Publications by authors named "D Sidi"
Article Synopsis
- * Recent advancements have improved 4D flow MRI by reducing imaging times and enhancing data processing, making the technique more applicable in clinical settings.
- * The method offers a variety of flow parameters for analyzing blood dynamics, including forward and reverse flow, and is becoming essential for studying cardiovascular issues like congenital heart defects and valvular diseases.
Tropical endomyocardial fibrosis (FET) is a leading cause of heart failure and the most common restrictive cardiomyopathy worldwide. Extensive fibrosis of the ventricular endocardium causing architectural distortion, impaired filling and valvular insufficiency define the disease. Confined to peculiar and limited geographical areas, the aetiology remains blurred and it carries a grim prognosis.
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- Access to cardiac surgery in low-income countries like Cambodia and Mozambique is limited, with a significant lack of data on patient outcomes and characteristics.
- A study conducted from 2001 to 2011 followed over 2,000 patients undergoing open-heart surgery, revealing challenges such as high rates of rheumatic and congenital heart diseases and significant loss to follow-up, particularly in Mozambique due to remoteness.
- The early postoperative mortality rates were relatively low (6.10% in Mozambique and 3.05% in Cambodia), suggesting that while cardiac surgery can be effectively performed, follow-up care remains a major issue that affects understanding long-term patient outcomes.
Tropical endomyocardial fibrosis (EMF) is a neglected disease of poverty that afflicts rural populations in tropical low-income countries, with some certain high-prevalence areas. Tropical EMF is characterized by the deposition of fibrous tissue in the endomyocardium, leading to restrictive physiology. Since the first descriptions in Uganda in 1948, high-frequency areas for EMF have included Africa, Asia, and South America.
View Article and Find Full Text PDFAcyl-CoA dehydrogenase family, member 9 (ACAD9) mutation is a frequent, usually fatal cause of early-onset cardiac hypertrophy and mitochondrial respiratory chain complex I deficiency in early childhood. We retrospectively studied a series of 20 unrelated children with cardiac hypertrophy and isolated complex I deficiency and identified compound heterozygosity for missense, splice site or frame shift ACAD9 variants in 8/20 patients (40%). Age at onset ranged from neonatal period to 9 years and 5/8 died in infancy.
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