Second mRNA Vaccination of COVID-19 in a Patient Who Developed Pericarditis after the First Vaccination.

The coronavirus infection 2019 (COVID-19) pandemic has led to the development of mRNA vaccines with proven efficacy. However, it remains unclear whether patients who developed pericarditis after the first COVID-19 mRNA would be fit to receive the second vaccination. Herein, we present the case of a 64-year-old man who visited our emergency department with substernal chest discomfort that began 4 days after his first mRNA COVID-19 vaccination. Acute pericarditis was diagnosed based on symptoms and ST-segment elevation on an electrocardiogram. Chest pain improved 2 days after treatment.Since there are no guidelines on whether to administer an additional vaccination to a patient who developed pericarditis after the initial vaccination, we considered whether or not to administer the additional vaccination. We informed the patient about the risks and benefits and decided to administer the second dose. He did not experience any major adverse reactions. The indications for the second vaccination need to be thoroughly considered.

Clinical significance of prehospital 12-lead electrocardiography in patients with ST-segment elevation myocardial infarction presenting with syncope: from a multicenter observational registry (K-ACTIVE study).

Patients with acute myocardial infarction (AMI) presenting with syncope have poor clinical outcomes partly due to a delay in the diagnosis. Although the impact of prehospital 12-lead electrocardiography (PHECG) on the reduction of first medical contact (FMC)-to-device time and subsequent adverse clinical events in patients with AMI has been demonstrated, the impact of PHECG for the patients presenting with syncope remains to be elucidated. This study aimed to explore the impact of PHECG on 30-day mortality in patients with ST-segment elevation myocardial infarction (STEMI) presenting with syncope. From a cohort of multi-center registry [Kanagawa-ACuTe cardIoVascular rEgistry (K-ACTIVE)], a total of 90 consecutive patients with STEMI presenting with syncope were included. The 30-day mortality were compared between patients with PHECG (PHECG group, n = 25) and those without PHECG (non-PHECG group, n = 65). There was no significant difference in the baseline clinical characteristics between the 2 groups. FMC-to-device time was significantly shorter in the PHECG group than in the non-PHECG group (122 [86, 128] vs. 131 [102, 153] min, p = 0.03) due to the shorter door-to-device time. Thirty-day mortality was significantly lower in the PHECG group than in the non-PHECG group (16.0 vs. 44.6%, p = 0.03). In conclusion, PHECG was associated with shorter FMC-to-device time and lower 30-day mortality in patients with STEMI presenting with syncope.

Anti-inflammatory effect of factor-Xa inhibitors in Japanese patients with atrial fibrillation.

Activated factor-X (FXa) plays an important role not only in the coagulation cascade, but also in pro-inflammatory responses. However, few data exist regarding the anti-inflammatory effect of FXa inhibitors in clinical practice. The aim of this study was to evaluate the anti-inflammatory and anti-atherosclerotic effects of FXa inhibitors in Japanese patients with non-valvular atrial fibrillation (NVAF). Eighty-three patients with NVAF were treated with FXa inhibitors from March 2013 to March 2015 at our institution. Of these, 55 patients who were not pretreated with warfarin or dabigatran (rivarixaban in 23 patients and apixaban in 32) were included in this study. We measured various inflammatory and coagulation markers at baseline and at 6 months after treatment. Plasma concentrations of pentraxin 3 (PTX3) (from 2.45 ± 1.31 to 1.97 ± 1.00 ng/mL, p = 0.0009) and fibrin and fibrinogen degradation products (FDP) D-dimer (from 1.18 ± 0.70 to 0.74 ± 0.32 µg/mL, p < 0.0001) decreased, while those of TM (from 2.9 ± 0.8 to 3.2 ± 0.9 FU/mL, p = 0.003) increased significantly at 6 months. Interestingly, change of each marker denoted the same tendency in both rivaroxaban and apixaban. In conclusion, the present study suggests that FXa inhibitors have not only an anti-coagulant effect but also anti-inflammatory effects in patients with NVAF. Further large-scale prospective study is necessary to evaluate whether changes in these markers will be associated with a lower risk for future cardiovascular events.

