18 research outputs found
High prevalence of muscular ventricular septal defect in neonates
Objectives.This study sought to use echocardiography to evaluate the prevalence of muscular ventricular septal defect in neonates.Background.Ventricular septal defect is usually asymptomatic and closes spontaneously. An increase in its prevalence has been noted recently. One reason is the improved detection of small defects, especially with the increased use of echocardiography. Therefore, one would expect a higher prevalence in neonates on the basis of echocardiographic screening.Methods.Color Doppler echocardiography was performed in 1,053 consecutive neonates 6 to 170 h old at Western Galilee Hospital, Israel. Data on the neonates, parents and family were obtained to analyze the influencing factors. The identified patients were followed up for 1 to 10 months or until ventricular septal defect closure.Results.Muscular ventricular septal defect was found in 56 (25 male, 31 female) of the 1,053 neonates, a prevalence of 53.2/1,000 live births. All neonates were asymptomatic. Six had a systolic murmur. Electrocardiographic findings were normal in 44 (97.8%) of 45 neonates followed up, and left ventricular hypertrophy occurred in 1 (2.2%). By echocardiography, 50 ventricular septal defects (89.3%) were single and 6 (10.7%) were multiple. The defects (range 1 to 5 mm in diameter, mean [±sd]2.3 ± 0.8) occurred anywhere along the muscular septum; 43 (76.8%) were detectable only on color Doppler imaging. The left atrium and left ventricle were mildly dilated. Of 45 neonates who were followed up for 6 to 10 months or until closure of the defects, 40 (88.9%) had defects that closed spontaneously. The risk of ventricular septal defect was not significantly associated with gestational age, birth weight, birth order, maternal age, diabetes, smoking, exposure to drugs or infection, paternal age, familial congenital heart disease, religion or consanguinity.Conclusions.There is a prevalence of muscular ventricular septal defect in neonates of 53.2/1,000 live births. The patients were asymptomatic, and 88.9% had defects that closed spontaneously within 1 to 10 months. These defects may be caused by environmental factors. In many cases, muscular ventricular septal defect may also result from delayed physiologic development
Clinical Significance of Conditions Presenting with ECG Changes Mimicking Acute Myocardial Infarction
Prevalence of valvar regurgitation by color Doppler echocardiography in neonates with normal hearts
Glycaemic control modifies the haptoglobin 2 allele-conferred susceptibility to coronary artery disease in Type 1 diabetes
Percutaneous coronary intervention in patients receiving enoxaparin or unfractionated heparin after fibrinolytic therapy for ST-segment elevation myocardial infarction in the ExTRACT-TIMI 25 trial
Objectives We sought to evaluate whether enoxaparin (ENOX) is superior to unfractionated heparin (UFH) as adjunctive therapy for patients with ST-segment elevation myocardial infarction (STEMI) who receive fibrinolytic therapy and subsequently undergo percutaneous coronary intervention (PCI) by analyzing data from the ExTRACT-TIMI 25 (Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial Infarction Treatment-Thrombolysis In Myocardial Infarction 25) trial.
Background Limited data are available on the use of ENOX compared with UFH as adjunctive therapy in STEMI patients treated with fibrinolytic therapy and subsequent PCI.
Methods A total of 20,479 STEMI patients who received fibrinolytic therapy were randomized to a strategy of ENOX throughout index hospitalization or UFH for at least 48 h, with blinded study drug to continue if PCI was performed. The primary end point of death or recurrent MI through 30 days was compared for ENOX versus UFH among the patients who underwent subsequent PCI (n = 4,676).
Results After initial fibrinolysis, fewer patients underwent PCI through 30 days in the ENOX versus the UFH group (22.8% vs. 24.2%; p = 0.027). Among patients who underwent PCI by 30 days, the primary end point occurred in 10.7% of ENOX and 13.8% of UFH patients (0.77 relative risk; p < 0.001). There were no differences in major bleeding for ENOX versus UFH (1.4% vs. 1.6%; p = NS). Results were similar when PCI was carried out in patients receiving blinded study drug during PCI (n = 2,178).
Conclusion Among patients treated with fibrinolytic therapy for STEMI who underwent subsequent PCI, ENOX administration was associated with a reduced risk of death or recurrent MI without difference in the risk of major bleeding. The strategy of ENOX support for fibrinolytic therapy followed by PCI is superior to UFH and provides a seamless transition from the medical management to the interventional management phase of STEMI without the need for introducing a second anticoagulant in the cardiac catheterization laboratory