Chapter 8.1

ACS

ACS

— is primarily caused by rupture of an atherosclerotic plaque with subsequent platelet adherence, activation, aggregation, and the activation of the clotting cascade. Ultimately, a thrombus composed of fibrin and platelets may develop, resulting in incomplete or complete occlusion of a coronary artery.

• ST-segment elevation MI (STEMI)

• non-ST segment elevation (NSTE)-ACS

ACS is a spectrum of disease encompassing — or —, which are classified according to ECG changes and underlying pathophysiology.3

MI type 1

The predominant cause of ACS in more than 90% of patients is atheromatous plaque rupture, fissuring, or erosion of an unstable atherosclerotic plaque. This is called an —, which generally occurs in coronary arteries where the stenosis occludes less than 50% of the lumen prior to the event, rather than a more stable 70% to 90% stenosis of the coronary artery.4

MI type 2

— is related to a reduction in myocardial oxygen supply or an increase in myocardial demand in the absence of a coronary artery process

MI type 3

— is defined as MI resulting in death without the possibility of measuring biomarkers, while MI types 4 and 5 occur during revascularization procedures

• STEMI

• NSTEMI

• An injury that transects the entire thickness of the myocardial wall results in a — which will result in the release of biomarkers, mainly troponins T or I, from the necrotic myocytes into the bloodstream.

• An — is limited to the subendocardial myocardium and is usually smaller and not as extensive as a STEMI

Troponin

NSTEMI differs from UA in that ischemia is severe enough to result in the release of what biomarker.

• adenosine diphosphate (ADP)

• thromboxane A2 (TXA2)

Following plaque rupture, a clot (a partially or completely occlusive thrombus) forms on top of the ruptured plaque. The thrombogenic contents of the plaque are exposed to blood elements. Exposure of collagen and tissue factor induce platelet adhesion and activation, which promote the release of platelet-derived vasoactive substances, including — and —. These produce vasoconstriction and potentiate platelet activation

glycoprotein (GP) IIb/IIIa

Furthermore, during platelet activation, a change in the conformation in the — surface receptors of platelets occurs that cross-links platelets to each other through fibrinogen bridges. This is considered the final common pathway of platelet aggregation

Fibrin

Simultaneously, the extrinsic coagulation cascade pathway is activated as a result of exposure of blood components to the thrombogenic lipid core and disrupted endothelium, which are rich in tissue factor. This leads to the production of thrombin (factor IIa), which converts fibrinogen to — through enzymatic activity. It stabilizes the clot and traps red blood cells, which gives the clot a red appearance. Therefore, the clot is composed of cross-linked platelets and fibrin strands.

• Inclusion of platelets gives the clot a white appearance.

Ventricular remodeling

It is a process that occurs in several cardiovascular (CV) conditions including HF and following an MI. It is characterized by left ventricular dilation and reduced pumping function of the left ventricle, leading to cardiac failure.

• ACE inhibitors

• ARBs

• β-blockers

• Aldosterone antagonists

Use of — can slow down or reverse ventricular remodeling through inhibition of the renin-angiotensin aldosterone system and/or through improvement in hemodynamics (decreasing preload or afterload).10 These agents also significantly improve survival in ACS patients.

Echocardiogram

At some point during hospitalization, prior to discharge, patients with a definite ACS should have their left ventricular function (LVF) evaluated. The most common way LVF is measured is using an — to calculate the patient’s left ventricular ejection fraction (LVEF, percent of blood pumped out of the left ventricle with each contraction)

40% (0.40)

LVF is one of the strongest predictors of mortality following MI. Patients with LVEF less than — are at high risk of death. LVEF is an important factor to consider when contemplating the use of several drugs, such as ACE inhibitors and aldosterone antagonists.

Cardiogenic shock

The most serious early complication of MI is—, occurring in approximately 7% of hospitalized patients presenting with STEMI. Mortality in patients with this and with MI is high, approaching 60%

ACS

The classic symptom of an — is:

• severe new-onset or increasing substernal angina

• at least 20 minutes in duration

• most often occurring at rest

• The pain may radiate to the shoulder, down the left arm, and to the back or jaw

12-lead ECG

Within 10 minutes of presentation to an ED with symptoms of ischemic chest discomfort, a — should be obtained and interpreted.

• If the first ECG is not diagnostic, additional ECGs should be performed every 15 to 30 minutes for the first hour if the patient is still symptomatic and the clinician has a high suspicion of ACS. When possible, an ECG should be performed by emergency medical system providers to reduce the delay until myocardial reperfusion

• ST-segment elevation (STE)

• ST-segment depression

• T-wave inversion

Key findings on review of an ECG that indicate myocardial ischemia or infarction are: —

• (a) symptoms of ischemia

• (b) ECG changes of new ischemia or development of pathological Q waves

• (c) imaging evidence of new loss of viable myocardium

• (d) new regional wall motion abnormality

• (e) identification of an intracoronary thrombus by angiography or autopsy

The diagnosis of MI is confirmed when the following conditions are met in a clinical setting consistent with myocardial ischemia: “Detection of a rise and/or fall of cardiac biomarkers with at least one value above the 99th percentile of the upper reference limit and with at least one of the following: —

• Patient symptoms

• PMH

• ECG

• Troponin

— are utilized to stratify patients into low, medium, or high risk of death, MI, or likelihood of failing pharmacotherapy and needing urgent coronary angiography and PCI