Impact of combined lipid lowering and blood pressure control on coronary plaque: myocardial ischemia treated by percutaneous coronary intervention and plaque regression by lipid lowering and blood pressure controlling assessed by intravascular ultrasonography (MILLION) study.

The aim of the study was to elucidate the aggressive reduction of both low-density lipoprotein cholesterol (LDL-C) and blood pressure (BP) reduced coronary atherosclerotic plaque volume compared with a standard treatment of LDL-C and BP in Japanese patients with coronary artery disease (CAD). This study is a prospective, randomized, and open-labelled with a blind-endpoint evaluation study. A total of 97 patients (81 men, mean age 62.0 ± 9.6) with CAD undergoing intravascular ultrasonography (IVUS)-guided percutaneous coronary intervention (PCI) were randomized, and 68 patients had IVUS examinations at baseline and at 18-24 months follow-up. Patients were randomly assigned to standard or aggressive strategies targeting LDL-C and a BP of 100 mg/dL and 140/90 mmHg vs. 70 mg/dL and 120/70 mmHg, respectively. The primary endpoint was the percent change in coronary plaque volume. Both standard and aggressive strategies succeeded to achieve target levels of LDL-C and BP; 74.9 ± 14.7 vs. 63.7 ± 11.9 mg/dL (NS) and 124.1 ± 9.4/75.8 ± 7.7 vs. 113.6 ± 9.6/65.8 ± 9.4 mmHg (systolic BP; NS, diastolic BP; p < 0.05), respectively. Both groups showed a significant reduction in the coronary plaque volume of -9.4 ± 10.7% and -8.7 ± 8.6% (NS) in standard and aggressive therapies, respectively. Both standard and aggressive intervention significantly regressed coronary plaque volume by the same degree, suggesting the importance of simultaneous reductions of LDL-C and BP for prevention of CAD.

Penetration rate of the placement of a drug-eluting stent for the treatment of superficial femoral artery lesions in Japan.

Stent placement for treating superficial femoral artery (SFA) lesions has been approved. The Zilver PTX stent, a drug-eluting stent (DES) for treating SFA lesions, has been available in Japan since 2012. However, the penetration rate of this DES has not yet been reported. This prospective multicenter registry study enrolled 314 patients (354 limbs) to be treated by stent placement in 2014 (UMIN000011551). The primary endpoint was the measurement of the penetration rate of the DES. The secondary endpoints were measuring the freedom from restenosis, freedom from target lesion revascularization (TLR), freedom from major adverse limb event (MALE), and the survival rate at 12 months postoperatively. Female patients comprised 28% participants. The mean age was 73.1 ± 9.2 years. A total of 56% patients had diabetes mellitus (DM), 36% patients were receiving hemodialysis, and 30% used cilostazol at baseline. The mean lesion length was 156 ± 101 mm, and the percentage of TASC II C/D lesions was 58%. Critical limb ischemia (CLI) was observed in 32% limbs. The penetration rates of the Zilver PTX stent were only 8%. The primary patency rate was similar between DES and bare-metal stents (BMS) at 12 months postoperatively (77 vs. 84%, p = 0.52). In this study, the rates of freedom from restenosis, freedom from TLR, freedom from MALE, and the survival rate at 12 months postoperatively were 83, 86, 85, and 89%, respectively. The penetration rate of a first-generation DES placement for treating SFA lesions is low in Japan. On the other hand, BMS is well utilized and its primary patency is acceptable.

A case of giant saphenous vein graft aneurysm successfully treated with catheter intervention.

The patient was a 67-year-old man who had undergone coronary artery bypass graft surgery using a saphenous vein graft (SVG) 22 years before. Computed tomography angiogram revealed a large aneurysm of the SVG (38 × 42 mm in diameter; 80-mm long) and total occlusion of the left anterior descending artery (LAD). We first performed percutaneous coronary intervention for chronic total occlusion of the native LAD with bi-directional approach via the SVG. One month later, we performed the trans-catheter embolization of the SVG and occluded the SVG using multiple coils. This case demonstrates that trans-catheter embolization after recanalization of native coronary artery is an effective strategy to treat an SVG aneurysm. © 2015 Wiley Periodicals, Inc.

