Cardiomyopathies — MCQs
Which protein is defective in dilated cardiomyopathy?
Which of the following is NOT a cause of restrictive cardiomyopathy (RCM)?
Which type of cardiomyopathy is associated with alcohol abuse?
Which of the following statements is false regarding restrictive cardiomyopathy?
Characteristic feature of hypertrophic obstructive cardiomyopathy is:-
Which finding on echocardiography suggests 'constrictive pericarditis'?
Radiological features of left ventricular heart failure are all, except -
Which one of the following is used in Cardiovascular imaging?
Which of the following is NOT a characteristic feature of mitral stenosis on X-ray?
Transesophageal echocardiogram (TEE) is preferred to transthoracic echocardiogram (TTE) in which of the following evaluations?
Cardiomyopathies Indian Medical PG Practice Questions and MCQs
Question 1: Which protein is defective in dilated cardiomyopathy?
- A. Tropomyosin
- B. Myosin
- C. Troponin
- D. Dystrophin (Correct Answer)
Explanation: ***Dystrophin*** - **Dystrophin** is a crucial protein in the **muscle cell membrane** that anchors the cytoskeleton to the extracellular matrix. - Defects in dystrophin lead to sarcolemmal fragility, causing muscle damage and can result in **dilated cardiomyopathy**, especially in conditions like **Duchenne muscular dystrophy** [1]. *Myosin* - **Myosin** is a fundamental **motor protein** involved in muscle contraction, forming the thick filaments. - While mutations in myosin can cause various cardiac conditions, like hypertrophic cardiomyopathy, direct primary defects in myosin are not typically identified as the cause of dilated cardiomyopathy [2]. *Troponin* - **Troponin** is a protein complex that regulates muscle contraction by controlling the interaction between actin and myosin, particularly in response to calcium. - Although troponins are vital for cardiac function and are released during myocardial injury, their primary defect is not typically implicated in the etiology of dilated cardiomyopathy [2]. *Tropomyosin* - **Tropomyosin** is a protein that winds around actin filaments and, along with troponin, regulates the binding of myosin to actin. - While essential for muscle contraction, direct defects in tropomyosin are not a common genetic cause of dilated cardiomyopathy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 574.
Question 2: Which of the following is NOT a cause of restrictive cardiomyopathy (RCM)?
- A. Fatty infiltration of myocardium (Correct Answer)
- B. Carcinoid syndrome
- C. Sarcoidosis
- D. Amyloidosis
Explanation: ***Fatty infiltration of myocardium*** - While fatty infiltration can occur in the heart, it is typically associated with **arrhythmogenic right ventricular cardiomyopathy (ARVC)**, a dilated cardiomyopathy [1], rather than restrictive cardiomyopathy. - **Restrictive cardiomyopathy** is characterized by stiff, non-compliant ventricular walls that impair diastolic filling, which is not the primary mechanism of fatty infiltration. *Amyloidosis* - **Amyloidosis** is a common cause of restrictive cardiomyopathy due to the deposition of **insoluble amyloid fibrils** in the myocardial interstitium [2]. - This deposition leads to **increased myocardial stiffness** and impaired diastolic function. *Sarcoidosis* - **Cardiac sarcoidosis** can cause restrictive cardiomyopathy by the infiltration of **non-caseating granulomas** into the myocardium [2]. - These granulomas lead to **fibrosis and thickening** of the ventricular walls, restricting ventricular filling. *Carcinoid syndrome* - **Carcinoid heart disease**, occurring in patients with carcinoid syndrome, can manifest as restrictive cardiomyopathy due to the deposition of **fibrous plaques** on the endocardium, particularly on the right side of the heart. - This fibrosis primarily affects the **valves and endocardial surface**, hindering ventricular filling and function.
Question 3: Which type of cardiomyopathy is associated with alcohol abuse?
