Valvular heart disease and heart failure US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Valvular heart disease and heart failure. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Valvular heart disease and heart failure US Medical PG Question 1: A 68-year-old man comes to the emergency department because of a 1-week history of difficulty breathing. He has had recurrent palpitations over the past 2 years. During this time, he has also had several episodes of anxiety despite no change in his daily life. He has occasional sharp chest pain localized to the left upper sternal border. He has no abdominal pain or leg swelling. Two years ago, he had streptococcal pharyngitis, which was promptly treated with a 10-day course of penicillin. He has never traveled outside of the country. His temperature is 36.5°C (97.7°F), pulse is 82/min, and blood pressure is 140/85 mm Hg. Physical examination shows a 3/6 holosystolic murmur that is loudest at the apex and radiates to the axilla with a mid-systolic click. Bilateral fine crackles are heard on lung auscultation. Which of the following is the most likely cause of this patient's symptoms?
- A. Inflammatory valve degeneration
- B. Ectopic production of serotonin
- C. Myxomatous valve degeneration (Correct Answer)
- D. Calcific valve degeneration
- E. Overproduction of catecholamines
Valvular heart disease and heart failure Explanation: ***Myxomatous valve degeneration***
- The presence of a **mid-systolic click** followed by a **holosystolic murmur** at the apex radiating to the axilla is highly characteristic of **mitral valve prolapse (MVP)** with **mitral regurgitation (MR)**.
- MVP is most commonly caused by **myxomatous degeneration** of the mitral valve leaflets, leading to their billowing into the left atrium during systole. The patient's recurrent palpitations, anxiety, and non-exertional chest pain are common symptoms associated with MVP, while difficulty breathing and crackles suggest **heart failure** from chronic MR.
*Inflammatory valve degeneration*
- **Inflammatory valve degeneration**, such as that seen in rheumatic heart disease, typically presents with a history of recurrent streptococcal infections leading to valvular scarring and dysfunction (e.g., mitral stenosis).
- While the patient had streptococcal pharyngitis, it was treated, and the clinical presentation with a mid-systolic click is more indicative of myxomatous changes rather than rheumatic inflammation.
*Ectopic production of serotonin*
- **Ectopic production of serotonin** occurs in settings like **carcinoid syndrome**, which typically involves flushing, diarrhea, bronchospasm, and can affect the right-sided heart valves primarily.
- The patient's symptoms are centered on left-sided heart issues and do not align with the broader systemic features of carcinoid syndrome.
*Calcific valve degeneration*
- **Calcific valve degeneration** commonly affects the **aortic valve** leading to **aortic stenosis** in older adults, characterized by a systolic ejection murmur heard at the right upper sternal border.
- It does not typically cause a mid-systolic click or affect the mitral valve in this manner, and the murmur description is inconsistent with aortic stenosis.
*Overproduction of catecholamines*
- **Overproduction of catecholamines**, as seen in conditions like **pheochromocytoma**, causes symptoms such as paroxysmal hypertension, palpitations, sweating, and anxiety.
- While some symptoms like palpitations and anxiety overlap, the specific cardiac murmur and signs of heart failure are not directly explained by catecholamine excess alone; a structural heart problem is more likely.
Valvular heart disease and heart failure US Medical PG Question 2: A 27-year-old woman with a history of a "heart murmur since childhood" presents following a series of syncopal episodes over the past several months. She also complains of worsening fatigue over this time period, and notes that her lips have begun to take on a bluish tinge, for which she has been using a brighter shade of lipstick. You do a careful examination, and detect a right ventricular heave, clubbing of the fingers, and 2+ pitting edema bilaterally to the shins. Despite your patient insisting that every doctor she has ever seen has commented on her murmur, you do not hear one. Transthoracic echocardiography would most likely detect which of the following?
- A. Mitral insufficiency
- B. Aortic stenosis
- C. Dynamic left ventricular outflow tract obstruction
- D. Positive bubble study (Correct Answer)
- E. Ventricular aneurysm
Valvular heart disease and heart failure Explanation: ***Positive bubble study***
- The patient's symptoms, including **cyanosis** (**bluish tinge to the lips**), **clubbing**, and **right ventricular heave**, suggest **Eisenmenger syndrome**, a late complication of a **left-to-right shunt** that has reversed due to pulmonary hypertension.
