ECG Interpretation - Hanumanthappa, Male 51 Years

Patient & Technical Details

• Date: 01-06-2026, 02:08 PM
• HR: 63 bpm | PR: 122 ms | QRS: 96 ms | QT/QTcBz: 420/430 ms
• P/QRS/T axis: 64°/10°/95° | RV5/SV1: 0.044/0.503 mV
• Settings: 25 mm/s, 10 mm/mV (standard)

Systematic Analysis

1. Rate & Rhythm

• Sinus rhythm at 63 bpm - normal rate.
• PR interval 122 ms - normal (no AV block).
• QRS duration 96 ms - normal (no bundle branch block).

2. Axis

• QRS axis ~10° - normal axis.

3. P Waves

• Present and upright in I, II - normal sinus origin.

4. QRS Complexes - KEY FINDING

• Low QRS voltage in precordial leads - the machine flags RV5 of only 0.044 mV (normally >0.7 mV), which is severely reduced.
• Poor R-wave progression across V1-V6: the R waves fail to grow normally from V1 to V4/V5. This pattern suggests loss of anterior myocardial forces.
• Low precordial voltage is defined as QRS amplitude <10 mm (1 mV) in all precordial leads (Goldman-Cecil Medicine).

5. ST Segments & T Waves

• No obvious acute ST elevation visible, but T-wave morphology across precordials is flattened/abnormal, consistent with ischemic repolarization changes or post-infarct pattern.

6. Limb Leads

• Low-amplitude complexes also in limb leads, consistent with global low voltage.

Automated Machine Diagnosis (confirmed on tracing)

1. Sinus rhythm
2. Possible extensive infarct - age undetermined - this is the most significant finding; the poor R-wave progression and anterior low voltage suggest an old (age-undetermined) extensive anterior myocardial infarction
3. Low QRS voltages in precordial leads
4. Abnormal ECG

Clinical Interpretation

Differential for Low Voltage (from Goldman-Cecil Medicine)

• Myocardial infarction (most relevant here given the pattern)
• Pericardial effusion
• Cardiomyopathy (dilated)
• Hypothyroidism
• Obesity
• Amyloidosis, Sarcoidosis
• COPD

Clinical Recommendations

1. Urgent history: Does the patient have a known prior MI? Any chest pain history? Risk factors (HTN, DM, smoking)?
2. Echocardiogram - essential to assess LV wall motion abnormalities, ejection fraction, and rule out pericardial effusion (another cause of low voltage).
3. Troponin / cardiac biomarkers - to rule out an acute/recent event if the patient is symptomatic.
4. Thyroid function tests (TSH) - to exclude hypothyroidism as a cause of low voltage.
5. Cardiology referral - this patient needs comprehensive evaluation given the pattern of extensive anterior infarction.
6. Risk stratification - if EF is reduced, this patient may need consideration for ICD prophylaxis and heart failure therapy (ACEi/ARB, beta-blocker).

Bottom line: This is an abnormal ECG showing sinus rhythm with low precordial QRS voltage and a pattern consistent with an old extensive anterior myocardial infarction (age undetermined). The patient requires echocardiography and clinical correlation urgently. There is no acute STEMI pattern, but silent or unrecognized prior large anterior MI is the leading diagnosis.

ECG in Context of Confirmed NSTEMI

Why This ECG Pattern Fits NSTEMI

Management Framework (Harrison's 22E + Sabiston)

Immediate / Acute Phase

• Nitrates - sublingual NTG 0.3-0.6 mg; switch to IV nitroglycerin (5-10 mcg/min, titrate up) if recurrent pain or uncontrolled BP. Avoid if SBP <90 mmHg or recent PDE-5 inhibitor use.
• Beta-blockers - start early (oral metoprolol preferred); reduce myocardial O2 demand. Avoid in acute/severe HF or cardiogenic shock.
• Oxygen - only if SpO2 <90%.

