Heart attacks without blocked arteries may signal a dangerous blind spot in cardiovascular care, particularly for patients managing autoimmune conditions. While cardiologists routinely clear major coronary vessels during emergency angiography, the microscopic circulation feeding heart muscle often escapes scrutiny—potentially missing a critical mechanism linking systemic inflammation to cardiac events.
This detailed case demonstrates how inflammatory surges can trigger genuine myocardial infarction through microvascular compromise rather than traditional arterial blockages. A 51-year-old woman with active vasculitis and rheumatoid arthritis developed acute chest pain with classic ST-segment changes and significantly elevated troponin levels (2,526 pg/mL). Despite clear major coronary arteries on angiography, specialized testing revealed severely impaired coronary flow reserve (1.7) and elevated microvascular resistance (32), confirmed by advanced PET imaging showing reduced myocardial blood flow globally.
The temporal correlation between inflammatory markers and cardiac injury suggests autoimmune flares directly compromise the heart's microscopic vessel network. This finding challenges the traditional binary of obstructed versus clear coronaries, revealing a third pathway where systemic inflammation creates cardiac ischemia through microvascular dysfunction. For the growing population with autoimmune diseases, this represents both vulnerability and opportunity—heightened cardiac monitoring during inflammatory flares could prevent missed diagnoses. However, detecting microvascular dysfunction requires sophisticated testing unavailable in most emergency settings, highlighting a significant gap between pathophysiology and clinical practice in this overlooked cause of heart attacks.