Authors: Ahmed Elsherif 1 ; Michelle Wyatt 2
Peer Reviewers: Stanley Oiseth 3 ; Joseph Alpert 4
Affiliations: 1 Suez Canal University; 2 Medical Editor at Lecturio; 3 Chief Medical Editor at Lecturio; 4 Tucson University, Arizona

Coronary heart disease (CHD), also called ischemic heart disease, includes coronary artery disease caused by atherosclerosis, stable angina, and acute coronary syndromes. Vasospastic angina occurs in patients with and without coronary artery disease, and stable angina refers to chest pain caused by fixed epicardial coronary artery obstruction.[1] The term acute coronary syndrome (ACS) applies to patients presenting with acute symptoms, usually chest pain, suspected of having unstable angina, or acute myocardial infarction (MI). Indeed, patients with acute MI can present without chest pain and may only have complaints of shortness of breath, diaphoresis, nausea, dizziness, or left arm pain. Patients with unstable angina do not have elevated lab test results for biomarkers of cardiac muscle damage (troponin), indicating myocardial cell death induced by ischemia. Individuals presenting with acute MI are divided into ST-elevation MI (STEMI) and non-ST-elevation myocardial infarction (NSTEMI); this distinction is essential for clinical management. Patients without ST segment elevation on ECG but with ST segment and T wave abnormalities indicating myocardial ischemia, plus positive cardiac enzymes, are diagnosed with NSTEMI. Those with ECG changes showing ST-elevations and positive cardiac enzymes are diagnosed with STEMI.[2] Coronary heart disease is the most common cause of death globally, increases with age, and at least 90% of CHD occurs in individuals with known risk factors. [3,4]

For further review of this topic, including links to lectures by specialists in the field, follow these links:

This article is not intended to substitute for professional medical advice and should not be relied on as health or personal advice. Always seek the guidance of your doctor or other qualified health professional with any questions you may have regarding your health or a medical condition.

Ischemic heart disease


Types of ischemic heart disease. Image by Lecturio.


Ischemic heart disease (IHD) describes a wide range of clinical conditions in which there is an imbalance between oxygen supply and the myocardial demand, resulting in ischemia to a portion of the myocardium. [5] IHD is classified into chronic, stable disease (stable angina) and acute, unstable disease (acute coronary syndromes).

Stable angina refers to chest pain when myocardial oxygen demand exceeds oxygen supply. Inadequate blood supply is most often due to coronary artery atherosclerotic disease.


The major coronary vessels are the right coronary artery (RCA), the left coronary artery (LCA), the left circumflex anterior artery (LCx), and the left anterior descending (LAD) artery.

Normal Coronary Circulation.
An individual’s specific coronary anatomy and dominance are clinically significant as the location of the thrombus results in varying clinical pictures (with different management indicated). Approximately 80–85% of people are “right-dominant,” [6,7] which means that the posterior descending artery (PDA) originates from the RCA. The other 15–20% are “left-dominant” (PDA originates from the LCx) or “codominant” (there are right and left PDAs originating from the RCA and LCx. The magnitude of an RCA infarct depends on the distance of the acute occlusion from the origin and the dominance of the vessel. A proximal RCA occlusion in a right-dominant patient can present with a right ventricular infarct and cardiogenic shock. In contrast, a distal RCA occlusion may present with a smaller area of inferoseptal infarct and inferior left ventricular (LV) dysfunction. Image by Lecturio.


IHD is the leading cause of death worldwide. It is considered the most common chronic illness in the United States, accounting for 42% of cardiovascular deaths. Stable angina occurs in about 14 % of patients with IHD, and unstable angina results in 1 million hospitalizations annually. [3,4]

Lifetime risk of coronary heart disease: [8]

  • At age 40: 49% in men and 32% in women
  • At age 75: 35% in men and 24% in women

Risk Factors

The most common risk factor of coronary heart disease is atherosclerosis of the epicardial coronary arteries,

esulting in partial or complete obstruction with subsequent inadequate perfusion of the myocardium supplied by its regional coronary artery.

Many risk factors contribute to the pathophysiology of coronary heart disease. Major modifiable risk factors include cigarette smoking, hypertension, diabetes mellitus, and hyperlipidemia. For the most part, atherosclerosis is an irreversible process. Defined risk factors can be reduced through lifestyle changes, including diet, exercise, maintaining a healthy weight, and smoking cessation. [9,10] Cholesterol-lowering medications such as statins may cause plaque regression in some cases.[11] Other risk factors for CHD include male gender, family history of CAD in a first-degree family member (< age 55 in men, < 65 in women), sedentary lifestyle, obesity, hyperglycemia, and psychological or emotional stress.[12]

Patients with MI at young ages (<30) may have familial lipid metabolism disorders, connective tissue disease, uncontrolled type 1 diabetes mellitus, or vasculitis. Coronary anomalies, substance abuse disorders, antiphospholipid syndrome, and hyperviscosity syndrome should also be considered during history taking.[13]

Pathophysiology of CHD

Stenosis of the coronary arteries can lead to an insufficient oxygen supply to the myocardial tissue or decreased coronary flow reserve, the ratio of maximum flow to resting flow. A vasodilatory stimulus in normal coronary arteries results in approximately a fourfold increase in flow rate compared to baseline. With progressive stenosis, baseline flow remains normal until the coronary artery is narrowed by 70%–75%. However, coronary flow reserve begins to decrease at 40%–50% diameter stenosis. Coronary flow reserve decreases to two times baseline at approximately 75% stenosis, indicating myocardial ischemia.[14,15]

Coronary Artery Disease

Drawings of a normal artery and an artery with an atherosclerotic plaque, as typically seen with coronary artery disease. The atherosclerotic plaque has an irregular morphology and may not involve the entire circumference of the artery, as depicted here. Image: “Coronary artery disease” by BruceBlaus. License: CC BY 3.0

Myocardial Oxygen Demand

Four major factors determine the oxygen demand of the myocardium:

  1. Heart rate
  2. Systolic blood pressure (afterload)
  3. Tension on the myocardial wall (preload)
  4. Myocardial contractility

Any clinical condition increasing these factors will also increase the myocardial oxygen demand and result in ischemia, such as tachycardia, hypertension, and ventricular hypertrophy.

