Introduction: Chest pain is a common reason for emergency room visits. Acute coronary syndrome (ACS) remains a high mortality etiology of chest pain. Spontaneous coronary artery dissection (SCAD) is a rare cause of ACS in the general population, but a relatively common cause of ACS in young women. Case: Patient is a 29-year-old female with history of anxiety and fibroids that presented with chest pain. She described the chest pain as sharp, substernal, non-radiating that lasted for 10 minutes after eating dinner. The pain improved with leaning forward and resolved when lying on her stomach. She had a second episode of chest pain after 2 hours with similar characteristics which lasted 10 minutes. She was 4 months post-partum. She reported having a sore throat 4 days prior to the presentation. Troponin peaked at 0.173. ECG showed diffuse ST-elevation and PR depression in V3-V6 I II III aVF. TTE showed LVEF 65% and no wall motion abnormalities. CTA coronary showed 50-60% narrowing of mid LAD. Cardiac MR showed mild hypokinesis of mid-anteroseptal wall with associated subendocardial to midmyocardial delayed enhancement with focal elevations in myocardial native T1 and T2, and LVEF 53%. Coronary catheterization showed 50-60% stenosis in the mid-LAD distal to the first diagonal artery, there was no improvement in the stenosis after administration of intra-coronary nitroglycerin, there were no septals noted to arise from this area, consistent with diagnosis of SCAD (figure 1). Diagnosis: On initial evaluation, the etiology of her chest pain appeared to be myopericarditis. However, using CTA coronary, cardiac MR and coronary catheterization findings, the pain was more consistent with type 1 NSTEMI in the setting of SCAD. Patient was started on IV heparin, metoprolol tartrate, and aspirin. Conclusions: SCAD is a life-threating and often missed etiology of ACS. It requires a high index of suspicion and should be in the differential diagnosis in young women presenting with chest pain.
Introduction: ST-elevation myocardial infarction (STEMI) is a known cause of cardiac arrest (CA). Little is known about the impact of targeted therapeutic management in CA patients with STEMI (SCA). Our aim was to investigate the effect of TTM on SCA. Methods: This was a retrospective cohort study using the 2019 Nationwide Inpatient Sample database to identify admissions in adults with diagnoses of CA and STEMI. Regression models were adjusted for demographic variables. Primary outcome was mortality, and secondary outcomes were length of stay (LOS) and total charge in USD. Results: Out of 13895 admissions with SCA, 440 underwent TTM. Compared to Non-TTM-SCA cohort, TTM-SCA cohort had fewer females (18.18% vs 31.03,p<0.05), more males (81.82% vs 68.97,p<0.05), lower mean age (62.17 vs 64.57,p<0.05), more Native American (2.27% vs 0.63%,p<0.05), less South region hospitals (25.00% vs 39.95%,p<0.05), less acute respiratory failure with hypercapnia (0.47% vs 8.53%,p<0.05), acute respiratory failure with hypoxia (1.94% vs 38.90%,p<0.001), history of cardiac arrest (0.11% vs 0.61%,p<0.01), ventricular fibrillation (2.27% vs 50.59%,p<0.001), cerebral infarction (0.29% vs 4.28%,p<0.05), more alcohol abuse (12.50% vs 4.72%,p<0.001), and more persistent vegetative state (1.14% vs 0.15%,p<0.05). Compared to Non-TTM-SCA, TTM-SCA group had similar mortality rates (38.64% vs 42.96%,p=0.3940), mortality OR 1.04 (95%CI 0.66-1.62,p=0.869), higher mean LOS 10.69 vs 6.25 days (95%CI 2.39-6.17,p<0.001), and higher mean total hospitalization charge $238960.90 vs $179880.10 (95%CI 18772.87-98404.78,p<0.01). Conclusion: In SCA patients, TTM presence had no difference in mortality rate, odds of mortality, but had higher mean LOS and total hospitalization charge. TTM was associated with fewer females, more males, lower mean age, more Native Americans, less acute respiratory failure, history of cardiac arrest, ventricular fibrillation, cerebral infarction, and more alcohol abuse and persistent vegetative state.
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