ArticleThe open cardiovascular medicine journal2009
Feto-placental atherosclerotic lesions in intrauterine fetal demise: role of parental cigarette smoking.
Article in The open cardiovascular medicine journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 13 citations in OpenAlex.
- Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants.The application of clinical genetics · 2014Review
- Severe intra- and periventricular hemorrhage: role of arteriolosclerosis related to maternal smoke.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The atherogenic effect of cigarette smoking is already recognizable in coronary arteries of fetuses in the last gestational weeks. In this study we analyzed the atherogenic effect of mother's and father's smoking habit on coronary arteries and even on adnexa of 30 human fresh fetuses died from 32 to 41 gestational weeks. In 12 cases only the mothers of the victims were cigarette smokers, in 7 cases only the fathers were smokers, whereas in 11 cases nobody smoked.We observed pre-atherosclerotic and initial atherosclerotic lesions of the adnexa in 21 cases, of which 11 cases had only mother smokers and 6 cases only father smokers. The atherogenic effect is statistically significant in both smoker groups, but stronger in maternal one. The atherosclerotic lesions found in umbilical and placental arteries are similar to those described in fetal coronary arteries: thickening of the arterial walls caused by proliferation and migration of the smooth muscle cells of the tunica media with loss of polarity and infiltration of the subendothelial connective tissue.
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Registered trials
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