Refractory angina is an independent predictor of adverse events in patients with vasospastic angina (VSA). The aim of this study was to investigate the relationship between coronary lumen complexity and refractory symptoms in patients with VSA. Seventeen patients with VSA underwent optical coherence tomography. The patients were divided into the refractory VSA group (n = 9) and the stable VSA group (n = 8). A shoreline development index was used to assess the coronary artery lumen complexity. Shear stress was estimated using a computational fluid dynamics model. No difference was observed in the baseline characteristics between the two groups. The refractory VSA group showed the higher shoreline development index (refractory VSA 1.042 [1.017–1.188] vs stable VSA 1.003 [1.006–1.025], p = 0.036), and higher maximum medial thickness (refractory VSA 184 ± 17 μm vs stable VSA 148 ± 31 μm, p = 0.017), and higher maximum shear stress (refractory VSA 14.5 [12.1–18.8] Pa vs stable VSA 5.6 [3.0–10.5] Pa, p = 0.003). The shoreline development index positively correlates with shear stress (R² = 0.46, P = 0.004). Increased medial thickness of the coronary arteries provokes lumen complexity and high shear stress, which might cause refractory symptoms in patients with VSA. The shoreline index could serve as a marker for irritability of the medial layer of coronary arteries and symptoms.

The release of lipid-laden plaque material subsequent to ST-segment elevation myocardial infarction (STEMI) may contribute to the no-reflow phenomenon. The aim of this study was to investigate the association between in vivo cholesterol crystals (CCs) detected by optical coherence tomography (OCT) and the no-reflow phenomenon after successful percutaneous coronary intervention (PCI) in patients with acute STEMI. We investigated 182 patients with STEMI. Based on the thrombolysis in myocardial infarction (TIMI) flow grade after PCI, patients were divided into a no-reflow group (n = 31) and a reflow group (n = 151). On OCT, CCs were defined as thin, high-signal intensity regions within a plaque. A multivariable logistic regression analysis was performed to determine predictors for the no-reflow phenomenon. The prevalence of CCs was higher in the no-reflow group than the reflow group (no-reflow group, 77% vs. reflow group, 53%; p = 0.012). The multivariable logistic model showed that the CC number, lipid arc and ostial lesions were positive independent predictors of no-reflow. The combination of a lipid arc ≥ 139°and CC number ≥ 12 showed good predictive performance for the no-reflow phenomenon (sensitivity, 48%; specificity, 93%; and accuracy, 86%). In vivo CCs at the culprit plaque are associated with the no-reflow phenomenon after PCI in patients with STEMI. The combination of the number of CCs and lipid arc can predict the no-reflow phenomenon after PCI with a high accuracy of 86%.

This image series shows the use of intravascular ultrasound and optical coherence tomography in the diagnosis and treatment of a patient with inferior STEMI.

Background: Kounis syndrome is the concurrence of acute coronary syndrome (ACS), including coronary spasm, acute myocardial infarction, and stent thrombosis due to an allergic and/or anaphylactoid insult.Case summary: We present two cases of Kounis syndrome likely triggered by insect bites, with plaque erosion demonstrated using optical coherence tomography (OCT). Three common findings were derived from this case series. First, the patients developed a rash after an insect bite followed by ACS. Second, immunoglobulin E levels were increased. Finally, OCT identified the aetiology of ACS in this case series as erosion of the culprit lesions.Discussion: Kounis syndrome, which is ACS following allergic reactions due to insect bites, is a rare complication. Kounis syndrome is probably not uncommon, but underdiagnosed. It is important for physicians to consider the treatment of Kounis syndrome in the complex course of ACS associated with allergic reactions. Furthermore, patients with a history of Kounis syndrome should avoid antigen exposure during secondary prophylaxis. In some cases, it may take several days from antigen exposure to the onset of ACS. Considering Kounis syndrome is beneficial for early diagnosis and appropriate treatment.

Aims: Early risk stratification of patients with acute heart failure (AHF) is critical for appropriate triage and outcome improvement. The serum sodium, blood urea nitrogen, age, serum albumin, systolic blood pressure, and natriuretic peptide level (SOB-ASAP) score can predict in-hospital mortality of AHF. However, the relationship between the SOB-ASAP score and long-term prognosis is unknown. This study investigated the determinants of the long-term prognosis of AHF by evaluating the SOB-ASAP score. Methods: This retrospective cohort study included all patients with acute decompensated heart failure who were admitted to our hospital between April 2017 and March 2018. And those who discharged were analysed retrospectively. The follow-up period was 3 years. Primary end point was all-cause death. Results: Total of 140 patients were analysed. The median SOB-ASAP score of entire cohort on admission was 3 points (interquartile range; 1–5). The Kaplan–Meier curve demonstrated that patients in the higher SOB-ASAP group (score ≥3) had a higher incidence of all-cause death (log-rank test; P < 0.001) than those in the lower SOB-ASAP (group score <3). Conclusions: At admission, the SOB-ASAP score may be useful for predicting the long-term prognosis of hospitalized patients with AHF.