Myocardial Oxygen Supply

The capacity of the blood to carry oxygen to the myocardium is affected by factors such as the hemoglobin level, oxygen tension, and the amount of extracted oxygen from hemoglobin to the tissue, which is related to 2,3 diphosphoglycerate levels. Another factor is coronary artery blood flow, which is affected by the following factors:

  • Coronary artery diameter–atherosclerosis is the most frequent cause of coronary artery narrowing and obstruction.
  • Coronary artery tone–reduces the oxygen supply without significant underlying atherosclerotic changes, as seen with vasospastic angina.
  • Perfusion pressure–determined by the pressure gradient from the aorta to the coronary arteries.
  • Heart rate–coronary artery flow occurs mainly during diastole; extreme tachycardia decreases the duration of diastole and blood flow into the coronary arteries.

Any clinical condition affecting these factors will reduce the myocardial oxygen supply and result in ischemia.[16]


Patients with coronary heart disease (CHD) can present with:

  1. Chronic disease–most commonly presents with stable angina, defined as substernal discomfort or pressure (the most widely used descriptor) precipitated by exertion or other stress, with radiation to the shoulder, jaw, or inner aspect of the arm relieved by rest or nitroglycerin in less than 10 minutes. It is typically triggered by physical exertion, psychological stress, or exposure to the cold. The same type and degree of exertion or stress (e.g., walking up 2 flights of stairs) produce the same symptoms. It usually subsides within 10 minutes after rest or taking nitroglycerin. Suspect ACS in angina lasting longer than 20 minutes. 
    • Note: Stable anginal pain is always of similar intensity and quality.
  2. Acute coronary syndromes (ACS)–almost always associated with rupture of an atherosclerotic plaque, followed quickly by partial or complete thrombosis of the affected artery. ACS is a term that includes unstable angina (UA) and acute myocardial infarction. Acute MI is divided into ST-segment elevation myocardial infarctions (STEMI), and non-ST-segment elevation myocardial infarction (NSTEMI), and their management differs.
  3. Unstable angina (UA) is defined as myocardial ischemia at rest or with minimal exertion in the absence of acute myocardial injury/necrosis. It may be characterized by: prolonged (>20 minutes) angina at rest; new onset of angina; angina that is increasing in frequency, duration, trigger threshold, or that which occurs after a recent episode of myocardial infarction. Many previously diagnosed UAs were probably NSTEMIs, which are now diagnosed with the sensitive biomarkers of necrosis, troponin I or T. [2]
    • Note: New-onset angina occurring for the first time is by definition unstable angina
  4. Sudden cardiac death (SCD)– unexpected death due to cardiac causes, usually within 1 hour of symptom onset in a person with or without known cardiac disease, or within 24 hours of last being seen well if the death is unwitnessed. SCD represents the first expression of CAD in many individuals who experience out-of-hospital cardiac arrest. Most cases are related to cardiac arrhythmias, and about 50% of all cardiac deaths are attributable to SCD.[17]
  5. Vasospastic angina–caused by vasospasm occurring at rest; may occur with or without underlying atherosclerosis in the coronary arteries.
  6. Post-infarction angina–occurs within 2 weeks after myocardial infarction.
  7. Silent myocardial ischemia–occurs without typical symptoms. It occurs more frequently in women, older adults, patients with diabetes (due to neuropathy), and patients with chronic kidney disease. Atypical symptoms such as dizziness, nausea, generalized weakness, malaise, and epigastric pain may be presenting complaints.



The classic presentation of a patient with stable ischemic heart disease starts with episodes of chest discomfort described as a sense of pressure, choking, heaviness, or tightness in the chest. The pain starts gradually, with the intensity increasing and decreasing (crescendo-decrescendo in nature) within minutes and typically lasts for 2–5 minutes and not longer than 20 minutes. Sometimes the pain is described as central substernal discomfort that the patient can’t localize but typically places his palm or clenched fist over the sternum. Typical pain radiates to one of the dermatomes between C8 to T4, most often to the left shoulder and left arm. It can also radiate to the interscapular region, back, epigastrium, and lower jaw.

Episodes of angina are provoked by physical exertion and emotional stress and are relieved within minutes by rest or sublingual nitroglycerin. Angina may be associated with shortness of breath, diaphoresis, dizziness, light-headedness, and fatigue.[5] Clinicians should inquire about risk factors such as smoking, hyperlipidemia, hypertension, and diabetes mellitus.


Physical examination is usually unremarkable in patients with stable angina when asymptomatic; however, clinicians should look for evidence of atherosclerosis at other sites, such as carotid bruits and peripheral vascular disease. A cardiac exam also evaluates for heart murmurs or extra sounds as evidence of valvular disease and left ventricular dysfunction.

Resting ECG

ECG is usually normal between attacks but may show evidence of previous myocardial infarction or conduction delays. During an episode of chest pain, reversible ST-segment depression (injury pattern) or elevation, with or without T-wave inversion, is suggestive of myocardial ischemia.

Resting ECG in a patient with stable angina during an episode of chest pain. Note the ST depression and T wave inversion in the lateral leads. These reversible changes are not seen after the pain resolves in a patient with stable CHD, and persistent changes with pain lasting more than 20 minutes signal an acute coronary syndrome with unstable angina. Image by Lecturio.

Exercise ECG (stress testing)

Noninvasive stress testing is used to establish the diagnosis and prognosis in patients with stable ischemic heart disease. Testing is done with a treadmill or bicycle for exercise, and imaging may be added with nuclear medicine testing, echocardiography, or cardiac MRI. A stress test with exercise treadmill testing (ETT) is generally safe in patients with no resting abnormalities on ECG. There is a small risk of death or MI in < 1 per 2500 tests. Contraindications are BP > 200/100 mm Hg, significant aortic stenosis, and hypertrophic cardiomyopathy. A treadmill ECG stress test is considered abnormal when horizontal or down-sloping ST-segment depression ≥ 1 mm at 60-80 ms after the J point is seen.[18]

In patients who cannot exercise due to physical limitations (e.g., leg amputation, severe arthritis), pharmacologic stress testing using vasodilators or dobutamine is an alternative to exercise for detecting physiologically significant coronary artery stenoses.


