title: Silent myocardial ischemia in patients with symptomatic intracranial atherosclerosis: associated factors.
abstract: OBJECTIVE
  Optimization of coronary risk evaluation in stroke patients has been encouraged. The relationship between symptomatic intracranial atherosclerosis and occult coronary artery disease (CAD) has not been evaluated sufficiently. We aimed to investigate the prevalence of silent myocardial ischemia in patients with symptomatic intracranial atherosclerosis and to identify factors associated with its presence.
  
  
  METHODS
  From 186 first-ever transient ischemic attack or ischemic stroke patients with intracranial stenoses, 65 fulfilled selection criteria, including angiographic confirmation of a symptomatic atherosclerotic stenosis and absence of known CAD. All patients underwent a maximal-stress myocardial perfusion single-photon emission computed tomography (SPECT). Lipoprotein(a) [Lp(a)], C-reactive protein, and homocysteine (Hcy) levels were determined before SPECT.
  
  
  RESULTS
  Stress-rest SPECT detected reversible myocardial perfusion defects in 34 (52%) patients. Vascular risk factors associated with a pathologic SPECT were hypercholesterolemia (P=0.045), presence of >2 risk factors (P=0.004) and high Lp(a) (P=0.023) and Hcy levels (P=0.018). Ninety percent of patients with high Lp(a) and Hcy levels had a positive SPECT. Existence of a stenosed intracranial internal carotid artery (ICA; odds ratio [OR], 7.22, 2.07 to 25.23; P=0.002) and location of the symptomatic stenosis in vertebrobasilar arteries (OR, 4.89, 1.19 to 20.12; P=0.027) were independently associated with silent myocardial ischemia after adjustment by age, sex, and risk factors.
  
  
  CONCLUSIONS
  More than 50% of the patients with symptomatic intracranial atherosclerosis and not overt CAD show myocardial perfusion defects on stress-rest SPECT. Stenosed intracranial ICA, symptomatic vertebrobasilar stenosis and presence of high Lp(a) and Hcy levels may characterize the patients at a higher risk for occult CAD.
authors.affiliation: Department of Neurology, Vall d'Hebron Universitary Hospital, Passeig Vall d'Hebron 119-129, 08035 Barcelona, Spain. juanfarenillas@terra.es
authors.forename: Juan F
authors.initials: JF
authors.lastname: Arenillas
authors.forename: Jaume
authors.initials: J
authors.lastname: Candell-Riera
authors.forename: Guillermo
authors.initials: G
authors.lastname: Romero-Farina
authors.forename: Carlos A
authors.initials: CA
authors.lastname: Molina
authors.forename: Pilar
authors.initials: P
authors.lastname: Chacón
authors.forename: Santiago
authors.initials: S
authors.lastname: Aguadé-Bruix
authors.forename: Joan
authors.initials: J
authors.lastname: Montaner
authors.forename: Gustavo
authors.initials: G
authors.lastname: de León
authors.forename: Joan
authors.initials: J
authors.lastname: Castell-Conesa
authors.forename: José
authors.initials: J
authors.lastname: Alvarez-Sabín
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000096:biosynthesis; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000473:pathology; D005080:Exercise Test; D005260:Female; D006710:Homocysteine / Q000097:blood; D006801:Humans; D002537:Intracranial Arteriosclerosis / Q000150:complications* / Q000175:diagnosis*; D017270:Lipoprotein(a) / Q000097:blood; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000175:diagnosis* / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D016017:Odds Ratio; D010477:Perfusion; D011877:Radionuclide Imaging; D012307:Risk Factors; D017256:Technetium Tc 99m Sestamibi / Q000494:pharmacology; D015899:Tomography, Emission-Computed, Single-Photon
chemical_list: D017270:Lipoprotein(a); D006710:Homocysteine; D002097:C-Reactive Protein; D017256:Technetium Tc 99m Sestamibi