Symptomatic atherosclerotic plaque progression in a first-generation carotid stent—case report: Management and 5-year clinical and imaging outcome

Abstract Background Restenosis in first-generation (single-layer, nitinol) carotid stents (FGS) is believed to represent an exaggerated healing response of (neo)intimal hyperplasia (NIH) formation. Rather than NIH, we describe symptomatic in-FGS unstable plaque (neo)atherosclerosis mandating re-revascularization. To halt continued plaque evolution, we propose a novel treatment strategy involving a micronet-covered stent to sequestrate the plaque from the vessel lumen. A durable long-term result is documented using multi-modal imaging. Case summary With a seemingly optimal result of FGS (Precise) symptomatic carotid lesion revascularization followed by optimal medical therapy, a late (≥3 years) progressive ISR arose. At year 11, crescendo ipsilateral transient ischaemic attacks occurred. Angiography showed an ulcerated tight lesion throughout stent length. Intravascular ultrasound (IVUS) revealed thin-cap fibroatheroma. Re-intervention was performed under distal protection. Undersized balloon predilatation caused symptomatic no-flow, and aspiration catheter was used to reduce the filter load. A micronet-covered stent (CGuard) was implanted and post-dilated to ensure full lumen gain; IVUS confirmed complete plaque sequestration. The optimal anatomic result remained unchanged throughout 5 years (ultrasound and computed tomography verification); this was accompanied by clinical cure. Discussion This is the first demonstration of in-FGS (neo)atherosclerosis resolution using a micronet-covered stent to sequestrate and insulate the atherosclerotic plaque. We show that ISR may be underlined by late atherosclerotic plaque progression via the FGS single-layer stent struts that may show vulnerable plaque phenotype and may be associated with cerebral ischaemia. The anatomically and clinically effective exclusion of the atherosclerotic plaque by a micronet-covered stent enabled lasting, optimal endovascular reconstruction and clinical cure.

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When Coadministration Cannot Be Avoided: Real World Experience of Direct Acting Antivirals for the Treatment of Hepatitis C Virus Infection in Patients on First Generation Anticonvulsants

Journal of Pharmacy Practice ◽

10.1177/0897190020977762 ◽

2020 ◽

pp. 089719002097776

Author(s):

Kayla M. Natali ◽

Humberto R. Jimenez ◽

Jihad Slim

Keyword(s):

Drug Interaction ◽

Hepatitis C ◽

Clinical Cure ◽

First Generation ◽

Virologic Response ◽

Hcv Infection ◽

Direct Acting Antivirals ◽

Chronic Hcv Infection ◽

Chronic Hcv ◽

Direct Acting

Background Coadministration of direct-acting antivirals (DAAs) for chronic hepatitis C virus (HCV) infection and first generation anticonvulsants is currently not recommended due to a drug-drug interaction that could potentially lead to subtherapeutic DAA levels and subsequent treatment failure. Currently, there is limited data evaluating this interaction and timely treatment of HCV infection with DAAs is imperative to prevent liver-related morbidity and mortality. Methods A retrospective case series evaluating clinical cure of chronic HCV infection, defined as sustained virologic response (SVR) 12 weeks after completion of DAA therapy, in patients from three inner-city clinics who remained on first generation anticonvulsants during the treatment course. Results A total of five patients received standard dose DAAs for treatment of chronic HCV infection while being maintained on first generation anticonvulsants. The most common HCV genotype was 1a (80%), followed by 1b (20%). The majority of patients were treated with glecaprevir/pibrentasvir (80%) for eight weeks and one patient was treated with ledipasvir/sofosbuvir for 12 weeks. Anticonvulsant regimens consisted of carbamazepine, phenytoin, phenytoin plus phenobarbital, phenytoin plus levetiracetam, and phenobarbital plus lacosamide. All five patients achieved sustained virologic response (SVR) despite this drug-drug interaction. Conclusion Although every effort to prevent concomitant use of DAAs and potent inducers should be made, clinical cure may still be achieved in patients whom cannot avoid this coadministration.

