Coronary Artery Disease and Angina — MCQs
Drug used for both the acute angina attack and prophylaxis of angina:
A 50-year-old man with a history of smoking, hypertension, and chronic exertional angina develops several daily episodes of chest pain at rest compatible with cardiac ischemia. The patient is hospitalized. All the following would be part of an appropriate management plan except one.
Most sensitive method of monitoring cardiovascular ischemia in the perioperative period is -
Treatment of choice for prinzmetal's angina
In the context of chest pain evaluation, which is the best way to differentiate between stable angina and NSTEMI?
A 56-year-old patient developed excruciating chest discomfort in the past 72 hours, relieved by GTN spray. Troponin I is normal, and the ECG shows features of left ventricular hypertrophy (LVH) with T wave flattening. The patient is already on statins, aspirin, and metoprolol 50 mg . What is the next best step in management?
Most common cause of death in Rheumatoid Arthritis?
Mobitz II heart block is seen with all except?
Stunning of myocardium without any acute coronary syndrome is:-
A 30 years old man presents with cramping gluteal pain after walking 500 meters. Which is the vessel involved?
Coronary Artery Disease and Angina Indian Medical PG Practice Questions and MCQs
Question 1: Drug used for both the acute angina attack and prophylaxis of angina:
- A. Isosorbide dinitrate (Correct Answer)
- B. Diltiazem
- C. Verapamil
- D. Dipyridamole
Explanation: ***Isosorbide dinitrate***- This drug is a **nitrate** available in multiple formulations that can be used for **both acute relief and prophylaxis of angina** [1].- **Sublingual isosorbide dinitrate** has a rapid onset (2-5 minutes) making it suitable for **acute angina attacks**, while **oral formulations** provide longer duration of action for **prophylactic management** [1].- It works by causing **vasodilation**, primarily of veins, reducing **preload** and myocardial oxygen demand, and also dilates coronary arteries.- This dual-use capability through different formulations makes it unique among the given options.*Diltiazem*- Diltiazem is a **calcium channel blocker** primarily used for the **prophylaxis of angina** by reducing heart rate and myocardial contractility [2].- While effective for prevention, its onset of action is **too slow for acute angina relief**.*Verapamil*- Verapamil, another **calcium channel blocker**, is also used for **angina prophylaxis** due to its effects on reducing heart rate and contractility.- Similar to diltiazem, it is **not suitable for acute angina attacks** because it does not provide rapid relief.*Dipyridamole*- Dipyridamole is a **vasodilator** and a **platelet aggregation inhibitor**, primarily used in the prevention of thromboembolic events or as a pharmacologic stress agent.- Although it causes vasodilation, it is **not recommended for acute angina relief** or as a primary prophylactic agent for angina due to the risk of **coronary steal phenomenon** in some patients.
Question 2: A 50-year-old man with a history of smoking, hypertension, and chronic exertional angina develops several daily episodes of chest pain at rest compatible with cardiac ischemia. The patient is hospitalized. All the following would be part of an appropriate management plan except one.
- A. Intravenous heparin
- B. Aspirin
- C. Beta-blockers
- D. Lidocaine (Correct Answer)
Explanation: ***Lidocaine*** - **Lidocaine** is an antiarrhythmic drug primarily used for the treatment of **ventricular arrhythmias**, particularly in the setting of acute myocardial infarction [3]. - It is not a standard component of initial management for **unstable angina** or **non-ST elevation myocardial infarction (NSTEMI)** in the absence of documented ventricular arrhythmias. *Intravenous heparin* - **Intravenous heparin** is critical in the management of unstable angina and NSTEMI to prevent further thrombus formation. - It works by potentiation of **antithrombin III**, which inhibits the activity of thrombin and factor Xa. *Aspirin* - **Aspirin** is an essential antiplatelet agent used immediately in patients with acute coronary syndromes [2]. - It inhibits **cyclooxygenase-1 (COX-1)**, reducing thromboxane A2 production and thus **platelet aggregation** [3]. *Beta-blockers* - **Beta-blockers** are indicated to reduce myocardial oxygen demand by decreasing heart rate, blood pressure, and myocardial contractility [1]. - They help to alleviate angina symptoms and improve outcomes in patients with acute coronary syndromes by balancing **myocardial oxygen supply and demand** [1].
