Table 1.

Traditional Pharmacological Approaches for Acute Coronary Syndrome (ACS)

Class of Medications	Mechanism of Action	Efficacy for Hard Clinical Outcomes in ACS
β-Blockers	Decrease heart rate, blood pressure, and contractility through antagonism of β1 receptors	Decrease mortality in ACS,^18–20 Intravenous use increases risk of cardiogenic shock,²² Long-term secondary prevention benefit is less certain in patients without heart failure or reduced left ventricularsystolic function²¹
Nitrates	Decrease preload through venodilation; vasodilate coronary arteries	No benefit on mortality^31,32
Calcium channel blockers	May vasodilate, reduce heart rate, or decrease contractility depending on specific drug	No clear benefit on mortality or reinfarction in ACS,³⁵ Increased reinfarction rate when nifedipine is used alone in ACS³⁴
Angiotensin-converling enzyme inhibitors	Block conversion of angiotensin 1 to angiotensin II and decrease systemic vascular resistance	Decrease mortality and heart failure when used in acute myocardial infarction.^31,32,37,38 Long-term secondary prevention benefit in patients with normal ejection fraction is less certain^41–44
Angiotensin II receptor blockers	Displace angiotensin II from the angiotensin II type 1 receptor and decrease systemic vascular resistance	Noninferiorto ACE-I in reducing mortality and cardiovascular events after ST-segment elevation myocardial infarction⁴⁷
Aldosterone antagonists	Competitively inhibit binding of aldosterone to receptors and prevent detrimental effects of renin–angiotensin–aldosterone system cascade	Reduce mortality and sudden cardiac death in patients with acute Ml with reduced ejection fraction and symptoms of heart failure or diabetes mellitus⁴⁸