What is the most likely diagnosis for an elderly male patient with hypertension, previous stroke, and abdominal aortic aneurysm (AAA), presenting with bilateral pitting edema, sinus tachycardia, and elevated brain natriuretic peptide (BNP), on Verapamil (calcium channel blocker)?

Most Likely Diagnosis: Verapamil-Induced Peripheral Edema

The most likely diagnosis is verapamil-induced peripheral edema, not heart failure. While the elevated BNP of 2300 pg/mL initially suggests cardiac pathology, the clinical presentation is inconsistent with decompensated heart failure, and verapamil is a well-known cause of dependent edema through peripheral vasodilation rather than cardiac dysfunction 1.

Clinical Reasoning Against Heart Failure

The absence of classic heart failure symptoms strongly argues against acute decompensation:

• No shortness of breath, orthopnea, or paroxysmal nocturnal dyspnea 2
• Clear lung fields on examination (no pulmonary congestion) 2
• The patient lacks the typical constellation of symptoms seen in acute heart failure requiring hospitalization 2

The sinus tachycardia (HR 120 bpm) is more consistent with:

• Compensatory response to verapamil's negative chronotropic effects being overcome 1
• Possible volume depletion if diuretics were recently initiated
• Underlying hypertension or anxiety rather than cardiac decompensation 2

Verapamil as the Primary Culprit

Verapamil causes peripheral edema through direct pharmacologic mechanisms unrelated to heart failure:

• Non-dihydropyridine calcium channel blockers like verapamil cause peripheral vasodilation, leading to increased capillary hydrostatic pressure and fluid extravasation into interstitial spaces 1
• This edema is gravitational (bilateral lower extremity pitting edema) and not associated with pulmonary congestion 1
• The FDA label explicitly warns that verapamil has negative inotropic effects, though these are usually compensated by afterload reduction in most patients 1

Critical distinction: Verapamil-induced edema occurs WITHOUT heart failure in the majority of cases 1.

Interpreting the Elevated BNP (2300 pg/mL)

This BNP level requires careful contextualization given multiple confounding factors:

Hypertension and Left Ventricular Hypertrophy

• Chronic hypertension causes left ventricular hypertrophy (LVH), which independently elevates BNP through increased wall stress 2, 3
• LVH is the most important predictor for elevated natriuretic peptides in hypertensive patients 2
• BNP elevation from LVH does not necessarily indicate acute decompensated heart failure 3

Previous Stroke and Cardiovascular Risk

• Patients with prior stroke have elevated cardiovascular risk and often have underlying diastolic dysfunction 2
• Diastolic dysfunction can cause BNP elevation even with normal systolic function and without acute symptoms 3, 4
• The BNP level of 2300 pg/mL could represent chronic elevation from baseline cardiac remodeling rather than acute decompensation 3, 5

Atrial Fibrillation Consideration

• The sinus tachycardia should prompt evaluation for paroxysmal atrial fibrillation, which independently elevates BNP regardless of ventricular function 3, 6
• Hypertensive patients with LVH have 3.4-fold greater odds of developing supraventricular tachycardia including atrial fibrillation 2

Renal Function Assessment

• Critical: Check serum creatinine and eGFR immediately 5
• Even mild-moderate chronic kidney disease reduces BNP clearance, artificially elevating levels 3, 5
• In patients with GFR <60 mL/min/1.73 m², BNP concentrations must be interpreted with caution 5

Diagnostic Algorithm

Immediate next steps to confirm diagnosis:

1. Discontinue or reduce verapamil dose 1

   • If edema resolves within 1-2 weeks, this confirms verapamil as the cause
   • Consider switching to an ACE inhibitor or ARB for hypertension management 2

2. Order echocardiography within 1-2 weeks (not emergently) 3, 4

   • Assess left ventricular ejection fraction to distinguish HFrEF from HFpEF 3
   • Evaluate for LVH, diastolic dysfunction, and valvular disease 3, 4
   • Check for right ventricular dysfunction given AAA history 3

3. Obtain comprehensive laboratory assessment 3, 5

   • Serum creatinine and eGFR (essential for BNP interpretation) 5
   • Electrolytes, liver function tests 2
   • Thyroid function (thyroid dysfunction affects BNP levels) 3, 4

4. Perform 12-lead ECG 3, 4

   • Evaluate for left ventricular hypertrophy 2
   • Screen for atrial fibrillation or other arrhythmias 2, 6
   • Assess for ischemic changes 3

Common Pitfalls to Avoid

Do not reflexively treat with diuretics based solely on elevated BNP and peripheral edema:

• Verapamil-induced edema does not respond well to diuretics because the mechanism is increased capillary permeability, not volume overload 1
• Aggressive diuresis in a patient without true heart failure can cause volume depletion, worsening the compensatory tachycardia 2

Do not assume elevated BNP always equals acute heart failure:

• BNP of 2300 pg/mL can represent chronic elevation from hypertension, LVH, renal dysfunction, or atrial arrhythmias 3, 5, 4
• The "grey zone" concept applies even at higher BNP levels when clinical presentation is discordant 3, 4

Do not overlook medication review:

• The European Heart Rhythm Association explicitly warns about bradyarrhythmias and AV block with verapamil, particularly at higher doses 2
• Verapamil should be avoided in patients with severe left ventricular dysfunction (EF <30%) or moderate-to-severe heart failure symptoms 1

Risk Stratification Despite Non-Acute Presentation

Even if this is not acute heart failure, the elevated BNP carries prognostic significance:

• Each 100 pg/mL increase in BNP confers 35% increased relative risk of death over 1.5-3 years 3, 4
• This patient requires optimization of cardiovascular risk factors and close outpatient follow-up 2
• The combination of hypertension, prior stroke, and AAA places this patient at very high cardiovascular risk 2

Ensure comprehensive aortic surveillance given AAA history:

• 27% of patients with AAA also have thoracic aortic aneurysm 2
• The 10-year risk of mortality from cardiovascular causes may be 15 times the risk of aorta-related death in AAA patients 2