Cardiovascular Disease Fellow PGY VI, United States
Disclosure(s):
Sharul Saxena, MD: No financial relationships to disclose
Background: While there exist guidelines on management of vasospasm and dissection, there are no instructions on management when ACS is driven by both forces occurring concomitantly. In the patients below, we achieved improvement by administering intracoronary nitroglycerin, nicardipine, and systemic cyproheptadine. This strategy can be utilized by clinicians in the future.
Methods: Patient is a 36-year-old female with history of polysubstance abuse, hypertension and hyperlipidemia who presents to the hospital for 3-day history of cheat pain. EKG on admission was significant for ST elevations in the inferior leads. Initial high sensitivity troponin assay was 21696 pg/mL. Urine drug screen was positive for opiates and benzodiazepines. Due to concern for inferior STEMI, the patient was taken emergently for coronary angiogram. Coronary angiogram showed severe diffuse spasm encompassing the left main to distal LAD and the distal left circumflex artery (Figure 1 and Figure 2). The RCA showed dissection in the mid PDA (Figure 3). LVGram revealed EF to be around 20-25%. No culprit lesion was found and acute coronary syndrome (ACS) was attributed to severe diffuse spasm and concomitant dissection. The patient was managed with intracoronary nitroglycerine and nicardipine and placement of an intraoartic balloon pump with mild improvement in vasospasm. Patient was also administered cyproheptadine for 2 days and she was brought down on Day 3 for relook angiogram.
Outcome: There was dramatic improvement in the diffuse vasospasm originally seen in the L system (Figure 4 & 5). The SCAD visualized in PDA remained angiographically persistent and stable. There was visualization of focal lesion in mid LAD. Unfortunately, in the attempt to perform IVUS of this lesion, patient developed iatrogenic spiral dissection from left main to LAD and LCX. As the patient already had low EF and was in danger of decompensation, percutaneous LVAD was rapidly implanted. Multiple stents were placed from LAD and LCX to LM with bifurcation stenting. Final angiography showing TIMI 3 flow in LM, LAD, and LCX system (Figure 4). In the days that followed, the percutaneous LVAD was weaned and removed, and patient was discharged home.
Conclusion: We demonstrate a case of diffuse coronary artery spasm in conjunction with coronary artery dissection, two pathologic entities rarely seen together. Major improvement was achieved after systemic cyproheptadine. We highlight an instance where vasospasm and dissection are seen together, result in cardiogenic shock, and the dramatic improvement seen post cyproheptadine.
