Ecdysterone (Ecd), an active ingredient in trianthema, has a strong anti‐inflammatory effect. This study aimed to explore the potential mechanism by which Ecd improves atherosclerosis (AS). Here, we systematically investigated the mechanism of Ecd in human umbilical vein endothelial cells (HUVECs) treated with oxidised low‐density lipoprotein (ox‐LDL). In ox‐LDL‐treated HUVECs, Ecd promoted HUVEC viability as well as inhibited ferroptosis and the secretion of inflammatory factors (TNF‐α, IL‐6 and IL‐1β). In addition, Ecd inhibited the expression of neutrophil cytoplasmic factor 2 (NCF2) and triggered the PI3K/AKT/Nrf2 signalling pathway, thereby alleviating the increase of ferroptosis in ox‐LDL‐treated HUVECs. More importantly, we constructed an AS mouse model by feeding ApoE^−/− mice with a high‐fat diet and found that Ecd treatment alleviated vasculopathy and arterial ferroptosis and inhibited the secretion of inflammatory factors in vivo, which could be reversed by overexpression of NCF2. Overall, this study showed that the protective effect of Ecd on AS is mainly achieved by inhibiting NCF2 and activating the PI3K/Akt/Nrf2 pathway to inhibit ferroptosis. Therefore, Ecd may be an effective drug to improve AS by inhibiting ferroptosis‐induced inflammation.

Objective: To investigate the predictive value of hyperhomocysteinaemia (HHcy) for obstructive coronary artery disease (CAD) in an Asian population in northern China. Methods: This retrospective study enrolled patients at their first cardiac assessment and assigned them to an obstructive CAD group or a non-obstructive CAD group according to the coronary angiography results. HHcy was defined as a homocysteine (Hcy) level > 15 µmol/l. Results: This study enrolled 2987 participants: 1172 in the non-obstructive CAD group and 1815 in the obstructive CAD group. Hcy level in the obstructive CAD group was significantly higher than in the non-obstructive CAD group. The proportion of patients with HHcy in the obstructive CAD group was significantly greater than in the non-obstructive CAD group. Multivariate logistic regression analysis demonstrated that HHcy was independently correlated with obstructive CAD in both young (aged ≤ 55 years) and old patients (aged > 55 years). HHcy showed a higher sensitivity (93.1%), specificity (86.1%) and accuracy (90.0%) for obstructive CAD. The odds ratio for HHcy was 84.2. The Kappa value (0.8) showed substantial agreement between obstructive CAD and HHcy. Conclusions: HHcy was associated with obstructive CAD and may be a potentially independent risk factor for obstructive CAD with good predictive value.

Kounis syndrome is a rare type of acute coronary syndrome caused by coronary spasm with or without atherosclerotic plaque erosion or rupture due to inflammatory factors released by allergic reactions. Due to a lack of awareness, Kounis syndrome is often underdiagnosed. Here, we for the first time report a case of Kounis syndrome induced by anisodamine. A 48-year-old woman presented with upper abdominal pain and vomiting after eating. She was diagnosed with gastrointestinal spasm and intramuscularly injected with 10 mg anisodamine. The patient subsequently developed chest pain and hypotension with erythematous rash. A systemic allergic reaction was diagnosed. Saline solution, promethazine and dexamethasone were administered immediately. A 12-lead electrocardiogram indicated ST-segment elevation in II, III and aVF leads. Emergent coronary angiography was recommended. According to a preoperative electrocardiogram, the ST-segment elevation in the II, III and aVF leads had disappeared. Coronary angiograph revealed no significant coronary stenosis. The patient was diagnosed with Kounis syndrome induced by anisodamine, showing acute ST-segment elevation myocardial infarction due to allergic coronary vasospasm. During the 9-month follow-up, the patient did not receive further anisodamine injections and remained free of chest pain. In conclusion, it is essential for clinicians to be aware of Kounis syndrome because of the wide range of triggers and its potentially fatal evolution if not identified in time.

