Unstable angina / non ST elevation myocardial infarction beta blockers


 * Associate Editors-In-Chief: ; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.; Smita Kohli, M.D.;

Mechanism of Benefit

 * In Unstable angina/NSTEMI, the primary benefits of beta blockers are due to inhibition of beta-1 adrenergic receptors, which results in a decrease in cardiac work and myocardial oxygen demand.
 * Slowing of the heart rate also has a favorable effect, acting not only to reduce myocardial oxygen demand(MVO2) but also to increase the duration of diastole and diastolic pressure-time, a determinant of forward coronary flow and collateral flow.

Indications

 * In the absence of contraindication(especially hypotension, heart failure and hemodyanamic instability), beta blockers should be initiated either orally or intravenously within first 24 hours.

Contra-indication

 * Patients with marked first-degree AV block (i.e., ECG PR interval greater than 0.24 s), any form of second- or third-degree AV block in the absence of a functioning implanted pacemaker, a history of asthma, severe LV dysfunction or HF (e.g., rales or S3 gallop) or at high risk for shock (see below) should not receive beta blockers on an acute basis.

Clinical Trial data
Two recent studies(GUSTO-I and COMMIT) have revealed that early aggressive beta blockade poses a substantial net hazard in hemodynamically unstable patients and should be avoided.

In the COMMIT study, the utility of early intravenous followed by oral beta blocker (metoprolol) was tested in 45,852 patients with MI (93% had STEMI, 7% had NSTEMI) which showed that neither the composite of death, reinfarction, or cardiac arrest nor death alone was reduced for up to 28 d in the hospital. Overall, a modest reduction in reinfarction and ventricular fibrillation (which was seen after day 1) was counterbalanced by an increase in cardiogenic shock, which occurred early (first day) and primarily in those who were hemodynamically compromised or in HF or who were stable but at high risk of development of shock. Risk factors for shock were older age, female sex, time delay, higher Killip class, lower blood pressure, previous hypertension, higher heart rate, and ECG abnormality.

In GUSTO-I retrospective analyses, the administration of intravenous atenolol combined with late oral administration was associated with higher mortality than late oral administration alone. The authors concluded that late oral administration of atenolol might be sufficient and may offer just as good of outcomes as that coupled with early IV administration. Overall, the rationale for beta-blocker use in all forms of CAD, including Unstable angina, is generally favorable, with the exception of initial heart failure.

==ACC / AHA Guidelines (DO NOT EDIT) ==

{{cquote|

Class I
1. Oral beta blocker therapy should be initiated within the first 24 h for patients who do not have 1 or more of the following: a- Signs of HF, b- Evidence of a low output state, c- Increased risk for cardiogenic shock, or d- Other relative contraindications to beta blockade (PR interval >0.24 sec, second or third degree heart block, active asthma, or reactive airway disease). (Level of Evidence: B)

Class IIa
1. It is reasonable to administer intravenous (IV) beta blockers at the time of presentation for hypertension to Unstable angina / NSTEMI patients who do not have 1 or more of the following: a- Signs of HF, b- Evidence of a low output state, c- Increased risk for cardiogenic shock, d- Other relative contraindications to beta blockade (PR interval >0.24 s, second or third degree heart block, active asthma, or reactive airway disease). (Level of Evidence: B)

Class III
1. It may be harmful to administer intravenous beta blockers to Unstable angina / NSTEMI patients who have contraindications to beta blockade, signs of HF or low output state, or other risk factors for cardiogenic shock. (Level of Evidence: A)}}