- A. Hypertrophic cardiomyopathy
- B. Dilated cardiomyopathy (Correct Answer)
- C. Pericarditis
- D. Myocarditis
Explanation: ### Dilated cardiomyopathy - Chronic **alcohol abuse** is a well-established cause of **dilated cardiomyopathy**, leading to weakening and enlargement of the ventricles [1]. - This condition results in impaired systolic function and can cause **heart failure** [1]. *Hypertrophic cardiomyopathy* - This condition is primarily characterized by **pathological thickening of the heart muscle**, often genetic, and is not directly caused by alcohol abuse. - It leads to issues with relaxation and filling of the heart, rather than dilation and weakness. *Pericarditis* - **Pericarditis** is the inflammation of the sac surrounding the heart (pericardium), most commonly caused by viral infections, autoimmune diseases, or injury. - It is not directly linked to alcohol abuse as a primary cause. *Myocarditis* - **Myocarditis** is the inflammation of the heart muscle, often triggered by viral infections, autoimmune reactions, or certain medications. - While heavy alcohol use can weaken the heart, myocarditis is primarily an inflammatory process not directly caused by alcohol.
Question 4: Which of the following statements is false regarding restrictive cardiomyopathy?
- A. Left ventricular hypertrophy is present.
- B. Filling pressure is decreased. (Correct Answer)
- C. In the early phase, systolic function is impaired.
- D. Heart failure is predominantly right-sided.
Explanation: Filling pressure is decreased. - In restrictive cardiomyopathy, the ventricles become stiff and noncompliant, impairing filling. - This leads to increased filling pressures (e.g., elevated left and right atrial pressures) as the heart attempts to fill adequately. Left ventricular hypertrophy is present. - Left ventricular hypertrophy is common in restrictive cardiomyopathy, particularly in conditions like amyloidosis and sarcoidosis, where infiltrative processes thicken the ventricular walls. - While the chambers are not dilated, the walls can be abnormally thick due to underlying pathology. In the early phase, systolic function is impaired. - In the early stages of restrictive cardiomyopathy, systolic function is typically preserved. The primary defect is diastolic dysfunction—impaired ventricular filling. - Systolic dysfunction may develop in later stages as the underlying disease progresses or due to severe volume overload. Heart failure is predominantly right-sided. - Right-sided heart failure symptoms (e.g., peripheral edema, ascites, jugular venous distension) are often prominent in restrictive cardiomyopathy. - Due to the rigid and non-compliant ventricles inhibiting filling, both ventricles are affected, but systemic venous congestion often dominates the clinical picture.
Question 5: Characteristic feature of hypertrophic obstructive cardiomyopathy is:-
- A. Increased size of ventricle
- B. Asymmetric hypertrophy of the interventricular septum (Correct Answer)
- C. Normal myofiber arrangement
- D. Increased size of atria
Explanation: ***Asymmetric hypertrophy of the interventricular septum*** - This is the **hallmark pathological finding** in **hypertrophic obstructive cardiomyopathy (HOCM)**, leading to dynamic outflow tract obstruction [1]. - The thickened septum impedes blood flow from the left ventricle, especially during systole [2]. *Increased size of ventricle* - While the ventricle may *appear* larger due to hypertrophy, it's specifically the **asymmetric septal thickening** that is characteristic, not a generalized increase in ventricular chamber size, which can be seen in dilated cardiomyopathy [1]. - In HOCM, the left ventricular **cavity size** often remains normal or is reduced due to the thickened walls, especially during systole [1]. *Normal myofiber arrangement* - A key microscopic feature of HOCM is **myofiber disarray**, not a normal arrangement [1]. - This disorganization of cardiac muscle cells contributes to the systolic dysfunction and electrical instability seen in the condition [2]. *Increased size of atria* - While **left atrial enlargement** can develop in HOCM due to increased left ventricular diastolic pressure and impaired relaxation, it is a **secondary adaptation** and not the primary defining characteristic of the disease itself [1]. - The fundamental pathology lies in the ventricular hypertrophy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 577-578. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 303-304.
Question 6: Which finding on echocardiography suggests 'constrictive pericarditis'?