Question 3: Most sensitive method of monitoring cardiovascular ischemia in the perioperative period is -
- A. NIBP
- B. ECG
- C. Pulse oximeter
- D. TEE (Correct Answer)
Explanation: ***TEE*** - **Transesophageal echocardiography (TEE)** is the most sensitive method for detecting perioperative myocardial ischemia because it can visualize **regional wall motion abnormalities** and changes in **ventricular function** much earlier than ECG. - **Ischemia** directly impairs the contractility of the affected myocardium, leading to subtle changes in wall motion that TEE can identify. *NIBP* - **Non-invasive blood pressure (NIBP)** monitoring can detect **hemodynamic changes** (like hypotension or hypertension) that may precede or accompany ischemia. - However, these changes are **non-specific** and occur relatively late, making NIBP a less sensitive indicator of early ischemia. *ECG* - **Electrocardiography (ECG)** monitors the electrical activity of the heart and can detect **ST-segment changes** indicative of ischemia. - While useful, ECG changes may appear later than wall motion abnormalities, and **silent ischemia** can be missed if the leads are not optimally placed or if the ischemia does not produce significant electrical changes. *Pulse oximeter* - A **pulse oximeter** measures **oxygen saturation** in the peripheral blood. - It is primarily used to assess **respiratory function** and tissue oxygenation, and it does not directly monitor myocardial ischemia or cardiac function.
Question 4: Treatment of choice for prinzmetal's angina
- A. Nitroglycerin
- B. Prazosin
- C. Beta-blockers
- D. Calcium Channel Blockers (CCBs) (Correct Answer)
Explanation: ***Calcium Channel Blockers (CCBs)*** - **Dihydropyridine** CCBs like nifedipine or amlodipine, and **non-dihydropyridine** CCBs like diltiazem or verapamil, are the **first-line agents** for Prinzmetal's angina [1]. - They work by **relaxing coronary smooth muscle**, preventing the vasospasm that causes the angina [1]. *Nitroglycerin* - **Nitroglycerin is effective** for acute relief of Prinzmetal's angina symptoms due to its **vasodilatory properties**. - However, it's typically used as **rescue therapy** and not as a long-term preventative treatment. *Beta-blockers* - Beta-blockers are **contraindicated** in Prinzmetal's angina as they can **worsen coronary vasospasm** by blocking beta-2 mediated vasodilation, leaving unopposed alpha-1 vasoconstriction [2]. - They can increase the **frequency and severity of attacks**. *Prazosin* - Prazosin is an **alpha-1 adrenergic blocker** used primarily for **hypertension** and benign prostatic hyperplasia. - While it can cause vasodilation, it is **not the treatment of choice** for Prinzmetal's angina and is less effective than CCBs in preventing coronary spasm.
Question 5: In the context of chest pain evaluation, which is the best way to differentiate between stable angina and NSTEMI?
- A. ECG
- B. Cardiac-biomarker (Correct Answer)
- C. Trans thoracic Echocardiography
- D. Multi uptake gated Acquisition scan
Explanation: **Cardiac-biomarker** - **Cardiac biomarkers**, particularly **troponin**, are crucial for differentiating between **unstable angina** and **NSTEMI** [1], [2]. In NSTEMI, there is evidence of **myocardial necrosis**, leading to elevated cardiac troponins [2]. - **Stable angina** and **unstable angina** do not involve myocardial necrosis, so troponin levels remain within the normal range [1]. *ECG* - While an **ECG** is essential in the initial assessment of chest pain, it may show **non-specific changes** in both **unstable angina** and **NSTEMI**, such as T-wave inversions or ST-segment depression [2]. - The definitive distinction of **NSTEMI** often relies on **sequential biomarker measurements**, as ECG changes alone may not be sufficient for diagnosis or differentiation from unstable angina [2]. *Trans thoracic Echocardiography* - **Echocardiography** can show **regional wall motion abnormalities** that might suggest ischemia, but these findings are not specific enough to differentiate between **stable angina** and **NSTEMI** immediately. - It is more useful for assessing **ventricular function**, identifying **valvular disease**, or detecting other causes of chest pain, rather than acute differentiation of coronary syndromes. *Multi uptake gated Acquisition scan* - A **MUGA scan** assesses **left ventricular ejection fraction** and wall motion, primarily used in evaluating global cardiac function and monitoring cardiotoxicity from chemotherapy. - It is **not a first-line diagnostic tool** for differentiating between acute coronary syndromes like **stable angina** and **NSTEMI** because it does not directly detect acute myocardial injury.
