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Beta blockers are indicated for the treatment of acute myocardial infarctions. During a myocardial infarction, systemic stress causes an increase in circulating catecholamines. [22] [23] This results an increase in heart rate and blood pressure, therefore increasing myocardial oxygen demand.
At least 10% of patients with STEMI do not develop myocardial necrosis (as evidenced by a rise in cardiac markers) and subsequent Q waves on EKG after reperfusion therapy. Such a successful restoration of flow to the infarct-related artery during an acute myocardial infarction is known as "aborting" the myocardial infarction.
As a result, there is dilatation of the chamber arising from the infarct region. The initial remodeling phase after a myocardial infarction results in repair of the necrotic area and myocardial scarring that may, to some extent, be considered beneficial since there is an improvement in or maintenance of LV function and cardiac output. Over time ...
Class Ib drugs shorten the action potential of myocardial cell and has a weak effect on the initiation of phase 0 of depolarization Treat and prevent ventricular arrhythmia during and immediately after myocardial infarction, though this is now discouraged given the increased risk of asystole; Ic Encainide; Flecainide; Moricizine; Propafenone
Myocardial infarction (heart attack) Since beta 1 receptor are mainly located in the heart, most beta 1 blockers take abnormalities associated with the heart as the target. [5] It treats medical conditions like hypertension, arrhythmias, heart failure, chest pain, myocardial infarction.
The treatment with β-blockers reduces the incidence of sudden heart failure when the patient has already had a myocardial infarction. The reason is probably because of their anti-arrhythmic effects and also anti-ischemic effects. [10] A β-blocker therapy is also useful in myocardial infarction, independent to heart failure.
Metoprolol is used for a number of conditions, including angina, acute myocardial infarction, supraventricular tachycardia, ventricular tachycardia, congestive heart failure, and prevention of migraine headaches. [4] It is an adjunct in the treatment of hyperthyroidism. [17]
Myocardial rupture is most common three to seven days after myocardial infarction, commonly of small degree, but may occur one day to three weeks later. In the modern era of early revascularization and intensive pharmacotherapy as treatment for MI, the incidence of myocardial rupture is about 1% of all MIs. [6]
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