Association of White Matter Hyperintensities and Cardiovascular Disease

Abstract

Cardiac and cerebrovascular diseases are currently the leading causes of mortality and disability worldwide. Both the heart and brain display similar vascular anatomy, with large conduit arteries running on the surface of the organ providing tissue perfusion through an intricate network of penetrating small vessels. Both organs rely on fine tuning of local blood flow to match metabolic demand. Blood flow regulation requires adequate functioning of the microcirculation in both organs, with loss of microvascular function, termed small vessel disease (SVD) underlying different potential clinical manifestations. SVD in the heart, known as coronary microvascular dysfunction, can cause chronic or acute myocardial ischemia and may lead to development of heart failure. In the brain, cerebral SVD can cause an acute stroke syndrome known as lacunar stroke or more subtle pathological alterations of the brain parenchyma, which may eventually lead to neurological deficits or cognitive decline in the long term. Coronary microcirculation cannot be visualized in vivo in humans, and functional information can be deduced by measuring the coronary flow reserve. The diagnosis of cerebral SVD is largely based on brain magnetic resonance imaging, with white matter hyperintensities, microbleeds, and brain atrophy reflecting key structural changes. There is evidence that such structural changes reflect underlying cerebral SVD. Here, we review interactions between SVD and cardiovascular risk factors, and we discuss the evidence linking cerebral SVD with large vessel atheroma, atrial fibrillation, heart failure, and heart valve disease.

Meta-analysis of the correlation between serum uric acid level and carotid intima-media thickness

“…Both the heart and brain exhibit similar vascular anatomy, with large ductal arteries extending from the surface of the organs and providing tissue perfusion through a complex network of small vessels. Both organs rely on fine-tuning of local blood flow to meet metabolic demands [7]. Atherosclerosis is the common pathological basis of cardiovascular and cerebrovascular diseases, and there is a strong correlation between carotid atherosclerosis and cardiovascular and cerebrovascular diseases.…”

Detecting Small Vessel Pathology in Cocaine Use Disorder

“…It is also conceivable that blood pressure in CUD patients may only temporarily be raised due to the acute effects of the drug, but not persistently, which may be why their blood pressure levels were normal at the time of the assessment. It is also of note that previous studies on microbleeds often recruited older participants with higher baseline measures of cardiovascular health, or focused on populations with vascular disease ( Frey et al, 2019 ; Moroni et al, 2020 ). However, we cannot rule out that other cardiovascular risk factors such as 24 h systolic blood pressure ( Abraham et al, 2016 ), levels of fasting glucose ( Park et al, 2007 ) or blood lipids ( Jimenez-Conde et al, 2010 ), which were not assessed in the present study, might have influenced lesion volume.…”

Altered microstructural pattern of white matter in Cushing’s disease identified by automated fiber quantification

“…It was also noteworthy that increased cardiovascular risk factors, including hypertension, hyperglycemia, and dyslipidemia, caused by elevated concentration of cortisol in patients with Cushing’s disease were also considered to be critical contributors to the white matter lesions ( Santos et al, 2015 , Williamson et al, 2018 ). Cardiovascular risk factors would result in loss of microvascular function with disordered cerebral hemodynamic, termed small vessel disease, and lead to ischemia and blood–brain barrier dysfunction which would further induce activated microglia, oligodendroglia apoptosis, clasmatodendritic astrocytosis and impair the white matter structure ( Black et al, 2009 , Moroni et al, 2020 ). Moreover, neurovascular decoupling following small vessel disease would fail to maintain the homeostasis of the cerebral microenvironment by compromising energy utilization and promoting aggregation of neurotoxic metabolites, such as amyloid-β peptide and tau protein ( Iadecola, 2017 ), subsequently inducing chronic brain damage in vulnerable tracts associated with neuropsychological deficits.…”