- A positive bubble study on echocardiography would confirm the presence of a **right-to-left shunt**, characteristic of Eisenmenger syndrome, by showing microbubbles crossing from the right to the left side of the heart.
*Mitral insufficiency*
- While mitral insufficiency can cause a murmur and heart failure symptoms, it does not typically lead to the **cyanosis** and **clubbing** described.
- The absence of a murmur, despite a history of one, points away from a significant current insufficiency.
*Aortic stenosis*
- Aortic stenosis is characterized by an **ejection systolic murmur** that would likely be heard on examination, contradicting the scenario where no murmur is audible.
- It usually presents with a different constellation of symptoms, such as angina, syncope, and heart failure, without the prominent cyanosis or clubbing seen here.
*Dynamic left ventricular outflow tract obstruction*
- This is characteristic of **hypertrophic obstructive cardiomyopathy (HOCM)**, which can cause exertional syncope.
- However, HOCM does not typically lead to **cyanosis**, a **right ventricular heave**, or **clubbing**, which are strong indicators of a right-to-left shunt.
*Ventricular aneurysm*
- A ventricular aneurysm is a bulging of the ventricular wall, often a complication of a **myocardial infarction**, which is unlikely in a 27-year-old with a history of a "heart murmur since childhood."
- It typically presents with symptoms related to heart failure, arrhythmias, or embolism, and would not explain the prominent **cyanosis** and **clubbing**.
Valvular heart disease and heart failure US Medical PG Question 3: A 50-year-old female presents with a holosystolic murmur heard best over the apex, radiating to the axilla. She has no signs of pulmonary hypertension or edema. What best explains her lack of symptoms?
- A. The aorta is compensating with increased compliance
- B. Mitral valve prolapse without regurgitation causes no hemodynamic changes
- C. The left atrium is compensating with increased compliance (Correct Answer)
- D. As long as preload in the left ventricle is maintained there would be no symptoms
- E. The right ventricle is compensating with decreased compliance
Valvular heart disease and heart failure Explanation: ***The left atrium is compensating with increased compliance***
- In **mitral regurgitation**, the initial compensatory mechanism involves the **left atrium stretching and increasing its compliance** to accommodate the regurgitant volume.
- This **prevents a significant rise in left atrial pressure**, thereby averting pulmonary congestion symptoms like edema or pulmonary hypertension.
*The aorta is compensating with increased compliance*
- **Aortic compliance** primarily affects **afterload** and is not a direct compensatory mechanism for mitral regurgitation.
- While aortic stiffening can exacerbate cardiac workload, increased compliance wouldn't specifically mitigate symptoms arising from left atrial volume overload.
*Mitral valve prolapse without regurgitation causes no hemodynamic changes*
- A **holosystolic murmur** best heard at the apex and radiating to the axilla is characteristic of **mitral regurgitation**, indicating actual blood flow back into the atrium during systole.
- **Mitral valve prolapse without regurgitation** might be silent or cause a mid-systolic click without significant hemodynamic changes, but this patient has clear evidence of regurgitation.
*As long as preload in the left ventricle is maintained there would be no symptoms*
- **Preload maintenance in the left ventricle** is important for maintaining cardiac output, but regurgitation itself diverts blood from forward flow.
- Symptoms in mitral regurgitation often arise from **increased left atrial pressure** and subsequent pulmonary congestion, even if left ventricular preload is sufficient to maintain some forward flow.
*The right ventricle is compensating with decreased compliance*
- **Right ventricular compliance** is primarily relevant to conditions affecting the pulmonary circulation or right heart.
- It would not directly compensate for left-sided volume overload in mitral regurgitation; in fact, prolonged left-sided heart failure can eventually lead to right ventricular dysfunction.
