Microvascular arterial disease of the brain and the heart: a shared pathogenesis

Abstract

Microvascular arterial disease in the heart manifest as coronary microvascular dysfunction. This condition causes microvascular angina and is associated increased morbidity and mortality. Microvascular arterial disease in the brain is referred to as cerebrovascular small vessel disease. This is responsible for 45% of dementias and 25% of ischaemic strokes. The heart and brain share similar vascular anatomy and common pathogenic risk factors are associated with the development of both coronary microvascular dysfunction and cerebrovascular small vessel disease. Microvascular disease in the heart and brain also appear to share common multisystem pathophysiological mechanisms. Further studies on diagnostic approaches, epidemiology and development of disease-modifying therapy seem warranted.

Figure 1.

Two clinical cases with angina and ‘heart-brain’ imaging. Top: Normal heart and brain MRI scans. A 42-year-old man with a history of multiple hospital attendances for chest pain underwent coronary angiography for investigation of coronary artery disease. The angiogram was normal. He then gave informed consent to take part in the CorCMR clinical trial. (A) Pharmacological stress imaging during intravenous infusion of adenosine, a drug which causes tachycardia and vasodilatation and an increase in blood flow in the heart. The images are calibrated hence absolute blood flow can be quantified in ml/min/g tissue, within the whole heart or in segments. In this case, there is normal augmentation of blood flow (bright orange, arrow) and no perfusion defects (i.e. no residual blue colour). (B) Cardiac MRI reveals normal myocardial blood flow at rest (uniform dark blue, arrow). (C) Normal MRI brain scan, axial T2 turbo spin echo scan, with no evidence of small vessel disease. Bottom: Small vessel disease in the heart and brain. A 59-year-old woman with a history of chest pain underwent coronary angiography for the investigation of coronary artery disease. The angiogram was normal. She then gave informed consent to take part in the CorCMR clinical trial. (A) Pharmacological stress MRI was undertaken to assess the capacity for blood flow augmentation achieved by infusion of intravenous adenosine which stimulates tachycardia and vasodilatation. The scan revealed a circumferential subendocardial perfusion defect (dark blue, arrow) that contrasts with the hyperaemia (bright orange) elsewhere in the heart. This feature is diagnostic of microvascular dysfunction within the sub-endocardium, supporting a clinical diagnosis of microvascular angina. (B) Cardiac MRI reveals normal blood flow at rest (upper panel—dark blue, arrow). (C) Brain MRI showing extensive periventricular and subcortical high T2-weighted white matter signal change (examples shown by blue arrows) in keeping with small vessel ischaemic damage. Furthermore, prominent cerebrospinal fluid (CSF) spaces in keeping with brain volume loss (atrophy) for age were noted. In summary, this patient has microvascular angina and brain imaging features of small vessel disease and early atrophy that portend a future risk of stroke and vascular dementia.