Málaga, (EFE).- A research group led by José María Pérez Pomares, professor at the University of Málaga (UMA), has discovered the cellular mechanism that causes coronary arterioventricular fistulas, a congenital anomaly that, in the most serious cases, it can cause death.
Dr. Pérez Pomares, professor and researcher at the Department of Animal Biology of the UMA and IBIMA-BIONAND Platform, has carried out this work in collaboration with researchers from the National Center for Cardiovascular Research (CNIC) in Madrid, the Maternal-Infant Hospital of Malaga, the Center for Applied Medical Research (CIMA) in Pamplona and the Necker Hospital and the Pasteur/Imagine Institute in Paris.
Its results have been published in the journal “Experimental and molecular medicine”, from the prestigious publishing group Nature.
What are coronary fistulas
Coronary fistulas are abnormal connections between different blood vessels of the coronary system, large arteries or veins (aorta, pulmonary or cava) or other parts of the heart, such as its chambers (atria and ventricles).
The most frequent type of coronary fistula is precisely this last type, which involves the connection of a coronary artery with the interior of the heart, which is the one studied in the aforementioned article.
It is estimated that between 0.21 and 5.8% of the population have coronary anomalies and that between 0.1 and 0.2% of patients who come for a hospital review of their coronary arteries have a fistula. It is a relatively low incidence rate, although it must be taken into account that in many cases the presence of this defect is not diagnosed, details EFE Pérez Pomares (Málaga, 1972).
Although fistulas are often small and are not serious or cause problems, allowing those affected to lead a normal life, larger ones can be associated with serious complications such as endocarditis (infection of the tissue that lines the heart internally), hypertrophy or dilation of the ventricular walls or sudden death.
“The pathology is correlated with other heart problems, the spectrum is highly variable,” says the UMA professor.
a congenital anomaly
It is known that this congenital deformation is generated during embryonic development, although until now the information available about its origin has been scarce.
Dr. Pérez Pomares, who for two years (2018-2020) chaired the Coronary Development, Anatomy and Pathology Working Group of the European Society of Cardiology, has led one of the few studies that explain the causes of this defect, a work that can help to improve the early diagnosis of this type of abnormalities and other associated pathologies.
The results of the investigation suggest that the appearance of discontinuities in the ventricular muscle wall is at the origin of this coronary defect.
The chambers of the heart are lined with three tissues: the endocardium, the innermost; the myocardium, the thick central muscular layer, which allows the contraction of the atria and ventricles and therefore blood circulation, and the epicardium, which covers the external surface of the organ.
When the endocardium and epicardium come into contact abnormally early during embryonic development, usually because the myocardium that separates the two layers presents thinner than normal regions or porous areas, a connection is generated between the surface and the interior. of the heart that will mature into a fistula.
To carry out this study, Dr. Pérez Pomares’ team has worked with genetic and experimental animal models – mouse and bird embryos – and has also been able to study human samples from a unique case of pediatric coronary fistula. These samples were provided by informed consent for use in research.
The results open the door to identify new candidate genes for the early diagnosis of these congenital anomalies and their associated risks. EFE