• fibrinolytics (eg, alteplase, reteplase, and tenecteplase)

• primary PCI

Patients with STEMI are at the highest risk of death; therefore, immediate reperfusion strategies should be initiated. The ACCF/AHA/ SCAI PCI guidelines define a target time to initiate reperfusion treatment as:

• within 30 minutes of first medical contact for —

• within 90 minutes from presentation for —

• (a) early restoration of blood flow to the infarct-related artery

• (b) prevention of death and other MI complications

• (c) prevention of coronary artery reocclusion

• (d) relief of ischemic chest discomfort

• (e) resolution of ST-segment and T-wave changes on the ECG

Short-term desired outcomes in a patient with ACS are:

primary PCI

Early reperfusion therapy with — of the infarct artery within 90 minutes from the time of hospital presentation is the reperfusion treatment of choice for patients with STEMI who present within 12 hours of symptom onset

primary PCI

For — in STEMI, the patient is taken from the ED to the cardiac catheterization laboratory and undergoes coronary angiography with either balloon angioplasty or, preferably, placement of a bare metal or drug-eluting intracoronary stent in the artery associated with the infarct.5

True

True or false

• Results of biochemical marker tests do not need to be available when the decision to proceed to primary PCI is made

True

True or false

• In addition, intracranial hemorrhage (ICH) and major bleeding risks from primary PCI are lower than the risks of severe bleeding events following fibrinolysis.

True

Patients presenting to facilities that do not have interventional cardiology services can be transferred when a protocol that minimizes delays has been established between institutions and if primary PCI can be performed within the first 120 minutes of first medical contact.

• True or false

  • Immediate transfer to a PCI-capable facility is recommended for patients who develop cardiogenic shock or acute severe HF, irrespective of the timing of presentation.

Fibrinolytic agent

Administration of a — is indicated in patients with STEMI who present to the hospital within 12 hours of the onset of chest discomfort, who are initially seen at a non-PCI capable hospital and who have an anticipated time from first medical contact-to-device greater than 120 minutes if transferred to a PCI capable hospital

Fibrinolytic agent

— therapy is preferred over primary PCI when there is no cardiac catheterization laboratory in a hospital and the delay from first medical contact-to-device would exceed 120 minutes if the patient was transferred to a PCI-capable hospital

False

True or False

• It is necessary to obtain the results of biochemical markers before initiating fibrinolytic therapy.

primary PCI

Because administration of fibrinolytics results in clot lysis, patients who are at high risk of major bleeding (including ICH) presenting with an absolute contraindication should not receive fibrinolytic therapy; — is preferred.

• alteplas

• reteplase

• tenecteplase

Generally, a more fibrin-specific agent such as — is preferred over a non-fibrin-specific agent such as streptokinase.

• Fibrin-specific fibrinolytics open a greater percentage of infarcted arteries.

• Intracranial Hemorrhage (ICH)

• Major Bleeding

What are the most serious side effects of fibrinolytic agents

False

True or false

• The risk of ICH is lower with fibrin-specific agents than with streptokinase.

NSTE-ACS

Fibrinolytic therapy is not indicated and should not be used in patients with — because increased mortality has been reported with these agents compared with controls in clinical trials

• PCI

• coronary artery bypass graft (CABG)

Clinical practice guidelines recommend coronary angiography followed by either — or — surgery revascularization as an early treatment (early invasive strategy) for patients with NSTE-ACS at an elevated risk for death or MI, including those with a high-risk score or patients with refractory angina, hemodynamic instability or electrical instability.

• ASA

• P2Y12 inhibitor antiplatelet (clopidogrel, prasugrel, or ticagrelor)

All patients undergoing PCI should receive — therapy indefinitely. A — should be administered concomitantly with ASA for at least 12 months following PCI for a patient with ACS

True

True or false

• A longer duration of P2Y12 inhibitor therapy may be considered for select patients with a low-bleeding risk receiving a drug-eluting stent (DES) because the risk of stent thrombosis is greater upon cessation of dual antiplatelet therapy (DAPT).

Stress testing

— is indicated in patients with NSTE-ACS when an initial ischemia-guided strategy is selected and for patients with STEMI where primary PCI was not performed and who do not have high-risk clinical characteristics for which earlier coronary angiography would be warranted

• Intranasal oxygen (If oxygen saturation is low)

• SL NTG

• ASA

• PSY12 Inhibitor

• Anticoagulant

According to ACC/ACCF/AHA STEMI and NSTE ACS practice guidelines, additional pharmacotherapy that all patients should receive within the first day of hospitalization, and preferably in the ED, are:

GP IIb/IIIa inhibitor (GPI) (ATE)

What class of drugs may be administered with unfractionated heparin (UFH) for patients with STEMI undergoing primary PCI.

NSTE-ACS

High-risk patients with what ACS should proceed to early angiography (within 24 hours) and select high-risk patients may receive a GPI?

IV NTG

What drug may be given in select patients still experiencing pain despite SL NTG?

True

True or false

• It is reasonable to administer morphine to patients with refractory angina as an analgesic and a venodilator that lowers preload.

Oral β-blockers

This class of drugs should be initiated within the first day in patients without cardiogenic shock or other contraindications.

True

True or false

• High-intensity statin therapy should be initiated or continued during hospitalization in all patients without contraindications.