Effects of sitagliptin on coronary atherosclerosis evaluated using integrated backscatter intravascular ultrasound in patients with type 2 diabetes: rationale and design of the TRUST study.

Patients with diabetes mellitus are at high risk for developing coronary artery disease (CAD), even if they are treated with statins. Several studies have shown the beneficial effects of dipeptidyl peptidase-4 (DPP-4) inhibitors on the cardiovascular system in an animal model. However, recent clinical trials using DPP-4 inhibitors have shown that these inhibitors fail to reduce the occurrence of cardiovascular events. Therefore, this study will be performed to evaluate the effects of sitagliptin, a DPP-4 inhibitor, on coronary atherosclerosis in patients with type 2 diabetes. This study will be a prospective, open-label, randomized multicenter trial performed in 6 centers in Japan. Stable CAD patients with type 2 diabetes who have undergone successful percutaneous coronary intervention under integrated backscatter (IB)-intravascular ultrasound (IVUS) guidance will be studied. They will be randomly assigned to either the sitagliptin group or a control group. After 48 weeks' treatment, the IVUS examination will be repeated in the same coronary artery as at baseline. The primary end point will be the percentage change in plaque volume measured using grayscale IVUS from baseline to the 48-week follow-up. This study will be the first multicenter trial to evaluate the effects of a DPP-4 inhibitor on coronary atherosclerosis evaluated using IB-IVUS, and the findings will clarify the anti-atherogenic effects of sitagliptin.

Effects of liraglutide, a glucagon-like peptide-1 analog, on left ventricular remodeling assessed by cardiac magnetic resonance imaging in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention.

The clinical efficacy of glucagon-like peptide-1 (GLP-1) analogs in patients with acute myocardial infarction (AMI) is uncertain. The purpose of the present study was to evaluate the effects of the GLP-1 analog liraglutide on left ventricular (LV) remodeling in patients with AMI. We retrospectively evaluated the effects of liraglutide on LV remodeling assessed by cardiac magnetic resonance imaging (CMRI) in 15 patients with type 2 diabetes who were successfully treated with primary percutaneous coronary intervention (PCI) for AMI. Patients were divided into two groups based on their hypoglycemic medication: liraglutide use (group L; n = 6) or standard therapy (group S; n = 9). The CMRI findings in the early phase and at the 6-month follow-up were compared. At the 6-month follow-up, group S showed increases in LV end-diastolic (from 64 to 74 mL/m(2), p = 0.08) and end-systolic (from 38 to 45 mL/m(2), p = 0.13) volume indexes, whereas no such increase was observed in group L. The LV mass index (LVMI) was significantly smaller in group L than in group S at baseline (64 vs. 75 g/m(2), p = 0.05) and at follow-up (56 vs. 78 g/m(2), p = 0.009). Multivariate regression analysis showed that liraglutide use was an independent negative predictor of LVMI (ß = -0.720, p = 0.003). In conclusion, liraglutide may be able to prevent the progression of LV remodeling and is associated with a lower LV mass in diabetic patients with AMI undergoing primary PCI.

Correlation between serum levels of proprotein convertase subtilisin/kexin type 9 (PCSK9) and atherogenic lipoproteins in patients with coronary artery disease.

