Cardiology — MCQs

Cardiology UK Medical PG Practice Questions and MCQs

Question 11: A 45-year-old man presents with progressive shortness of breath and fatigue. Echocardiogram shows severe aortic stenosis with valve area 0.8 cm² and mean gradient 50 mmHg. He is symptomatic with exertional dyspnea. What is the most appropriate management?

A. Medical management with diuretics
B. Balloon aortic valvuloplasty
C. Aortic valve replacement (Correct Answer)
D. ACE inhibitors
E. Observation

Explanation: ***Aortic valve replacement***- This patient has **severe aortic stenosis** (valve area 0.8 cm², mean gradient 50 mmHg) and is **symptomatic** with exertional dyspnea, which are clear indications for intervention.- For symptomatic severe aortic stenosis, **aortic valve replacement** (either surgical or transcatheter) is the definitive treatment to improve survival and alleviate symptoms, as per current guidelines (Class I recommendation).*Medical management with diuretics*- Medical therapy, such as diuretics, can provide **symptom relief** for heart failure in aortic stenosis but does not address the underlying mechanical obstruction or improve long-term survival.- Relying solely on medical management for severe, symptomatic AS leads to a very **poor prognosis**, with high mortality rates within a few years.*Balloon aortic valvuloplasty*- **Balloon aortic valvuloplasty (BAV)** offers only temporary hemodynamic improvement and is typically considered a **bridge to definitive AVR** in critically ill patients or for **congenital AS**.- It is not the preferred definitive treatment for calcific severe aortic stenosis in adults due to a high rate of **restenosis** and potential complications.*ACE inhibitors*- **ACE inhibitors** and other vasodilators are generally contraindicated or used with extreme caution in severe aortic stenosis due to the risk of precipitating **severe hypotension** by reducing preload and systemic vascular resistance.- These medications do not alleviate the fixed outflow obstruction and can worsen symptoms like **syncope** or lead to cardiogenic shock.*Observation*- **Observation** is appropriate only for patients with **asymptomatic severe aortic stenosis** or those with mild to moderate disease.- The presence of symptoms like exertional dyspnea indicates a high risk of adverse cardiovascular events, including sudden cardiac death, and necessitates prompt **aortic valve replacement**.

Question 12: A 55-year-old man presents with progressive shortness of breath and fatigue over 6 months. Echocardiogram shows concentric left ventricular hypertrophy with preserved ejection fraction. Cardiac catheterization shows normal coronary arteries. What is the most likely diagnosis?

A. Ischemic cardiomyopathy
B. Dilated cardiomyopathy
C. Hypertrophic cardiomyopathy
D. Heart failure with preserved ejection fraction (Correct Answer)
E. Constrictive pericarditis

Explanation: ***Heart failure with preserved ejection fraction*** - The patient's symptoms of **shortness of breath** and **fatigue** combined with an echocardiogram showing **concentric left ventricular hypertrophy** and **preserved ejection fraction** (typically >50%) are diagnostic criteria for **HFpEF**. - **Normal coronary arteries** on cardiac catheterization further support a non-ischemic etiology, making HFpEF the most likely diagnosis, often secondary to chronic **hypertension**. *Ischemic cardiomyopathy* - This condition is characterized by **systolic dysfunction** (reduced ejection fraction) and ventricular remodeling due to **coronary artery disease**. - The patient has **preserved ejection fraction** and **normal coronary arteries**, which rules out ischemic cardiomyopathy as the primary cause. *Dilated cardiomyopathy* - This is defined by **ventricular chamber dilation** and impaired **systolic function** leading to a reduced ejection fraction. - The echocardiogram shows **concentric left ventricular hypertrophy** (thickened walls), not ventricular dilation, and a preserved ejection fraction. *Hypertrophic cardiomyopathy* - While it involves **left ventricular hypertrophy**, it is typically **asymmetric** (often septal) and often genetic in origin, sometimes leading to LV outflow tract obstruction. - The patient's presentation with acquired **concentric hypertrophy** and symptoms of heart failure is more consistent with HFpEF, often due to chronic pressure overload. *Constrictive pericarditis* - This condition results from a stiff or calcified **pericardium** that restricts diastolic filling, often with a normal myocardium and characteristic pericardial findings on imaging. - The presence of significant **concentric left ventricular hypertrophy** points to a primary myocardial pathology rather than an extrinsic pericardial restriction.

