ABSTRACT
BACKGROUND: Familial hypercholesterolemia (FH) is a genetic disorder, causing an increased risk of coronary heart disease (CHD) if untreated. Silent brain infarctions and white matter hyperintensities (WMHIs) observed on T2-weighted magnetic resonance images (MRI) are associated with increased risk for stroke and myocardial infarction. Age is a strong predictor of WMHIs. PURPOSE: To use MRI to assess the presence of clinically silent brain lesions in older FH patients, and to compare the occurrence and size of these lesions in older FH patients with middle-aged FH patients and healthy controls. MATERIAL AND METHODS: A total of 43 older (age >or= 65 years) FH patients with the same FH North Karelia mutation, living in Finland, were identified. In this comprehensive cohort, 1.5 T brain MRI was available for 33 individuals (age 65-84 years, M/F 9/24, mean duration of statin treatment 15.3 years). This group was divided into two age categories: 65-74 years (FHe1 group, n=23) and 75-84 years (FHe2 group, n=10). Infarcts, including lacunas, and WMHIs on T2-weighted images were recorded. Data from brain MRI were compared to those of a group of middle-aged FH patients with CHD (n=19, age 48-64 years) and with middle-aged healthy controls (n=29, age 49-63 years). RESULTS: Only two (6%) of the older FH patients had clinically silent brain infarcts detected by MRI. The amount of large WMHIs (>5 mm in diameter) was similar in the FHe1 group compared with the groups of middle-aged FH patients and healthy controls, even though the FHe1 group was 13 years older. The total amount of WMHIs and the amount of large WMHIs were greatest in the FHe2 group. CONCLUSION: FH patients aged 65 to 74 years receiving long-term statin treatment (15 years) did not have more WMHIs on brain MRI compared to middle-aged FH patients and healthy controls.
Subject(s)
Cerebral Infarction/diagnosis , Hyperlipoproteinemia Type II/diagnosis , Hyperlipoproteinemia Type II/genetics , Image Processing, Computer-Assisted , Magnetic Resonance Imaging , Age Factors , Aged , Aged, 80 and over , Brain/pathology , Cohort Studies , Cross-Sectional Studies , Female , Genetic Carrier Screening , Humans , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Hyperlipoproteinemia Type II/drug therapy , Male , Middle Aged , Receptors, LDL/genetics , Reference ValuesABSTRACT
BACKGROUND: Clinically silent brain lesions detected with magnetic resonance imaging (MRI) are associated with increased risk for stroke, while stroke risk is controversial in familial hypercholesterolemia (FH). PURPOSE: To determine whether the occurrence and size of clinically silent brain lesions in FH patients with coronary heart disease (CHD) is higher than in neurologically healthy controls without CHD. MATERIAL AND METHODS: Brain MRI (1.5T) was performed on 19 DNA-test-verified FH patients with CHD and on 29 cardiovascularly and neurologically healthy controls, all aged 48 to 64 years. All patients were on cardiovascular medication. Intracranial arteries were evaluated by MR angiography. Infarcts, including lacunas, and white matter T2 hyperintensities (WMHI), considered as signs of small vessel disease, were recorded. A venous blood sample was obtained for assessment of risk factors. Carotid and femoral intima-media thicknesses (IMT), assessed with ultrasound, were indicators of overall atherosclerosis. RESULTS: On intracranial MR angiography, three patients showed irregular walls or narrowed lumens in intracranial carotid arteries. No silent infarcts appeared, and no differences in numbers or sizes of WMHIs between groups were recorded. Patients had greater carotid and femoral IMTs, and a greater number of carotid and femoral plaques. Cholesterol-years score, level of low-density lipoprotein (LDL) cholesterol, and level of high-sensitivity C-reactive protein (hsCRP) of the FH-North Karelia patients were higher than those of the controls, while the level of high-density lipoprotein (HDL) cholesterol in controls was higher. CONCLUSION: FH patients with CHD and adequate cardiovascular risk-factor treatment showed no difference in the amount or size of clinically silent brain lesions compared to controls, despite patients' more severe atherosclerosis.
Subject(s)
Atherosclerosis/complications , Cerebrovascular Disorders/diagnosis , Cerebrovascular Disorders/etiology , Coronary Disease/complications , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Hyperlipoproteinemia Type II/complications , Hyperlipoproteinemia Type II/drug therapy , Aged , Carotid Arteries/diagnostic imaging , Carotid Arteries/pathology , Carotid Stenosis/diagnosis , Carotid Stenosis/diagnostic imaging , Cerebral Arteries/diagnostic imaging , Cerebral Veins/diagnostic imaging , Female , Humans , Magnetic Resonance Angiography , Magnetic Resonance Imaging , Male , Middle Aged , Risk Factors , UltrasonographyABSTRACT
Myopericarditis is a rare extraintestinal complication of inflammatory bowel disease (IBD). It has also been described as a side-effect of the treatment of IBD. We report a 37-year-old-woman with Crohn's disease who had several mild episodes of myopericarditis, two of which were associated with a pleural effusion, and two with conduction abnormalities in the atrioventricular node. During the last episode, a nodal rhythm was followed by a third-degree atrioventricular block and a prolonged pause, resulting in loss of consciousness and convulsions. A permanent pacemaker was implanted. Our patient is also human lymphocyte antigen (HLA) B27-positive. HLA B27 is known to be associated with conduction disturbances in the AV node. Recurrent myopericarditis can be a sign of IBD.
