Impaired glucose tolerance and cardiovascular disease: the possible role of post-prandial hyperglycemia.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic and epidemiological concepts without systematic search criteria or original data
PubMed 15131534 · doi:10.1016/j.ahj.2003.11.020
What was done
This is a narrative review synthesizing literature on the contribution of the post-prandial state and impaired glucose tolerance to atherosclerosis and cardiovascular disease. The authors examined evidence linking 2-hour post-challenge glycemia from oral glucose tolerance tests to cardiovascular outcomes and reviewed proposed cellular mechanisms.
What was found
No numbers were reported in the abstract. The abstract states that in individuals with impaired glucose tolerance and normal fasting glycemia, the post-prandial phase shows rapid blood glucose spikes. It reports that 2-hour post-challenge glycemia is an independent risk factor for cardiovascular disease and that acute hyperglycemia promotes free radical production, endothelial dysfunction, a prothrombotic state, and inflammation.
Why it matters
The paper highlights post-prandial glycemic excursions as potential therapeutic targets for cardiovascular risk reduction in impaired glucose tolerance, rather than relying solely on fasting glucose measurements.
Limits
The abstract reports no quantitative data, effect sizes, sample size, or systematic search criteria. The oral glucose tolerance test is noted to be non-physiological, and intervention evidence demonstrating clinical event reduction from targeting post-prandial hyperglycemia is identified as needing future study.
Cited by
- supports Elevated blood sugar damages the single-cell endothelial lining of blood vessels within a short period, leading to inflammation and clotting.