospital for an acute myocardial infarction, Ann ] Jeina has been taking the bile salt sequestrant cholestyramine and the HMG-CoA rednctase inhibitor pravastatin to lower her blood cholesterol levels (see Chapter 34). She also takes 160 mg acetylsalicylic acid (ASA aspirin) each day. At her most recent visit to her cardiologist, she asked whether she shonld... 

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