Cardiology Practice Questions

Q: What TIMI score on angiography denotes complete occlusion of a coronary artery?

0. The **TIMI (Thrombolysis in Myocardial Infarction)** flow grade is a scoring system used during coronary angiography to assess the degree of blood flow through a coronary artery [1]. It is a critical prognostic indicator in patients with Acute Coronary Syndrome (ACS). ### Explanation of Options: * **TIMI 0 (Correct):** This represents **complete occlusion** of the coronary artery [3]. There is no flow beyond the point of obstruction. This is typically seen in the culprit vessel of an ST-elevation myocardial infarction (STEMI). * **TIMI 1:** This denotes **penetration without perfusion**. Contrast material passes beyond the area of obstruction but fails to opacify the entire distal coronary bed. * **TIMI 2:** This is **partial perfusion**. Contrast material opacifies the entire distal vessel, but the rate of entry and clearance is significantly slower than in a normal vessel. * **TIMI 3:** This represents **full perfusion** (normal flow) [3]. Contrast opacifies the distal vessel as rapidly as it does in a normal, non-obstructed artery. ### Clinical Pearls for NEET-PG: * **Goal of PCI:** The primary objective of Primary Percutaneous Coronary Intervention (PCI) is to restore **TIMI 3 flow** [3]. * **TIMI Risk Score:** Do not confuse the *TIMI Flow Grade* (angiographic) with the *TIMI Risk Score* (clinical). The Risk Score (0-7) predicts 14-day mortality in UA/NSTEMI based on parameters like age ≥65, ≥3 CAD risk factors, and ST-segment changes [2]. * **No-Reflow Phenomenon:** This occurs when a patient has TIMI 0-1 flow despite the mechanical opening of the epicardial artery, usually due to microvascular dysfunction or distal embolization.

Q: All of the following are true about hypertrophic obstructive cardiomyopathy except?

Dilatation of ventricles. Hypertrophic Obstructive Cardiomyopathy (HOCM) is a genetic disorder characterized by primary myocardial hypertrophy without an underlying systemic cause (like hypertension) [1]. **Why Option C is the correct answer:** In HOCM, the hallmark is **concentric or asymmetric hypertrophy**, which leads to a **reduction in ventricular cavity size** rather than dilatation. The ventricular walls become thick and non-compliant, resulting in diastolic dysfunction. Ventricular dilatation is a feature of *Dilated Cardiomyopathy (DCM)* or the "burnt-out" end-stage of HOCM, but it is not a characteristic feature of the disease itself. **Analysis of Incorrect Options:** * **Option A (Asymmetric septal hypertrophy):** This is the most common anatomical pattern in HOCM. The interventricular septum is significantly thicker than the posterior wall (Septum:LV wall ratio > 1.3:1) [1]. * **Option B (Dilatation of atria):** Due to a stiff, non-compliant left ventricle (diastolic dysfunction) and often associated mitral regurgitation (caused by SAM), the left atrium undergoes pressure and volume overload, leading to **Left Atrial Enlargement (LAE)**. * **Option C (Outflow obstruction):** The hypertrophy of the subaortic septum, combined with the **Systolic Anterior Motion (SAM)** of the mitral valve, creates a dynamic Left Ventricular Outflow Tract (LVOT) obstruction [1]. **NEET-PG High-Yield Pearls:** * **Inheritance:** Autosomal Dominant; most common mutation involves **Beta-myosin heavy chain** or Myosin-binding protein C [1]. * **Murmur:** Harsh systolic ejection murmur at the left sternal border. * **Dynamic Maneuvers:** Murmur **increases** with Valsalva and standing (decreased preload) and **decreases** with squatting and handgrip (increased preload/afterload). * **Histology:** Myocardial fiber **disarray** [1]. * **Drug of Choice:** Beta-blockers (to increase diastolic filling time). Avoid Nitrates, Diuretics, and Digoxin.

Q: Which of the following auscultatory signs is absent in mitral stenosis when atrial fibrillation is present?

Presystolic accentuation. In **Mitral Stenosis (MS)**, the classic murmur is a low-pitched mid-diastolic rumble [1]. Toward the end of diastole, there is typically a **presystolic accentuation** of this murmur. This accentuation is caused by **atrial systole** (atrial kick), which increases the pressure gradient across the narrowed mitral valve, accelerating blood flow into the ventricle just before the mitral valve closes [1]. In **Atrial Fibrillation (AF)**, there is no coordinated atrial contraction. Since the "atrial kick" is lost, the terminal increase in blood flow across the valve disappears, leading to the **absence of presystolic accentuation**. **Analysis of Other Options:** * **Mid-diastolic murmur:** This is caused by the passive flow of blood across the stenosed valve during the early and mid-phases of diastole [1]. It persists in AF, though its duration may vary with cycle length. * **Variable first heart sound (S1):** In AF, the R-R interval is irregular. The intensity of S1 depends on the duration of diastole (the position of leaflets at the onset of ventricular systole). Therefore, a variable S1 is a *characteristic* finding of AF. * **Loud P2:** This indicates pulmonary hypertension secondary to MS [1]. It is a reflection of pulmonary artery pressure and is not dependent on the cardiac rhythm. **High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of AF":** Whenever a patient with MS develops AF, the presystolic accentuation disappears, and the S1 becomes variable in intensity. * **S1 in MS:** S1 is loud/tapping in MS because the leaflets are held wide open by high atrial pressure until the very start of systole [1]. If the valve is heavily calcified, S1 becomes soft. * **Opening Snap (OS):** The A2-OS interval is inversely proportional to the severity of MS (shorter interval = more severe MS) [2].

