How should I manage a 55-year-old man with several days of chest tightness, blood pressure controlled on losartan 60 mg and amlodipine 5 mg, low‑density lipoprotein cholesterol (LDL‑C) of 45 mg/dL, sinus rhythm on ECG with possible left‑ventricular hypertrophy (LVH), and reduced left‑ventricular ejection fraction (LVEF) of 40 % but no dyspnea?

Management of Chest Tightness with Reduced LVEF and Suspected LVH

Immediate Priority: Rule Out Acute Coronary Syndrome

This patient requires urgent evaluation for acute coronary syndrome given several days of chest tightness with reduced LVEF of 40%, even with controlled blood pressure and excellent LDL control. 1

• Obtain high-sensitivity cardiac troponin immediately and repeat at appropriate intervals to rule out NSTEMI 1
• Perform urgent invasive coronary angiography if troponin is elevated or if high clinical suspicion exists, as this patient has reduced LVEF (<40%) which places him in a high-risk category 1
• ECG changes suggesting LVH do not exclude acute ischemia as the cause of chest tightness 1

Medication Optimization for Reduced LVEF

Given LVEF of 40%, this patient has heart failure with reduced ejection fraction (HFrEF) and requires guideline-directed medical therapy regardless of whether chest tightness is ischemic. 1

Essential Medications to Initiate:

• Add an ACE inhibitor or ARB (he is already on losartan 60mg, which should be continued and potentially uptitrated to 100mg daily) to prevent symptomatic heart failure and reduce mortality 1
• Initiate an evidence-based beta-blocker (carvedilol, metoprolol succinate, or bisoprolol) immediately to reduce mortality in patients with reduced LVEF, regardless of whether this is post-MI or non-ischemic 1
• Add a mineralocorticoid receptor antagonist (spironolactone or eplerenone) as this patient has LVEF <40%, which is a Class I indication to reduce all-cause and cardiovascular mortality 1
• Continue statin therapy given his history warrants secondary prevention, even though LDL is already at 45 mg/dL 1

Critical Medication Considerations:

• Do NOT use non-dihydropyridine calcium channel blockers (verapamil or diltiazem) in this patient with LVEF 40%, as they may be harmful and worsen heart failure 1
• The amlodipine 5mg he is currently taking is acceptable as a dihydropyridine calcium channel blocker for blood pressure control 1
• Avoid digoxin unless atrial fibrillation develops requiring rate control 1

Addressing the Left Ventricular Hypertrophy

The combination of LVH on ECG with reduced LVEF of 40% suggests a primary cardiomyopathic process rather than simple hypertensive heart disease, despite controlled blood pressure. 2

Diagnostic Workup Needed:

• Obtain transthoracic echocardiography with Doppler to measure maximum diastolic wall thickness, calculate left ventricular mass index, assess wall thickness/radius ratio, and evaluate for left ventricular outflow tract obstruction with both resting gradients and provocative maneuvers 2, 3
• Assess for asymmetric septal hypertrophy (≥15 mm), systolic anterior motion of mitral valve, or LVOT gradient ≥30 mmHg at rest or with provocation to evaluate for hypertrophic cardiomyopathy 3
• Obtain family history of cardiomyopathy, sudden cardiac death, or heart failure 3
• Consider cardiac MRI to assess for late gadolinium enhancement patterns, myocardial fibrosis, and to differentiate between ischemic and non-ischemic cardiomyopathy 4

LVH-Specific Treatment:

• Losartan demonstrates superior efficacy for LVH regression compared to all other antihypertensive classes, including beta-blockers, and should be uptitrated to 100mg daily if blood pressure tolerates 2, 5
• The established hierarchy for LVH regression is: ARBs (losartan) > ACE inhibitors > beta-blockers 2
• Treatment-induced reduction in left ventricular mass is significantly and independently associated with reduction in major cardiovascular events, stroke, and cardiovascular/all-cause mortality 1, 2

Management Algorithm Based on Echocardiographic Findings

If Hypertrophic Cardiomyopathy with Obstruction is Found:

• Immediately discontinue amlodipine and avoid all vasodilators (including ACE inhibitors, ARBs, nitrates, dihydropyridine calcium channel blockers) as these worsen LVOT obstruction and can precipitate hemodynamic collapse 3
• Initiate non-vasodilating beta-blockers as first-line therapy with goal resting heart rate 60-65 bpm 3
• Consider non-dihydropyridine calcium channel blockers (verapamil or diltiazem) as second-line if beta-blockers fail 3
• Assess sudden cardiac death risk using established markers (family history of sudden death, unexplained syncope, non-sustained VT, massive LVH ≥30mm, abnormal BP response to exercise) 3

If Non-Obstructive Cardiomyopathy is Confirmed:

• Continue losartan and uptitrate to 100mg daily 2
• Continue amlodipine for blood pressure control 6, 7, 8
• Add beta-blocker for HFrEF management 1
• Add mineralocorticoid receptor antagonist 1

Sudden Cardiac Death Risk Stratification

With LVEF of 40% and possible LVH, this patient requires evaluation for primary prevention ICD. 1

• If this is ischemic cardiomyopathy (≥40 days post-MI) with LVEF ≤30% on guideline-directed medical therapy, ICD is reasonable (Class IIa) 1
• If non-sustained VT is present with LVEF ≤40% and inducible VF or sustained VT at electrophysiological study, ICD is reasonable (Class IIa) 1
• Reassess LVEF after 3 months of optimal medical therapy before making final ICD decision 1

Common Pitfalls to Avoid

• Do not assume chest tightness is non-cardiac simply because blood pressure is controlled and LDL is low—acute coronary syndrome must be excluded first 1
• Do not use non-dihydropyridine calcium channel blockers in patients with LVEF ≤40% as they are potentially harmful 1
• Do not delay beta-blocker initiation in patients with reduced LVEF, as this is a Class I recommendation with Level A evidence for mortality reduction 1
• Do not overlook mineralocorticoid receptor antagonist in patients with LVEF <40%, as this is also Class I for mortality reduction 1
• Do not assume LVH is purely hypertensive when LVEF is reduced—consider primary cardiomyopathy and obtain detailed echocardiography 2, 3