A 68-year-old man comes to the clinic for a routine follow-up regarding his heart failure.… — USMLE Step 3

A 68-year-old man comes to the clinic for a routine follow-up regarding his heart failure. Two months ago, he was hospitalized for an acute heart failure exacerbation. During that admission, his lisinopril was discontinued after his serum creatinine acutely worsened from a baseline of $1.9 \text{ mg/dL}$ to $3.8 \text{ mg/dL}$ and his serum potassium peaked at $6.1 \text{ mEq/L}$ . Since discharge, he has adhered to a low-sodium diet and his weight has remained stable. He currently has no orthopnea or lower extremity edema but reports dyspnea when walking up one flight of stairs or carrying groceries. His past medical history includes heart failure with reduced ejection fraction (most recent echocardiogram 1 month ago showed a left ventricular ejection fraction of $25\%$ ), type 2 diabetes mellitus, chronic kidney disease, and coronary artery disease.

Current medications include carvedilol $25 \text{ mg}$ twice daily, dapagliflozin $10 \text{ mg}$ daily, furosemide $40 \text{ mg}$ daily, atorvastatin $40 \text{ mg}$ daily, and aspirin $81 \text{ mg}$ daily.

Vital signs are:
Temperature: $37.0^\circ\text{C}$ ( $98.6^\circ\text{F}$ )
Blood pressure: $118/75 \text{ mm Hg}$
Pulse: $66/\text{min}$ and regular
Respirations: $16/\text{min}$

Physical examination shows a jugular venous pressure of $7 \text{ cm H}_2\text{O}$ . The lungs are clear to auscultation bilaterally. Cardiac examination reveals a regular rate and rhythm with normal S1 and S2; no murmurs, rubs, or gallops are heard. The extremities have trace, bilateral, non-pitting edema.

Laboratory studies show:
Sodium: $138 \text{ mEq/L}$
Potassium: $5.2 \text{ mEq/L}$
Bicarbonate: $24 \text{ mEq/L}$
Creatinine: $2.7 \text{ mg/dL}$ (estimated glomerular filtration rate: $24 \text{ mL/min/1.73 m}^2$ )

Which of the following is the most appropriate pharmacologic intervention to further reduce this patient's risk of all-cause mortality?

Initiate isosorbide dinitrate and hydralazineAnswer
B
Initiate sacubitril-valsartan
C
Initiate spironolactone
D
Initiate ivabradine
E
Initiate digoxin

Answer

The most appropriate intervention is to initiate isosorbide dinitrate and hydralazine.

The correct answer is to initiate isosorbide dinitrate and hydralazine. This patient has symptomatic heart failure with reduced ejection fraction (HFrEF) and requires further optimization of guideline-directed medical therapy to reduce mortality. Standard next steps typically include a mineralocorticoid receptor antagonist (MRA) or transitioning to an angiotensin receptor-neprilysin inhibitor (ARNI). However, this patient's current estimated glomerular filtration rate is

24 \text{ mL/min/1.73 m}^2

and his potassium is

5.2 \text{ mEq/L}

. Furthermore, he has a documented history of severe acute kidney injury and hyperkalemia on an ACE inhibitor. In patients with HFrEF who are intolerant to RAAS inhibitors due to renal insufficiency or hyperkalemia, the combination of isosorbide dinitrate and hydralazine is recommended to reduce both morbidity and all-cause mortality. Because it does not cause hyperkalemia or rely on renal clearance, it is uniquely suited for this specific clinical phenotype.

Step-by-Step Solution

Identify the patient's current disease state and management goal.

The patient has symptomatic heart failure with reduced ejection fraction (NYHA Class II-III) despite optimal tolerated medical therapy (beta-blocker and SGLT2 inhibitor). The goal is to reduce all-cause mortality.

Recognizing the ongoing symptoms and the specific prompt requirement (mortality reduction) dictates the next step in guideline-directed medical therapy (GDMT).

Evaluate the patient's physiological limitations using current vitals and laboratory results.

The patient has severe chronic kidney disease (eGFR

24 \text{ mL/min/1.73 m}^2

), borderline hyperkalemia (Potassium

5.2 \text{ mEq/L}

), and a resting heart rate of

66/\text{min}

. He also has a documented history of severe acute kidney injury and hyperkalemia caused by an ACE inhibitor.

These parameters act as strict filters to determine which evidence-based therapies are safe to initiate.

Apply the physiological limitations to rule out standard GDMT additions.

An MRA (spironolactone) and an ARNI (sacubitril-valsartan) are contraindicated due to the eGFR being

< 30 \text{ mL/min/1.73 m}^2

and potassium being

> 5.0 \text{ mEq/L}

. Ivabradine is contraindicated because the resting heart rate is

< 70/\text{min}

Overlooking these absolute contraindications would lead to life-threatening adverse drug events, such as profound hyperkalemia or bradycardia.

Select the appropriate alternative therapy that meets the management goal.

Isosorbide dinitrate and hydralazine is selected.

This combination is a Class 2a recommendation for reducing morbidity and mortality in patients with current or prior symptomatic HFrEF who are intolerant to first-line RAAS inhibitors due to renal insufficiency or hyperkalemia.

Key Concept

In patients with symptomatic heart failure with reduced ejection fraction (HFrEF) who cannot tolerate RAAS inhibitors or ARNIs due to renal insufficiency or hyperkalemia, the combination of isosorbide dinitrate and hydralazine is indicated to reduce all-cause mortality.

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