Question 13: A 25-year-old woman presents with a 2-week history of fever, weight loss, and a new heart murmur. Blood cultures grow Streptococcus viridans. Echocardiogram shows vegetation on the mitral valve. What is the most likely diagnosis?

A. Rheumatic fever
B. Infective endocarditis (Correct Answer)
C. Myocarditis
D. Pericarditis
E. Cardiomyopathy

Explanation: ***Infective endocarditis***- The constellation of fever, weight loss, a **new heart murmur**, **positive blood cultures** for ***Streptococcus viridans***, and **vegetation on the mitral valve** seen on echocardiogram are all classic diagnostic criteria for infective endocarditis.- ***Streptococcus viridans***, a common inhabitant of the oral flora, is a frequent cause of **subacute infective endocarditis**, particularly affecting previously damaged or sometimes normal heart valves. It directly explains the vegetations.*Rheumatic fever*- This condition is an immune-mediated sequela of a preceding **Group A Streptococcus (GAS)** pharyngitis, not directly caused by ***Streptococcus viridans*** bacteremia.- While it can cause **carditis** and valvular damage (often **mitral regurgitation**), the pathology is an inflammatory process, not direct bacterial colonization forming vegetations.*Myocarditis*- Myocarditis involves inflammation of the **myocardium** (heart muscle), typically presenting with symptoms such as chest pain, heart failure, or arrhythmias.- It does not primarily manifest with a **new heart murmur** due to valvular dysfunction, nor does it cause **valvular vegetations** directly.*Pericarditis*- Pericarditis is inflammation of the **pericardium**, often causing sharp, positional chest pain and sometimes a **pericardial friction rub**.- This condition does not cause **valvular vegetations** or a new heart murmur resulting from damage to the heart valves themselves.*Cardiomyopathy*- Cardiomyopathy is a primary disease of the **heart muscle**, leading to impaired pumping function (e.g., dilated, hypertrophic) and symptoms of **heart failure**.- It is a structural and functional abnormality of the heart muscle and does not explain the acute infectious process (fever, bacteremia) or the specific presence of **vegetations** on a heart valve.

Question 14: A 50-year-old man presents with progressive shortness of breath and ankle swelling. Chest X-ray shows cardiomegaly and pulmonary edema. ECG shows atrial fibrillation. Echocardiogram shows severe mitral regurgitation. What is the most likely cause of his symptoms?

A. Ischemic heart disease
B. Mitral valve disease (Correct Answer)
C. Hypertensive heart disease
D. Cardiomyopathy
E. Pericardial disease

Explanation: ***Mitral valve disease***- The echocardiogram directly reveals **severe mitral regurgitation (MR)**, which is the primary cause for the patient's symptoms of **shortness of breath**, **pulmonary edema**, and **ankle swelling**, indicating **heart failure** due to **volume overload** in the left atrium and pulmonary circulation.- Severe MR leads to significant **left atrial enlargement** and increased pressure, which are major factors contributing to the development of **atrial fibrillation (AF)** observed on the ECG.*Ischemic heart disease*- While **ischemic heart disease (IHD)** is a very common cause of heart failure and can lead to functional MR due to ventricular remodeling or papillary muscle dysfunction, the most prominent and *direct* finding in this case is the documented **severe mitral regurgitation** itself.- The question's focus on severe valvular pathology makes valvular disease a more specific explanation for the immediate symptoms than general IHD, without further evidence of acute coronary events.*Hypertensive heart disease*- **Hypertensive heart disease** typically causes **left ventricular hypertrophy** and can lead to heart failure with preserved or reduced ejection fraction.- While hypertension can contribute to cardiac remodeling, the explicit finding of **severe mitral regurgitation** as the primary echocardiographic abnormality points more directly to a valvular etiology as the immediate cause of the patient's acute decompensation.*Cardiomyopathy*- **Cardiomyopathy** results in primary myocardial dysfunction leading to ventricular dilation and heart failure symptoms, which can include secondary (functional) mitral regurgitation.- However, if the severe mitral regurgitation is *primary* (e.g., due to leaflet prolapse or chordal rupture), then **mitral valve disease** is the direct root cause; if it is secondary, the cardiomyopathy would be the *underlying* cause, but the symptoms are explicitly mediated by the severe MR.*Pericardial disease*- **Pericardial diseases** such as constrictive pericarditis or cardiac tamponade primarily affect **diastolic filling** and cause symptoms related to elevated systemic venous pressure and reduced cardiac output.- These conditions do not typically present with **severe mitral regurgitation** as the main pathology explaining the pulmonary edema and cardiomegaly.

