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Biomedical subjects

L A Pearce

Publications and source records attributed to L A Pearce.

47 records · Page 3Linked to original sources
PubMed1969

Histamine and spermidine content in brain during development.

Histamine concentration in fetal rat brain is high at 17 days gestation but decreases sharply just before birth. Values subsequently increase to a maximum postnatal concentration 5 to 10 days after birth, and then steadily decline to low adult values by time of weaning. Spermidine follows a pattern similar to that of histamine but with a 24- to 48-hour lag. The developmental pattern for histamine in the central nervous system is different from that for other neural amines. It appears that the marked fetal and neonatal changes in brain histamine correlate best with periods of rapid cell proliferation and growth during brain maturation.

Animals↗
PubMedDate not supplied

Increased risk of intracranial hemorrhage when aspirin is combined with warfarin: A meta-analysis and hypothesis.

BACKGROUND: Oral anticoagulation with vitamin K antagonists increases the risk of intracranial hemorrhage; whether addition of aspirin to oral anticoagulation augments this risk is unclear. METHODS: Meta-analysis of randomized clinical trials in which aspirin was added to oral anticoagulants. RESULTS: Six randomized clinical trials were identified, including a total of 3,874 participants. Use of aspirin with oral anticoagulants was associated with more than double the frequency of intracranial hemorrhage (relative risk = 2.4, 95% CI = 1.2-4.8, p = 0.02). CONCLUSION: We hypothesize that aspirin when added to oral vitamin K antagonists may increase the risk of intracranial hemorrhage, but this observation requires confirmation. The magnitude of this effect is uncertain, and the clinical importance is likely different for different patient populations.

Aspirin↗
PubMedDate not supplied

Cardioembolic vs. noncardioembolic strokes in atrial fibrillation: frequency and effect of antithrombotic agents in the stroke prevention in atrial fibrillation studies.

BACKGROUND: While atrial fibrillation (AF) increases the risk of cardioembolic stroke, some ischemic strokes in AF patients are noncardioembolic. OBJECTIVES: To assess ischemic stroke mechanisms in AF and to compare their responses to antithrombotic therapies. METHODS: On-therapy analyses of ischemic strokes occurring in 3,950 participants in the Stroke Prevention in Atrial Fibrillation I-III clinical trials. Strokes were classified by presumed mechanism according to specified neurologic features by neurologists unaware of antithrombotic therapy. RESULTS: Of 217 ischemic strokes, 52% were classified as probably cardioembolic, 24% as noncardioembolic, and 24% as of uncertain cause (i.e., 68% of classifiable infarcts were deemed cardioembolic). Compared to those receiving placebo or no antithrombotic therapy, the proportion of cardioembolic stroke was lower in patients taking adjusted-dose warfarin (p = 0.02), while the proportion of noncardioembolic stroke was lower in those taking aspirin (p = 0.06). Most (56%) ischemic strokes occurring in AF patients taking adjusted-dose warfarin were noncardioembolic vs. 16% of strokes in those taking aspirin. Adjusted-dose warfarin reduced cardioembolic strokes by 83% (p < 0.001) relative to aspirin. Cardioembolic strokes were particularly disabling (p = 0.05). CONCLUSIONS: Most ischemic strokes in AF patients are probably cardioembolic, and these are sharply reduced by adjusted-dose warfarin. Aspirin in AF patients appears to primarily reduce noncardioembolic strokes. AF patients at highest risk for stroke have the highest rates of cardioembolic stroke and have the greatest reduction in stroke by warfarin.

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