• Aspirin 325 mg loading, then 75-100 mg daily (lifetime)
• Add a P2Y12 inhibitor:
  • Ticagrelor 180 mg loading then 90 mg BD (preferred over clopidogrel)
  • Or Clopidogrel 300-600 mg loading then 75 mg daily if ticagrelor not available
• DAPT should continue for 12 months post-ACS

• Fondaparinux (preferred, less bleeding) or LMWH (enoxaparin) or UFH during hospitalization

• High-intensity statin immediately (Atorvastatin 40-80 mg or Rosuvastatin 20-40 mg) - stabilizes plaque, reduces recurrent events

Risk Stratification - Key Step for This Patient

Long-Term Secondary Prevention

Special Concern in This Patient

1. Assess LV ejection fraction - if EF <35-40%, the patient may need ICD prophylaxis consideration
2. Rule out LV thrombus (common after large anterior MI - needs anticoagulation if present)
3. Identify wall motion abnormalities defining the infarct territory
4. Assess for mechanical complications (MR, VSD)

Clinical Significance of LVEF 58% in This NSTEMI

What It Tells Us

Revised Management Plan with LVEF 58%

What CHANGES with Preserved EF

• Eplerenone/spironolactone (only for EF ≤40% post-MI)
• Routine anticoagulation for LV thrombus (low risk)
• ICD workup (EF too good)

ACE Inhibitor - Still Indicated?

• Reduce risk of recurrent MI and cardiovascular death
• Beneficial in patients with CAD even without HF (HOPE trial data)
• Especially relevant here given extensive anterior territory involvement

Invasive Strategy - Still Urgent

• Coronary angiography should still be performed within 24 hours if GRACE score >140
• Aim to identify the culprit lesion (likely LAD territory given anterior pattern)
• PCI to the culprit lesion if anatomy is suitable
• Good EF actually makes him a better procedural candidate with lower periprocedural risk

Summary - Good Prognostic Sign

NSTEMI + LVEF 58% = favorable short-term prognosis

Key goals now:
1. Coronary angiography ± PCI (within 24h if high GRACE)
2. DAPT x 12 months (Aspirin + Ticagrelor)
3. Statin + ACE inhibitor + Beta-blocker lifelong
4. Aggressive risk factor modification
5. Cardiac rehab after discharge
6. Repeat echo at 6-8 weeks to confirm EF is maintained

Intermittent Prick-like Shoulder Sensation in This NSTEMI Patient

Differential Diagnosis

1. POST-INFARCTION PERICARDITIS / DRESSLER SYNDROME ⚠️ - Top Priority

• Sharp/pleuritic chest pain radiating to left shoulder (phrenic nerve irritation from pericardial/diaphragmatic involvement)
• Fever >38°C without other explanation
• Pericardial friction rub on auscultation
• New/worsening pericardial or pleural effusion on echo
• Raised ESR, CRP, leukocytosis

"Pericarditis, usually with fever, can also develop after myocardial infarction (Dressler syndrome)." (Murray & Nadel's Textbook of Respiratory Medicine)

2. Referred Cardiac Ischemia to Shoulder

• Residual ischemia from the culprit coronary lesion (LAD territory) can refer pain to the left shoulder, arm, or jaw via C8-T4 dermatomal overlap
• Intermittent nature fits with demand ischemia during activity
• Critical to distinguish from pericarditis as management differs significantly

3. Musculoskeletal / Cervical Cause

• Cervical radiculopathy (C5-C6 nerve root) - prick-like, dermatomal, exacerbated by neck movement
• Brachial plexus irritation - cervical rib or positional compression
• Shoulder bursitis/tendinitis - can mimic referred cardiac pain
• These are diagnoses of exclusion in an acute NSTEMI patient

Immediate Bedside Assessment

Investigations to Order Now

Management Based on Likely Cause

• Aspirin is actually first-line here (1-2g TDS x 2 weeks, then taper) - already on it for his NSTEMI
• Colchicine 0.5 mg BD x 3 months - significantly reduces recurrence
• Avoid NSAIDs (ibuprofen/indomethacin) in post-MI pericarditis - may impair infarct healing
• Avoid corticosteroids unless refractory - associated with infarct complications

• Optimize anti-ischemic therapy (beta-blocker dose, nitrates)
• Expedite coronary angiography - do not delay

• Can be managed conservatively after cardiac causes excluded

Bottom Line

In a 51-year-old male with NSTEMI, prick-like shoulder pain must be treated as pericarditic or ischemic in origin until proven otherwise. Examine for a friction rub, repeat ECG for PR depression or new ST changes, and check echo for pericardial effusion. If left shoulder and positional - Dressler/pericarditis is the leading diagnosis.