Question 6: A 56-year-old patient developed excruciating chest discomfort in the past 72 hours, relieved by GTN spray. Troponin I is normal, and the ECG shows features of left ventricular hypertrophy (LVH) with T wave flattening. The patient is already on statins, aspirin, and metoprolol 50 mg . What is the next best step in management?
- A. LMWH (Low Molecular Weight Heparin)
- B. Increase beta blocker dose
- C. IV NTG Drip
- D. Add Clopidogrel (Correct Answer)
- E. Arrange urgent coronary angiography
Explanation: ***Add Clopidogrel*** - The patient presents with **unstable angina** (chest discomfort relieved by GTN, normal troponin, and ECG changes indicative of ischemia) and is already on aspirin, statins, and a beta-blocker. - Adding **clopidogrel** (or another P2Y12 inhibitor) is crucial for **dual antiplatelet therapy (DAPT)**, which is a cornerstone in the management of unstable angina/NSTEMI to prevent further thrombotic events. - This is the **immediate next step** to optimize medical therapy before considering invasive strategies. *LMWH (Low Molecular Weight Heparin)* - While **anticoagulation** is important in acute coronary syndromes and would be appropriate to add, the question asks for the **next best step** given the patient's existing management. - LMWH would typically be added alongside DAPT, but establishing dual antiplatelet therapy takes priority. *Increase beta blocker dose* - The patient is already on metoprolol 50 mg, and while **titrating beta-blockers** is important for symptom control and reducing myocardial oxygen demand, the immediate priority in unstable angina is to address the underlying thrombotic process with DAPT. - Beta-blocker optimization can be done after ensuring adequate antiplatelet therapy. *IV NTG Drip* - **Intravenous nitroglycerin (IV NTG)** is used to relieve ongoing chest pain and reduce preload/afterload, especially in severe or refractory symptoms. - However, the patient's chest discomfort was already **relieved by GTN spray**, indicating that immediate pain control with IV NTG is not the most urgent next step compared to preventing further thrombotic events with DAPT. *Arrange urgent coronary angiography* - While **coronary angiography** is indicated in high-risk unstable angina, the immediate next step is to **optimize medical management** with dual antiplatelet therapy. - Angiography timing depends on risk stratification; in a stable patient already on aspirin, beta-blockers, and statins, adding clopidogrel first ensures optimal antiplatelet coverage before any invasive procedure. - Early invasive strategy (angiography within 24-72 hours) would be appropriate after medical stabilization.
Question 7: Most common cause of death in Rheumatoid Arthritis?
- A. Hepatic failure
- B. ARDS
- C. Pulmonary fibrosis
- D. Ischemic heart disease (Correct Answer)
Explanation: ***Ischemic heart disease*** - Patients with **rheumatoid arthritis (RA)** have a significantly increased risk of developing **cardiovascular diseases**, including ischemic heart disease. [1] - This heightened risk is due to chronic systemic inflammation, accelerated atherosclerosis, and potential side effects of RA treatments contributing to **endothelial dysfunction**. [1] *Hepatic failure* - While certain medications used to treat RA, such as **methotrexate**, can cause liver toxicity, hepatic failure is not the most common cause of death in RA patients. [2] - Regular **liver enzyme monitoring** helps in detecting and managing medication-induced liver issues. *ARDS* - **Acute Respiratory Distress Syndrome (ARDS)** can occur in severely ill patients, but it is not a direct or most common complication of rheumatoid arthritis nor a primary cause of death. [2] - RA can affect the lungs (e.g., interstitial lung disease), but ARDS is typically a severe, acute event triggered by other conditions like **sepsis** or trauma. *Pulmonary fibrosis* - **Interstitial lung disease (ILD)**, including pulmonary fibrosis, is a known extra-articular manifestation of RA and can be a significant cause of morbidity and mortality. [2] - However, **cardiovascular events**, particularly ischemic heart disease, still surpass pulmonary fibrosis as the leading cause of death in RA patients.
Question 8: Mobitz II heart block is seen with all except?