BACKGROUND: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a key regulator of serum low-density lipoprotein (LDL) cholesterol levels. Recently, PCSK9 has additionally been related to metabolic risk factors such as the levels of triglycerides, apolipoprotein B (apoB), insulin, and glucose, as well as body mass index. The purpose of this study was to investigate correlations between serum levels of PCSK9 and apoB-containing atherogenic lipoproteins in patients with coronary artery disease (CAD). METHODS: Serum levels of PCSK9 and lipoprotein(a) [Lp(a)]; small, dense LDL; and oxidized LDL were measured in 101 patients with CAD who were not receiving lipid-lowering therapy. RESULTS: Serum hetero-dimer PCSK9 levels were positively correlated with serum levels of Lp(a) (r = 0.195, p = 0.05); small, dense LDL (r = 0.336, p = 0.0006); and oxidized LDL (r = 0.268, p = 0.008). Multivariate regression analyses showed that serum hetero-dimer PCSK9 was a significant predictor of serum levels of Lp(a) (ß = 0.235, p = 0.01); small, dense LDL (ß = 0.143, p = 0.03); and oxidized LDL (ß = 0.268, p = 0.008). CONCLUSIONS: Serum PCSK9 levels were positively correlated with serum levels of Lp(a); small, dense LDL; and oxidized LDL in patients with CAD. This suggests that the interaction between serum PCSK9 and apoB-containing lipoproteins plays a role in establishing the atherosclerotic status of patients. TRIAL REGISTRATION: UMIN Clinical Trials Registry, UMIN ID: C000000311 .

Comparison of the effects of pitavastatin versus pravastatin on coronary artery plaque phenotype assessed by tissue characterization using serial virtual histology intravascular ultrasound.

Thin-cap fibroatheroma (TCFA) is the most common type of vulnerable plaque and is the precursor of plaque rupture. However, rupture of a TCFA is not the only mechanism underlying thrombus formation or acute coronary syndrome. Although statin therapy changes the composition of coronary artery plaques, the effects of statins, particularly different types of statins, on plaque phenotype have not been fully examined. This study compared the effects of pitavastatin versus pravastatin on coronary artery plaque phenotype assessed by virtual histology (VH) intravascular ultrasound (IVUS) in patients with angina pectoris (AP). Coronary atherosclerosis in nonculprit lesions was evaluated using VH-IVUS at baseline and 8 months after statin therapy; analyzable IVUS data were obtained from 83 patients with stable AP (39 patients treated with pitavastatin and 44 with pravastatin) and 36 patients with unstable AP (19 patients treated with pitavastatin and 17 with pravastatin). Pitavastatin had a strong effect on reducing pathologic intimal thickening (PIT), especially in patients with unstable AP, but had no impact on VH-TCFA or fibroatheroma (FA). By contrast, pravastatin had weak effects on reducing PIT, VH-TCFA, or FA. Increases in the number of calcified plaques were observed for both statins. In conclusion, pitavastatin and pravastatin changed coronary artery plaque phenotype as assessed by VH-IVUS in patients with AP. However, the effects of these statins on coronary artery plaque phenotype were different.

Impact of combined lipid lowering with blood pressure control on coronary plaque regression: rationale and design of MILLION study.

A line of epidemiological studies suggests that the accumulation of coronary risk factors promotes the progression of coronary atherosclerosis. Recent clinical studies showed that aggressive low-density lipoprotein (LDL) cholesterol-lowering therapy using statins could regress coronary atheroma and reduce major cardiovascular events. Additionally, therapy that controlled amlodipine-based blood pressure reduced major cardiovascular events in patients with hypertension compared with an atenolol-based regimen. An open-label randomized multicenter study is primarily planned to evaluate the changes in coronary atheroma volume using intravascular ultrasonography 18-24 months after intensive lowering of LDL-cholesterol and blood pressure compared with a standard therapy indicated by current guidelines in Japanese patients with coronary artery disease (CAD). The secondary endpoints include changes in serum lipid levels, inflammatory markers, glucose markers and blood pressure. In total, 100 subjects with CAD who are undergoing percutaneous coronary intervention will be tested. The MILLION study will provide new evidence and therapeutic standards for the prevention of CAD in Japanese patients by controlling both LDL-C levels and blood pressure.

Statin treatment alters serum n-3 to n-6 polyunsaturated fatty acids ratio in patients with dyslipidemia.