Question 15: A 40-year-old man presents with progressive dyspnea on exertion and fatigue over 3 months. Echocardiogram shows dilated left ventricle with ejection fraction of 25%. He has no history of coronary artery disease or hypertension. What is the most likely diagnosis?

A. Ischemic cardiomyopathy
B. Dilated cardiomyopathy (Correct Answer)
C. Hypertrophic cardiomyopathy
D. Restrictive cardiomyopathy
E. Pericardial disease

Explanation: ***Dilated cardiomyopathy***- The classic presentation involves progressive **heart failure symptoms** (dyspnea, fatigue) accompanied by **left ventricular dilation** and severe **systolic dysfunction (EF < 40%)** on echocardiogram.- Since the patient has no history of **coronary artery disease (CAD)** or hypertension, this presentation strongly suggests **idiopathic dilated cardiomyopathy**, the most common form of non-ischemic cardiomyopathy.*Ischemic cardiomyopathy*- This diagnosis requires evidence of significant **coronary artery disease** or prior **myocardial infarction** causing the systolic dysfunction, which is explicitly absent in this case.- The underlying pathology is due to myocardial scarring and stunning resulting from **myocardial ischemia**.*Hypertrophic cardiomyopathy*- This condition is primarily characterized by unexplained **left ventricular hypertrophy** leading to impaired **diastolic filling**, not typically a dilated chamber.- While end-stage hypertrophic cardiomyopathy can involve systolic failure, the initial defining feature is a thickened, **non-dilated LV**.*Restrictive cardiomyopathy*- Defined by abnormally rigid, non-compliant ventricles leading to severe impairment of **diastolic filling** (restrictive physiology), usually with **preserved systolic function**.- The echocardiogram findings typically show normal LV size, often with **biatrial enlargement**, not **LV dilation** and low ejection fraction.*Pericardial disease*- Conditions like constrictive pericarditis mainly impair cardiac filling and stroke output due to external compression, affecting **diastolic function**.- Pericardial disease does not typically cause the primary myocardial disease necessary to result in such severe **left ventricular systolic dysfunction** and remodeling.

Question 16: A 60-year-old man presents with crushing central chest pain lasting 45 minutes. His ECG shows ST depression in leads V4-V6. Troponin I is elevated at 0.8 ng/ml (normal <0.04). What is the most likely diagnosis?

A. Unstable angina
B. NSTEMI (Correct Answer)
C. STEMI
D. Pericarditis
E. Aortic dissection

Explanation: ***NSTEMI***- This diagnosis is defined by evidence of myocardial necrosis (elevated **Troponin I**) in the setting of clinical symptoms of ischemia (crushing chest pain) and ECG changes (ST **depression**).- ST depression indicates **subendocardial ischemia** and differentiates it from STEMI, where transmural ischemia causes ST elevation.*Unstable angina*- The definition of unstable angina requires cardiac biomarkers (**Troponin** and CK-MB) to be **normal**, ruling it out when Troponin is elevated.- While symptoms and ECG (ST depression) are consistent with ACS, the presence of myocardial injury confirms infarction, not just unstable angina.*STEMI*- This diagnosis requires persistent **ST segment elevation** (or new LBBB) on the ECG, reflecting transmural myocardial ischemia.- The patient's ECG showing only ST **depression** (V4-V6) definitively excludes a primary STEMI diagnosis.*Pericarditis*- The pain associated with pericarditis is typically sharp, **pleuritic**, and improves when leaning forward, unlike crushing ischemic pain.- ECG classically shows **diffuse ST elevation** and **PR segment depression**, findings absent in this presentation.*Aortic dissection*- Pain is usually described as **tearing or ripping** and often radiates to the back, which differs from crushing ischemic pain.- While it is a life-threatening cause of chest pain, it characteristically does not cause primary **Troponin** elevation or ischemic ST changes.