- A. Sarcoidosis
- B. Cushing syndrome (Correct Answer)
- C. Coronary artery disease
- D. Hypothyroidism
Explanation: ***Cushing syndrome*** - Cushing syndrome is primarily associated with **hormonal imbalances** (excess cortisol) and does not directly cause primary conduction system disease leading to Mobitz II heart block. - While it can lead to cardiovascular complications like hypertension and atherosclerosis, these do not typically manifest as direct abnormalities in **AV nodal conduction** causing Mobitz II block. *Sarcoidosis* - **Cardiac sarcoidosis** can infiltrate the myocardium and the cardiac conduction system, leading to various arrhythmias, including **Mobitz II AV block**. - Granulomas can directly damage the **AV node** or His-Purkinje system, impairing conduction. *Coronary artery disease* - **Ischemia or infarction** from coronary artery disease can affect the blood supply to the AV node or His bundle, causing conduction disturbances [1]. - Acute myocardial infarction, especially an **anterior MI**, can damage the His-Purkinje system, commonly leading to **Mobitz II AV block** [1]. *Hypothyroidism* - Severe **hypothyroidism** can affect myocardial function and the cardiac conduction system. - It can lead to various bradyarrhythmias, including **Mobitz II AV block**, due to slowed electrical impulses and metabolic derangements affecting cardiac cells.
Question 9: Stunning of myocardium without any acute coronary syndrome is:-
- A. Restrictive cardiomyopathy
- B. Subendocardial infarction
- C. Transmural infarction
- D. Takotsubo cardiomyopathy (Correct Answer)
Explanation: ***Takotsubo cardiomyopathy*** - This condition involves **transient systolic dysfunction** of the left ventricle, often triggered by severe emotional or physical stress, mimicking a heart attack but without **coronary artery obstruction**. - The apical and mid-ventricular segments of the left ventricle become akinetic or hypocinetic, causing the heart to take on a shape resembling an octopus trap (**takotsubo**). *Restrictive cardiomyopathy* - This is a condition where the walls of the ventricles become **stiff** and **lose their flexibility**, preventing the heart from filling properly. - It is typically caused by conditions like **amyloidosis** or **sarcoidosis**, leading to impaired diastolic function, not transient stunning. *Subendocardial infarction* - This refers to a **heart attack** that affects only the **inner layer** of the heart muscle (**subendocardium**) due to reduced blood flow [2]. - It is a form of **acute coronary syndrome** where there is irreversible myocardial necrosis, unlike the temporary dysfunction in stunning [1]. *Transmural infarction* - This is a **severe form of heart attack** where the entire thickness of the heart muscle wall is affected, usually due to a **complete blockage of a coronary artery** [2]. - This also represents **acute coronary syndrome** with widespread myocardial necrosis, which is fundamentally different from a reversible stunning of the myocardium [1].
Question 10: A 30 years old man presents with cramping gluteal pain after walking 500 meters. Which is the vessel involved?
- A. Saphenous venous insufficiency
- B. Femoral venous insufficiency
- C. Arterial disease with femoral artery involvement
- D. Arterial disease with aorto-iliac involvement (Correct Answer)
Explanation: ***Arterial disease with aorto-iliac involvement*** - **Cramping gluteal pain** that occurs predictably after walking a specific distance (**claudication**) is highly indicative of **peripheral arterial disease (PAD)** [1]. - Involvement of the **aorto-iliac arteries** (e.g., common iliac, internal iliac) restricts blood flow to the gluteal muscles and thigh, causing claudication in this region [1]. *Saphenous venous insufficiency* - This condition involves dysfunction of the **superficial venous system**, leading to symptoms like **varicose veins**, aching, swelling, and skin changes, but typically not **cramping cluteal claudication** with exertion. - Symptoms are usually relieved with elevation and worsen with prolonged standing. *Femoral venous insufficiency* - Refers to dysfunction of the **deep venous system** in the thigh, causing symptoms similar to saphenous insufficiency (e.g., swelling, pain, skin changes), but again, not typically **exertional gluteal claudication**. - It’s often associated with a history of **deep vein thrombosis (DVT)**. *Arterial disease with femoral artery involvement* - While **femoral artery disease** would cause claudication, the primary location of pain would be in the **calf** or **thigh** (below the knee) rather than predominantly the gluteal region. - Claudication originating in the **gluteal muscles** suggests a more proximal arterial obstruction affecting blood supply to the hip and buttock [1].
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