BACKGROUND: The effects of statins on serum n-3 to n-6 polyunsaturated fatty acids (PUFAs) levels have not been fully evaluated. We examined the effects of two types of statins (rosuvastatin and pitavastatin) on serum PUFAs levels and their ratios in patients with dyslipidemia. FINDINGS: A total of 46 patients who were not receiving lipid-lowering therapy were randomly assigned to receive either 2.5 mg/day of rosuvastatin or 2 mg/day of pitavastatin. Serum PUFAs levels were measured at baseline, at 4 weeks, and at 12 weeks. Rosuvastatin was used to treat 23 patients, and the remaining 23 patients were treated using pitavastatin. Serum docosahexaenoic acid (DHA) levels decreased significantly at 12 weeks in both groups (rosuvastatin: from 169.6 to 136.3 µg/mL, p = 0.006; pitavastatin: from 188.6 to 153.9 µg/mL, p = 0.03). However, serum levels of eicosapentaenoic acid (EPA) and arachidonic acid (AA) did not change. In addition, the EPA/AA ratio did not change, whereas the DHA/AA ratio decreased significantly at 12 weeks in both groups (rosuvastatin: from 0.99 to 0.80, p = 0.01; pitavastatin: from 1.14 to 0.91, p = 0.003). No adverse events were observed during the study period. CONCLUSIONS: In this small, open-label, pilot study, rosuvastatin and pitavastatin decreased serum DHA levels and the DHA/AA ratio in patients with dyslipidemia.

Low serum docosahexaenoic acid is associated with progression of coronary atherosclerosis in statin-treated patients with diabetes mellitus: results of the treatment with statin on atheroma regression evaluated by intravascular ultrasound with virtual histology (TRUTH) study.

BACKGROUND: Diabetes mellitus (DM) accelerates plaque progression despite the use of statin therapy. The purpose of the present study was to evaluate the determinants of atheroma progression in statin-treated patients with DM. METHODS: Coronary atherosclerosis in nonculprit lesions in a vessel undergoing percutaneous coronary intervention (PCI) was evaluated using virtual histology intravascular ultrasound. The study included 50 patients with DM who had been taking statin therapy for 8 months at the time of PCI. RESULTS: Twenty-six patients (52%) showed atheroma progression (progressors) and the remaining 24 patients (48%) showed atheroma regression (regressors) after 8 months of follow-up. Fewer progressors than regressors received intensive lipid-lowering therapy with pitavastatin (31% vs. 50%, p = 0.17) and the frequency of insulin use was higher in progressors (31% vs. 13%, p = 0.18). However, neither of these differences reached statistical significance. Risk factor control at baseline and at the 8-month follow-up did not differ between the 2 groups except for serum levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Univariate regression analysis showed that serum EPA (r = -0.317, p = 0.03) and DHA (r = -0.353, p = 0.02) negatively correlated with atheroma progression. Multivariate stepwise regression analysis showed that low serum DHA and pravastatin use were significant independent predictors for atheroma progression during statin therapy (DHA: ß = -0.414, type of statin: ß = -0.287, p = 0.001). CONCLUSIONS: Low serum DHA is associated with progression of coronary atherosclerosis in statin-treated patients with DM. TRIAL REGISTRATION: UMIN Clinical Trials Registry, UMIN ID: C000000311.

Elevation of urinary liver-type fatty acid-binding protein as predicting factor for occurrence of contrast-induced acute kidney injury and its reduction by hemodiafiltration with blood suction from right atrium.

