DOI: 10.1161/circ.148.suppl_1.18940 ISSN: 0009-7322

Abstract 18940: Can the Religious Observation of Fasting Cause Prinzmetal’s Angina?

Natasha Qureshi, Kirtivardhan Vashistha, Syed Ali, Yumiko Kanei
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

CASE DESCRIPTION: A 73-year-old male with HTN, HLD, CAD/MI status post PCI to the RCA and LAD (2021), and former tobacco use presented with acute, severe, left-sided chest pain with nausea, diaphoresis and dizziness. He started fasting and adjusted his sleep schedule 3 days prior for Ramadan, but did not miss any of his medications including isosorbide and ranolazine. He was chest pain free on arrival, but subsequently developed severe chest pain becoming bradycardic, hypotensive and hypoxic. At that time the EKG (Figure 1) showed ST elevation (STEMI) in leads II, III and aVF with high degree atrioventricular block. He was started on intravenous fluids and a vasopressor but had spontaneous resolution of symptoms within 10 minutes. Emergent coronary angiography revealed stable 70% stenosis of an ostial left circumflex (LCx) artery and non-obstructive CAD of the RCA. Labs revealed normal blood glucose, negative urine toxicology and mild elevation of troponin (trended serially). Echocardiogram was normal with no regional wall motion abnormalities. He was treated as vasospastic angina with addition of a calcium channel blocker without recurrence of his symptoms.

DISCUSSION: Vasospastic angina is an important cause of acute coronary syndrome. Our patient had severe vasospastic angina while being treated for CAD for over 10 years. No prior studies have linked fasting to vasospasm. We hypothesize that fasting and a diurnal sleep schedule may contribute to worsened episodes in susceptible individuals due to hormonal changes including glucose shifts and an increase in catecholamines and cortisol. Increased catecholamine levels may induce spasm by stimulation of alpha receptors in the coronary arteries, and cortisol can induce vascular inflammation, potentiating negative effects. We highlight the importance of keeping high clinical suspicion for a diagnosis of vasospasm, as well as the need to further understand the complex pathophysiology to counsel patients in the future.

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