- A. Pericardial thickening and septal bounce (Correct Answer)
- B. Increased wall thickness
- C. Global hypokinesis
- D. Pericardial effusion
Explanation: ***Pericardial thickening and septal bounce*** - **Pericardial thickening** is a direct anatomical feature of constrictive pericarditis, indicating the fibrotic and inflamed state of the pericardium. - **Septal bounce**, or interventricular septal motion variation with respiration, is a highly specific sign of constriction, due to exaggerated ventricular interdependence. *Increased wall thickness* - This finding is more characteristic of **hypertrophic cardiomyopathy** or **hypertensive heart disease**, where the myocardial muscle itself thickens. - While it can impair diastolic function, it doesn't indicate a primary pericardial issue. *Global hypokinesis* - **Global hypokinesis** refers to reduced overall contractility of the heart muscle, typically seen in conditions like **dilated cardiomyopathy** or significant **ischemic heart disease**. - This indicates systolic dysfunction, whereas constrictive pericarditis primarily affects diastolic filling. *Pericardial effusion* - A **pericardial effusion** is an accumulation of fluid around the heart, which can cause **cardiac tamponade** if severe. - While effusions can sometimes precede or coexist with constrictive pericarditis, the fluid itself is not the hallmark of constriction, which is defined by a thickened, rigid pericardium.
Question 7: Radiological features of left ventricular heart failure are all, except -
- A. Kerley B lines
- B. Cardiomegaly
- C. Increased flow in upper lobe veins
- D. Oligemic lung fields (Correct Answer)
Explanation: ***Oligemic lung fields*** - **Oligemic lung fields** are characteristic of conditions like severe **pulmonary hypertension** or **pulmonary embolism** post-embolus, leading to reduced blood flow to the lungs, not left ventricular heart failure. - In left ventricular heart failure, the primary issue is **pulmonary venous congestion** and **edema**, leading to increased, not decreased, pulmonary vascular markings. *Kerley B lines* - **Kerley B lines** are often seen in left ventricular heart failure, indicating **interstitial pulmonary edema**. - They represent thickened, edematous interlobular septa due to increased hydrostatic pressure in the pulmonary capillaries. *Cardiomegaly* - **Cardiomegaly** (enlarged heart) on chest X-ray is a common finding in left ventricular heart failure, reflecting ventricular dilation and/or hypertrophy due to chronic increased workload. - This enlargement is often due to the heart's compensatory mechanisms attempting to maintain cardiac output. *Increased flow in upper lobe veins* - **Increased flow in upper lobe veins** (cephalization of pulmonary vessels) is an early sign of pulmonary venous hypertension in left ventricular heart failure. - Due to elevated left atrial pressure, blood is preferentially shunted to the less gravitationally dependent upper lobes.
Question 8: Which one of the following is used in Cardiovascular imaging?
- A. Second generation CT
- B. Third generation CT
- C. Spiral CT
- D. Multidetector CT (Correct Answer)
Explanation: **Explanation:** **Multidetector CT (MDCT)** is the gold standard for cardiovascular imaging because it overcomes the two biggest challenges in cardiac radiology: **cardiac motion** and **respiratory motion**. 1. **Why MDCT is correct:** MDCT utilizes multiple rows of detectors, allowing for sub-millimeter isotropic resolution and high temporal resolution. When combined with **ECG-gating** (synchronizing data acquisition with the diastolic phase of the cardiac cycle), it allows for motion-free imaging of the coronary arteries. Modern MDCT (64-slice and above) can image the entire heart in a single breath-hold, making it essential for Coronary CT Angiography (CCTA). 2. **Why other options are incorrect:** * **Second and Third Generation CT:** These are historical iterations. Second-generation used a "translate-rotate" motion with a fan beam, and Third-generation used a "rotate-rotate" motion. While Third-generation is the basis for modern scanners, the basic configuration lacked the speed and detector density required to freeze cardiac motion. * **Spiral (Helical) CT:** While a prerequisite for MDCT, early single-slice spiral CTs were too slow to capture the heart without significant motion artifacts and could not provide the necessary spatial resolution for small vessels like the coronary arteries. **High-Yield Clinical Pearls for NEET-PG:** * **Temporal Resolution:** The time required to acquire data for one image. High temporal resolution is vital to "freeze" the heart. * **Electron Beam CT (EBCT):** Historically known as the "Ultrafast CT," it was the previous gold standard for Calcium Scoring but has been largely replaced by MDCT. * **Calcium Scoring (Agatston Score):** Performed on MDCT to predict the risk of future adverse cardiac events. * **Beta-blockers:** Often administered before a Cardiac CT to lower the heart rate (ideally <60-65 bpm) to improve image quality.
