Post-myocardial infarction

P-Blockers and ACE inhibitors are also indicated for post-myocardial infarction for the reduction of cardiovascular morbidity and mortality, as are aldosterone antagonists, in post-myocardial infarction patients with reduced left ventricular systolic function and diabetes or signs and symptoms of heart failure.2,48... 

NRT should be used with caution in patients within 2 weeks post-myocardial infarction, those with serious arrhythmias, and those with serious or worsening angina. 

Using plasma procainamide levels as a guide to therapy, it has been demonstrated (K13), contrary to evidence derived from uncontrolled trials (E2), that procainamide is valuable for preventing as well as controlling ventricular arrhythmias which develop in the immediate post-myocardial infarct period and are one of the main causes of death at this time. 

Congestive heart failure (CHF) post-myocardial infarction (Ml) To improve survival of stable patients with left ventricular systolic dysfunction (ejection fraction 40% or less) and clinical evidence of CHF after an acute Ml. 

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...

Plasminogen, an inactive precursor, is activated to plasmin which as a protease is able to break down fibrin clots. The thrombolytic agents in use promote the conversion of plasminogen to plasmin at the site of a thrombus. Indications include post-myocardial infarction treatment. The thrombolytic must be administered within 6 hours for an optimal effect. Other indications are treatment of acute pulmonary thromboembolism, deep-vein thrombosis, acute arterial thrombosis and thromboembolism, as well as in the clearance of arteriovenous catheters and can-nulae. Agents are streptokinase, anistreplase, urokinase, alteplase, reteplase and tenecteplase. 

Left ventricular dysfunction Post-myocardial infarction Non-diabetic nephropathy Type 1 diabetic nephropathy Type 2 diabetes mellitus Proteinuria Hyperkalaemia Bilateral renal artery stenosis disease... 

Post-myocardial infarction Chronic obstructive Bradycardia... 

Blocker therapy has been shown to reduce post-myocardial infarction mortality by approximately 20% and is well accepted as a part of the postinfarction therapeutic regimen. In patients without any organic heart disease, a proarrhythmic effect is less common, and Class I agents may be safe and effective for the suppression of symptomatic VPC. 

Lidocaine Post-myocardial infarct arrhythmias Ventricular tachycardia... 

Post myocardial infarction left ventricular function, lower resting heart rate... 

It is indicated in pulmonary hypertension, prophylaxis of angina pectoris, post myocardial infarction therapy, CHF and acute LVF. It is not recommended for acute attacks of angina. 

Flecainide Sodium channel (INa) blockade Dissociates from channel with slow kinetics no change in action potential duration Supraventricular arrhythmias in patients with normal heart do not use in ischemic conditions (post-myocardial infarction) Oral hepatic, and kidney metabolism half life 20 h Toxicity Proarrhythmic... 

Men aged over 50 years with established CAD have an ED incidence of 40% and in those post myocardial infarction or post vascular surgery the incidence ranges from 39% to 64%, depending on diagnostic criteria (15). 

Post-surgical and post-myocardial infarction ventricular septal defect... 

The vast majority of ventricular septal defects (VSD) are congenital. Acquired VSDs are almost always a consequence of septal rupture following myocardial infarction, traumatic VSDs as a consequence of sharp or blunt chest trauma are exceptionally rare. Typically the post myocardial infarction ventricular septal defect (PMIVSD) occurs within the first week after the event (41). In the current era of thrombolysis about 0.2% of patients develop a VSD as a result of septal necrosis. Medical management of these patients is limited and carries a 30-day mortality of 94% compared with 47% who were treated surgically (42). 

Amplatzer post myocardial infarction ventricular septar defects (VSD) occluder. 

Post-myocardial infarction -blockade Timolol Propanolol Reduced CHD and total mortality, reinfarction Norwegian Timolol Study BHAT >5,600 13... 

Michal, E., Basu, S., and Kuo, H.-C. Methods and Compositions for Treating Post-Myocardial Infarction Damage, 2006-447340 2007218118 (2007). 

There is strong evidence that beta-blockers can reduce mortality by up to 23% post myocardial infarction. Beta-blockers should be used to reduce the risk of further cardiovascular disease events irrespective of whether the blood pressure is raised or not. There is no evidence that any beta-blocker is more effective than another in secondary prevention, hence a beta-blocker which is well tolerated and that can be taken once or twice daily should be used. Atenolol, bisoprolol or metoprolol are suitable agents. These agents are not specifically licensed post myocardial infarction but all are licensed for angina and the doses for this indication should be used i.e. 

ACE inhibitors reduce morbidity and mortality post myocardial infarction in patients with left ventricular systolic dysfunction (LVSD). This is thought to be mediated via their action on the renin-angiotensin system. More recent evidence from the HOPE study (2000) has established that ACE inhibitors given to high risk CVD patients who had not got low ejection fraction or heart failure resulted in benefits in terms of reduced morbidity and mortality. 

The NICE clinical guidelines on secondary prevention of myocardial infarction (2007) now recommend that ACE inhibitors should be used in all patients post myocardial infarction with or without LVSD (i.e. ejection fraction <40%). 

Within the HOPE study ramipril was the agent of choice and this would be an appropriate ACE inhibitor to use post-myocardial infarction. Ramipril is licensed for use post myocardial infarction at a dose of 2.5 mg twice daily initially (started in hospital 3-10 days after infarction), increased after 2 days to 5 mg twice daily. Maintenance doses are 2.5 mg-5 mg twice daily. 

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