Valvular heart disease and heart failure US Medical PG Question 4: A 64-year-old woman with a history of rheumatic fever presents to her primary care clinician complaining of excessive fatigue with walking and difficulty lying flat. She had no prior physical limitations, but recently has been unable to walk more than 3 blocks without needing to stop and rest. Her cardiac exam is notable for a late diastolic murmur heard best at the apex in the left lateral decubitus position with no radiation. What is the most likely diagnosis?
- A. Aortic Stenosis
- B. Tricuspid Regurgitation
- C. Mitral Regurgitation
- D. Aortic Regurgitation
- E. Mitral Stenosis (Correct Answer)
Valvular heart disease and heart failure Explanation: ***Mitral Stenosis***
- A **late diastolic murmur heard best at the apex** in the left lateral decubitus position is a classic finding of **mitral stenosis**.
- History of **rheumatic fever** is a strong risk factor for mitral stenosis due to scarring and thickening of the mitral valve leaflets. **Fatigue with exertion** and **dyspnea on lying flat (orthopnea)** are common symptoms of left atrial enlargement and pulmonary congestion.
*Aortic Stenosis*
- Characterized by a **systolic ejection murmur** best heard at the right upper sternal border, radiating to the carotids.
- While it can cause exertional dyspnea and fatigue, the murmur timing and location do not match the patient's presentation.
*Tricuspid Regurgitation*
- Presents with a **holosystolic murmur** best heard at the left sternal border, often increasing with inspiration.
- Unlike mitral stenosis, it is more commonly associated with right-sided heart failure symptoms like peripheral edema and ascites.
*Mitral Regurgitation*
- Characterized by a **holosystolic murmur** that radiates to the axilla, best heard at the apex.
- Although also associated with rheumatic fever and causing fatigue, the timing of the murmur (systolic vs. diastolic) differentiates it from mitral stenosis.
*Aortic Regurgitation*
- Presents with an **early diastolic decrescendo murmur** best heard at the left sternal border.
- While it can cause dyspnea on exertion, its murmur is distinctly different from the late diastolic murmur described.
Valvular heart disease and heart failure US Medical PG Question 5: An 85-year-old man presents to his primary care provider after feeling "lightheaded." He said he helped his wife in the garden for the first time, but that while moving some bags of soil he felt like he was going to faint. He had a big breakfast of oatmeal and eggs prior to working in the garden. He has no significant past medical history and takes a baby aspirin daily. Physical exam reveals an elderly, well-nourished, well-built man with no evidence of cyanosis or tachypnea. Vital signs show normal temperature, BP 150/70, HR 80, RR 18. Cardiac exam reveals crescendo-decrescendo systolic murmur. What is the most likely cause of this patient's diagnosis?
- A. Infection
- B. Atherosclerosis
- C. Calcification (Correct Answer)
- D. Congenital defect
- E. Malnutrition
Valvular heart disease and heart failure Explanation: ***Calcification***
- The patient's age (85 years old) and the presence of a **crescendo-decrescendo systolic murmur** strongly suggest **aortic stenosis**. The most common cause of aortic stenosis in the elderly is **degenerative calcification** of the aortic valve.
- His **lightheadedness** upon exertion (moving bags of soil) is consistent with symptoms of aortic stenosis, as the narrowed valve restricts blood flow to the brain during increased demand.
*Infection*
- While infective endocarditis can cause new murmurs and systemic symptoms, it typically presents with **fever**, **fatigue**, and signs of infection, which are not described in this patient.
- The type of murmur in endocarditis is often **regurgitant** or can have a rapidly changing character, rather than the classic crescendo-decrescendo systolic murmur of aortic stenosis.
*Atherosclerosis*
- Although atherosclerosis is a common process in the elderly and can affect large vessels, it does **not** directly cause aortic stenosis. The valve pathology is primarily a **degenerative calcific process** rather than atherosclerotic plaque formation.
- While atherosclerosis and calcific aortic stenosis share some risk factors (age, hypertension, hyperlipidemia), the mechanism of valve narrowing is through progressive **calcification and fibrosis** of the valve leaflets, not atheroma formation.
*Congenital defect*
- While a **bicuspid aortic valve** is a common congenital defect that can lead to aortic stenosis, symptoms typically present much earlier in life (40s-60s) due to accelerated calcification.
