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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.
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.
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.
Elevated homocysteine is significantly associated with chronic total coronary occlusion, particularly in elderly and those with hypertension and diabetes.
To describe the evolution of ventricular septal defects in infants from intra-uterine diagnosis to the age of 3 years or until documented echocardiographic closure of the defect, as well as any relationship between closure rate, time and foetal echocardiographic features.
Between January, 2004 and December, 2006, 268 cases of congenital cardiac defect were detected in 14,993 pregnancies referred to our hospital for routine foetal echocardiography; of these cases, 125 had isolated ventricular septal defect. The mothers were scheduled for regular ultrasonography every 2 weeks from diagnosis until the ventricular septal defect closed or 3 years postnatally.
Of the 125 cases of ventricular septal defects, the pregnancy was terminated in 25, four resulted in death, two defects closed spontaneously in utero, 55 closed at a mean age of 13.7 months postnatally, 17 were treated with surgery, nine remained unclosed, and 13 cases were lost to follow-up. Only 7.7% of muscular ventricular septal defects remained patent as compared with 35.7% of perimembranous ventricular septal defects (p is less than 0.01). Muscular ventricular septal defects closed earlier than perimembranous ventricular septal defects. All the ventricular septal defects less than or equal to 3 millimetres closed, whereas only 79.5% of the defects greater than 3 millimetres closed before the age of 3 years; 60.9% of the defects less than or equal to 3 millimetres closed before the age of 1 year as compared with 41.7% of the defects greater than 3 millimetres. The velocity of right-to-left flow was negatively correlated with closure rate but not related to closure period.
Ventricular septal defects can close in utero or during the postnatal period, and both the size and site play a role in the natural history, with small and muscular ventricular septal defects having a high closure rate and early closure.
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