Although contrast-induced acute kidney injury (CI-AKI) has a great impact on patients' prognosis, few data exist regarding predictors of CI-AKI in patients with severe renal dysfunction who have undergone contrast angiography. Therefore, we prospectively studied 25 patients with renal dysfunction, which was defined as the estimated glomerular filtration rate (eGFR) level <45 ml/min/1.73 m(2), undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI). We performed hemodiafiltration with blood suction from the right atrium (RA-HDF). The mean level of urinary liver-type fatty acid-binding protein (L-FABP) at baseline was significantly higher in the CI-AKI group than in the non-CI-AKI group (59.8 ± 45.6 vs 13.4 ± 11.9 µg/gCr, P = 0.0003). Multivariate regression analysis demonstrated that baseline urinary L-FABP was an independent significant predictor of CI-AKI (ß = 0.741, P = 0.013). Receiver-operating characteristic analysis showed that baseline urinary L-FABP exhibited 100 % sensitivity and 81.8 % specificity for predicting CI-AKI when the cutoff value was defined as 19.0 µg/gCr. Interestingly, the incidence of CI-AKI after CAG or PCI was reduced in the RA-HDF group in a comparison with 41 control patients (12 % vs 27 %) with eGFR level <45 ml/min/1.73 m(2) who underwent PCI before the introduction of RA-HDF. In conclusion, baseline L-FABP levels can be a predictor for occurrence of CI-AKI. We suggest that RA-HDF may prevent the development of CI-AKI in patients with severe renal dysfunction undergoing coronary procedures, although further large-scale prospective study is necessary to confirm our conclusions.

Impacts of age on coronary atherosclerosis and vascular response to statin therapy.

Age is a well-established risk factor for cardiovascular disease. Recent trials using intravascular ultrasound (IVUS) have shown that lipid-lowering therapy with statins halts the progression or induces the regression of coronary artery plaques. However, impacts of age on coronary atherosclerosis and vascular response to statin therapy have not been fully evaluated. The effects of 8-month statin therapy on coronary atherosclerosis were evaluated using virtual histology-IVUS. IVUS data were analyzed from 119 patients who were divided into two groups according to age: elderly patients (≥65 years, n = 72) and non-elderly patients (<65 years, n = 47). No patients were taking statins or other lipid-lowering therapies at baseline. At baseline, external elastic membrane (EEM) volume (17.27 vs. 14.95 mm(3)/mm, p = 0.02) and plaque volume (9.49 vs. 8.11 mm(3)/mm, p = 0.03) in the elderly patients were significantly greater than in the non-elderly patients. The EEM volume (-2.4 %, p = 0.007) and plaque volume (-3.1 %, p = 0.007) after 8-month of statin therapy had significantly decreased in the non-elderly patients but not in the elderly patients. A significant positive correlation was observed between age and percentage change in plaque volume (r = 0.265, p = 0.004). A multivariate regression analysis showed that age was a significant predictor of the percentage change in plaque volume during statin therapy (ß = 0.223, p = 0.02). Coronary atherosclerosis was more advanced and vascular responses to statin therapy were attenuated in the elderly patients compared to the non-elderly patients.

Lipoprotein(a) is associated with necrotic core progression of non-culprit coronary lesions in statin-treated patients with angina pectoris.

BACKGROUND: Statin therapy results in regression and stabilization of coronary artery plaques, and reduces the incidence of coronary artery disease. However, statin therapy does not effectively halt the accumulation of necrotic core in all patients. The purpose of the present study was to identify the predictors associated with necrotic core progression during statin therapy. METHODS: Coronary atherosclerosis in non-culprit lesions was evaluated using virtual histology intravascular ultrasound at baseline and 8 months after statin therapy. One hundred nineteen patients were divided into 2 groups based on necrotic core progression or regression during an 8-month follow-up period. RESULTS: Patients with necrotic core progression had higher serum lipoprotein(a) [Lp(a)] levels than patients with regression at baseline (16 mg/dL vs. 12 mg/dL, p = 0.02) and at the 8-month follow-up (17 mg/dL vs. 10 mg/dL, p = 0.006). Patients with necrotic core progression had a higher fibro-fatty plaque volume (1.28 mm³/mm vs. 0.73 mm³/mm, p = 0.002), and less necrotic core (0.56 mm³/mm vs. 1.04 mm³/mm, p < 0.0001) and dense calcium (0.35 mm³/mm vs. 0.56 mm³/mm, p = 0.006) plaque volumes at baseline than patients with regression. Multivariate logistic regression analysis showed that Lp(a) was a significant independent predictor associated with necrotic core progression during statin therapy (odds ratio [OR]: 3.514; 95% confidence interval [CI]: 1.338-9.228; p = 0.01). CONCLUSIONS: Serum Lp(a) is independently associated with necrotic core progression in statin-treated patients with angina pectoris.