Q: Which of the following is NOT an X-ray feature of Atrial Septal Defect?

Left atrial enlargement. **Explanation:** In **Atrial Septal Defect (ASD)**, the underlying pathophysiology is a left-to-right shunt at the atrial level [2]. Because the pressure gradient between the atria is low and the mitral valve remains competent, the left atrium (LA) decompresses directly into the right atrium. Consequently, the LA does not undergo volume or pressure overload, making **Left Atrial Enlargement (LAE)** a characteristically absent feature in ASD. If LAE is present, one must suspect associated Mitral Regurgitation or Lutembacher Syndrome. **Analysis of Options:** * **Right Atrial Enlargement (Option A):** The shunted blood flows from the LA to the RA, leading to volume overload and subsequent enlargement of the RA [1] and Right Ventricle. * **Pulmonary Plethora (Option C):** Increased blood flow through the right heart is pumped into the pulmonary circulation, resulting in prominent pulmonary vascular markings (plethora) on X-ray [1]. * **Small Aortic Knuckle (Option D):** Due to the significant left-to-right shunt, the stroke volume entering the systemic circulation (left ventricle to aorta) is relatively reduced, making the aortic knuckle appear small or inconspicuous. **High-Yield Clinical Pearls for NEET-PG:** * **Lutembacher Syndrome:** The combination of ASD and acquired Mitral Stenosis (leads to significant LAE). * **ECG in ASD:** Look for RBBB (Right Bundle Branch Block) and Right Axis Deviation (ostium secundum) [2] or Left Axis Deviation (ostium primum). * **Auscultation:** Characterized by a **fixed, wide splitting of S2** and a mid-diastolic flow murmur at the tricuspid area.

Q: Which of the following statements regarding peripartum cardiomyopathy is true?

Subsequent pregnancies carry a risk.. **Explanation:** Peripartum Cardiomyopathy (PPCM) is an idiopathic form of heart failure characterized by left ventricular systolic dysfunction (LVEF <45%) occurring toward the end of pregnancy or in the months following delivery, where no other cause of heart failure is found. **Why Option D is Correct:** Subsequent pregnancies carry a significant risk of recurrence and clinical deterioration. Even if the patient’s Left Ventricular (LV) function returns to normal, there is a **20% risk of relapse** in future pregnancies. If the LV function has not normalized, the risk of maternal mortality and severe heart failure is extremely high, and subsequent pregnancy is generally contraindicated. **Analysis of Incorrect Options:** * **Option A:** While serious, the mortality rate is not 40-50%. With modern management (including ACE inhibitors postpartum, beta-blockers, and bromocriptine), the mortality rate has decreased to approximately **5-10%**. * **Option B:** PPCM is not specifically associated with long-term hypertension. While hypertensive disorders of pregnancy are risk factors for developing PPCM, the cardiomyopathy itself does not cause chronic hypertension. * **Option C:** Pre-eclampsia is a major **risk factor** for PPCM, but it does not "cause" it in a direct physiological sense. PPCM is thought to be triggered by the cleavage of prolactin into a cardiotoxic 16kDa fragment. **High-Yield Clinical Pearls for NEET-PG:** * **Timing:** Most commonly presents in the **1st month postpartum**. * **Risk Factors:** Advanced maternal age (>30), multiparity, twin pregnancy, and pre-eclampsia. * **Management:** Standard HF therapy, but **ACE inhibitors/ARBs are contraindicated until after delivery** (teratogenic). * **Bromocriptine:** Emerging therapy that inhibits prolactin secretion, potentially blocking the production of the cardiotoxic 16kDa fragment.

Q: A 58-year-old man presents with chest pain that occurs on exertion and resolves with rest. The pain is not present at rest and always remits spontaneously within a few minutes. His blood pressure is mildly elevated at 145/85 mmHg, and his ECG shows normal sinus rhythm. What is the most appropriate investigation?