Stress-ECG showing ST-segment-depression (arrow) in columns C and D. An exercise treadmill test (ETT) is used to detect ischemia with exercise that is not present at rest. While exercising, this patient has at least 2 mm of ST depression indicative of ischemia. Some patients may have chest pain or arrhythmia provoked by stress testing. Planar or downsloping ST-segment depression of ≥ 1 mm is indicative of ischemia. Image: “Stress-ECG with ST-segment-depression (arrow) in columns C and D” by J. Heuser. License: CC BY-SA 3.0

Nuclear Cardiology Imaging

Stress myocardial perfusion imaging can show areas of diminished uptake of radioactive isotope by the myocardium at rest or during exercise. It helps diagnose CAD in patients with abnormal resting ECGs and equivocal ETTs and can be performed either with an ETT or a pharmacologic stress test. [19] A stress test with single-photon emission CT (SPECT) uses 99mTc-labeled agents, such as 99mTc-sestamibi. For patients who cannot complete an adequate exercise stress test, a vasodilator stress test with SPECT imaging uses agents such as dipyridamole, adenosine, or regadenoson (Lexiscan).


Angiography visualizes the locations and severity of coronary artery stenoses and is indicated when coronary revascularization is considered.

CT angiography is rapidly becoming the diagnostic test of choice when coronary artery disease is suspected. Coronary computed tomography angiography (CCTA) evaluates the extent of CAD and helps in planning potential interventional or surgical therapy. CCTA has high sensitivity and a corresponding low rate of false negatives. The CAD-RADS (Reporting and Data System) classifies findings based on the degree of maximal coronary stenosis to help guide management.[48]


General measures for all patients with CHD include discussion of lifestyle modification and control of the previously mentioned risk factors. It is essential to assess the extent and severity of atherosclerosis affecting different body organs.

Medical Treatment

  1. Antiplatelet therapy: Low-dose aspirin or clopidogrel (if aspirin is contraindicated due to allergy or intolerance) should be prescribed for all patients. Newer agents include ticagrelor and prasugrel.
  2. Antianginal therapy: Nitrates cause venous and arterial dilatation, thus lowering myocardial oxygen demand by reducing the preload and afterload on the heart. Sublingual nitroglycerin should be taken during an angina attack; it often relieves the pain within 2–3 minutes. It can also be taken prophylactically before strenuous exercise. Isosorbide mono-and dinitrate are long-acting nitrates taken regularly once or twice daily.
  3. Beta-blockers: work by lowering myocardial oxygen demand by reducing heart rate and contractility. Therapy aims to relieve angina and ischemia; beta-blockers also reduce mortality and re-infarction rates after MI.
  4. Calcium channel antagonists: also lower myocardial oxygen demand; they reduce blood pressure and decrease contractility.

Coronary Revascularization


A coronary angiogram is pictured in this photo, with the outline of the major coronary arteries filled with radiopaque dye. Note the left main coronary artery, the LAD, and its branches. Image: “A coronary angiogram” by Bleiglass. License: CC BY-SA 3.0

It is appropriate to manage stable angina with medical therapy. [20] Percutaneous coronary intervention (PCI) or surgery should be considered in patients with:

  • Low exercise capacity or ischemia at a low workload
  • Large areas of affected myocardium on imaging
  • Impaired LV function with ejection fraction <40%

PCI is mainly used in patients with single-vessel or 2-vessel disease with suitable anatomy, and coronary artery bypass graft (CABG) surgery is more often used in patients with 3-vessel or left main coronary disease.[21]


Several prognostic indicators determine the outcome of CHD:

  • LV function: Increased left ventricular end-diastolic pressure, increased ventricular volume, and reduced ejection fraction are associated with a poor prognosis.
  • Location and severity of coronary artery stenosis: Stenosis of the left anterior descending (LAD) artery (“the widow-maker”) is associated with greater risk and poor prognosis.
  • Number and severity of risk factors: patients with multiple risk factors for atherosclerotic cardiovascular disease (ASCVD) are associated with an increased risk of myocardial infarction with a worse prognosis.
  • The annual mortality rate in patients with stable ischemic heart disease has improved with medical treatments; the 1-year rate of cardiovascular death is 1.9%, with an all-cause mortality rate of 2.9%.[22]

Vasospastic Angina


Vasospastic angina is characterized by sudden-onset coronary artery spasm that leads to a reduction in coronary blood flow, causing chest pain without exertion that lasts less than 15–30 minutes. Formerly called Prinzmetal’s angina or variant angina, vasospastic angina is promptly relieved by short-acting nitrates even in the absence of underlying CAD. Myocardial ischemia causing ECG changes in patients with vasospastic angina is due to transient vasospasm with or without underlying CAD.


Vasospastic angina is an uncommon cause of myocardial ischemia, responsible for approximately 5% of angina cases. [23] Patients are generally younger (< age 50) than those with stable or unstable angina secondary to coronary artery atherosclerosis. This syndrome has a higher incidence in Japan compared to Western countries, with a higher prevalence in women. The overall incidence has decreased significantly over the past 30 years, possibly due to the increased use of calcium channel blockers to treat hypertension.


Coronary vasospasm can be associated with risk factors such as stress, smoking, cocaine or amphetamine use, nitrate withdrawal, and vasoconstrictor medications such as triptans. Rarely, coronary artery vasospasm may be triggered after CABG surgery or near a stent.[24] Generally, the specific trigger is unknown. Many patients don’t display the classical coronary risk factors except for smoking. Vasospastic angina (VSA) is associated with systemic vasomotor disorders such as migraine and Raynaud phenomenon, which suggests it may be part of a more generalized vascular disorder.


The underlying mechanism of VSA is unclear, and many theories have been put forward in recent years. Vasospasm occurs in response to local vasoconstrictor stimuli in the coronary segment. Impaired regulation of myofibril contraction in smooth muscle cells of coronary vessels causes smooth muscle hyperactivity, resulting in vasospasm. Abnormalities of the endothelium, such as a defect in nitric oxide synthase (NOS), can lead to reduced nitric oxide levels, a natural vasodilator. Coronary artery vasospasm can result from impairment of K+ ATP-dependent channels and hyperactivity of an intracellular enzyme rho-kinase. Sudden vasoconstriction from any of these mechanisms leads to decreased coronary blood flow, causing myocardial hypoxia and angina. Other factors have been suggested in the pathogenesis of coronary artery spasm, including autonomic nervous system dysfunction, magnesium deficiency, chronic low-grade inflammation, and increased oxidative stress. Genetic factors may be involved, as there is a 3-fold greater incidence in Japanese people. [25] It is possible that certain genetic mutations predispose to coronary artery spasm, such as those affecting the endothelial NOS gene.

Clinical Features: Symptoms of Vasospastic Angina

Patients experience very severe central chest pain, the same type of pain as classic angina. These attacks tend to happen at rest or during regular activity. Some patients may also experience these attacks during or after exercise, especially with coexisting fixed coronary artery stenosis. Other symptoms include shortness of breath and palpitations. Patients typically experience angina attacks in clusters, more often from midnight to early morning.

