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Published on: April 25, 2014
Myocardial perfusion in cardiac amyloidosis
Liza Chacko1,2, Tushar Kotecha1,2, Adam Ioannou1,2
1National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.
Insights
Cardiac amyloidosis causes severe myocardial ischemia, impacting clinical outcomes. Cardiovascular magnetic resonance (CMR) and histology reveal reduced blood flow and capillary damage, highlighting complex pathophysiology.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Pathology
Background:
- Cardiac involvement is a primary determinant of outcomes in systemic amyloidosis.
- Myocardial ischemia is hypothesized to contribute to cellular damage in cardiac amyloidosis.
Purpose of the Study:
- To assess the presence and mechanisms of myocardial ischemia in cardiac amyloidosis.
- Utilize cardiovascular magnetic resonance (CMR) with multiparametric mapping and histopathological assessment.
Main Methods:
- Quantitative stress perfusion CMR with myocardial blood flow (MBF) mapping in 93 cardiac amyloidosis patients and 97 controls.
- Histopathological analysis of 24 myocardial biopsies and 3 explanted hearts from patients with cardiac amyloidosis.
Main Results:
- Patients with cardiac amyloidosis exhibited severely reduced stress MBF compared to controls (1.04 ± 0.51 ml/min/g).
- Myocardial perfusion abnormalities correlated with amyloid burden, cardiac function, and biomarkers.
- Histology revealed amyloid infiltration in arteries, reduced capillary density, and abnormal vascular endothelial growth factor staining.
Conclusions:
- Cardiac amyloidosis is linked to severe inducible myocardial ischemia, detectable by CMR and histology.
- Pathophysiology involves amyloid infiltration of arteries, capillary rarefaction, and disruption, alongside cardiac dysfunction.
Aims:
Cardiac involvement is the main driver of clinical outcomes in systemic amyloidosis and preliminary studies support the hypothesis that myocardial ischaemia contributes to cellular damage. The aims of this study were to assess the presence and mechanisms of myocardial ischaemia using cardiovascular magnetic resonance (CMR) with multiparametric mapping and histopathological assessment.
Methods And Results:
Ninety-three patients with cardiac amyloidosis (CA) (light-chain amyloidosis n = 42, transthyretin amyloidosis n = 51) and 97 without CA (three-vessel coronary disease [3VD] n = 47, unobstructed coronary arteries n = 26, healthy volunteers [HV] n = 24) underwent quantitative stress perfusion CMR with myocardial blood flow (MBF) mapping. Twenty-four myocardial biopsies and three explanted hearts with CA were analysed histopathologically. Stress MBF was severely reduced in patients with CA with lower values than patients with 3VD, unobstructed coronary arteries and HV (CA: 1.04 ± 0.51 ml/min/g, 3VD: 1.35 ± 0.50 ml/min/g, unobstructed coronary arteries: 2.92 ± 0.52 ml/min/g, HV: 2.91 ± 0.73 ml/min/g; CA vs. 3VD p = 0.011, CA vs. unobstructed coronary arteries p < 0.001, CA vs. HV p < 0.001). Myocardial perfusion abnormalities correlated with amyloid burden, systolic and diastolic function, structural parameters and blood biomarkers (p < 0.05). Biopsies demonstrated abnormal vascular endothelial growth factor staining in cardiomyocytes and endothelial cells, which may be related to hypoxia conditions. Amyloid infiltration in intramural arteries was associated with severe lumen reduction and severe reduction in capillary density.
Conclusion:
Cardiac amyloidosis is associated with severe inducible myocardial ischaemia demonstrable by histology and CMR stress perfusion mapping. Histological evaluation indicates a complex pathophysiology, where in addition to systolic and diastolic dysfunction, amyloid infiltration of the epicardial arteries and disruption and rarefaction of the capillaries play a role in contributing to myocardial ischaemia.
