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Chronic total coronary occlusion is among the most complex coronary artery diseases. Elevated homocysteine is a risk factor for coronary artery diseases. However, few studies have assessed the relationship between homocysteine and chronic total coronary occlusion.
Methods:
1295 individuals from Southwest China were enrolled in the study. Chronic total coronary occlusion was defined as complete occlusion of coronary artery for more than three months. Homocysteine was divided into quartiles according to its level. Univariate and multivariate logistic regression models, receiver operating characteristic curves, and subgroup analysis were applied to assess the relationship between homocysteine and chronic total coronary occlusion.
Results:
Subjects in the higher homocysteine quartile had a higher rate of chronic total coronary occlusion (P < 0.001). After adjustment, the odds ratio for chronic total coronary occlusion in the highest quartile of homocysteine compared with the lowest was 1.918 (95% confidence interval 1.237–2.972). Homocysteine ≥ 15.2 μmol/L was considered an independent indicator of chronic total coronary occlusion (odds ratio 1.53, 95% confidence interval 1.05–2.23; P = 0.0265). The area under the receiver operating characteristic curve was 0.659 (95% confidence interval, 0.618–0.701; P < 0.001). Stronger associations were observed in elderly and in those with hypertension and diabetes.
Conclusions:
Elevated homocysteine is significantly associated with chronic total coronary occlusion, particularly in elderly and those with hypertension and diabetes.
Some authors have shown that hyperhomocysteinemia (HHCY) is a risk factor for stroke/TIA mainly in patients with associated other risk factors such as hypertension, dyslipidemia, smoking and carotid atherosclerosis. The mechanism through HHCY acts is only postulated but experimental evidence suggest that endothelial dysfunction generated by reactive oxygen species, platelet activation and thrombus formation play a key role in the pathophysiologic mechanisms of HHCY. It has also been demonstrated that HHCY can represent an independent risk factor for venous thromboembolism and the association between HHCY with factor V Leiden further increase the risk of deep venous thrombosis. Here we reported a case of A 16 year-old woman presented to our emergency room complaining of headache and showing a right facial paresis, a mild defect of motility in her upper right arm, a slurred speech with NIHSS (National Institute of Health Stroke Scale) =7. Magnetic resonance study plus MRI venography were performed which showed an ischemic lesion in the left frontal area and occlusion of the longitudinal superior venous sinus. Her plasma levels of homocysteine was increased (91 µmol/L), so anticoagulation with LMWH and then with warfarin and a therapy with folic acid was started. After a cycle of rehabilitation she was discharged with full recovery. As stroke could have serious impact on the quality of life, HHCY should be considered in all patients with stroke or TIA and eventually treated
A thrombophilic defect is an abnormality in the coagulation system that predisposes an individual to thrombosis. This chapter examines the role that the acquired thrombophilic defects play in the magnitude of early pregnancy loss, with particular reference to Primary Antiphospholipid syndrome, hyperhomocysteinemia and Acquired protein C resistance. Antiphospholipid syndrome (APS) is now recognized to be the most important treatable cause of recurrent miscarriage. The potential of thromboelastography as a clinical tool to overcome many of the above limitations in hemostasis testing in our recurrent pregnancy-loss population is promising. The success of thromboprophylactic treatment for women with recurrent miscarriage associated with APS has resulted in women with unexplained recurrent miscarriage frequently demanding similar treatment. Recurrent miscarriage is a distressing condition that affects at least 1% of couples trying to achieve a successful pregnancy. Recurrent miscarriage is a heterogeneous condition and no single abnormality will account for all cases.
This chapter, reviews mitochondrial and other selective metabolic causes of stroke. In MELAS, despite the microangiopathic findings in the brain and muscles, the stroke-like episodes are more likely attributed to mitochondrial and metabolic dysfunction in neural tissue and glia rather than to ischemic vascular pathology. Kearns Sayre syndrome (KSS) is a mitochondrial disorder caused by large heteroplasmic deletions in mtDNA. Brain infarction, presumably secondary to cardioembolic sources, may occur. Hyperhomocysteinemia is a clinical syndrome caused by several enzyme deficiencies in methionine metabolism. Patients with homocystinuria have markedly elevated plasma homocysteine concentrations. Most patients present with peripheral venous thrombosis, including pulmonary embolism. Stroke, peripheral arterial occlusions, or myocardial infarction can be the initial presentation. The increased tendency for thrombosis usually presents as an ischemic stroke. Metabolic stroke due to hypoxemia and vascular insufficiency may occur in methylmalonic acidemia. Metabolic causes of stroke are quite heterogeneous.
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