Fractional flow reserve (FFR) has become the gold standard for evaluating coronary lesion-specific ischemia. However, FFR is an invasive method that may cause possible complications in the coronary artery and requires expensive equipment, which limits its use. Promising noninvasive diagnostic methods, such as computed tomography angiography–derived FFR (CT-FFR) and the quantitative flow ratio (QFR), have been proposed. In this study, we evaluated the diagnostic performance of the QFR and CT-FFR in predicting coronary lesion-specific ischemia, with the FFR serving as the reference standard. Patients with suspected or known coronary artery disease who underwent coronary CT angiography revealing 30–90% diameter stenosis in the main coronary artery (≥ 2.0 mm reference diameter) were enrolled. The FFR was measured during invasive coronary angiography (within 15 days after coronary CT angiography). An FFR ≤ 0.8 was the reference standard for coronary lesion-specific ischemia. A total of 103 vessels from 92 consecutive patients (aged 59.8 ± 9.2 years; 60.9% were men) were evaluated. The diagnostic performance of a QFR ≤ 0.80 for predicting coronary lesion-specific ischemia demonstrated good diagnostic accuracy, sensitivity, and specificity (92.2%, 87.2%, and 96.4%, respectively), with an area under the receiver operating characteristic curve (AUC) of 0.987 (P < 0.0001). The diagnostic performance of a CT-FFR ≤ 0.80 for predicting coronary lesion-specific ischemia also demonstrated good diagnostic accuracy, sensitivity, and specificity (96.1%, 95.7%, and 96.4%, respectively), with an AUC of 0.967 (P < 0.0001). However, there was no significant difference in the AUC between a QFR ≤ 0.80 and a CT-FFR ≤ 0.80 for predicting coronary lesion-specific ischemia (P = 0.319). There was an excellent correlation between the QFR and FFR (r = 0.856, P < 0.0001). The CT-FFR and FFR also showed a good direct correlation (r = 0.816, P < 0.0001). The QFR and CT-FFR are strongly correlated with the FFR and can provide excellent clinical diagnostic performance for coronary lesion-specific ischemia detection.

Pheochromocytoma is a rare endocrine tumor arising from chromaffin cells and having extensive and profound effects on the cardiovascular system by continuously or intermittently releasing catecholamines. The clinical manifestations of pheochromocytoma are diverse, and the typical triad, including episodic headache, palpitations, and sweating, only occurs in 24% of pheochromocytoma patients, which often misleads clinicians into making an incorrect diagnosis. We herein report the case of a patient with intermittent chest pain and elevated myocardial enzymes for 2 years who was diagnosed with pheochromocytoma. A 49-year-old woman presented with intermittent chest pain for 2 years. Two years ago, the patient experienced chest pain and was diagnosed with acute myocardial infarction, with 25% stenosis in the left circumflex. The patient still had intermittent chest pain after discharge. Two hours before admission to our hospital, the patient experienced chest pain with nausea and vomiting, lasting for 20 min. Troponin I and urinary norepinephrine and catecholamine levels were elevated. An electrocardiogram indicated QT prolongation and ST-segment depression in leads II, III, aVF, and V3-V6. A coronary computed tomography angiogram revealed no evidence of coronary artery disease. Echocardiography showed left ventricular enlargement and a decreased posterior inferior wall motion amplitude. Contrast-enhanced computed tomography demonstrated an inhomogeneous right adrenal mass. The patient successfully underwent laparoscopic right adrenalectomy, and histopathology confirmed adrenal pheochromocytoma. During the first-year follow-up visits, the patient was asymptomatic. The abnormal changes on echocardiography and electro-cardiogram disappeared. Clinicians should be aware of pheochromocytoma. A timely and accurate diagnosis of pheochromocytoma is essential for alleviating serious cardiac complications.

Takotsubo cardiomyopathy (TCM) is characterized by reversible left ventricular dysfunction triggered by emotional or physical stress. Only 1%-2% of patients with acute coronary syndrome are diagnosed with TCM. Although obstructive coronary artery disease is frequently considered to be the cause of chest pain, TCM should be considered in some clinical settings. In this case, clinicians did not make a timely and accurate diagnosis for TCM due to a lack of knowledge until the third hospitalization with a left ventriculogram. A 55-year-old postmenopausal woman had intermittent chest pain following emotionally stressful events three times in the past 3 years. Cardiac troponin levels increased after each instance of symptom onset. A transthoracic echocardiogram showed reversible left ventricular dysfunction. The patient underwent three coronary angiograms without evidence of coronary artery disease. A left ventriculogram was first performed at the third hospitalization and revealed apical akinesia with ballooning of the apical region and consistent hypercontractile basal segments. The diagnosis of TCM was confirmed. The patient was treated with an angiotensin-converting-enzyme inhibitor (perindopril) and a β-blocker (metoprolol). No complications occurred during the patient’s hospitalization. The patient was told to avoid stressful events. During the 9-mo follow-up visit, the patient was asymptomatic with an ejection fraction of 55%. Clinicians should be conscious of the possibility of TCM, especially in postmenopausal women presenting with clinical manifestations similar to acute coronary syndrome without coronary occlusion.