Question 17: A 65-year-old man presents with progressive shortness of breath on exertion and orthopnea. Chest X-ray shows cardiomegaly and upper lobe blood diversion. Echocardiogram shows ejection fraction of 35%. What is the most appropriate first-line medication?

A. Furosemide
B. ACE inhibitor (Correct Answer)
C. Beta-blocker
D. Spironolactone
E. Digoxin

Explanation: ***ACE inhibitor***- It is a cornerstone medication for **Heart Failure with Reduced Ejection Fraction (HFrEF)** (EF < 40%), offering significant reduction in morbidity and all-cause mortality.- It works by inhibiting the conversion of **Angiotensin I to Angiotensin II**, blocking the deleterious effects of the **Renin-Angiotensin-Aldosterone System (RAAS)**, which includes harmful cardiac remodeling.*Furosemide*- Furosemide is a **loop diuretic** primarily used to relieve symptoms of volume overload (e.g., **pulmonary congestion** and orthopnea) by increasing fluid excretion.- While crucial for symptom management, it is *not* considered a first-line drug for improving long-term **survival or prognosis** in HFrEF.*Beta-blocker*- Beta-blockers (e.g., Carvedilol) are also essential **mortality-reducing agents** in HFrEF by blocking detrimental sympathetic nervous system activation.- Although the second major pillar of HFrEF therapy, they are typically initiated after or concurrently with an ACE inhibitor (or ARNI), usually once the patient is **euvolemic**.*Spironolactone*- This is an **Aldosterone Antagonist** used primarily in patients with persistent severe symptoms (NYHA Class II-IV) and low EF who are already receiving an ACEi/ARNI and a Beta-blocker.- It provides further prognostic benefit and prevents **potassium loss**, but is added after the two foundational therapies are established.*Digoxin*- Digoxin is used primarily for **symptom control** and to reduce the risk of hospitalization, especially in patients with coexisting **atrial fibrillation**.- Unlike ACE inhibitors and Beta-blockers, it does *not* provide a primary **mortality benefit** and is generally reserved for refractory cases.

Question 18: A 67-year-old man presents with progressive shortness of breath and ankle swelling over 3 months. Examination reveals elevated JVP, bilateral crepitations, and pitting edema. His NT-proBNP is 2500 pg/ml. What is the most appropriate initial investigation?

A. Chest X-ray
B. Echocardiogram (Correct Answer)
C. CT pulmonary angiogram
D. Coronary angiography
E. Exercise stress test

Explanation: ***Echocardiogram*** - The patient's presentation with progressive **shortness of breath**, **ankle swelling**, elevated **JVP**, bilateral **crepitations**, and a significantly elevated **NT-proBNP (2500 pg/ml)** is highly suggestive of **heart failure**. - An echocardiogram is the **most appropriate initial investigation** as it directly visualizes cardiac structure, assesses **left ventricular function (ejection fraction)**, identifies **valvular disease**, and evaluates chamber sizes, providing crucial information for diagnosis and guiding treatment.*Chest X-ray* - While a chest X-ray can show signs of **pulmonary congestion** (e.g., **cardiomegaly**, **pulmonary edema**, **pleural effusions**) that are consistent with heart failure, it does not provide information on **cardiac function** or **valvular pathology**. - It is a useful adjunct but cannot quantify the severity of heart failure or pinpoint the underlying cause of cardiac dysfunction, which an echocardiogram can. *CT pulmonary angiogram* - This investigation is primarily indicated for diagnosing **pulmonary embolism (PE)**, a condition that can cause acute shortness of breath. - However, the patient's symptoms are progressive over 3 months, indicating a more chronic process, and the features of **fluid overload** (ankle swelling, elevated JVP) are more characteristic of heart failure than PE. *Coronary angiography* - Coronary angiography is an invasive procedure used to assess for **coronary artery disease (CAD)**, which is a common underlying cause of heart failure. - It is typically reserved for patients where CAD is strongly suspected as the etiology of heart failure and revascularization is being considered, usually after non-invasive assessments like an echocardiogram. *Exercise stress test* - An exercise stress test evaluates for **myocardial ischemia** in patients with suspected coronary artery disease who are stable and able to exert themselves. - Given the patient's symptoms of progressive shortness of breath and clear signs of **heart failure decompensation**, an exercise stress test is contraindicated and inappropriate as an initial investigation.

