Treatment Time and In-Hospital Mortality Among Patients With ST-Segment Elevation Myocardial Infarction, 2018-2021.

Importance: Recognizing the association between timely treatment and less myocardial injury for patients with ST-segment elevation myocardial infarction (STEMI), US national guidelines recommend specific treatment-time goals. Objective: To describe these process measures and outcomes for a recent cohort of patients. Design, Setting, and Participants: Cross-sectional study of a diagnosis-based registry between the second quarter of 2018 and the third quarter of 2021 for 114 871 patients with STEMI treated at 648 hospitals in the Get With The Guidelines-Coronary Artery Disease registry. Exposures: STEMI or STEMI equivalent. Main Outcomes and Measures: Treatment times, in-hospital mortality, and adherence to system goals (75% treated ≤90 minutes of first medical contact if the first hospital is percutaneous coronary intervention [PCI]-capable and ≤120 minutes if patients require transfer to a PCI-capable hospital). Results: In the study population, median age was 63 (IQR, 54-72) years, 71% were men, and 29% were women. Median time from symptom onset to PCI was 148 minutes (IQR, 111-226) for patients presenting to PCI-capable hospitals by emergency medical service, 195 minutes (IQR, 127-349) for patients walking in, and 240 minutes (IQR, 166-402) for patients transferred from another hospital. Adjusted in-hospital mortality was lower for those treated within target times vs beyond time goals for patients transported via emergency medical services (first medical contact to laboratory activation ≤20 minutes [in-hospital mortality, 3.6 vs 9.2] adjusted OR, 0.54 [95% CI, 0.48-0.60], and first medical contact to device ≤90 minutes [in-hospital mortality, 3.3 vs 12.1] adjusted OR, 0.40 [95% CI, 0.36-0.44]), walk-in patients (hospital arrival to device ≤90 minutes [in-hospital mortality, 1.8 vs 4.7] adjusted OR, 0.47 [95% CI, 0.40-0.55]), and transferred patients (door-in to door-out time <30 minutes [in-hospital mortality, 2.9 vs 6.4] adjusted OR, 0.51 [95% CI, 0.32-0.78], and first hospital arrival to device ≤120 minutes [in-hospital mortality, 4.3 vs 14.2] adjusted OR, 0.44 [95% CI, 0.26-0.71]). Regardless of mode of presentation, system goals were not met in most quarters, with the most delayed system performance among patients requiring interhospital transfer (17% treated ≤120 minutes). Conclusions and Relevance: This study of patients with STEMI included in a US national registry provides information on changes in process and outcomes between 2018 and 2021.

Systems of Care for ST-Segment-Elevation Myocardial Infarction: A Policy Statement From the American Heart Association.

The introduction of Mission: Lifeline significantly increased timely access to percutaneous coronary intervention for patients with ST-segment-elevation myocardial infarction (STEMI). In the years since, morbidity and mortality rates have declined, and research has led to significant developments that have broadened our concept of the STEMI system of care. However, significant barriers and opportunities remain. From community education to 9-1-1 activation and emergency medical services triage and from emergency department and interfacility transfer protocols to postacute care, each critical juncture presents unique challenges for the optimal care of patients with STEMI. This policy statement sets forth recommendations for how the ideal STEMI system of care should be designed and implemented to ensure that patients with STEMI receive the best evidence-based care at each stage in their illness.

Efficacy of a Novel Mitochondrial-Derived Peptide in a Porcine Model of Myocardial Ischemia/Reperfusion Injury.

With the complexities that surround myocardial ischemia/reperfusion (MI/R) injury, therapies adjunctive to reperfusion that elicit beneficial pleiotropic effects and do not overlap with standard of care are necessary. This study found that the mitochondrial-derived peptide S14G-humanin (HNG) (2 mg/kg), an analogue of humanin, reduced infarct size in a large animal model of MI/R. However, when ischemic time was increased, the infarct-sparing effects were abolished with the same dose of HNG. Thus, although the 60-min MI/R study showed that HNG cardioprotection translates beyond small animal models, further studies are needed to optimize HNG therapy for longer, more patient-relevant periods of cardiac ischemia.

Clinical Case of the Month: A 56-Year-Old Man with Sudden Onset Abdominal Pain.

Acute abdominal pain is one of the most common presentations encountered in the emergency department (ED). The differential diagnosis of acute abdominal pain is extensive and identifying the underlying etiology can be challenging. Spontaneous renal artery thrombosis is a rare cause of acute abdominal pain. We review a case of acute presentation of renal artery thrombosis in a patient without risk factors for thromboembolism, and highlight the importance of considering this rare cause of abdominal pain.

Zofenopril Protects Against Myocardial Ischemia-Reperfusion Injury by Increasing Nitric Oxide and Hydrogen Sulfide Bioavailability.