Patients with variant coronary syndrome often have asymptomatic ischemic episodes. If coronary artery spasm causes a prolonged disturbance in coronary blood flow, it can (uncommonly) lead to myocardial infarction even in the absence of underlying CAD.

Syncope may also occur if there are disturbances to the heart rhythm, such as asystole, atrioventricular block, or ventricular tachyarrhythmias. Fatal arrhythmias may cause sudden cardiac death.


Definitive vasospastic angina is diagnosed when chest pain responds to nitrates, and there are transient ischemic ECG changes seen, or if coronary arteriography documents >90% spasmodic constriction during an anginal episode.
Suspected vasospastic angina is diagnosed if nitrate-responsive angina is present, but no definite ECG changes or coronary spasm can be documented.


Electrocardiography is one of the essential keys to diagnosing vasospastic angina. ECG changes demonstrate transient ST-segment elevation (≥ 0.1 mV), ST-segment depression (≥ 0.1 mV), and may also include a taller T wave and negative U wave. These changes must be in at least two contiguous leads, be evident during the attack of chest pain, and resolve when the pain dissipates. An episode can often be induced by having the patient hyperventilate. Arrhythmias may occur during an episode of variant angina and manifest as ventricular tachycardia, atrioventricular block, or bradyarrhythmias.
If silent episodes of coronary spasm or arrhythmias are suspected, then a 24-hour Holter ambulatory monitor can be done, which records rhythm changes during symptomatic episodes.

ECG recorded in a patient with an episode of variant angina showing 2:1 sinus bradycardia with a prolonged PR interval, significant ST elevation (5–6 mm) in the inferior leads, and anterior ST depression. Image: by Ruisi M, Ruisi P, Rosero H, Schweitzer P. License: CC BY 3.0

Coronary Angiography

Diagnostic coronary arteriography is recommended if vasospastic angina is suspected by the history and ECG findings. It may either confirm the diagnosis or detect a high-grade fixed coronary obstruction.

Focal coronary artery spasm significantly reduces the diameter of the lumen, causing temporary occlusion and myocardial ischemia. Vasospasm can occur in normal-appearing arteries or arteries affected by atherosclerosis. The right coronary artery is most commonly affected; involvement of more than one artery is a negative prognostic factor. VSA is underdiagnosed, and documentation of myocardial ischemia with a demonstration of coronary artery spasm can be done with coronary angiography and a provocative stimulus such as acetylcholine or ergonovine.

Coronary angiography in a patient with vasospastic angina. A: Coronary angiography demonstrates 95% stenosis in the proximal LAD artery (arrow in A) after administering intravenous ergonovine, which also provoked the patient’s typical chest pain; C: After injection of intracoronary nitroglycerin, the apparent stenosis completely resolved (arrow in C), thus documenting vasospasm. Image: Coronary angiographyby W. Choi. License: CC BY 4.0, cropped by Lecturio.


With vasospastic angina, cardiac enzymes are not elevated (troponins and CK-MB).

Exercise Testing

Stress testing with ECG monitoring has variable results. ECG changes with exercise such as ST elevation or ST depression may point to fixed artery stenosis or coronary artery spasm.


Myocardial infarction and life-threatening arrhythmias include ventricular tachyarrhythmias or bradyarrhythmias, sinus arrest, or even an AV block from a severe ischemic episode following vasospasm. Sudden cardiac arrest, with or without syncope, can occur due to ischemia-induced ventricular fibrillation. Atherosclerosis can also occur later at the site of vasospasm, leading to local coronary thrombosis.


Medical Treatment

Sublingual nitroglycerin is used for VSA attacks; calcium channel blockers (CCB), such as diltiazem or amlodipine, are effective in preventing ischemia. Long-acting nitrates (e.g., isosorbide mononitrate) can be added if a CCB is not sufficient to control the episodes. Documentation of suppression of both symptomatic and more commonly occurring asymptomatic episodes by ambulatory electrocardiographic monitoring is needed. Regular physical activity/exercise can also help treat VSA. [26]

An implantable cardioverter-defibrillator (ICD) is recommended for patients with documented life-threatening ventricular arrhythmias.

Note: Drugs to avoid:

  • Non-selective beta-blockers (e.g., propranolol) can worsen vasospasm
  • Aspirin at high doses because it inhibits prostacyclin production, but low dose aspirin is permitted
  • Triptans used to treat acute migraines (e.g., sumatriptan) 
  • Fluorouracil (5-fluorouracil) may cause coronary artery spasm.


Myocardial infarction and life-threatening arrhythmias occur in approximately 25% of untreated patients.[27] Therapy appears to decrease the frequency of life-threatening events. If the condition is controlled early on, it can have a favorable prognosis. Complications, such as acute myocardial infarction and cardiac death, typically occur early on after the onset of angina. Patients who have coronary spasm in multiple arteries are prone to having fatal arrhythmias. Individuals who do not have coexisting coronary artery stenosis generally have a more benign prognosis and better survival than those with severely diseased arteries and coronary artery vasospasm. [28]

Review Questions

  1. An 18-year-old man presents to the emergency department with severe chest pain radiating to the back. ST-elevation is seen on the ECG, but his cardiac enzymes are normal. A coronary artery catheterization reveals a normal study. What is the most likely diagnosis?
    1. Stable angina
    2. Unstable angina
    3. Ludwig angina
    4. Vasospastic angina
    5. Vincent angina
  2. A 35-year-old Japanese woman comes to the clinic complaining of chest pain. For the last three years, she has had intermittent chest pain, mostly at night, that lasts up to 10 minutes. It awakens her from sleep and is associated with nausea and sweating. An electrocardiogram is unremarkable. What would be the most likely finding on a Holter monitor during an episode of chest pain?
    1. Normal ECG
    2. PR segment depression in most leads
    3. Prolonged QT interval
    4. Transient ST-segment elevation in the inferior leads
    5. Bradycardia with no other ECG changes
  3. A 56-year-old man who has been diagnosed with vasospastic angina comes to the emergency department with an acute episode of chest pain. Which of the following would be the initial drug of choice for this patient?
    1. Nitroglycerin patch
    2. Sublingual nitroglycerin
    3. Oral nitroglycerin
    4. Verapamil
    5. Amlodipine

Answers: 1D, 2D, 3B

Acute Coronary Syndrome (ACS)


Simple diagram delineating the differences in the clinical presentation and classification of ACS. Patients with symptoms of ACS require an ECG and labs drawn for troponin levels within 10 minutes of presentation in an emergency department, and if normal, repeat troponin levels in 2 to 3 hours to assess for changes consistent with NSTEMI. Image: “Abbreviations used for ACS (Acute coronary syndrome)” by J. Heuser. License: CC BY-SA 3.0


The term acute coronary syndrome (ACS) refers to patients with suspicion or confirmation of acute myocardial ischemia or infarction, associated with symptoms of chest pain or pressure, with or without dyspnea, nausea, and diaphoresis. The three types of ACS are non-ST-elevation myocardial infarction (NSTEMI), ST-elevation MI (STEMI), and unstable angina (UA).