- An 85-year-old presenting with new symptoms is more likely to have age-related **degenerative calcific aortic stenosis** rather than a late manifestation of an undiagnosed congenital defect.
*Malnutrition*
- Malnutrition is not directly associated with the development of a crescendo-decrescendo systolic murmur or **aortic stenosis**.
- While severe malnutrition can cause various systemic issues, it does not explain the specific cardiac findings and exertional symptoms described in this well-nourished patient.
Valvular heart disease and heart failure US Medical PG Question 6: A 36-year-old man presents to his primary care physician because of shortness of breath. He is an office worker who has a mostly sedentary lifestyle; however, he has noticed that recently he feels tired and short of breath when going on long walks with his wife. He also has had a hacking cough that seems to linger, though he attributes this to an upper respiratory tract infection he had 2 months ago. He has diabetes that is well-controlled on metformin and has smoked 1 pack per day for 20 years. Physical exam reveals a large chested man with wheezing bilaterally and mild swelling in his legs and abdomen. The cause of this patient's abdominal and lower extremity swelling is most likely due to which of the following processes?
- A. Excessive protease activity
- B. Damage to kidney tubules
- C. Hyperplasia of mucous glands
- D. Defective protein folding
- E. Right ventricular dysfunction secondary to pulmonary hypertension (Correct Answer)
Valvular heart disease and heart failure Explanation: ***Right ventricular dysfunction secondary to pulmonary hypertension***
- This patient's long history of smoking, chronic cough, and wheezing suggest significant **chronic obstructive pulmonary disease (COPD)**, which leads to **hypoxemia** and **pulmonary hypertension**.
- **Pulmonary hypertension** increases the workload on the **right ventricle**, eventually leading to **right heart failure** (cor pulmonale), characterized by peripheral edema (leg swelling) and ascites (abdominal swelling).
*Excessive protease activity*
- While excessive protease activity (e.g., elastase) is implicated in the pathogenesis of **emphysema** by destroying alveolar walls, it does not directly cause peripheral edema and ascites.
- This process primarily leads to **airflow obstruction** and **gas exchange abnormalities**, which can indirectly contribute to pulmonary hypertension but is not the direct cause of the peripheral edema.
*Damage to kidney tubules*
- **Acute tubular necrosis** or chronic kidney disease can cause edema due to impaired fluid and electrolyte balance, but the patient's symptoms (dyspnea, wheezing, smoking history) point strongly to a primary pulmonary and cardiac etiology.
- While diabetes can cause nephropathy, there is no information to suggest acute kidney injury or chronic kidney disease leading to such severe edema.
*Hyperplasia of mucous glands*
- **Hyperplasia of mucous glands** in the bronchi is characteristic of **chronic bronchitis**, contributing to the chronic cough and airway obstruction.
- This pathology primarily affects airway clearance and airflow, rather than directly causing systemic edema or ascites.
*Defective protein folding*
- **Defective protein folding**, such as in **alpha-1 antitrypsin deficiency**, can lead to early-onset emphysema and liver disease.
- While this could fit with a pulmonary presentation, it is less common than smoking-induced COPD and does not directly explain the edema and ascites caused by right heart failure.
Valvular heart disease and heart failure US Medical PG Question 7: A 70-year-old male presents for an annual exam. His past medical history is notable for shortness of breath when he sleeps, and upon exertion. Recently he has experienced dyspnea and lower extremity edema that seems to be worsening. Both of these symptoms have resolved since he was started on several medications and instructed to weigh himself daily. Which of the following is most likely a component of his medical management?
- A. Lidocaine
- B. Verapamil
- C. Carvedilol (Correct Answer)
- D. Aspirin
- E. Ibutilide
Valvular heart disease and heart failure Explanation: ***Carvedilol***
- The patient exhibits classic symptoms of **heart failure**, such as **dyspnea on exertion**, **orthopnea** (shortness of breath when he sleeps), and **lower extremity edema**.
- **Beta-blockers** like carvedilol are essential for managing **chronic heart failure** by reducing myocardial oxygen demand and improving cardiac function.