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Therapies Targeted at Non-Coding RNAs in Prevention and Limitation of Myocardial Infarction and Subsequent Cardiac Remodeling—Current Experience and Perspectives

International Journal of Molecular Sciences ◽

10.3390/ijms22115718 ◽

2021 ◽

Vol 22 (11) ◽

pp. 5718

Author(s):

Michal Kowara ◽

Sonia Borodzicz-Jazdzyk ◽

Karolina Rybak ◽

Maciej Kubik ◽

Agnieszka Cudnoch-Jedrzejewska

Keyword(s):

Myocardial Infarction ◽

Atherosclerotic Plaque ◽

Cardiac Remodeling ◽

Therapeutic Option ◽

Circular Rna ◽

Plaque Progression ◽

Cardiac Damage ◽

Non Coding Rna ◽

Causes Of Mortality ◽

Long Non Coding Rna

Myocardial infarction is one of the major causes of mortality worldwide and is a main cause of heart failure. This disease appears as a final point of atherosclerotic plaque progression, destabilization, and rupture. As a consequence of cardiomyocytes death during the infarction, the heart undergoes unfavorable cardiac remodeling, which results in its failure. Therefore, therapies aimed to limit the processes of atherosclerotic plaque progression, cardiac damage during the infarction, and subsequent remodeling are urgently warranted. A hopeful therapeutic option for the future medicine is targeting and regulating non-coding RNA (ncRNA), like microRNA, circular RNA (circRNA), or long non-coding RNA (lncRNA). In this review, the approaches targeted at ncRNAs participating in the aforementioned pathophysiological processes involved in myocardial infarction and their outcomes in preclinical studies have been concisely presented.

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Non-invasive Serial Monitoring of Atherosclerotic Plaque Progression and Thrombosis with PET-CT in a Rabbit Model

The American Journal of Cardiology ◽

10.1016/j.amjcard.2013.01.353 ◽

2013 ◽

Vol 111 (7) ◽

pp. 13B

Author(s):

Zhang Ming Duo ◽

Zhao Quan Ming

Keyword(s):

Atherosclerotic Plaque ◽

Rabbit Model ◽

Plaque Progression ◽

Non Invasive ◽

Pet Ct

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Temporal and spatial changes in wall shear stress during atherosclerotic plaque progression in mice

Royal Society Open Science ◽

10.1098/rsos.171447 ◽

2018 ◽

Vol 5 (3) ◽

pp. 171447 ◽

Cited By ~ 5

Author(s):

R. Xing ◽

A. M. Moerman ◽

Y. Ridwan ◽

M. J. Daemen ◽

A. F. W. van der Steen ◽

...

Keyword(s):

Shear Stress ◽

Wall Shear Stress ◽

Mouse Model ◽

Atherosclerotic Plaque ◽

Proximal Part ◽

Plaque Progression ◽

Plaque Composition ◽

Spatial Changes ◽

Temporal And Spatial ◽

Wall Shear

Wall shear stress (WSS) is involved in atherosclerotic plaque initiation, yet its role in plaque progression remains unclear. We aimed to study (i) the temporal and spatial changes in WSS over a growing plaque and (ii) the correlation between WSS and plaque composition, using animal-specific data in an atherosclerotic mouse model. Tapered casts were placed around the right common carotid arteries (RCCA) of ApoE −/− mice. At 5, 7 and 9 weeks after cast placement, RCCA geometry was reconstructed using contrast-enhanced micro-CT. Lumen narrowing was observed in all mice, indicating the progression of a lumen intruding plaque. Next, we determined the flow rate in the RCCA of each mouse using Doppler Ultrasound and computed WSS at all time points. Over time, as the plaque developed and further intruded into the lumen, absolute WSS significantly decreased. Finally at week 9, plaque composition was histologically characterized. The proximal part of the plaque was small and eccentric, exposed to relatively lower WSS. Close to the cast a larger and concentric plaque was present, exposed to relatively higher WSS. Lower WSS was significantly correlated to the accumulation of macrophages in the eccentric plaque. When pooling data of all animals, correlation between WSS and plaque composition was weak and no longer statistically significant. In conclusion, our data showed that in our mouse model absolute WSS strikingly decreased during disease progression, which was significantly correlated to plaque area and macrophage content. Besides, our study demonstrates the necessity to analyse individual animals and plaques when studying correlations between WSS and plaque composition.

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