The Joint Task Force of the European Society of Cardiology, American College of Cardiology Foundation, the American Heart Association, and the World Heart Federation (ESC/ACCF/AHA/WHF) defined acute MI in 2018 as the presence of acute myocardial injury detected by abnormal cardiac biomarkers in the setting of evidence of acute myocardial ischemia. [2] 

The definition of MI was further refined by developing a clinical classification according to the assumed proximate cause of the myocardial ischemia:

  • Type 1: an MI caused by acute atherothrombotic CAD, usually precipitated by plaque disruption 
  • Type 2: an MI consequent to increased oxygen demand or decreased supply, including that due to coronary dissection, vasospasm, emboli, microvascular dysfunction. Many of these patients have CAD that will modulate the ischemic threshold and depends on the severity of any given stressor that might cause ischemia [29] This type also includes supply/demand mismatches without underlying CAD such as seen with arrhythmias, anemia, or severe hypotension. [2, 30]
  • Type 3: Patients with a typical presentation of myocardial ischemia/infarction (symptoms and ECG changes) who died before blood for biomarkers could be drawn or before their appearance in the blood.
  • Type 4a: an MI associated with percutaneous coronary intervention (PCI) or from procedure-related complications associated with decreased coronary blood flow.
  • Type 4b: an intervention-related MI with stent/scaffold thrombosis
  • Type 5: an MI associated with coronary artery bypass graft surgery (CABG) 


Diagnosis Clinical features ECG findings Laboratory findings
Unstable angina Ischemic chest pain that occurs at rest or with previously tolerated levels of exertion None, or ST-segment depressions None
Non-ST-elevation myocardial infarction (NSTEMI) Ischemic chest pain in any setting None or ST-segment depressions Elevated troponin
ST-elevation myocardial infarction (STEMI) Ischemic chest pain in any setting ST-segment elevations Elevated troponin

Note: It is difficult to distinguish between ACS entities based on clinical symptoms alone.


ACS is a subcategory of ischemic heart disease, the leading cause of death worldwide. [31]

  • Mean age at onset: 68
  • Male to female ratio: 3:2
  • 70% of ACSs are NSTEMIs


The most common cause of acute coronary syndromes is an acute thrombus in an atherosclerotic coronary artery, with infrequent causes being cocaine use, coronary spasm, and coronary artery dissection. [32] Endocarditis, vasculitis, or emboli from heart valve prostheses are rare causes.

Plaque Rupture

Image: Heart showing irregular dark brown area indicating irreversibly damaged (dead/necrotic) muscle caused by acute myocardial infarction. Figure B is a longitudinal cross-section of the coronary artery with plaque buildup and an occlusive thrombus (blood clot) resulting from plaque rupture. By: National Heart Lung and Blood Institute (NIH). License: Public Domain


The pathology of ACS can be traced back to ischemia resulting from reduced coronary blood flow leading to myocardial cell injury or death. After the initial lipid-laden atherosclerotic plaque rupture in a coronary artery occurs, there is platelet aggregation, fibrin deposition, and thrombus formation. A complete vessel occlusion typically leads to ST-elevation myocardial infarction (STEMI), causing irreversible tissue damage. Myocardial necrosis begins after as little as 15 to 20 minutes of coronary occlusion. [33] After 6–12 hours, the damage can be seen by light microscopy in the form of loss of cross-striations and contraction bands. This is followed 24–72 hours later by pyknotic then lost nuclei, and heavy neutrophilic infiltrates. Grossly, the center of the infarct is yellow-tan. At 3–7 days, dead myofibers are starting to be phagocytosed by macrophages at the infarct borders. At 7–10 days, granulation tissue (new vessels and fibroblasts) is seen at the margins. At 10–14 days, there is well-established (“organizing”) granulation tissue with prominent new blood vessels and collagen deposition. Between 2 and 8 weeks, there is decreased cellularity, and collagen deposition continues. After 2 months, a dense collagenous scar is formed.

Images showing the temporal evolution of pathological changes in STEMI are shown below.

Clinical Features

There is often sudden, severe, substernal chest pain, typically radiating into the left shoulder and left arm. It can also radiate to the jaw, teeth, or the right side of the body. Pain in patients with ACS often occurs without previous exertion, improves only slightly or not at all with nitroglycerin or rest, and lasts longer than 15 minutes.

The pain can be described as an unbearable, cramp-like tightness in the chest. In addition, dyspnea, sense of impending doom, weakness, nausea, and diaphoresis are typical. Radiation into the upper abdomen, spine, or neck can also occur. A drop in blood pressure and tachycardia, accompanied by cold sweating, can be signs of early cardiogenic shock. Infarcts often happen during the early hours of the morning. [32] History should include contraindications to thrombolytic therapy.

Silent myocardial ischemia (or silent infarctions) especially affect diabetic patients with neuropathy. In these patients, about 85% of ischemic episodes occur without chest pain, suggesting that clinical angina only represents a small fraction of actual ischemic events. Medications that reduce anginal chest pain also reduce episodes of silent ischemia. [34]

Infarction pain can also be atypical, manifesting as upper abdominal pain, feeling of faintness combined with vagal symptoms such as sweating, dyspnea, nausea, or vomiting. These painless or atypical presentations occur in about one-third of all cases. [35]

Physical examination may occasionally show evidence of LV dysfunction such as basilar rales, an S3 or S4 gallop, hypotension, or peripheral hypoperfusion in patients with UA or NSTEMI. The exam is also important to exclude other potential causes of the patient’s symptoms, both cardiac and noncardiac.


In addition to the medical history and physical examination, a 12-lead ECG and lab testing for the cardiac biomarker troponin are essential.