Benefit of prehospital electrocardiogram on door-to-device time in ST-segment elevation myocardial infarction with cardiogenic shock: Data from the Kanagawa Acute Cardiovascular Registry.

BACKGROUND: The benefit of prehospital 12­lead electrocardiogram (PH-ECG) performed by emergency medical service personnel at the site of first medical contact (FMC) in patients with ST-segment elevation myocardial infarction (STEMI) with cardiogenic shock (CS-STEMI) remains unclear. This study aimed to investigate the effect of PH-ECG on door-to-device time in patients with CS-STEMI. METHODS: This study enrolled CS-STEMI (Killip class IV) patients who were transferred directly to hospitals by ambulance (n = 517) from the Kanagawa Acute Cardiovascular Registry database. Patients were divided into PH-ECG (+) (n = 270) and PH-ECG (-) (n = 247) groups. Patients who experienced out-of-hospital cardiac arrest, who did not undergo emergent coronary intervention, or whose data were missing were excluded. Patient characteristics, FMC-to-door time, door-to-device time, and in-hospital mortality were compared between the groups. RESULTS: The patient backgrounds of the PH-ECG (+) and PH-ECG (-) groups were comparable. The peak creatinine kinase level was greater in the PH-ECG (+) group than in the PH-ECG (-) group [2756 (1292-6009) IU/ml vs. 2270 (957-5258) IU/ml, p = 0.048]. The FMC-to-door time was similar between the two groups [25 (20-33) min vs. 27 (20-35) min, p = 0.530], while the door-to-device time was significantly shorter in the PH-ECG group [74 (52-103) min vs. 83 (62-111) min, p = 0.007]. In-hospital mortality did not differ between the two groups (18 % vs. 21 %, p = 0.405). Multivariable logistic regression analyses revealed that PH-ECG (+) was independently associated with a door-to-device time < 60 min [odds ratio (95 % confidence intervals): 1.88 (1.24-2.83), p = 0.003]. CONCLUSIONS: PH-ECG was significantly associated with shorter door-to-device times in patients with CS-STEMI. Further studies with larger populations and more defined protocols are required to evaluate the utility of PH-ECG in patients with CS-STEMI.

A case of hyperchylomicronemia associated with GPIHBP1 autoantibodies and fluctuating thyroid autoimmune disease.

Recent studies have reported that patients with autoimmune hyperchylomicronemia caused by glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1 (GPIHBP1) autoantibodies are associated with rheumatoid arthritis, systemic lupus erythematosus, Sjogren's syndrome, Hashimoto's thyroiditis, Basedow's disease, and immune thrombocytopenia. We report a rare case of hyperchylomicronemia due to GPIHBP1 autoantibodies and fluctuating thyroid autoimmune disease. A 28-year-old woman, diagnosed with Hashimoto's thyroiditis at 26 years of age, started taking 50 µg/day of levothyroxine sodium. She had an episode of acute pancreatitis at 27 years of age; her serum triglyceride (TG) level was 1291 mg/dL at that time. The patient was referred to our hospital because her hyperchylomicronemia (hypertriglyceridemia) did not improve on treatment with pemafibrate and eicosapentaenoic acid (EPA). Serum total cholesterol and TG levels were 237 mg/dL and 2535 mg/dL, respectively, while plasma pre-heparin lipoprotein lipase (LPL) mass was 15 ng/mL (26.5-105.5 ng/mL). We diagnosed her as Basedow's disease based on autoimmune antibodies and ultrasound examination. Targeted exome sequencing revealed no pathogenic variants in the LPL or GPIHBP1 genes. The serum GPIHBP1 autoantibody level was 686.0 U/mL (<58.4 U/mL) and GPIHBP1 mass was 301.9 pg/mL (570.6-1625.6 pg/mL). The patient showed hyperchylomicronemia during periods of hypothyroidism and hyperthyroidism, whereas GPIHBP1 autoantibodies were positive during episode of hyperchylomicronemia but negative during periods of normal TG levels. Based on these findings, the patient was diagnosed with hyperchylomicronemia due to GPIHBP1 autoantibodies and treated with rituximab. GPIHBP1 autoantibodies remained undetectable and TG levels were controlled at approximately 200 mg/dL.

