Proprotein convertase subtilisin/kexin type 9 (PCSK9) circulates as mature and furin-cleaved forms, but their biological functions are uncertain. We investigated whether their levels associate with prognosis in patients with acute ST elevation myocardial infarction (STEMI).We enrolled 160 statin-naïve patients with acute STEMI and followed for 3 years. PCSK9 subtype levels were determined by an enzyme-linked immunosorbent assay before and at five timepoints up to 48 h after emergent coronary intervention. The occurrence of coronary and cardiac events was compared between subjects stratified by the PCSK9 level.One hundred and twenty-six patients completed 3 years of follow-up. In the acute phase, both PCSK9 subtype levels decreased, and thereafter increased from 6 to 48 h (mature: from 198 ± 67 to 334 ± 116 ng/mL, furin-cleaved: from 20 ± 7 to 39 ± 16 ng/mL, both p < 0.01). Major cardiac events occurred in 46 patients. The furin-cleaved/mature PCSK9 ratio at 48 h after coronary intervention predicted the likelihood of experiencing of events; patients in the third tertile had lower event-free survival than those in the first and second tetiles in Kaplan-Meier analysis (p = 0.004). Multivariate Cox regression analysis revealed that this ratio had a greater impact (HR: 1.92; 95% CI: 1.06-3.45, p = 0.03) on events than other known atherosclerosis risk factors.The furin-cleaved/mature PCSK9 ratio was associated with 3-year cardiovascular events in statin-naïve patients with acute STEMI, suggesting a potential link between furin cleavage process of PCSK9 and its effect on prognosis. (249 words).
Lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular diseases; however, its role in acute coronary syndrome (ACS) remains unclear.
A 54-year-old woman with multiple sclerosis treated with interferon-β (IFN-β)-1b for 15 years presented with sustained hypertension (240/124 mmHg) and retinal bleeding. She had proteinuria, anemia, thrombocytopenia, elevated serum creatinine levels, and haptoglobin depletion. Intravenous nicardipine stabilized her blood pressure, but her renal function and platelet count deteriorated. The initial disintegrin-like metalloprotease with thrombospondin type 1 motif 13 (ADAMTS13) activity was 28% of normal without its inhibitor. The subsequent peripheral appearance of schistocytes suggested thrombotic microangiopathy (TMA). After IFN-β-1b cessation, the platelet count increased, and the blood pressure stabilized. The ADAMTS13 activity normalized, although the creatinine level did not. TMA may develop after the long-term use of IFN-β without adverse events.
Coronary sinus ostial atresia is rare and usually not clinically relevant, but it should be noted in cases of cardiac resynchronization therapy. A rare case of successful left ventricular lead implantation for cardiac resynchronization therapy via the left superior vena cava in a patient with coronary sinus ostial atresia is reported. The persistent left superior vena cava associated with these cases tends to be smaller than usual in its diameter and difficult to identify, since the direction of venous drainage is reversed. Therefore, in the present case, it was useful to use a small-diameter, soft inner catheter as a guiding catheter to perform selective imaging and avoid vascular injury. In addition, it appeared to be important to plan the surgical strategy using prior imaging information, since it would be difficult to obtain the backup needed for lead insertion.Learning objective: Cardiac resynchronization therapy via the left superior vena cava with coronary sinus ostial atresia is generally possible without problems if prior imaging information is available, such as three-dimensional computed tomography and the venous phase of coronary angiography. It is important to determine whether there is a persistent left superior vena cava before the procedure. Thromboprophylaxis remains controversial in this situation.〉.
Vaccination is important for the prevention of coronavirus-induced disease 2019 (COVID-19) caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) and to protect persons with a high risk for complications. There have been reports of myopericarditis following COVID-19 vaccination, especially in adolescent males and young adults. Breakthrough infections, such as the Delta or Omicron variant of SARS-CoV-2, have raised great concern about the necessity for repeated doses of the vaccine. A case of myopericarditis after the second dose of COVID-19 mRNA-1273 (Moderna) vaccine in a 23-year-old man with a prior episode of viral myopericarditis is presented. He received the second dose of the COVID-19 mRNA vaccine, after which he developed persistent midsternal chest pain and he was subsequently transferred to our emergency department. An echocardiogram showed a trivial inferior pericardial effusion with diffuse left ventricular systolic dysfunction. He was treated with colchicine from the first day of hospitalization with a diagnosis of myopericarditis. His chest pain had resolved by the third day, and left ventricular wall motion was dramatically improved by the seventh day of hospitalization. A strong response to the second vaccination in the present case suggests that the prior history of myopericarditis is evidence of strong congenital or acquired immunological features in this individual. Individuals with such a strong immune response may be more likely to develop myopericarditis after mRNA vaccination. Immunization against COVID-19 is currently recommended from a risk-benefit standpoint. We advised the patient to avoid additional COVID-19 mRNA vaccines because of this episode. The risk of COVID-19 weighed against myopericarditis associated with the mRNA vaccination should be considered on a case-by-case basis. This case may help us better understand the mechanism of myopericarditis following COVID-19 mRNA vaccination.
Objective Non-alcoholic fatty liver disease is a risk factor for atrial fibrillation. We assessed whether liver fibrosis markers are associated with atrial remodeling indicators in patients with atrial fibrillation in whom fatty liver disease has not been identified. Methods In this prospective, observational study, 174 patients with atrial fibrillation without chronic liver disease who underwent catheter ablation were enrolled. Using blood collected from the right atrium, type IV collagen (COL4), type IV collagen 7S (COL4-7S), and tumor necrosis factor-α concentrations were measured as markers of liver fibrosis and inflammation. The left atrial volume and P-wave duration were used as atrial remodeling indicators. Results Left atrial volume was significantly positively correlated with COL4, COL4-7S, and tumor necrosis factor-α concentrations. COL4-7S concentrations were significantly positively correlated with tumor necrosis factor-α concentrations and the P-wave duration. To exclude the effect of alcohol consumption, a multiple regression analysis was performed for left atrial volume in patients with a <30-g daily alcohol intake (n = 124). Age, sex, and COL4-7S were significant explanatory variables (R = 0.44, adjusted R2 = 0.142, COL4-7S standardized β = 0.20). Conclusion Liver fibrosis may be involved in atrial remodeling via inflammation in patients with atrial fibrillation who do not have obvious fatty liver disease.
