Search

Aim: According to recent clinical trials, a combination of direct oral anticoagulants with antiplatelet drugs is often recommended for atrial fibrillation patients who receive drug-eluting stents (DESs). Although the optimal combination comprises direct factor Xa inhibitors and a P2Y 12 receptor antagonist (or aspirin), their influence on vascular responses to DESs remains unclear., Methods: Pigs were given either aspirin and clopidogrel (dual antiplatelet therapy [DAPT] group), aspirin and rivaroxaban (AR group), or clopidogrel and rivaroxaban (CR group), followed by everolimus-eluting stent (Promus Element) implantation into the coronary artery. Stented coronary arteries were evaluated via intravascular optical coherence tomography (OCT) and histological analysis at 1 and 3 months., Results: OCT revealed lower neointimal thickness in the DAPT group and comparable thickness among all groups at 1 and 3 months, respectively. Histological analyses revealed comparable neointimal area among all groups and the smallest neointimal area in the CR group at 1 and 3 months, respectively. In the DAPT and AR groups, the neointima continued to grow from 1 to 3 months. A shortened time course for neointima growth was observed in the CR group, with rapid growth within a month (maintained for 3 months). A higher incidence of in-stent thrombi was observed in the AR group at 1 month; no thrombi were found in either group at 3 months. More smooth muscle cells with contractile features were found in the CR group at both 1 and 3 months., Conclusions: Our results proved the noninferiority of the combination of rivaroxaban with an antiplatelet drug, particularly the dual therapy using rivaroxaban and clopidogrel, compared to DAPT after DES implantation.

Dipeptidyl peptidase-4 (DPP-4) inhibitors have potential as a treatment for atherosclerosis. However, it is unclear whether DPP-4 inhibitors stabilize atherosclerotic plaque or alter the composition of complex plaque. Sixteen Watanabe heritable hyperlipidemic rabbits aged 10-12 weeks with atherosclerotic plaque in the brachiocephalic artery detected by iMap ™ intravascular ultrasound (IVUS) were divided into a DPP-4 inhibitor group and a control group. Linagliptin was administered to the DPP-4 inhibitor group via nasogastric tube at a dose of 10 mg/kg/day for 16 weeks, and control rabbits received the same volume of 0.5% hydroxyethylcellulose. After evaluation by IVUS at 16 weeks, the brachiocephalic arteries were harvested for pathological examination. IVUS revealed that linagliptin significantly reduced the plaque volume and vessel volume (control group vs. DPP-4 inhibitor group: ∆plaque volume, 1.02 ± 0.96 mm 3 vs.  - 3.59 ± 0.92 mm 3 , P = 0.004; ∆vessel volume,  - 1.22 ± 2.36 mm 3 vs.  - 8.66 ± 2.33 mm 3 , P = 0.04; %change in plaque volume, 6.90 ± 5.62% vs.  - 15.06 ± 3.29%, P = 0.005). With regard to plaque composition, linagliptin significantly reduced the volume of fibrotic, lipidic, and necrotic plaque (control group vs. DPP-4 inhibitor group: ∆fibrotic volume, 0.56 ± 1.27 mm 3 vs.  - 5.57 ± 1.46 mm 3 , P = 0.04; ∆lipidic volume, 0.24 ± 0.24 mm 3 vs.  - 0.42 ± 0.16 mm 3 P = 0.04; ∆necrotic volume, 0.76 ± 0.54 mm 3 vs.  - 0.84 ± 0.25 mm 3 , P = 0.02). Pathological examination did not show any significant differences in the %smooth muscle cell area or %fibrotic area, but infiltration of macrophages into plaque was reduced by linagliptin treatment (%macrophage area: 12.03% ± 1.51% vs. 7.21 ± 1.65%, P < 0.05). These findings indicate that linagliptin inhibited plaque growth and stabilized plaque in Watanabe heritable hyperlipidemic rabbits.

We report an autopsy case of a coronary aneurysm with massive adventitial inflammation post-percutaneous coronary intervention with sirolimus-eluting stent (SES) insertion in the left circumflex (LCX) coronary artery for ischemic heart disease 3 years prior to death. The internal elastic membrane was disrupted opposite the site of the eccentric LCX plaque due to injury during stenting, and the adventitia showed massive inflammatory cell infiltration, mainly consisting of eosinophils. The LCX showed aneurysmal dilatation with inflammatory cell infiltration. Inappropriate SES implantation attracted chronic inflammation. Chronic inflammation can lead to the development of coronary artery aneurysms.

Patients with atrial fibrillation (AF) are at risk of cardioembolism.(1,2)) Atrial thrombus formation associated with AF typically occurs in the left atrial appendage (LAA);(3)) therefore, transesophageal echocardiography (TEE) is important for detection of such a thrombus and measurement of LAA flow velocity.(4,5)) LAA closure is routinely performed during mitral valve surgery in patients with AF to prevent cardiogenic stroke.(6)) We report the case of a 65-year-old woman with severe mitral regurgitation (MR) and AF in whom a giant thrombus formed almost immediately after mitral and tricuspid valvuloplasty and concurrent LAA resection. No atrial thrombus or spontaneous echo contrast (SEC) was detected by TEE before the surgery. However, a giant intramural thrombus was detected in the left atrium 7 days after surgery. It was thought that the atrial dysfunction as well as the change in morphology of the left atrium resulting from the severe MR complicated by AF and congestive heart failure produced a thrombotic substrate. This case suggests that careful surveillance for thrombus formation and careful maintenance of anticoagulation therapy are needed throughout the perioperative period even if no SEC or thrombus is detected before surgery.