*Lidocaine*
- **Lidocaine** is primarily an **antiarrhythmic drug** used for acute treatment of **ventricular arrhythmias**, not for chronic heart failure management.
- It works by blocking sodium channels and has no direct benefit in addressing the underlying pathophysiology of heart failure.
*Verapamil*
- **Verapamil** is a **non-dihydropyridine calcium channel blocker** typically used for hypertension, angina, and supraventricular tachyarrhythmias.
- It can have **negative inotropic effects**, which are generally contraindicated or used with extreme caution in patients with **systolic heart failure** due to its potential to worsen cardiac function.
*Aspirin*
- **Aspirin** is an **antiplatelet agent** used for primary or secondary prevention of **atherosclerotic cardiovascular disease** (e.g., in patients with coronary artery disease).
- It does not directly manage the symptoms or pathophysiology of **heart failure** unless there is a coexisting ischemic etiology.
*Ibutilide*
- **Ibutilide** is an **antiarrhythmic drug** specifically used for the rapid conversion of **atrial flutter and atrial fibrillation** of recent onset to sinus rhythm.
- It is not a medication used for the long-term management of **heart failure** symptoms described in the patient.
Valvular heart disease and heart failure US Medical PG Question 8: A 72-year-old woman comes to the emergency department because of a 2-week history of worsening shortness of breath, lower extremity swelling, and a 3-kg (6.6-lb) weight gain. Crackles are heard on auscultation of the chest. Cardiac examination shows a dull, low-pitched early diastolic sound at the 5th left intercostal space that becomes louder in the left lateral decubitus position at end-expiration. Which of the following is the most likely cause of these auscultation findings?
- A. Increased ventricular contractility
- B. Increased capacity of the pulmonary circulation
- C. Decreased left-ventricular filling pressure
- D. Increased left ventricular end-systolic volume
- E. Decreased left myocardial compliance (Correct Answer)
Valvular heart disease and heart failure Explanation: ***Decreased left myocardial compliance***
- A dull, low-pitched early **diastolic sound (S3 gallop)**, heard best in the left lateral decubitus position at end-expiration, indicates **rapid ventricular filling** into a ventricle with altered diastolic properties. This finding, along with worsening shortness of breath, lower extremity swelling, and weight gain, suggests **heart failure with impaired ventricular filling**.
- Decreased left myocardial compliance (increased stiffness) means the left ventricle cannot **relax and fill properly** during diastole. The S3 occurs when blood rapidly decelerates as it enters the stiff, non-compliant ventricle, creating the characteristic sound.
- This represents **diastolic dysfunction** (heart failure with preserved ejection fraction - HFpEF), which is common in elderly patients with hypertension and is characterized by a stiff ventricle with increased filling pressures.
*Increased ventricular contractility*
- Increased ventricular contractility would lead to a more forceful ejection of blood during systole, not an early diastolic filling sound.
- This would not explain the S3 gallop or the signs of heart failure with fluid retention.
*Increased capacity of the pulmonary circulation*
- Increased pulmonary circulation capacity would help accommodate fluid and prevent pulmonary congestion, which contradicts the symptoms of crackles and shortness of breath.
- The patient has **decreased** capacity to handle the fluid volume, leading to pulmonary edema.
*Decreased left-ventricular filling pressure*
- Decreased LV filling pressure would imply less fluid overload and better cardiac function, contrary to the clinical presentation.
- An S3 gallop and signs of heart failure (crackles, edema, weight gain) indicate **increased** filling pressures from impaired ventricular function.
*Increased left ventricular end-systolic volume*
- Increased end-systolic volume indicates **systolic dysfunction** (reduced ejection fraction), where the ventricle cannot adequately eject blood, leaving residual volume after contraction.
- While systolic dysfunction can also produce an S3 gallop due to volume overload, the specific clinical description emphasizes a **diastolic filling abnormality** (sound during early diastole in a specific position that optimizes detection of ventricular filling).
- The S3 in systolic dysfunction is primarily due to **volume overload**, whereas the S3 here is attributed to blood entering a **stiff ventricle** with impaired compliance, which is the primary pathophysiologic mechanism being tested.
