Materiały źródłowe

• #1 Atrial Septal Defect – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535440/

  Atrial septal defect (ASD) is one of the most common types of congenital heart defects, occurring in about 25% of children. An ASD occurs when the communication between the right and left atria fails to close. ASD encompasses defects in the true septal membrane and other abnormalities that permit communication between the atria. […] ASDs occur as singular defects but are associated with Mendelian inheritance, aneuploidy, transcription errors, mutations, and maternal exposures. ASDs are noted in patients with syndromes such as Down, Treacher-Collins, thrombocytopenia-absent radii, Turner, and Noonan. These conditions occur as a result of Mendelian inheritance. Maternal exposure to rubella and drugs like cocaine and alcohol may also predispose the unborn fetus to developing an ASD. […] Atrial septation begins during the 4th week of gestation and involves a complex series of developmental events. The process starts with the growth of the primary atrial septum, or septum primum, from the roof of the primitive atrium toward the endocardial cushions. The caudal end of the septum primum becomes covered by mesenchymal cells derived from the embryonic endocardium, forming the mesenchymal cap.

• #2 Atrial Septal Defect (ASD) – Pediatrics – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/pediatrics/congenital-cardiovascular-anomalies/atrial-septal-defect-asd

  Atrial septal defects account for about 6 to 10% of cases of congenital heart disease (1). Most cases are isolated and sporadic, but some are part of a genetic syndrome (eg, mutations of chromosome 5, Holt-Oram syndrome). The combination of an atrial septal defect and atrioventricular conduction disturbance may be associated with a mutation in the NKX2-5 homeobox gene. […] In atrial septal defect, shunting is left to right initially (see figure Atrial septal defect). Some small ASDs, often just a stretched patent foramen ovale, close spontaneously during the first few years of life. Persistent moderate to large ASDs result in large shunts, leading to right atrial and right ventricular volume overload. If unrepaired, these large shunts may lead to pulmonary artery hypertension, elevated pulmonary vascular resistance, and right ventricular hypertrophy by the time people are in their 30s or 40s. The absolute size of the defect in millimeters should not be taken in isolation, as the significance of the size of the defect varies with the age and size of the patient, and it is of lesser importance than the physiologic consequences of the degree of shunting through the defect (1). Atrial arrhythmias, such as supraventricular tachycardia (SVT), atrial flutter, or atrial fibrillation, may also occur. The presence of an atrial shunt, even if predominantly left-to-right, may be associated with a paradoxical embolus due to a transient right-to-left shunt. Ultimately, the increase in the pulmonary artery pressure and vascular resistance may result in a bidirectional atrial shunt with cyanosis (Eisenmenger syndrome) during mid to late adulthood (most commonly over the age of 40).

• #3 Atrial Septal Defect (ASD) | Dayton Children’s Hospital

  https://www.childrensdayton.org/kidshealth/a/asd

  An atrial septal defect (ASD) sometimes called a hole in the heart is a type of congenital heart defect in which there is an abnormal opening in the dividing wall between the upper filling chambers of the heart (the atria). […] ASDs happen during fetal development of the heart. The heart develops from a large tube, dividing into sections that will eventually become its walls and chambers. If there’s a problem during this process, a hole can form in the wall that divides the left atrium from the right. […] In some cases, the tendency to develop an ASD might be inherited (genetic). Genetic syndromes can cause extra or missing pieces of chromosomes that can be associated with ASD. Most ASDs, though, have no clear cause. It’s also not clear why ASDs are more common in girls than in boys. […] An ASD that isn’t treated in childhood can lead to health problems later, including an abnormal heart rhythm (an atrial arrhythmia) and problems in how well the heart pumps blood.

• #4 Atrial Septal Defect – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535440/

  Atrial septal defect (ASD) is one of the most common types of congenital heart defects, occurring in about 25% of children. An ASD occurs when the communication between the right and left atria fails to close. ASD encompasses defects in the true septal membrane and other abnormalities that permit communication between the atria. […] ASDs occur as singular defects but are associated with Mendelian inheritance, aneuploidy, transcription errors, mutations, and maternal exposures. ASDs are noted in patients with syndromes such as Down, Treacher-Collins, thrombocytopenia-absent radii, Turner, and Noonan. These conditions occur as a result of Mendelian inheritance. Maternal exposure to rubella and drugs like cocaine and alcohol may also predispose the unborn fetus to developing an ASD. […] Atrial septation begins during the 4th week of gestation and involves a complex series of developmental events. The process starts with the growth of the primary atrial septum, or septum primum, from the roof of the primitive atrium toward the endocardial cushions. The caudal end of the septum primum becomes covered by mesenchymal cells derived from the embryonic endocardium, forming the mesenchymal cap.