CT coronary angiography. **Explanation:** The patient presents with classic symptoms of **Stable Angina** (exertional chest pain relieved by rest) [1]. According to current clinical guidelines (such as NICE and ESC), **CT Coronary Angiography (CTCA)** is now the first-line investigation for patients with new-onset stable chest pain where coronary artery disease (CAD) cannot be excluded by clinical assessment alone [4]. **Why CT Coronary Angiography is correct:** CTCA is a non-invasive anatomical test with a very high **negative predictive value**. It is preferred over functional stress tests because it can directly visualize the coronary arteries to detect or rule out atherosclerosis and stenosis, guiding further management effectively in stable patients [1], [4]. **Why the other options are incorrect:** * **A. Fasting blood lipids:** While important for risk stratification and long-term management, lipid profiles do not diagnose the cause of the acute presenting symptom (chest pain) [4]. * **B. Urgent invasive coronary angiography:** This is reserved for patients with Acute Coronary Syndrome (ACS) or those with high-risk features/refractory symptoms [1]. This patient is currently stable and pain-free at rest. * **C. Repeat ECG in 1 week:** A resting ECG is often normal in stable angina. Delaying investigation by a week without a definitive diagnostic plan is inappropriate and risks missing significant CAD. **Clinical Pearls for NEET-PG:** * **Gold Standard for CAD:** Invasive Coronary Angiography (but not the first-line for stable, low-to-intermediate risk patients). * **First-line for Stable Angina:** CT Coronary Angiography [4]. * **Definition of Stable Angina:** Chest pain that is (1) Constricting/heavy, (2) Precipitated by exertion, and (3) Relieved by rest or nitrates within 5 minutes [2]. * **ECG Finding:** The most common ECG finding during an actual episode of stable angina is **ST-segment depression** [3].

Question 1

All of the following statements are TRUE about infectious endocarditis EXCEPT?

Accepted Answer

Fatality rates for right-sided disease are greater than those for left-sided disease.

Answer

Cardiac valve leaflets are susceptible to infection because of their limited blood supply.

Answer

Streptococcus viridans is the most common organism implicated in left-sided disease.

Answer

More than three-fourths of cases of right-sided endocarditis are caused by Staphylococcus aureus.

Question 2

What TIMI score on angiography denotes complete occlusion of a coronary artery?

Accepted Answer

0

Answer

1

Answer

2

Answer

3

Question 3

A 42-year-old man with known valvular heart disease develops a fever for 1 week. He appears unwell; findings include a pansystolic murmur at the apex that radiates to the axilla and a soft S1 sound. He has petechiae on his conjunctival sac, linear hemorrhages under a few fingernails, and painful, tender, and erythematous nodules on some of the distal fingertips. Which of the following is the most responsible mechanism for these physical findings?

Accepted Answer

Vascular phenomena

Answer

Direct bacterial invasion

Answer

Immune response

Answer

Valvular damage

Question 4

All of the following are true about hypertrophic obstructive cardiomyopathy except?

Accepted Answer

Dilatation of ventricles

Answer

Asymmetric septal hypertrophy

Answer

Dilatation of atria

Answer

Outflow obstruction

Question 5

Which of the following auscultatory signs is absent in mitral stenosis when atrial fibrillation is present?

Accepted Answer

Presystolic accentuation

Answer

Mid-diastolic murmur

Answer

Variable first heart sound

Answer

Loud P2

Question 6

Which of the following is NOT an X-ray feature of Atrial Septal Defect?

Accepted Answer

Left atrial enlargement

Answer

Right atrial enlargement

Answer

Pulmonary plethora

Answer

Small aortic knuckle

Question 7

SABE is most commonly due to?

Accepted Answer

Streptococcus pneumoniae

Answer

Staphylococcus aureus

Answer

Streptococcus viridans

Answer

HACEK group bacteria

Question 8

Which of the following statements regarding peripartum cardiomyopathy is true?

Accepted Answer

Subsequent pregnancies carry a risk.

Answer

It has a 40-50% mortality even with treatment.

Answer

It is associated with a long-term increased incidence of hypertension.

Answer

Pre-eclampsia causes peripartum cardiomyopathy.

Question 9

A previously healthy 65-year-old woman presents with acute stroke. Examination reveals acute bilateral lower extremity deep vein thrombosis. Echocardiogram with agitated saline contrast shows bubbles crossing into the left atrium. Which of the following is most likely responsible for her symptoms?

Accepted Answer

Patent foramen ovale

Answer

Bicuspid aortic valve

Answer

Tetralogy of Fallot

Answer

Transposition of the great vessels

Question 10

A 58-year-old man presents with chest pain that occurs on exertion and resolves with rest. The pain is not present at rest and always remits spontaneously within a few minutes. His blood pressure is mildly elevated at 145/85 mmHg, and his ECG shows normal sinus rhythm. What is the most appropriate investigation?

Accepted Answer

CT coronary angiography

Answer

Fasting blood lipids

Answer

Urgent invasive coronary angiography

Answer

Repeat ECG in 1 week

Cardiology — MCQs

Cardiology — MCQs

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