Valvular heart disease and heart failure US Medical PG Question 9: A 71-year-old woman with a past medical history of type 2 diabetes, hypercholesterolemia, and hypertension was admitted to the hospital 8 hours ago with substernal chest pain for management of acute non-ST-elevated myocardial infarction (NSTEMI). The ECG findings noted by ST-depressions and T-wave inversions on anterolateral leads, which is also accompanied by elevated cardiac enzymes. Upon diagnosis, management with inhaled oxygen therapy, beta-blockers and aspirin, and low-molecular-weight heparin therapy were initiated, and she was placed on bed rest with continuous electrocardiographic monitoring. Since admission, she required 2 doses of sublingual nitroglycerin for recurrent angina, and the repeat troponin levels continued to rise. Given her risk factors, plans were made for early coronary angiography. The telemetry nurse calls the on-call physician because of her concern with the patient's mild confusion and increasing need for supplemental oxygen. At bedside evaluation, The vital signs include: heart rate 122/min, blood pressure 89/40 mm Hg, and the pulse oximetry is 91% on 6L of oxygen by nasal cannula. The telemetry and a repeat ECG show sinus tachycardia. She is breathing rapidly, appears confused, and complains of shortness of breath. On physical exam, the skin is cool and clammy and appears pale and dull. She has diffuse bilateral pulmonary crackles, and an S3 gallop is noted on chest auscultation with no new murmurs. She has jugular venous distention to the jaw-line, rapid and faint radial pulses, and 1+ dependent edema. She is immediately transferred to the intensive care unit for respiratory support and precautions for airway security. The bedside sonography shows abnormal hypodynamic anterior wall movement and an ejection fraction of 20%, but no evidence of mitral regurgitation or ventricular shunt. The chest X-ray demonstrates cephalization of pulmonary veins and pulmonary edema. What is the most appropriate next step in the stabilization of this patient?
- A. Obtain blood cultures and start preliminary broad-spectrum antibiotics
- B. Start intravenous fluids and epinephrine therapy
- C. Intubate the patient and perform an emergency cardiocentesis
- D. Initiate dopamine therapy and diuresis (Correct Answer)
- E. Insert two large-bore intravenous catheters and start rapid fluid resuscitation
Valvular heart disease and heart failure Explanation: ***Initiate dopamine therapy and diuresis***
- This patient is presenting with **cardiogenic shock** secondary to extensive NSTEMI, characterized by **hypotension**, signs of **end-organ hypoperfusion** (confusion, cool clammy skin), **pulmonary edema** (crackles, dyspnea, elevated jugular venous pressure), and **severely reduced ejection fraction**. Dopamine is a vasopressor that can increase cardiac output and blood pressure.
- **Diuresis** with loop diuretics such as furosemide is crucial to reduce the fluid overload contributing to the pulmonary edema and jugular venous distention.
*Obtain blood cultures and start preliminary broad-spectrum antibiotics*
- While infection is a concern in critically ill patients, there are **no signs of infection** in this clinical presentation. The patient's symptoms are clearly attributable to acute cardiac decompensation.
- A delay in treating cardiogenic shock to investigate for infection would be detrimental and potentially fatal.
*Start intravenous fluids and epinephrine therapy*
- Intravenous fluids would **worsen the existing pulmonary edema and fluid overload** in a patient with an ejection fraction of 20% and clinical signs of volume overload (crackles, JVD, S3 gallop).
- Epinephrine is a potent vasopressor but is generally reserved for more severe shock refractory to other inotropes, or in cases of **cardiac arrest**, not typically first-line for cardiogenic shock with significant pulmonary congestion.
*Intubate the patient and perform an emergency cardiocentesis*
- While the patient is confused and has respiratory distress, **intubation** should be considered after hemodynamic stabilization, if respiratory failure persists or worsens.
- **Cardiocentesis** is indicated for **cardiac tamponade**, which is not supported by the absence of an effusion on bedside sonography and the finding of hypodynamic anterior wall movement, which points to pump failure.
*Insert two large-bore intravenous catheters and start rapid fluid resuscitation*
- This patient is in **cardiogenic shock with clear evidence of fluid overload**, including pulmonary edema and elevated jugular venous pressure.