Question 9: Which of the following is NOT a characteristic feature of mitral stenosis on X-ray?
- A. Double contour of the right border
- B. Elevation of the left main bronchus
- C. Widening of the carinal angle
- D. Prominence of veins in the lower lobes (Correct Answer)
Explanation: In Mitral Stenosis (MS), the narrowing of the mitral valve leads to increased pressure in the left atrium (LA), causing **Left Atrial Enlargement (LAE)** and subsequent pulmonary venous hypertension. ### Why Option D is the Correct Answer In MS, pulmonary venous hypertension leads to a phenomenon called **Cephalization** (Antler sign). Due to perivascular edema in the lower lobes, there is reflex vasoconstriction of the lower lobe veins and compensatory dilatation of the **upper lobe veins**. Therefore, prominence of veins in the *lower* lobes is incorrect; they are actually constricted, while upper lobe veins are prominent. ### Explanation of Incorrect Options (Features of LAE) * **Double contour of the right border:** As the LA enlarges, its right border pushes toward the right and overlaps the right atrium, creating a "double shadow" or "double density" sign on a PA view. * **Elevation of the left main bronchus:** An enlarging LA pushes the left main bronchus upward, making it more horizontal. * **Widening of the carinal angle:** The subcarinal angle (normally 60–75°) increases to >90° as the LA expands superiorly between the two main bronchi. ### High-Yield Clinical Pearls for NEET-PG * **Straightening of the left cardiac border:** This occurs due to a prominent pulmonary artery segment and an enlarged left atrial appendage (filling the "mitral surf"). * **Kerley B Lines:** Horizontal lines at the lung bases indicating chronic pulmonary venous hypertension and interstitial edema. * **Most sensitive view for LAE:** Lateral view with barium swallow (shows posterior indentation of the esophagus). * **Walking Man Sign:** On a lateral X-ray, the posterior displacement of the left main bronchus resembles a person walking.
Question 10: Transesophageal echocardiogram (TEE) is preferred to transthoracic echocardiogram (TTE) in which of the following evaluations?
- A. Evaluation of pericardial diseases
- B. Evaluation of tricuspid wall vegetations
- C. Evaluation of left ventricular apical thrombi
- D. Evaluation of left atrial appendage thrombi (Correct Answer)
Explanation: **Explanation:** The preference for Transesophageal Echocardiography (TEE) over Transthoracic Echocardiography (TTE) is primarily determined by the anatomical proximity of the esophagus to the posterior structures of the heart. **Why Option D is Correct:** The **Left Atrial Appendage (LAA)** is a posterior structure that is difficult to visualize clearly on TTE due to its depth and interference from ribs and lung tissue. TEE uses a high-frequency transducer positioned in the esophagus, directly behind the left atrium. This provides superior spatial resolution, making TEE the **gold standard** for detecting LAA thrombi, especially in patients with atrial fibrillation prior to cardioversion. **Analysis of Incorrect Options:** * **A. Pericardial diseases:** TTE is the initial investigation of choice for pericardial effusion and tamponade as it provides an excellent global view of the pericardial space and hemodynamics. * **B. Tricuspid wall vegetations:** The tricuspid valve is an anterior structure. While TEE is more sensitive for small vegetations, TTE is generally sufficient and preferred as the first-line evaluation for right-sided valves. * **C. Left ventricular (LV) apical thrombi:** The LV apex is the structure furthest from the TEE probe but closest to the TTE transducer (apical four-chamber view). TTE (often with contrast) is superior for visualizing the LV apex. **High-Yield Clinical Pearls for NEET-PG:** * **TEE is superior for:** Left atrial appendage thrombi, prosthetic valve dysfunction, infective endocarditis (detecting small vegetations/abscesses), and aortic dissection. * **TTE is superior for:** Routine screening, apical thrombi, and initial assessment of pericardial effusions. * **Rule of Thumb:** If the structure is **posterior** (LA, LAA, Mitral Valve, Aorta), think **TEE**. If the structure is **anterior** (RV, LV apex, Pericardium), think **TTE**.
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