Stavros K Kakkos1, Andrew N Nicolaides2, Ioanna Charalambous3, Dafydd Thomas4, Argyrios Giannopoulos1, A Ross Naylor5, George Geroulakos6, Anne L Abbott7. 1. Department of Vascular Surgery, Imperial College, London, United Kingdom. 2. Department of Vascular Surgery, Imperial College, London, United Kingdom. Electronic address: anicolaides1@gmail.com. 3. Vascular Screening and Diagnostic Center, Nicosia, Cyprus. 4. Department of Neurology, St. Mary's Hospital, London, United Kingdom. 5. Department of Vascular Surgery, Leicester Royal Infirmary, Leicester, United Kingdom. 6. Department of Vascular Surgery, Imperial College, London, United Kingdom; Department of Vascular Surgery, Ealing Hospital, London, United Kingdom. 7. School of Public Health and Preventive Medicine, Monash University, Melbourne, Australia; Preventive Health Division of Baker IDI Heart and Diabetes Institute, Melbourne, Australia; Stroke Division of the Florey Institute of Neuroscience and Mental Health, Melbourne, Australia.
Abstract
OBJECTIVE: To determine baseline clinical and ultrasonographic plaque factors predictive of progression or regression of asymptomatic carotid stenosis and the predictive value of changes in stenosis severity on risk of first ipsilateral cerebral or retinal ischemic events (including stroke). METHODS: A total of 1121 patients with asymptomatic carotid stenosis of 50% to 99% in relation to the bulb diameter (European Carotid Surgery Trial [ECST] method) underwent six monthly clinical assessments and carotid duplexes for up to 8 years (mean follow-up, 4 years). Progression or regression was considered present if there was a change of at least one grade higher or lower, respectively, persisting for at least two consecutive examinations. RESULTS: Regression occurred in 43 (3.8%), no change in 856 (76.4%), and progression in 222 (19.8%) patients. Younger age, high grades of stenosis, absence of discrete white areas in the plaque, and taking lipid lowering therapy were independent baseline predictors of increased incidence of regression. High serum creatinine, male gender, not taking lipid lowering therapy, low grades of stenosis, and increased plaque area were independent baseline predictors of progression. One hundred and thirty first ipsilateral cerebral or retinal ischemic events, including 59 strokes, occurred. Forty (67.8%) of the strokes occurred in patients whose stenosis was unchanged, 19 (32.2%) in those with progression, and zero in those with regression. For the entire cohort, the 8-year cumulative ipsilateral cerebral ischemic stroke rate was zero in patients with regression, 9% if the stenosis was unchanged, and 16% if there was progression (average annual stroke rates of 0%, 1.1%, and 2.0%, respectively; log-rank, P = .05; relative risk in patients with progression, 1.92; 95% confidence interval, 1.14-3.25). For patients with baseline stenosis 70% to 99% in relation to the distal internal carotid (North American Symptomatic Carotid Endarterectomy Trial [NASCET] method), in the absence of progression (n = 349), the 8-year cumulative ipsilateral cerebral ischemic stroke rate was 12%. In the presence of progression (n = 77), it was 21% (average annual stroke rates of 1.5% and 2.6%, respectively; log-rank, P = .34). Only nine (30%) of the 30 strokes occurred in the progression group. CONCLUSIONS: Progressive asymptomatic carotid stenosis identified a subgroup with about twice the risk of ipsilateral stroke compared with those without progression. However, the clinical value of screening for progression simply for selecting patients for carotid procedures is limited because of the low frequency of progression and its relatively low associated stroke rate. The cost effectiveness of screening for change in stenosis severity to better direct current optimal medical treatment needs testing.