Accurate and timely diagnosis of acute MI due to thrombosis is crucial, as management includes antithrombotic medications and possibly PCI. Most patients will have acute obstructive atherosclerotic coronary artery stenoses with acute thrombosis (type 1 MI). However, some patients with chest pain who meet the diagnostic criteria for acute MI based on the finding of an elevated troponin may not have an acute thrombotic event (type 2 MI). Patients with myocardial injury unrelated to coronary artery disease can present with myocarditis, coronary artery spasm, decreased oxygen supply due to severe tachyarrhythmias, or increased oxygen demand due to severe anemia. [30]

The differential diagnosis of chest pain includes:

  • Other cardiac conditions: aortic dissection, aortic aneurysm, myocarditis, stress cardiomyopathy (Takotsubo), pericarditis
  • Pulmonary: Pulmonary embolism, tension pneumothorax, pleuritis, pneumonia 
  • Gastrointestinal: Esophageal rupture, perforated peptic ulcer, non-perforated peptic ulcer, esophagitis, esophageal spasm, esophageal reflux, pancreatitis, cholangitis, cholecystitis, choledocholithiasis, biliary colic
  • Chest wall: Costochondritis, rib fracture, cervical disc disease, herpes zoster before the rash appears, neuropathic pain, fibromyalgia
  • Psychiatric: Anxiety disorders (panic disorder, hyperventilation), depression, somatic symptom disorder

Laboratory Tests

Assessment of cardiac enzymes is important to differentiate between the different entities of ACS. Various institutions use troponin I or troponin T, which are specific and sensitive biomarkers of myocardial injury. HIgh-sensitivity troponin assays are available and use a sex-specific cutoff concentration [36]. CK-MB is used less often than in the past.

  • Unstable angina (UA) is characterized by a lack of increase in troponin levels. 
  • NSTEMI and STEMI are characterized by the destruction of cardiac muscle tissue, resulting in elevated cardiac biomarkers.

Note: Even without an initial increase in troponin, an infarct cannot immediately be excluded, and testing must be repeated in 2–3 hours. 

Troponin levels provide information about the presence and extent of myocardial damage. The determination of troponin I or T is considered the gold standard. It increases within 3 to 6 hours after the infarction. About 70% of patients show an increase 3 hours after the incident, and that number rises to 90% six hours after the event. This timeline stresses the necessity to measure cardiac enzymes again at a later time, even when the initial result was negative. Increased troponin levels on high-sensitivity assays confer an increased risk of adverse prognosis. [37]

CK-MB is specific to myocardial infarction but does not start  to rise until 4 hours after the occurrence of ischemia. A CK-MB concentration of between 6–20% of the total CK indicates myocardial damage. Resampling of CK-MB levels can be used to detect early reinfarction because the initial levels would have returned to baseline 36 to 48 hours after infarction. 

Troponin levels can also be used for detecting reinfarction. They should be measured immediately when reinfarction is suspected and repeated in 3 to 6 hours; a 20% increase in the second sample supports the diagnosis. [2]

Table of other biomarkers elevated in MI (in addition to troponin):

Parameter  Beginning of increase Maximum Normal levels
Troponin 3–8 hours 12 hours 1–2 weeks
CK-MB 3–12 hours 24 hours 2–3 days
Myoglobin 1–4 hours 4 hours 1 day
LDH 6–12 hours 2–4 days 1–2 weeks
AST 4 hours 48 hours 3–6 days


  • ECG can be normal with no specific changes, so a repeat ECG is needed every 15–30 minutes if suspicion of MI is high or the patient continues to be symptomatic.
  • In patients with NSTEMI, there is a less than total occlusion of a coronary artery, causing a subendocardial MI (not through the entire heart muscle wall)
  • ECG may show ST-segment depression or nonspecific T wave inversion (TWI), and by definition of an NSTEMI, there is no ST elevation


Echocardiography is a valuable tool that can be used in the diagnostic workup of ACS. It  provides direct visualization of the heart to assess:

  • Site/size of segmental wall motion abnormalities
  • LV systolic function
  • Presence of complications (aneurysm, valvular insufficiency, ventricular septal rupture, and pericardial effusion)

Coronary angiography

Coronary computed tomographic angiography (CCTA) is a valuable noninvasive test for the assessment of coronary artery disease (CAD) in selected patients with suspected coronary syndromes. It can determine the exact location and extent of coronary vessel stenosis and guide further management, including the need for revascularization. It can also exclude the presence of CAD.[38]

Invasive coronary angiography should be performed in high-risk patients with spontaneous ischemia despite appropriate medical therapy. This will help determine whether revascularization is needed either by PCI or CABG.[39]

Risk Assessment

Initial evaluation of a patient with ACS must include an assessment of the risk of an acute cardiac ischemic event. Low-risk patients can be observed for several hours for repeat lab draws for troponin levels and repeat ECGs. If the findings of that brief evaluation are normal, the patient can have further testing as an outpatient. Patients who are not low-risk should be hospitalized for further evaluation and treatment.  [40] 

Risk assessment tools such as the Global Registry of Acute Coronary Events (GRACE) or Thrombolysis in Myocardial Infarction (TIMI) algorithms take into account a patient’s risk variables that are predictive of major cardiac events (death, MI, or recurrent ischemia).

Risk Factors

  • Age > 65
  • Three of more ASCVD risk factors (hypertension, diabetes, smoking, hyperlipidemia, family history of CAD in a first-degree relative (< age 55 in men and < 65 in women)
  • Known CAD or previous MI
  • Two or more episodes of anginal chest pain at rest in the previous 24 hours
  • Aspirin use in the past 7 days
  • ST-segment deviation 
  • Elevated troponin or CK-MB

Treatment of ACS: UA and NSTEMI

The initial treatment of patients with unstable angina (UA) or acute non-ST elevation myocardial infarction (NSTEMI) is similar to that used in an acute ST-elevation myocardial infarction (STEMI) but without fibrinolysis. An elevation in biomarkers (troponin) may not be detectable for several hours after presentation. The treatment of UA and NSTEMI are similar; STEMI is discussed separately in the next section.

Many steps may be accomplished simultaneously by members of the emergency team. These include examination, lab draw (for troponin, CBC, chemistry panel, coagulation testing), establishing IV access, ECG, applying a cardiac monitor, and supplemental oxygen if O2 saturation <90% or if  there is respiratory distress. Hyperoxia has a vasoconstrictor effect on the coronary arteries, and supplemental oxygen is no longer used in every patient with chest pain.