Question 19: A 58-year-old man presents with progressive dyspnea and fatigue over 6 months. Echocardiogram shows severe mitral regurgitation with flail posterior leaflet. LV function normal. He is symptomatic on exertion. What is the most appropriate management?

A. Medical management
B. Mitral valve replacement
C. Mitral valve repair (Correct Answer)
D. Heart transplantation
E. Balloon mitral valvuloplasty

Explanation: ***Mitral valve repair***- Guidelines recommend surgical intervention for symptomatic patients with severe primary **mitral regurgitation** (MR) and preserved LV function (LVEF >60%).- **Repair is preferred** over replacement for degenerative MR (like a flail posterior leaflet) as it preserves the subvalvular apparatus, associated with superior long-term **left ventricular** function and survival.*Medical management*- Medical therapy (e.g., diuretics, vasodilators) is indicated only for patients deemed **not surgical candidates** or for asymptomatic patients with chronic MR being monitored.- In severe, primary MR that is symptomatic, delaying definitive surgical intervention increases the risk of irreversible **Left Ventricular (LV) dysfunction**.*Mitral valve replacement*- While a definitive surgical option, replacement is generally reserved for cases where **mitral repair** is technically unfeasible or has failed.- Replacement carries a higher perioperative risk and involves the long-term risks associated with a prosthetic valve, such as the need for lifetime **anticoagulation** with a mechanical valve.*Heart transplantation*- This option is reserved for patients with severe, **end-stage heart failure** refractory to optimal medical and surgical treatments.- It is not indicated in this patient, as the description clearly states they have **normal LV function**.*Balloon mitral valvuloplasty*- This procedure is strictly indicated for patients with severe **mitral stenosis**, particularly of **rheumatic etiology**.- It is contraindicated in patients with predominant severe **mitral regurgitation**, especially if caused by a structural defect like a **flail leaflet**.

Question 20: A 63-year-old man presents with progressive dyspnea and bilateral ankle swelling. Chest X-ray shows cardiomegaly and pulmonary edema. BNP is 2500 pg/mL. Echocardiogram shows EF 25%. What is the most appropriate initial medication?

A. Furosemide
B. ACE inhibitor (Correct Answer)
C. Beta-blocker
D. Spironolactone
E. Digoxin

Explanation: ***ACE inhibitor*** - **ACE inhibitors** are considered **first-line therapy** for patients with **Heart Failure with reduced Ejection Fraction (HFrEF)**, such as this patient with an EF of 25% and symptoms. - They work by blocking the **renin-angiotensin-aldosterone system (RAAS)**, leading to **vasodilation**, reduced cardiac remodeling, and significant improvements in **morbidity and mortality**. *Furosemide* - **Furosemide** is a loop diuretic primarily used for **symptomatic relief of congestion** (dyspnea, edema, pulmonary edema) in heart failure. - While often administered initially in acute decompensated heart failure, it does **not improve long-term mortality** or alter the disease progression; it addresses symptoms, not the underlying pathophysiology as the initial disease-modifying agent. *Beta-blocker* - **Beta-blockers** are also cornerstone therapy for HFrEF, improving **mortality and morbidity** by reducing sympathetic overactivity and remodeling. - However, they are typically initiated *after* ACE inhibitors (or ARNI/ARB) and only once the patient is **clinically stable and euvolemic**, as starting them in a congested patient can worsen heart failure symptoms. *Spironolactone* - **Spironolactone**, an **aldosterone antagonist**, is a **mortality-reducing agent** in HFrEF, particularly in patients with persistent symptoms or more severe disease. - It is usually added to an existing regimen of ACE inhibitors/ARBs and beta-blockers, not as the very first initial medication. *Digoxin* - **Digoxin** can improve symptoms and reduce hospitalizations in HFrEF by enhancing cardiac contractility and slowing heart rate in atrial fibrillation. - However, it does **not improve mortality** and is typically reserved for patients who remain symptomatic despite optimal guideline-directed medical therapy with ACE inhibitors, beta-blockers, and aldosterone antagonists.

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Cardiology — MCQs

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