Q-Bank Breakdown: Systolic vs diastolic heart failure — Why Every Answer Choice Matters

You’re cruising through your cardio Q-bank, and then a “heart failure” vignette shows up with five answer choices that all sound plausible. This is where most points are won or lost: not just knowing the right diagnosis, but knowing why each distractor is wrong. Let’s do a full Step-style breakdown of systolic vs diastolic heart failure—with a vignette, the correct answer, and a systematic teardown of every answer choice.

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The Clinical Vignette (Q-bank style)

A 72-year-old woman comes to clinic for progressive shortness of breath and decreased exercise tolerance for 6 months. She has a history of long-standing hypertension and type 2 diabetes. She reports waking up at night gasping for air and needs three pillows to sleep. On exam, BP is 168/92 mm Hg, HR 86/min, lungs have bibasilar crackles, and there is 1+ pitting edema at the ankles. A chest radiograph shows pulmonary vascular congestion. BNP is elevated. Transthoracic echocardiography shows:

• Left ventricular ejection fraction: 65%
• Concentric left ventricular hypertrophy
• Left atrial enlargement
• Impaired ventricular relaxation on Doppler

Question: What is the most likely underlying pathophysiology?

Answer choices

A. Decreased myocardial contractility due to loss of viable myocardium after infarction
B. Impaired ventricular relaxation with increased ventricular stiffness
C. Autoimmune destruction of cardiac myocytes causing dilated cardiomyopathy
D. Ventricular septal rupture leading to acute biventricular failure
E. Infiltration of myocardium by amyloid causing restrictive cardiomyopathy

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Stepwise Interpretation: What type of HF is this?

This patient has classic heart failure symptoms (orthopnea, PND, crackles, edema, high BNP) but with preserved EF (65%) and a history of chronic hypertension plus concentric LVH.

That combination points to:

• HFpEF = diastolic heart failure
• Main problem: filling, not pumping

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Correct Answer: B. Impaired ventricular relaxation with increased ventricular stiffness

Why B is correct

In diastolic HF (HFpEF):

• EF is normal or preserved (often $\ge 50\%$)
• The LV is often thick and stiff (concentric hypertrophy)
• The ventricle can contract normally, but it doesn’t relax well → high LV end-diastolic pressure → pulmonary congestion

High-yield physiologic framing:

• Primary dysfunction: impaired relaxation + decreased compliance
• Key hemodynamic result: $\uparrow$ LVEDP → $\uparrow$ pulmonary venous pressure → dyspnea/orthopnea/PND
• Remodeling pattern: concentric hypertrophy (pressure overload—think HTN, aortic stenosis)

Most common risk factors for HFpEF (Step favorites):

• Hypertension (biggest)
• Obesity
• Lung disease/OSA (often paired in real patients)
• Diabetes
• Elderly
• Female
  (“HOLD EF” is a common memory hook)

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Why the other choices are wrong (and what they really describe)

A. Decreased myocardial contractility due to loss of viable myocardium after infarction

Why it’s tempting: Ischemic heart disease is the most common cause of HF overall.

Why it’s wrong here: That describes systolic HF (HFrEF), which features:

• Reduced EF (often $<40\%$)
• Eccentric remodeling/dilation (volume overload pattern)
• Typical echo: dilated LV + poor contraction

Board clue mismatch: This patient has EF 65% and concentric LVH, not a dilated ventricle.

High-yield:

• Systolic HF = impaired contractility → $\downarrow$ SV → $\uparrow$ LVEDV → dilation
• Common causes: ischemic cardiomyopathy, dilated cardiomyopathy, chronic MR/AR

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C. Autoimmune destruction of cardiac myocytes causing dilated cardiomyopathy

Why it’s tempting: Dilated cardiomyopathy is common and causes HF symptoms.

Why it’s wrong: “Autoimmune destruction” is not a typical Step 1/2 primary association for dilated cardiomyopathy in this presentation. Dilated cardiomyopathy is classically linked to:

• Alcohol
• Coxsackie B viral myocarditis
• Doxorubicin
• Peripartum
• Hemochromatosis
• Genetic causes (e.g., TTN mutations)

And importantly, dilated cardiomyopathy → systolic dysfunction → low EF, not preserved EF.

High-yield echo pattern:

• Dilated cardiomyopathy: dilated chambers, thin walls, reduced EF, functional MR/TR possible

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D. Ventricular septal rupture leading to acute biventricular failure

Why it’s tempting: Mechanical complications of MI are fair game.

Why it’s wrong: The vignette describes chronic progressive symptoms over 6 months, not sudden deterioration. VSD rupture after MI causes:

• Acute heart failure (often cardiogenic shock)
• New harsh holosystolic murmur at the left sternal border
• Occurs 3–5 days post-MI (macrophage-mediated tissue breakdown)

Board clue mismatch: No acute post-MI timeline, no new loud murmur, and echo findings are consistent with chronic hypertensive remodeling.

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E. Infiltration of myocardium by amyloid causing restrictive cardiomyopathy

Why it’s tempting: Restrictive cardiomyopathy can have preserved EF and diastolic dysfunction, so it feels close.

Why it’s wrong here: The patient’s story screams hypertensive HFpEF: longstanding HTN + concentric LVH. Amyloidosis typically has extra clues:

• Signs of systemic amyloid (nephrotic syndrome, neuropathy, macroglossia, carpal tunnel)
• Echo may show thickened ventricular walls but not “true hypertrophy” (it’s infiltration), and may have a granular/sparkling appearance
• ECG classically shows low voltage despite increased wall thickness (discordance)

High-yield restrictive cardiomyopathy causes:

• Amyloidosis
• Sarcoidosis
• Hemochromatosis
• Radiation fibrosis
• Endomyocardial fibrosis (e.g., Loeffler)

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Quick Comparison Table: Systolic vs Diastolic HF (USMLE essentials)

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“BNP is elevated”—so what?

BNP (and NT-proBNP) rise with ventricular wall stretch, so they can be elevated in both HFpEF and HFrEF. BNP helps you:

• Support HF over non-cardiac dyspnea
• Track severity/response in many settings

But BNP does not by itself tell you systolic vs diastolic—echo does.

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High-yield distractor instincts (how to avoid traps)

When you see HF symptoms, lock onto one of two big forks:

1) What’s the EF?

• Low EF → think HFrEF
• Preserved EF → think HFpEF (then ask: HTN/AS vs restrictive causes)

2) What’s the remodeling pattern?

• Concentric LVH = pressure overload = HFpEF
• Dilated LV = volume overload/contractility failure = HFrEF

3) Acute vs chronic?

• Mechanical complications of MI (papillary muscle rupture, VSD rupture, free wall rupture) are acute, time-linked to MI, and usually dramatic.

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Mini Rapid-Fire: Classic presentations you should recognize

• HFpEF: elderly woman + long-standing HTN + concentric LVH + S4 + normal EF
• HFrEF: post-MI or alcoholic with dilated LV + S3 + reduced EF
• Amyloid restrictive CM: HF symptoms + thick walls on echo + low voltage ECG
• Post-MI VSD rupture: day 3–5 + shock + loud new holosystolic murmur

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Takeaway

This vignette is diastolic heart failure (HFpEF): impaired relaxation and increased stiffness from chronic hypertension causing concentric LVH, leading to elevated filling pressures and pulmonary congestion despite a normal EF. The distractors each map to a different cardiomyopathy or acute catastrophe—recognizable if you train yourself to anchor on EF, remodeling pattern, and timeline.