Background: Elevated homocysteine levels have been associated with a higher risk of cardiovascular disease. Because folate intake can reduce homocysteine levels, we investigated the association between dietary folate intake and nonfatal myocardial infarction.
Methods: We conducted a case-control study in three tertiary hospitals of Pamplona, Spain, between 1999 and 2001. Study physicians enrolled 171 patients less than 80 years of age with a first nonfatal myocardial infarction and 171 control patients matched by age, sex, hospital and calendar month. We excluded patients with any prior major cardiovascular disease. Participants were interviewed about medical factors and life-style and completed a food frequency questionnaire previously validated in Spain. We calculated energy-adjusted intakes of folate and estimated relative risks (RRs) of myocardial infarction and 95% confidence intervals (CIs) using conditional logistic regression. Relative risks were adjusted for conventional risk factors.
Results: Only 6% of participants were taking vitamin supplements. The main sources of folate were green leafy vegetables, green beans, oranges, peppers and lettuces. The estimated matched RR of myocardial infarction for the top three quartiles of folate intake (, above 340 microg/day) was 0.57 (CI = 0.35-0.94), compared with the lowest quartile of intake. The multivariate adjusted RR was 0.51 (CI = 0.24-1.06). There was no apparent dose effect above this threshold.
Conclusions: Our results in a Mediterranean population with natural plant foods as the main source of folate provide further evidence to support the hypothesis that dietary folate intake may be an independent protective factor for myocardial infarction. The magnitude of the effect, its biological plausibility, and the consistency across studies offer support for a causal association.
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http://dx.doi.org/10.1097/00001648-200211000-00015 | DOI Listing |
BMC Neurol
January 2025
Department of Neurosurgery, Gifu University Graduate School of Medicine, 1-1, Yanagido, Gifu, 501-1194, Japan.
Background: Tyrosine kinase inhibitors (TKIs) improve prognosis in chronic myeloid leukemia (CML). Nilotinib and ponatinib, second- and third-generation TKIs, respectively, have been reported to cause adverse vascular occlusive events such as myocardial infarction and peripheral arterial disease. However, little is known about the risk of cerebral infarction associated with severe cerebrovascular stenosis, which is a late complication of TKIs.
View Article and Find Full Text PDFNat Cardiovasc Res
January 2025
Department of Cardiology, Boston Children's Hospital, Boston, MA, USA.
Nat Cardiovasc Res
January 2025
Institute of Developmental and Regenerative Medicine, University of Oxford, Oxford, UK.
Arrhythmias are a hallmark of myocardial infarction (MI) and increase patient mortality. How insult to the cardiac conduction system causes arrhythmias following MI is poorly understood. Here, we demonstrate conduction system restoration during neonatal mouse heart regeneration versus pathological remodeling at non-regenerative stages.
View Article and Find Full Text PDFEur J Pharmacol
January 2025
Academy of Integrated Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Electronic address:
Dihydrotanshinone I (DHT) is an active ingredient derived from Salvia miltiorrhiza. Previous studies have demonstrated that DHT can improve cardiac function in rats with myocardial ischemia-reperfusion injury (IR). However, the mechanism by which DHT improves myocardial injury in rats still requires further research.
View Article and Find Full Text PDFHeart Lung
January 2025
University of Foggia, Department of Medical and Surgical Sciences, Foggia, Italy. Electronic address:
Background: It is crucial to distinguish type-1 myocardial infarction (T1MI) from type-2 myocardial infarction (T2MI) at admission and during hospitalization to avoid unnecessary invasive exams and inappropriate admissions to the acute cardiac care unit.
Objectives: The purpose of the study was to define a simple profile derived from commonly used biomarkers to differentiate T1MI from T2MI.
Methods: We prospectively enrolled in an observational study 213 iconsecutive patients with a provisional diagnosis of non-ST-elevation acute myocardial infarction (NSTEMI) admitted to the Cardiology Department.
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