What is the likely cause of death in a patient with sudden cardiac death due to coronary artery disease, elevated troponin (cardiac enzyme), coagulopathy (bleeding disorder), and hematemesis (vomiting blood), with lab results showing hypercoagulability (high PTT (partial thromboplastin time)) and impaired coagulation (INR (international normalized ratio) unreadable)?

Likely Cause of Death in This Patient

This patient most likely died from massive pulmonary embolism with right ventricular failure, complicated by coagulopathy and gastrointestinal bleeding. The combination of elevated troponin, markedly prolonged PTT with unreadable INR, and hematemesis in the context of sudden cardiac death points to PE as the primary mechanism, with the coagulopathy either contributing to or resulting from the catastrophic event 1.

Primary Mechanism: Pulmonary Embolism with RV Failure

Elevated troponin in the setting of sudden cardiac death strongly suggests massive PE with transmural right ventricular infarction despite patent coronary arteries 1. The European Society of Cardiology guidelines document that:

• Troponin elevation occurs in 50% of patients with clinically massive PE, compared to only 0-35% in non-massive PE 1
• Positive troponin in PE carries an in-hospital mortality of 44% versus 3% for negative troponin (OR 15.2; 95% CI 1.2-190.4) 1
• Transmural RV infarction despite patent coronary arteries has been documented in autopsies of patients who died from massive PE 1

The troponin elevation reflects right ventricular myocardial injury from acute RV afterload and strain, not coronary artery disease 1, 2. While the patient had underlying coronary disease, the acute troponin rise in the context of sudden death with coagulopathy is more consistent with PE-related RV failure 2.

Coagulopathy Pattern Analysis

The combination of high PTT with unreadable INR suggests either severe consumptive coagulopathy (DIC) or massive anticoagulant effect 1. This pattern can occur in two scenarios:

Disseminated Intravascular Coagulation (DIC)

• Massive PE can trigger DIC through widespread endothelial injury and tissue factor release 1
• DIC causes both thrombosis (PE) and bleeding (hematemesis) simultaneously
• The unreadable INR suggests either extreme prolongation beyond the assay's measurement range or interference from severe coagulopathy 1

Excessive Anticoagulation

• If the patient was on anticoagulation for coronary disease, supratherapeutic levels could explain the coagulopathy 1
• However, this would not explain the sudden cardiac death mechanism unless it led to catastrophic bleeding

Hematemesis as Contributing Factor

The gastrointestinal bleeding (hematemesis) likely represents either:

1. Consequence of severe coagulopathy from DIC triggered by massive PE 1
2. Stress ulceration from the acute hemodynamic collapse and shock state
3. Complication of anticoagulation if the patient was being treated for coronary disease or PE 1

The bleeding itself could have contributed to hemodynamic instability and cardiovascular collapse, but the elevated troponin and sudden cardiac death pattern suggest the primary mechanism was PE with RV failure 1.

Why Not Primary Acute Coronary Syndrome?

Several factors argue against acute MI from coronary disease as the primary cause:

• The coagulopathy pattern (high PTT, unreadable INR) is not typical for uncomplicated MI 1
• Massive GI bleeding with coagulopathy suggests a systemic process beyond isolated coronary thrombosis
• The combination of findings is more consistent with PE causing RV strain, troponin elevation, and triggering DIC 1, 2
• ACC/AHA guidelines note that troponin elevation can occur from multiple non-coronary causes including pulmonary embolism 1

Integrated Pathophysiologic Sequence

The most likely sequence of events:

1. Massive pulmonary embolism caused acute RV pressure overload 1
2. RV myocardial injury from increased afterload led to troponin elevation 1, 2
3. Hemodynamic collapse from RV failure and reduced cardiac output 1
4. DIC triggered by massive PE and shock state, causing coagulopathy 1
5. GI bleeding (hematemesis) resulted from the coagulopathy 1
6. Sudden cardiac death occurred from cardiovascular collapse due to massive PE with RV failure 1

Critical Diagnostic Pitfalls

Do not assume troponin elevation always indicates primary coronary disease - the ACC/AHA guidelines explicitly state that troponin can be elevated from pulmonary embolism, and this must be interpreted in clinical context 1. The European Society of Cardiology emphasizes that while RV myocardium may not be the only source of troponin in PE, elevated levels are repeatedly associated with worse prognosis 1.

The coagulopathy pattern is the key distinguishing feature - isolated acute MI would not typically cause high PTT with unreadable INR and hematemesis, whereas massive PE with DIC explains all findings 1.