BACKGROUND: Zofenopril, a sulfhydrylated angiotensin-converting enzyme inhibitor (ACEI), reduces mortality and morbidity in infarcted patients to a greater extent than do other ACEIs. Zofenopril is a unique ACEI that has been shown to increase hydrogen sulfide (H2S) bioavailability and nitric oxide (NO) levels via bradykinin-dependent signaling. Both H2S and NO exert cytoprotective and antioxidant effects. We examined zofenopril effects on H2S and NO bioavailability and cardiac damage in murine and swine models of myocardial ischemia/reperfusion (I/R) injury. METHODS AND RESULTS: Zofenopril (10 mg/kg PO) was administered for 1, 8, and 24 hours to establish optimal dosing in mice. Myocardial and plasma H2S and NO levels were measured along with the levels of H2S and NO enzymes (cystathionine ß-synthase, cystathionine γ-lyase, 3-mercaptopyruvate sulfur transferase, and endothelial nitric oxide synthase). Mice received 8 hours of zofenopril or vehicle pretreatment followed by 45 minutes of ischemia and 24 hours of reperfusion. Pigs received placebo or zofenopril (30 mg/daily orally) 7 days before 75 minutes of ischemia and 48 hours of reperfusion. Zofenopril significantly augmented both plasma and myocardial H2S and NO levels in mice and plasma H2S (sulfane sulfur) in pigs. Cystathionine ß-synthase, cystathionine γ-lyase, 3-mercaptopyruvate sulfur transferase, and total endothelial nitric oxide synthase levels were unaltered, while phospho-endothelial nitric oxide synthase(1177) was significantly increased in mice. Pretreatment with zofenopril significantly reduced myocardial infarct size and cardiac troponin I levels after I/R injury in both mice and swine. Zofenopril also significantly preserved ischemic zone endocardial blood flow at reperfusion in pigs after I/R. CONCLUSIONS: Zofenopril-mediated cardioprotection during I/R is associated with an increase in H2S and NO signaling.

CLINICAL CASE OF THE MONTH: A Review of Situs Inversus and Dextrocardia.

A 21-year-old woman at 25 weeks gestation presented to the emergency department with chief complaints of decreased appetite for one week, fever, runny and stuffy nose, and generalized muscle pains.

Clinical case of the month. A 29-year-old man with acute onset blurry vision, weakness, and gait abnormality. Stroke.

A 29-year-old man, with no significant past medical history, was in his usual state of health until the afternoon of admission. The patient was seated at work eating lunch when he suddenly noticed that his vision became blurry. He covered his right eye and had no visual difficulty but noted blurry vision upon covering his left eye. At this point, the patient tried to stand up, but had difficulty walking and noticed he was "falling toward his left." Facial asymmetry when smiling was also appreciated. The patient denied any alteration in mental status, confusion, antecedent or current headaches, aura, chest pains, or shortness of breath. He was not taking any prescribed medications and had no known allergies. The patient denied any prior hospitalization or surgery. He denied use of tobacco, alcohol, or illicit drugs, and worked as a maintenance worker in a hotel. His family history is remarkable for his father who died of pancreatic cancer in his 50s and his mother who died of an unknown heart condition in her late 40s. Vital signs on presentation to the emergency department included temperature of 97.6 degrees F; respiratory rate of 18 per minute; pulse of 68 per minute; blood pressure of 124/84 mmHg; pulse oximetry of 99% on ambient air. His body mass index was 24 and he was complaining of no pain. The patient had no carotid bruits and no significant jugular venous distention. Cardiovascular exam revealed a regular rate and rhythm with no murmurs. Neurological exam revealed left-sided facial weakness, dysarthria, and preserved visual fields. He was able to furrow his brow. Gait deviation to the left was present, and Romberg sign was negative. Deep tendon reflexes were 2+ throughout, and no other focal neurological deficit was present. The patient was admitted to the hospital with a diagnosis of stroke. Electrocardiogram, fasting lipid profile, computed tomography (CT) scan of head, magnetic resonance imaging (MRI) of head and neck, and transthoracic echo with bubble study were ordered. The initial head CT did not reveal bleeding. He was started on aspirin (ASA). On the second hospital day, the symptoms improved with resolution of dysarthria. His ataxia had also improved. Fasting lipid profile revealed mildly elevated low-density lipoprotein and total cholesterol. His head MRI revealed an acute right thalamic stroke. Echocardiography was significant only for a patent foramen ovale (PFO) with transit of agitated saline "bubbles" from right atrium to left heart within three cardiac cycles (Figure). Doppler ultrasound of extremities revealed no evidence of deep venous thrombosis. A complete resolution of symptoms occurred by the third hospital day. The patient was discharged on full dose aspirin and a statin and was referred for consideration of enrollment in a PFO closure versus medical management trial.

Surgical, medical, and percutaneous therapies for patients with multivessel coronary artery disease.

Patients with multivessel coronary artery disease (CAD) are now faced with a number of treatment choices, including coronary artery bypass graft surgery, medical therapy, and percutaneous coronary interventions (using bare-metal or drug-eluting stents). Each carries certain benefits and risks: bypass surgery is favored in the subset of patients with multivessel disease and diabetes or impaired left ventricular systolic function who are able to receive a left internal mammary artery graft; medical therapy consisting of beta-blockers, angiotensin-converting enzyme inhibitors, statins, aspirin, and nitrates is offered to patients with stable angina. Percutaneous procedures have previously been limited in their efficacy by restenosis and resulting morbidity, but contemporary stenting procedures appear to show equivalent mortality and morbidity outcomes (to bypass surgery) at 5 years. Drug-eluting stents are the newest percutaneous technique and show significant reduction in restenosis compared with older catheter-based therapies, but further investigation is needed to definitively define the role of drug-eluting stents in the treatment of multivessel CAD. This review summarizes the data comparing medical, surgical, and percutaneous treatment approaches for patients with multivessel CAD.