Radial versus femoral access in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction: A propensity-matched analysis from real-world data of the K-ACTIVE registry.

BACKGROUND: The access site for primary percutaneous coronary intervention (PCI) for patients with ST-elevation myocardial infarction (STEMI) recently shifted from femoral to radial. However, few real-world data on Japanese patients exist. METHODS: To elucidate the clinical selection and impact of the access site in STEMI patients, we analyzed a Japanese observational prospective multicenter registry of acute myocardial infarction (K-ACTIVE: Kanagawa ACuTe cardIoVascular rEgistry) in 2015 to 2021. Data were analyzed in the entire population and a propensity score-matched population adjusted for confounding factors. Major adverse cardiac event (MACE) was defined as cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke. Bleeding Academic Research Consortium (BARC) type 3 or 5 was used to assess bleeding events. MACE plus BARC type 3 or 5 bleeding were considered composite events. Clinical outcomes were followed for 30 days. RESULTS: The 6802 STEMI patients included 4786 patients with radial access (70.3 %) and 2016 with femoral access (29.7 %). Femoral access tended to be selected for more severe conditions than radial access. The median door-to-device time in the radial access group was significantly shorter than the femoral access group in the entire population (75 min versus 79 min, p < 0.01). After propensity score matching (each group, n = 1208), the incidence of MACE tended to be lower in the radial access group [risk ratio (RR) 0.83, 95 % confidence interval (CI) 0.63-1.09, p = 0.17]. The incidence of BARC 3 or 5 bleeding was significantly less in the radial access group (RR 0.47, 95%CI 0.23-0.97, p = 0.04). The incidence of composite events was significantly less in the radial access group (RR 0.74, 95%CI 0.57-0.96, p = 0.02). CONCLUSION: In STEMI patients undergoing primary PCI, in comparison to femoral access, radial access reduced composite events in the entire population and the matched population, through a reduction in MACE and BARC 3 or 5 bleeding.

Statin treatment for coronary artery plaque composition based on intravascular ultrasound radiofrequency data analysis.

BACKGROUND: Systemic therapy with statin has been shown to lower the risk of coronary events; however, the in vivo effects of statin therapy on plaque volume and composition are less understood. METHODS: We conducted a prospective, open-labeled, randomized, multicenter study in 11 centers in Japan. A total of 164 patients were randomized to receive either 4 mg/d of pitavastatin (intensive lipid-lowering therapy) or 20 mg/d of pravastatin (moderate lipid-lowering therapy). Analyzable intravascular ultrasound data were obtained for 119 patients at baseline and at 8-month follow-up. The primary end point was the difference of volume changes in each of the 4 main plaque components (fibrosis, fibrofatty, calcium, and necrosis), assessed by virtual histology intravascular ultrasound, between the 2 groups. RESULTS: The mean low-density lipoprotein cholesterol level at follow-up was significantly lower in the pitavastatin than in the pravastatin group (74 vs 95 mg/dL, P < .0001). During the 8-month follow-up period, statin therapy reduced the absolute and relative amount of fibrofatty component (pitavastatin: from 1.09 to 0.81 mm(3)/mm, P = .001; pravastatin: from 1.05 to 0.83 mm(3)/mm, P = .0008) and increased in the amount of calcium (pitavastatin: from 0.42 to 0.55 mm(3)/mm, P < .0001; pravastatin: from 0.44 to 0.55 mm(3)/mm, P = .005), whereas volume changes in both plaque components were not statistically different between the 2 groups. CONCLUSIONS: Both pitavastatin and pravastatin altered coronary artery plaque composition by significantly decreasing the fibrofatty plaque component and increasing the calcified plaque component.