Antianginal therapy with nitroglycerin is indicated for patients with chest pain and suspected ACS. Nitrates are venodilators at low doses and  arteriolar dilators at higher doses; they may prevent recurrent ischemia in patients with unstable angina. Sublingual nitroglycerin is given every 5 minutes for 3 doses, unless there are contraindications to nitrates. These include hypotension, severe aortic stenosis, hypertrophic cardiomyopathy, suspected right ventricular infarct, marked bradycardia or tachycardia, or recent use of a phosphodiesterase 5 inhibitor (e.g., sildenafil). Patients with ongoing or recurrent chest pain should receive IV nitroglycerin titrated to symptom relief unless adverse effects develop. IV morphine is given for relief of severe chest pain if not relieved.

Beta-blockers diminish symptoms and the risk of MI in patients with ACS who are not already taking a beta-blocker. If there are no contraindications (decompensated heart failure, advanced atrioventricular (AV) block, hypotension), oral or IV metoprolol should be initiated.

Calcium-channel blockers cause arterial vasodilation, increase coronary artery blood flow, and decrease blood pressure. Oral diltiazem is recommended for patients with contraindications to beta-blockers. Diltiazem is contraindicated in patients with LV systolic dysfunction or pulmonary vascular congestion.

Dual antiplatelet therapy (aspirin plus clopidogrel or similar) should be given to patients with ACS unless there are contraindications such as aspirin allergy or active bleeding. [41]

Anticoagulation therapy should be administered to all patients with ACS unless contraindicated. Unfractionated IV heparin is given if a cardiac catheterization is planned; otherwise, low molecular weight heparins (enoxaparin or dalteparin) or fondaparinux (a selective factor Xa inhibitor) are indicated. Bivalirudin is a direct thrombin inhibitor that is recommended as an alternative anticoagulant for patients needing PCI. [42] Fibrinolytic therapy is not recommended for patients with NSTEMI.

High-dose statin therapy is recommended in all patients with UA/NSTEMI regardless of cholesterol levels unless contraindicated. These doses of statins promote plaque stabilization and restore endothelial function, and reduction in ischemic events is not seen with lower doses. [43]

Some hospitals use ACE inhibitors for patients with NSTEMI unless hypotension is an issue in the first few hours; there is long-term benefit in MI patients with hypertension, diabetes, or stable chronic kidney disease. The evidence is more apparent in patients with STEMI.[44]

Acute Myocardial Infarction: STEMI

Diagnosis: ECG in STEMI

Sequence of ECG changes in patients with STEMI:

  • A hyperacute T wave is often the first change. It is tall, peaked, and symmetric in at least two contiguous leads.
  • Elevation of the J point and convex ST-segment elevation are the hallmarks of acute myocardial infarction
  • The ST-segment elevation becomes more prominent, and its form becomes convex or rounded upward.
  • The ST segment merges with the T wave in an “injury current” or so-called “tombstone” pattern. Reciprocal ST-segment depressions are usually observed in other leads.
  • The ST-segment eventually returns to baseline, an initial Q wave develops, and R wave amplitude is lost. If ST-segment elevation lasts >3 weeks, suspect a ventricular aneurysm in the infarcted region.
  • The T wave becomes inverted and may remain inverted or return upright.
  • The R wave amplitude becomes markedly reduced, the Q wave deepens, and the T wave remains inverted or becomes positive. These usually occur within 2 weeks, but they can occur after several hours.

A left bundle branch block (LBBB) often obscures ST-segment changes in acute STEMI; a new LBBB is associated with high mortality, and these patients benefit significantly from reperfusion therapy. In the setting of LBBB, Q waves in two of leads  I, aVL, V5, and V6 or R wave regression from V1 to V4 suggest acute MI.

Right bundle branch block (RBBB) usually does not mask typical ST elevation except in rare cases of isolated true posterior MI, which has tall right precordial R waves and ST depression.

ECG in a patient with an ST-Elevation Myocardial Infarction (STEMI). Note the ST segment elevation with an injury current pattern in leads II, III, and aVF, consistent with an inferior wall MI, and reciprocal changes with ST depression in V4, V5, and aVL. Image: HWI akut. By: JHeuser. License: CC BY-SA 3.0

Timing of ECG changes depending on the phase of the infarction:[33]

  • Early acute phase: Begins within minutes, persists, and evolves over several hours after the infarction, typically characterized by pointed elevation of the T-wave, which is called a hyperacute T-wave (hyperacute pattern). 
  • Acute phase: ST segments evolve from concave to convex, and when blended with the injury pattern of blended ST-T waves, take on the “tombstone” appearance. Reciprocal changes occur (ST-segment depressions) in leads opposite those with ST elevations and are associated with larger areas of injury.
  • Evolved acute phase: The ST-elevation and R-spike decrease, so-called “poor R-wave progression” occurs, and pathologic Q or QS waves develop.
  • Chronic phase: ST changes usually resolve completely in 2 weeks for inferior MI and may take longer for large anterior MIs. Symmetrical TWI can resolve within weeks to months or persist indefinitely. More than 6 months after the infarction, the changes of the QRS complex remain.

Localization of Infarction

The ECG leads depicting the characteristic ST changes in STEMIs provide information about which coronary artery is most likely obstructed and the location of the infarction. They are less useful for localization in NSTEMIs.


Localization of Infarction

ECG ST-segment elevation

Extensive anterior MI (LAD artery) I, aVL, V1-6
Anterior MI (LAD) V1-6
Lateral MI (distal LAD or LCx) I, aVL, V5-6
Anteroseptal MI (proximal LAD) V1-V4
Inferior MI (RCA) II, III, aVF
Posterior MI (left circumflex artery) V7-9, inverse in V1-V2
Right ventricle (proximal RCA) V4R to V6R

LAD: left anterior descending artery
LCx: left circumflex artery
RCA: right coronary artery


  • Cardiac catheterization is considered the gold standard and should be performed as quickly as possible in the case of STEMI. 
  • Echocardiography is a diagnostic tool that helps to detect wall motion abnormalities, determine LV function, and exclude complications, such as cardiac valvular defects.
  • MRI cardioangiography may serve as another means of detecting wall motion abnormalities and determining the size of infarction scars.

Treatment of STEMI

Partial myocardial salvage can be achieved by reperfusion within 3 to 6 hours, and the longer the duration of ischemia, the lesser amount of salvageable tissue there will be.

Initial Management of Myocardial infarction 

Testing for cardiac biomarkers and treatment with antianginal therapy, beta-blockers, antiplatelet agents, anticoagulants, and statins are the same as listed above for patients with NSTEMI.


