Unstable Angina, Non-St-Elevation Myocardial Infarction-Acute Coronary Syndrome



Unstable Angina, Non-St-Elevation Myocardial Infarction-Acute Coronary Syndrome


Talal T. Attar

Rebecca Miller



INTRODUCTION


Epidemiology

The 2020 Heart Disease and Stroke Statistics update of the American Heart Association (AHA) has reported that in the United States the prevalence of coronary heart disease (CHD) is 6.7% in persons 20 years of age or older. The prevalence of myocardial infarction (MI) is 3.0% in that population, with an MI every 40 seconds in the United States.

The median age at acute coronary syndrome (ACS) presentation is 65.6 years in males and 72 years in females.


PATHOGENESIS

ACS is the result of a sudden imbalance between myocardial oxygen consumption (MVO2) and demand. Coronary artery obstruction caused by atherosclerotic lesions is the most common cause of such imbalance. In the acute phase, the obstruction and the associated myocardial ischemia are caused by plaque rupture with superimposed obstructive thrombus. They can also be caused by hemorrhage inside the plaque core. Distal embolization from the ruptured plaque and the associated thrombus can also cause microvascular obstruction, resulting in myocardial ischemia or necrosis.


CLINICAL PRESENTATION

ACS, usually caused by sudden reduction in coronary blood flow, is a clinical term that encompasses a spectrum of presentations associated with acute myocardial ischemia. The classic presenting symptom of ACS is anginal chest pain. A dull, deep, ill-defined discomfort is felt in the substernal region with common radiation to the left arm. At times, the symptoms could be atypical with either unusual location of the pain (neck, back, epigastric region, etc) or the chest pain is replaced with “angina-equivalent” symptoms. These symptoms could be cardiovascular such as dyspnea, or at times can mimic gastric symptoms such as nausea and epigastric burning.

With clinically suggestive symptoms, electrocardiographic (ECG) findings divide ACS syndromes. With the presence of ST elevation, the presentation is characterized as ST-elevation myocardial infarction (STEMI). In the presence of ST depression, transient ST elevation, or T-wave inversion, the presentation is characterized as unstable angina (UA) or non-ST-elevation myocardial infarction (NSTE-ACS). A key branch point between those two syndromes is the presence of elevated cardiac biomarkers.

A normal ECG and negative cardiac biomarkers do not completely exclude an ischemic etiology if the clinical features of the presentation are highly suggestive. Such a scenario is classified as UA.




MANAGEMENT


Antianginal Therapy


Oxygen

Supplemental oxygen therapy should be administered to patients presenting with possible UA or NSTE-ACS with oxygen saturation below 90% or in respiratory distress.7,8 There is no evidence to support supplemental oxygen therapy in all patients with UA or NSTE-ACS because it may increase coronary vascular resistance and increase the risk of mortality in those without hypoxemia.7,18


Nitrates

Nitroglycerin reduces cardiac oxygen demand by primarily reducing cardiac preload, modestly reducing afterload, dilating coronary arteries, and increasing collateral blood flow to ischemic myocardial tissue. Sublingual nitroglycerin (0.3-0.4 mg) should be administered every 5 minutes for up to three doses in patients with continued ischemic pain.7 Nitroglycerin infusion is appropriate for patients with refractory ischemic symptoms, heart failure, or hypertension. Nitrate therapy is contraindicated within 24 hours of sildenafil or vardenafil administration or within 48 hours of tadalafil administration because of the risk of severe hypotension.7,8 Patients with right ventricular infarction may develop severe hypotension following the administration of nitroglycerin or other agents that reduce preload, so its use is contraindicated in such patients.7


Analgesics

Morphine is an opioid commonly used to alleviate acute or chronic pain; in the setting of UA or NSTE-ACS, morphine is a venodilator and can modestly reduce systolic blood pressure and heart rate by increasing vagal tone.7 Morphine (1-5 mg) may be given intravenously every 5 to 30 minutes as needed for chest pain refractory to nitrates and beta-blockers, but empiric use of morphine in all patients with ACS is associated with worse clinical outcomes and impaired absorption of oral antiplatelet medications.7,19 Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, naproxen, and celecoxib interfere with the antiplatelet activity of aspirin, and are associated with an increased risk of major adverse cardiovascular outcomes and should be avoided in patients with NSTE-ACS.7,20,21










Beta-blockers

Beta-blockers prevent sympathetic activation of beta-receptors in the myocardium, thus reducing heart rate, contractility, and blood pressure, and, subsequently, myocardial oxygen consumption. An oral beta-blocker should be initiated within 24 hours of presentation, provided there are no signs of heart failure or reduced cardiac output, increased risk of cardiogenic shock (age older than 70 years, heart rate >110 beats per minute, systolic pressure <120 mm Hg, late presentation after symptom onset), or other contraindications to beta-blocker therapy.7,8,22 Beta-blocker therapy is associated with reductions in cardiac ischemia, reinfarction, and ventricular arrhythmias, as well as increased long-term survival.7,8,23


Calcium Channel Blockers

Verapamil and diltiazem are non-dihydropyridine (non-DHP) calcium channel blockers that relax coronary vascular smooth muscle and reduce heart rate and blood pressure, thus increasing myocardial oxygen delivery and reducing myocardial oxygen demand. Oral non-DHP calcium channel blockers are recommended when beta-blockers are unsuccessful in relieving myocardial ischemia, contraindicated, or cause intolerable side effects.7


Ranolazine

Ranolazine reduces ventricular tension and myocardial oxygen consumption with minimal effect on blood pressure and heart rate. Ranolazine is approved for treatment of chronic angina, and the MERLIN-TIMI (Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST-Elevation Acute Coronary Syndromes-Thrombosis in Myocardial Infarction) 36 trial failed to demonstrate statistically significant reduction in major cardiovascular events in patients with ACS.24


Anticoagulant Therapy

Anticoagulants inhibit thrombin generation and activity, and have been shown to reduce ischemic outcomes in NSTE-ACS.7 Anticoagulation is recommended for all patients presenting with NSTE-ACS, regardless of initial treatment strategy, unless contraindicated.19


Unfractionated Heparin

Unfractionated heparin (UFH) enhances the activity of anti-thrombin III, inactivating thrombin and preventing the conversion of fibrinogen to fibrin. The anticoagulant effect and pharmacokinetics of UFH varies widely between patients.8 Weight-based dosing provides more consistent anticoagulation than fixed dosing of UFH.7 UFH is dosed as a 60 IU/kg bolus (up to 4000 IU) followed by 12 IU/kg/hour infusion (up to 1000 IU/hour) for 48 hours or until coronary angiography or percutaneous coronary intervention (PCI) is performed.7,8

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May 8, 2022 | Posted by in CARDIOLOGY | Comments Off on Unstable Angina, Non-St-Elevation Myocardial Infarction-Acute Coronary Syndrome
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