- **Rapid fluid resuscitation would exacerbate heart failure** and worsen respiratory compromise due to increased preload.
Valvular heart disease and heart failure US Medical PG Question 10: Background: Beta-blockers reduce mortality in patients who have chronic heart failure, systolic dysfunction, and are on background treatment with diuretics and angiotensin-converting enzyme inhibitors. We aimed to compare the effects of carvedilol and metoprolol on clinical outcome.
Methods: In a multicenter, double-blind, randomized parallel group trial, we assigned 1511 patients with chronic heart failure to treatment with carvedilol (target dose, 25 mg twice daily) and 1518 to metoprolol (target dose, 50 mg twice daily). The patients were required to have chronic heart failure (NYHA II-IV), the previous admission for a cardiovascular indication, an ejection fraction of < 0.35, and to have been treated optimally with diuretics and angiotensin-converting enzyme inhibitors unless not tolerated. The primary endpoints were all-cause mortality and the composite endpoint of all-cause mortality or all-cause admission. The analysis was done by intention-to-treat.
Findings: The mean study duration was 58 months (SD, 6). The mean ejection fraction was 0.26 (SD, 0.07) and the mean age was 62 years (SD, 11). The all-cause mortality was 34% (512 of 1511) for carvedilol and 40% (600 of 1518) for metoprolol (hazard ratio, 0.83 [95% CI 0.74-0.93], p = 0.0017). The reduction in all-cause mortality was consistent across pre-defined subgroups. The incidence of side effects and drug withdrawals did not differ significantly between the 2 study groups.
Based on the best interpretation of the results of this clinical trial, which of the following statements is most accurate?
- A. The study was underpowered and unable to arrive at a statistically significant conclusion.
- B. Metoprolol demonstrated a significant improvement in all-cause mortality in patients with heart failure compared to carvedilol.
- C. The results are likely biased due to trial design, and therefore non-generalizable.
- D. Carvedilol demonstrated a significant improvement in all-cause mortality in patients with heart failure as compared to metoprolol. (Correct Answer)
- E. There is no appreciable, statistically significant difference in overall mortality between the 2 treatment arms.
Valvular heart disease and heart failure Explanation: ***Carvedilol demonstrated a significant improvement in all-cause mortality in patients with heart failure as compared to metoprolol.***
- The study explicitly states that the all-cause mortality for carvedilol was 34% compared to 40% for metoprolol, with a **hazard ratio of 0.83** and a **p-value of 0.0017**.
- A p-value of < 0.05 indicates statistical significance, and a hazard ratio less than 1 favors the intervention (carvedilol), showing a **20% relative risk reduction** in mortality.
*The study was underpowered and unable to arrive at a statistically significant conclusion.*
- The p-value of 0.0017 for all-cause mortality is well below the conventional significance level of 0.05, indicating a **statistically significant result**.
- With **over 1500 patients in each arm** and mean follow-up of 58 months, the study was sufficiently powered to detect a difference, as evidenced by the significant findings.
*Metoprolol demonstrated a significant improvement in all-cause mortality in patients with heart failure compared to carvedilol.*
- The data shows that **metoprolol had a higher all-cause mortality (40%)** compared to carvedilol (34%), meaning metoprolol was associated with worse outcomes.
- The hazard ratio of 0.83, favoring carvedilol, clearly refutes any claim of metoprolol providing a significant improvement over carvedilol.
*There is no appreciable, statistically significant difference in overall mortality between the two treatment arms.*
- The **p-value of 0.0017** is statistically significant, indicating that the observed difference in mortality is unlikely due to chance.
- The **6% absolute difference** in mortality (40% vs. 34%) is both statistically and clinically appreciable in a chronic condition like heart failure.
*The results are likely biased due to trial design, and therefore non-generalizable.*
- The study was a **multicenter, double-blind, randomized parallel group trial**, which is a robust design aimed at minimizing bias.
- The "intention-to-treat" analysis further strengthens the generalizability by reflecting real-world clinical practice where patients may not always adhere to assigned treatments.
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