For patients with STEMI, a method for coronary reperfusion is chosen based on the patient’s presentation and availability of the cardiac catheterization team. Reperfusion therapy with PCI (goal < 90 minutes from first medical contact) is optimal for patients with STEMI and is the preferred approach for patients within 12 hours of the onset of symptoms and evidence of ongoing ischemia. Primary PCI is much preferred to fibrinolysis. In some cases, it can be done up to 12 hours of symptom onset in high-risk patients or with ongoing ischemia.

PCI is highly effective, has little morbidity, and patients recover completely within a few hours. Its main disadvantage is restenosis (recurrence of arterial blockage), seen in 5 to 20% of patients.[21] 

Reperfusion with surgical CABG is recommended for left main coronary artery disease, or if there is multiple-vessel disease involving the left anterior descending artery with LV dysfunction or diabetes. 

CABG is performed using the internal thoracic artery or a reverse saphenous vein from the leg. One end of the bypass is attached to the aorta and the other to the obstructed coronary artery beyond the obstruction. Open chest surgery with general anesthesia is required. The advantages of CABG include its high effectiveness and the durability of the result. Its main disadvantage is the need for open-chest surgery, which results in increased procedural morbidity, requires a 4 to 7-day hospital stay, and several weeks for a full recovery.

If PCI is not available within 120 minutes (including transfer time), then  fibrinolysis is indicated in patients with symptoms that have already lasted more than 2 to 3 hours if there are no absolute contraindications. A regimen of a tissue plasminogen activator (t-PA) plus IV heparin has better efficacy and lower mortality than streptokinase.[45] Longer-acting agents (tenecteplase, reteplase) are now given more commonly than alteplase. Timing is critical, ideally less than 30 minutes from initial medical contact (ambulance or ED) to drug administration (“door-to-needle time”). It should be delivered <10 min of STEMI confirmation on the ECG (do not wait for troponin levels if the clinical presentation is typical). The benefit from thrombolytic therapy is maximal when given < 2 hours of symptom onset.

Among patients with STEMI who have undergone fibrinolysis, early recurrence of ischemia by threatened reocclusion has been observed in 20 to 30% of patients, thrombotic coronary reocclusion in 5 to 15 %, and reinfarction in 3 to 5 % [46]. Reinfarction occurs at a median of 2 to 4 days after fibrinolytic therapy and is associated with increased mortality. 

Absolute Contraindications of Fibrinolytic Therapy

  • Previous hemorrhagic stroke at any time
  • Ischemic stroke within 3 months
  • Known intracranial neoplasm
  • Closed head injury within 3 months
  • Active bleeding, or bleeding diathesis
  • Suspected aortic dissection

Relative Contraindications

  • Severe uncontrolled hypertension > 180/110
  • History of ischemic stroke > 3 months
  • Prolonged CPR > 10 minutes
  • Major surgery < 3 weeks
  • Recent (within 2–4 weeks) internal bleeding

Coronary Angiography after Fibrinolysis (Rescue PCI) 

It is indicated in cases with:

  • Failure of reperfusion evidenced by < 50% resolution of ST-segment elevation > 90 min after completion of fibrinolytic treatment
  • Spontaneous recurrent ischemia while in a hospital
  • High-risk features: extensive ST-segment elevation, signs of heart failure, and hypotension (systolic blood pressure < 100 mm Hg)

Complications of STEMIs

STEMI complications can be classified into early and late. Reinfarction, arrhythmias (both atrial and ventricular), and heart failure can all occur shortly after MI or a couple of weeks later. Within the first 18 hours of the initial MI, a recurrent elevation in cardiac biomarker levels alone should not be relied upon to diagnose reinfarction and requires recurrent ST-segment elevation on ECG and at least one other supporting criterion (e.g., chest pain, hemodynamic decompensation). For patients, more than 18 hours from the initial MI, a rise in troponin and at least one additional criterion are sufficient for the diagnosis of reinfarction. 

Other early complications include sudden cardiac death (SCD), and potentially life-threatening AV block or ventricular tachyarrhythmias may happen in the first 24 hours. A few days after STEMI, patients can develop acute left heart failure (HF) and pulmonary edema resulting from acute pump failure or acute mitral valve insufficiency secondary to papillary muscle dysfunction. The most serious complication is cardiogenic shock, associated with mortality rates exceeding 50%.[47]

Late complications of STEMI include pericarditis, presenting either in the first week after an MI or with Dressler syndrome a couple of weeks later. Dressler syndrome, also called “post-cardiac injury” syndrome is noninfectious pericarditis that occurs 2–20 weeks post-MI secondary to the deposition of anticardiac antibody immune complexes in the pericardium, pleura, and lungs that elicit an inflammatory response. Other late complications are atrial and ventricular aneurysms which may precipitate thrombus formation and increased risk of thromboembolism. Finally, ventricular wall rupture leading to pericardial effusion and cardiac tamponade is a serious potential late complication after MI.

This table shows the timing of complications after STEMI:

Time Complications
0–24 h Ventricular arrhythmia, HF, Cardiogenic shock
1–3 days Postinfarction fibrinous pericarditis
3–14 days Free wall rupture with tamponade, papillary muscle rupture with mitral regurgitation, Interventricular septal rupture due to macrophage-mediated structural degradation, LV pseudoaneurysm (risk of rupture)
2 weeks to several months Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus)


Since 95% of acute coronary syndrome cases are manifestations of CHD, an appropriate goal for both patients and clinicians is the prevention of ASCVD by risk factor reduction. Lifestyle changes address healthy food choices, regular physical activity, maintaining a body mass index (BMI) below 25 (or similar reasonable goal for specific patients), and smoking cessation. Other risk factor reduction includes adequate control of hypertension, hyperlipidemia, and diabetes with medication in addition to lifestyle changes.

Review Questions

  1. What do typical ECG changes in a patient with acute STEMI look like?
    1. ST-segment depression with direct transition into a T-wave
    2. ST-segment elevation with negative preterminal T-wave
    3. A pointed depression of the T-wave, the so-called “anoxic” T wave
    4. Q-wave
    5. A monophasic ST-segment elevation with direct transition into a T-wave
  2. What is the best laboratory test for acute MI?
    1. LDH
    2. Troponin I
    3. CK-MB
    4. Myoglobin
    5. AST
  3. Which medication is contraindicated when a patient has also taken sildenafil?
    1. Aspirin
    2. P2Y12 inhibitors (e.g., clopidogrel)
    3. Nitroglycerin
    4. Heparin
    5. Warfarin

Answers: 1E, 2B, 3C

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