An 84-year-old man presented to the emergency department (ED) of a small community hospital with shortness of breath and diaphoresis. Approximately 2 weeks prior, the patient presented to the same ED and was diagnosed with clostridium difficile colitis. He was hospitalized for 2 days and treated with antibiotics and intravenous hydration, then transferred to a skilled nursing facility for continued antibiotics and acute rehabilitation. He was discharged home from the skilled nursing facility 5 days later. The patient was home for 1 week when he noticed mild shortness of breath on exertion, which lasted for 3 days until it suddenly developed into severe difficulty breathing 2 hours before he arrived in the ED by ambulance. The patient denied any chest pain, palpitations, cough, fever, or chills. His history was otherwise unremarkable. The patient also denied any history of previous MI, congestive heart failure, or other known cardiac disease. There was no history of chronic obstructive pulmonary disease or other lung disease. The patient's other past medical history included diabetes, gastroesophageal reflux disease, hyperlipidemia, hypertension, and the recent clostridium difficile infection. His surgical history was notable for bilateral knee operation and a right hip replacement. Home medications included lisinopril, finasteride, lovastatin, lantus, nifedipine, omeprazole, and tamsulosin. 

On arrival to the ED, the patient was afebrile with a blood pressure of 158/75 mmHg, pulse of 113 beats per minute, 22 respirations per minute, and pulse oximetry of 88% on nonrebreather oxygen mask. On physical examination, the patient exhibited severe respiratory distress with accessory muscle use, bibasilar rales, scattered rhonchi, and scattered wheezes. He was tachycardic with a regular rhythm and a 1/6 systolic murmur; 3+ pitting ankle edema was also noted. No jugular venous distension or pulse deficits were appreciated. The patient's abdomen was moderately distended, but soft and non-tender. There was no tenderness of his lower extremities. 

A 12 lead ECG showed sinus tachycardia at 112 beats per minute (Figure 3). Axis and PR intervals were normal. The QRS interval was prolonged (>120 ms), and there was a dominant S wave in V1, a broad monophasic R wave in lateral leads (I, aVL, V5-V6), absence of Q waves in lateral leads (I, V5-V6), and a prolonged R wave peak time (>60 ms) in left precordial leads (V5-6), consistent with an LBBB diagnosis.⁶ (Figure 1) Evaluating according to the modified Sgarbossa criteria, there were no ST segment elevations in the same direction as the QRS vectors in leads V1, V2, V3, and V4 (negative criterion). There were no ST segment depressions in any leads (negative criterion). The ST/S ratio was not less than −0.25 in any leads (negative criterion). In short, this patient did not meet the modified Sgarbossa criteria for an MI. Before laboratory test results were available, the patient was placed on bilevel positive airway pressure after failure to raise oxygen saturation with nonrebreather mask. Furosemide was given intravenously for suspected acute congestive heart failure and fluid overload. A chest radiography showed central vascular congestion and bilateral small pleural effusions (Figure 4). Laboratory test results showed a white blood cell count of 17,700 K/cmm (reference range,¹⁰ 4000-11,000 K/cmm) with a high percent neutrophils at 86.4% (reference range,¹⁰ 50-70%). Reflex lactic acid was 2.3 mmol/L (reference range,¹⁰ 0.7-2.1 mmol/L). Blood urea nitrogen was 43 mg/dL (reference range,¹⁰ 8-20 mg/dL) and serum creatinine was 1.67 mg/dL (reference range,¹⁰ 0.70-1.30 mg/dL) with estimated glomerular filtration rate of 39 mL/min (reference range,¹⁰ 90-140 mL/min). B-type natriuretic peptide was elevated at 27,218 pg/mL (reference range,¹⁰ <100 pg/mL), confirming congestive heart failure; serum troponin I was mildly elevated at 0.187 ng/mL (reference range,¹⁰ <0.04 ng/mL), suggestive of myocardial injury. Nitroglycerin, aspirin, and clopidogrel were administered for suspected myocardial infarction. After consultation with the receiving hospital, the patient was started on a heparin drip and transported to a tertiary center for advanced cardiac work-up and management. The patient was taken directly for cardiac catheterization, at which point an acute coronary occlusion was confirmed. 

MIs often present with classic symptoms of chest pain and shortness of breath. However, in a review¹¹ of more than 430,000 patients with confirmed acute MI, one-third had no chest pain on presentation to the hospital. Patients who were older, were women, or had diabetes most frequently presented without chest pain, and patients with MI without chest pain had a 23.3% in-hospital mortality rate compared with 9.3% among patients with MI chest pain.¹¹ Another study¹² found that the rate of missed acute MI was 2.1% and varied from 0% to 29% across various EDs where patients with acute MI were mistakenly discharged. Women, those who listed shortness of breath as their chief complaint, and those with a normal or nondiagnostic ECG were less likely to be hospitalized.¹² 

Our patient was elderly and diabetic; he presented with no chest pain. His chief concern was shortness of breath and his ECG was nondiagnostic for an MI due to LBBB. LBBB makes diagnosing acute MI by ECG difficult because of the hidden nature of ST segment elevations or depressions within the QRS complexes. Patients with chest pain and new LBBB should be assumed to have ST-elevation MI (STEMI).¹³ However, this guideline is not helpful when patients do not present with chest pain or if the chronicity of the LBBB is unknown, as in the present case. Serum troponin levels are highly sensitive and specific tests for MIs¹⁴; however, acute coronary syndrome may be difficult to determine if troponin levels are negative or only slightly elevated, as in cases of very recent MI, since it takes approximately 3 hours for troponin levels to become elevated after myocardial injury. 

In this case, making a quick, definitive diagnosis of acute MI was difficult. Our case was further confounded with a negative modified Sgarbossa criteria. To aid clinicians, the American College of Cardiology has proposed an algorithm for suspected MI in patients with LBBB with negative Sgarbossa criteria.¹⁵ This management algorithm recommends that patients with suspected MI and LBBB (new or old) with acute heart failure or hemodynamic instability undergo emergent percutaneous coronary intervention or fibrinolysis regardless of Sgarbossa criteria.¹⁵ In patients without heart failure or hemodynamic instability, a negative Sgarbossa criteria result should be followed up by an echocardiogram and/or serum cardiac biomarkers.¹⁵ The American College of Cardiology algorithm accounts for cases that would be missed according to modified Sgarbossa criteria without overtreating patients with LBBB. We agree with this conservative approach and believe clinical judgement at the patient bedside is paramount in preventing serious complications or death from missing an MI because of negative Sgarbossa criteria. 

LBBB complicates ECG interpretations in the diagnosis of acute MI because of repolarization abnormalities hiding ST segment changes consistent with myocardial ischemia. The modified Sgarbossa criteria provides a 3-criterion algorithm to diagnose MI in patients with LBBB that is highly sensitive and highly specific (91% and 90%, respectively). As such, it is a good tool that should be known and used by clinicians in acute care settings. However, it is possible that this tool could miss an MI, as illustrated in our case. Our patient, who was elderly and had diabetes presented with a respiratory complaint, demonstrated an LBBB on ECG and did not meet the modified Sgarbossa criteria for MI. This patient was treated appropriately with the diagnosis of acute STEMI, confirmed with cardiac catheterization that found coronary artery occlusion. This case is a reminder that high index of suspicion for atypical presentations and good clinical judgement should never replace any diagnostic algorithm.