Analysis of Plasma Homocysteine Levels in Patients with Unstable Angina

Tavares, José Roberto; D’Almeida, Vânia; Diniz, Daniela C.; Terzi, Carolina A.; Cruz, Edison N.; Stefanini, Edson; Andriollo, A; Paola, Ângelo A. V. de; Carvalho, Antônio Carlos

doi:10.1590/s0066-782x2002001100008

Cited by 9 publications

(8 citation statements)

References 44 publications

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“…Although this trial did not assess secondary stroke prevention, other clinical studies have shown a significant reduction in the occurrence of stroke. 15,16 Combined, these findings suggest that the mechanism of cerebrovascular disease may not be similar to vasoocclusive disease in other parts of the body, such as the heart. Thus, folic acid supplementation might be selectively beneficial to cerebral pathologic lesions by mechanisms not necessarily pertinent to atherosclerosis, or even to the action of homocysteine.…”

Section: Discussionmentioning

confidence: 95%

“…14 Blood homocysteine levels are higher in patients with unstable angina. 15 In addition to being a risk factor, elevated homocysteine is also implicated in poorer outcomes and greater myocardial injury in unstable angina and NSTEMI. 16 In epidemiologic studies, low homocysteine levels seemed to confer better longterm outcomes in patients with coronary heart disease.…”

Section: Introductionmentioning

confidence: 99%

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Folic Acid-Based Intervention in Non-ST Elevation Acute Coronary Syndromes

Imasa

Gomez

Nevado

2009

Asian Cardiovasc Thorac Ann

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Homocysteinemia is a risk factor for cardiovascular diseases. Folic acid combined with vitamins B(6) and B(12) is effective in lowering homocysteine levels. This randomized placebo-controlled study was designed to determine the effect of a folic acid-based supplement on secondary prevention of clinical events in non-ST-segment elevation acute coronary syndromes. The study comprised 240 patients with either unstable angina or non-ST-elevation myocardial infarction in the previous 2 weeks who were randomized to a folate group (n =116) or a placebo group (n =124). The folate group received 1 mg folic acid, 400 microg vitamin B(12), and 10 mg vitamin B(6) daily. Clinical outcomes within 6 months were assessed. The composite endpoint of death, nonfatal acute coronary syndrome, and serious re-hospitalization was significantly higher in the folate group; serious re-hospitalization alone was significantly higher in this group. Advanced age and diabetes increased susceptibility to the composite outcome. Folic acid-based supplementation is not beneficial and may even be harmful in the secondary prevention of cardiovascular events in patients with unstable angina and non-ST-elevation myocardial infarction. Further studies on the safety of such supplements are suggested. Controlled Clinical Trials Registry no. ISRCTN30249553.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Folic Acid-Based Intervention in Non-ST Elevation Acute Coronary Syndromes

Imasa

Gomez

Nevado

2009

Asian Cardiovasc Thorac Ann

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“…Hyperhomocysteinemia is a consequence of a wide range of determinants: genetic, such as HCU by CBS deficiency; physiological, such as diet rich in methionine and/or poor in B vitamins; medications, such as antifolate drugs [31,32]; or pathological, such as renal disease, hypertension and diabetes mellitus [33].…”

Section: Discussionmentioning

confidence: 99%

Homocysteine Induces Oxidative–Nitrative Stress in Heart of Rats: Prevention by Folic Acid

et al. 2010

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Hyperhomocysteinemia is a risk factor for cardiovascular disease, stroke, and thrombosis; however, the mechanisms by which homocysteine triggers these dysfunctions are not fully understood. In the present study, we investigated the effect of chronic hyperhomocysteinemia on some parameters of oxidative stress, namely thiobarbituric acid reactive substances, an index of lipid peroxidation, 2',7'-dichlorofluorescein (H(2)DCF) oxidation, activities of antioxidant enzymes named superoxide dismutase and catalase, as well as nitrite levels in heart of young rats. We also evaluated the effect of folic acid on biochemical alterations elicited by hyperhomocysteinemia. Wistar rats received daily subcutaneous injection of homocysteine (0.3-0.6 μmol/g body weight) and/or folic acid (0.011 μmol/g body weight) from their 6th to the 28th day of life. Controls and treated rats were killed 1 h and/or 12 h after the last injection. Results showed that chronic homocysteine administration increases lipid peroxidation and reactive species production and decreases enzymatic antioxidant defenses and nitrite levels in the heart of young rats killed 1 h, but not 12 h after the last injection of homocysteine. Folic acid concurrent administration prevented homocysteine effects probable by its antioxidant properties. Our data indicate that oxidative stress is elicited by chronic hyperhomocystenemia, a mechanism that may contribute, at least in part, to the cardiovascular alterations characteristic of hyperhomocysteinemic patients. If confirmed in human beings, our results could propose that the supplementation of folic acid can be used as an adjuvant therapy in cardiovascular alterations caused by homocysteine.

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“…Homocysteine (He) was first reported as a cause of atherosclerosis in 1969 8 , and has been gaining more importance as a risk factor for coronary artery disease [9][10][11][12][13][14][15] with its intriguing possible participation in the pathogenesis of endothelial dysfunction. An amino acid formed exclusively by demethylation of dietary methionine or by catabolism, it contains a thiole group (SH-) and does not participate in protein synthesis 16 .…”

Section: Discussionmentioning

confidence: 99%

Homocisteína plasmática total e fator von Willebrand no diabete melito experimental

Lópes¹,

Neves²,

D’Almeida³

et al. 2007

Arq. Bras. Cardiol.

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SummaryObjectives: To determine the plasma homocysteine and von Willebrand factor levels as markers of endothelial dysfunction in rats with diabetes mellitus induced by streptozotocin.Methods: Thirty-five adult male rats (Rattus norvegicus albinus) (weight between 180-200g) were randomized into three groups: control group (n=10), which received no drugs or vehicles; sham group (n=10), which received streptozotocin solution; and diabetic group (n=15), which received streptozotocin. Eight weeks after diabetes mellitus induction, the animals were weighed and anesthesized; blood samples were collected from abdominal aorta for plasma total homocysteine, von Willebrand factor and glucose levels. Conclusion: Reduced homocysteine levels and increased von Willebrand factor levels were observed in diabetes mellitus induced by streptozotocin; nevertheless, there were no correlations between them and with final glucose levels.

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Analysis of Plasma Homocysteine Levels in Patients with Unstable Angina

Abstract: Objective -To determine the prevalence of hyperhomocystinemia in patients with acute ischemic syndrome of the unstable angina type. Methods -

Cited by 9 publications

References 44 publications

Folic Acid-Based Intervention in Non-ST Elevation Acute Coronary Syndromes

Folic Acid-Based Intervention in Non-ST Elevation Acute Coronary Syndromes

Homocysteine Induces Oxidative–Nitrative Stress in Heart of Rats: Prevention by Folic Acid

Homocisteína plasmática total e fator von Willebrand no diabete melito experimental

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