OBJECTIVE: To determine baseline clinical and ultrasonographic plaque factors predictive of progression or regression of asymptomatic carotid stenosis and the predictive value of changes in stenosis severity on risk of first ipsilateral cerebral or retinal ischemic events (including stroke). METHODS: A total of 1121 patients with asymptomatic carotid stenosis of 50% to 99% in relation to the bulb diameter (European Carotid Surgery Trial [ECST] method) underwent six monthly clinical assessments and carotid duplexes for up to 8 years (mean follow-up, 4 years). Progression or regression was considered present if there was a change of at least one grade higher or lower, respectively, persisting for at least two consecutive examinations. RESULTS: Regression occurred in 43 (3.8%), no change in 856 (76.4%), and progression in 222 (19.8%) patients. Younger age, high grades of stenosis, absence of discrete white areas in the plaque, and taking lipid lowering therapy were independent baseline predictors of increased incidence of regression. High serum creatinine, male gender, not taking lipid lowering therapy, low grades of stenosis, and increased plaque area were independent baseline predictors of progression. One hundred and thirty first ipsilateral cerebral or retinal ischemic events, including 59 strokes, occurred. Forty (67.8%) of the strokes occurred in patients whose stenosis was unchanged, 19 (32.2%) in those with progression, and zero in those with regression. For the entire cohort, the 8-year cumulative ipsilateral cerebral ischemic stroke rate was zero in patients with regression, 9% if the stenosis was unchanged, and 16% if there was progression (average annual stroke rates of 0%, 1.1%, and 2.0%, respectively; log-rank, P = .05; relative risk in patients with progression, 1.92; 95% confidence interval, 1.14-3.25). For patients with baseline stenosis 70% to 99% in relation to the distal internal carotid (North American Symptomatic Carotid Endarterectomy Trial [NASCET] method), in the absence of progression (n = 349), the 8-year cumulative ipsilateral cerebral ischemic stroke rate was 12%. In the presence of progression (n = 77), it was 21% (average annual stroke rates of 1.5% and 2.6%, respectively; log-rank, P = .34). Only nine (30%) of the 30 strokes occurred in the progression group. CONCLUSIONS: Progressive asymptomatic carotid stenosis identified a subgroup with about twice the risk of ipsilateral stroke compared with those without progression. However, the clinical value of screening for progression simply for selecting patients for carotid procedures is limited because of the low frequency of progression and its relatively low associated stroke rate. The cost effectiveness of screening for change in stenosis severity to better direct current optimal medical treatment needs testing.
Authors: Robert J Dempsey; Tomy Varghese; Daren C Jackson; Xiao Wang; Nirvedh H Meshram; Carol C Mitchell; Bruce P Hermann; Sterling C Johnson; Sara E Berman; Stephanie M Wilbrand Journal: J Neurosurg Date: 2017-03-10 Impact factor: 5.115
Authors: Leo H Bonati; Stavros Kakkos; Joachim Berkefeld; Gert J de Borst; Richard Bulbulia; Alison Halliday; Isabelle van Herzeele; Igor Koncar; Dominick Jh McCabe; Avtar Lal; Jean-Baptiste Ricco; Peter Ringleb; Martin Taylor-Rowan; Hans-Henning Eckstein Journal: Eur Stroke J Date: 2021-05-11
Authors: Joseph Kamtchum-Tatuene; Luca Saba; Mirjam R Heldner; Michiel H F Poorthuis; Gert J de Borst; Tatjana Rundek; Stavros K Kakkos; Seemant Chaturvedi; Raffi Topakian; Joseph F Polak; Glen C Jickling Journal: Circ Res Date: 2022-06-17 Impact factor: 23.213
Authors: Kosmas I Paraskevas; Dimitri P Mikhailidis; Hediyeh Baradaran; Alun H Davies; Hans-Henning Eckstein; Gianluca Faggioli; Jose Fernandes E Fernandes; Ajay Gupta; Mateja K Jezovnik; Stavros K Kakkos; Niki Katsiki; M Eline Kooi; Gaetano Lanza; Christos D Liapis; Ian M Loftus; Antoine Millon; Andrew N Nicolaides; Pavel Poredos; Rodolfo Pini; Jean-Baptiste Ricco; Tatjana Rundek; Luca Saba; Francesco Spinelli; Francesco Stilo; Sherif Sultan; Clark J Zeebregts; Seemant Chaturvedi Journal: J Stroke Date: 2021-05-31 Impact factor: 6.967