Microvascular function variation in a healthy population: Insights from Oxygenation-Sensitive CMR
Bibliographic record
Abstract
Microvascular dysfunction has significant impacts on patient prognosis even in absence of obstructive coronary artery disease, and may predict future cardiovascular events. Factors like age, sex, and body composition contribute to vascular dysfunction over the lifetime. In otherwise healthy individuals the impact of these factors is unclear. Oxygenation-sensitive cardiovascular magnetic resonance imaging (OS-CMR) is a validated methodology to examine vascular function which exploits the blood oxygen level dependent effect, in which deoxygenated hemoglobin acts as an innate contrast agent in a magnetic field. Through varied OS-CMR signal intensities, regional tissue oxygenation changes during vasodilation are detected. Previous research utilizing OS-CMR observed blunted vascular function in many cardiovascular pathologies. Vasoactive breathing maneuvers, a period of paced hyperventilation followed by a voluntary maximal breath hold, are an endogenous alternative to pharmaceutical vasodilation in OS-CMR. Carbon dioxide variations, inducing vasoconstriction during hyperventilation and vasodilation during the breath hold, act on endothelial cells to modulate vascular tone. The breathing-induced myocardial oxygenation reserve (B-MORE) describes the myocardial oxygenation response during breathing maneuvers. This endothelial-dependent mechanism may provide a valuable assessment of microvascular function, based on meaningful biomarkers instead of secondary surrogate markers such as blood flow or tracer uptake. Previous work demonstrated a transmural gradient of vascular function during endothelial-independent adenosine vasodilation in subjects with risk factors but no cardiovascular disease. In a similar cohort, breathing maneuvers may provide valuable insight into microvascular dysfunction before the onset of cardiovascular disease. The thesis aims to investigate tissue oxygenation variation as a marker of microvascular function in healthy subjects, providing a better understanding of microvascular dysfunction pathophysiology in such populations. The included study retrospectively assessed the impact of demographic factors on global and regional B-MORE in healthy adults from 4 prospective OS-CMR studies in Montreal, Canada. We hypothesize that demographic factors will impart slight changes to microvascular function across the lifetime, differentially impacting B-MORE. This thesis includes the first study investigating factors impacting B-MORE in healthy subjects. Several factors differentially impacted microvascular function within the cohort. This indicates that in a healthy population, sex and body composition, including height and body size analysis, are associated with microvascular function and thus lead to baseline value variations. Female sex-specific risk factors may be associated with reduced function (lower B-MORE values). Further research is needed to fully understand the impact of healthy aging on the microvasculature over the lifetime, as it may be impacted by factors not assessed in this study. Future work should investigate the prognostic value and utility of B-MORE as a marker of microvascular function. Blunted B-MORE may indicate an increased risk for cardiovascular events. As breathing maneuvers employ endothelial-dependent vasodilation it is possible that slight B-MORE variations seen in healthy subjects reflect the biological spectrum of microvascular (endothelial) function. If validated by the invasive reference standards of microvascular function, this methodology could provide a non-invasive and informative test of microvascular function and tissue status. Given the relationship of B-MORE to factors affecting the vasculature in healthy individuals, it appears to be a sensitive marker to detect microvascular dysfunction at an early, subclinical stage. A methodology of this nature may be instrumental in diagnosing early microvascular disease, improving the prognosis of those at risk of ischemic heart disease
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.002 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.001 | 0.000 |
| Open science | 0.000 | 0.001 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.001 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".