• #5 Atrial Septal Defect – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535440/

  The septum secundum begins to form to the right of the septum primum, growing caudally from the atrial roof and partially covering the ostium secundum. The space between the septum primum and septum secundum forms the foramen ovale. In the fetus, the foramen ovale enables oxygen-rich blood to bypass the lungs by flowing directly from the right atrium to the left atrium. After birth, pulmonary vascular resistance decreases, leading to a reduction in right atrial pressure. This pressure change causes the septum primum to close the foramen ovale, completing the separation of the atria. […] Normally, the pressure in the right atrium is significantly lower than in its left counterpart, causing blood to flow from the left atrium to the right atrium, resulting in a left-to-right shunt. The size of the defect determines the significance of the shunt. Significant shunts have a pulmonary (Qp) to systemic (Qs) flow ratio greater than 1.5:1 (Qp/Qs 1.5). Chronic volume overload from high pulmonary blood flow leads to remodeling of the pulmonary vasculature.

• #6 Clinical manifestations and diagnosis of atrial septal defects in adults – UpToDate

  https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-atrial-septal-defects-in-adults

  Atrial septal defect (ASD) is the most common congenital heart lesion in adults and is often asymptomatic until adulthood. Diagnosis is important, as timely ASD repair improves outcomes. […] ASDs result from lack of sufficient tissue to completely septate the atria and are classified according to their location in the atrial septum, as described in the following sections. The location of the defect in relation to adjacent cardiac structures defines the anomalies associated with the ASD and impacts the natural history and requirements for repair. […] Atrial septation begins as early as the fifth week of gestation. The septum primum arises from the superior portion of the common atrium and grows caudally to the endocardial cushions located between the atria and ventricles, eventually closing the orifice (ostium primum) between the atria. A second orifice (the ostium secundum) develops in the septum primum; this orifice is covered by another septum (the septum secundum) that arises on the right atrial side of the septum primum. The septum secundum grows caudally and covers the ostium secundum. However, the septum secundum does not completely divide the atria, but leaves an oval orifice (the foramen ovale) that is covered but not sealed on the left side by the flexible flap of the septum primum.

• #7 Atrial Septal Defect – TeachMePaediatrics

  https://teachmepaediatrics.com/cardiology/congenital-heart-defects/atrial-septal-defect/

  The atrial septum is formed from two separate endocardial cushions, beginning during the 4th week of gestation. The primary atrial septum is the septum primum, which grows from cranial to caudal; so from the roof of the atrium down towards the atrioventricular endocardial cushions. This closes off the ostium primum. The ostium secundum develops again from the atrial roof and grows downwards towards the septum primum. The space formed between septum primum and secundum is known as the foramen ovale (FO). FO closes shortly after birth when vascular resistance changes: systemic BP increases with decreasing pulmonary pressure, with a decrease in right atrium pressure. […] Occurs when there is incomplete occlusion of ostium secundum by septum secundum, or too much reabsorption of septum primum from atrium roof (during apoptosis in forming foramen secundum).

• #8 Ostium Secundum Atrial Septal Defects: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/890991-overview

  A secundum atrial septal defect can result from inadequate formation of the septum secundum so that it does not completely cover the ostium secundum. More often, the ostium secundum is excessively large because of increased resorption so that septum secundum cannot cover it. […] Although heart failure from secundum ASD rarely occurs in children, this complication can often occur in adults. Adults also demonstrate a propensity for atrial dysrhythmias, including atrial flutter and fibrillation, presumably caused by chronic right atrial dilation. These complications may not be reversible if closure is delayed. […] The presence of this phenomenon has been identified as a potential risk factor for stroke due to embolization into the systemic arterial circulation. […] Isolated secundum atrial septal defect occasionally demonstrates familial inheritance in an autosomal dominant pattern, particularly when associated with prolonged atrioventricular conduction (ie, prolonged PR interval on ECG). Familial secundum ASD also occurs in Holt-Oram Syndrome.

• #9 Atrial Septal Defect (ASD) – Pediatrics – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/pediatrics/congenital-cardiovascular-anomalies/atrial-septal-defect-asd

  Atrial septal defects account for about 6 to 10% of cases of congenital heart disease (1). Most cases are isolated and sporadic, but some are part of a genetic syndrome (eg, mutations of chromosome 5, Holt-Oram syndrome). The combination of an atrial septal defect and atrioventricular conduction disturbance may be associated with a mutation in the NKX2-5 homeobox gene. […] In atrial septal defect, shunting is left to right initially (see figure Atrial septal defect). Some small ASDs, often just a stretched patent foramen ovale, close spontaneously during the first few years of life. Persistent moderate to large ASDs result in large shunts, leading to right atrial and right ventricular volume overload. If unrepaired, these large shunts may lead to pulmonary artery hypertension, elevated pulmonary vascular resistance, and right ventricular hypertrophy by the time people are in their 30s or 40s. The absolute size of the defect in millimeters should not be taken in isolation, as the significance of the size of the defect varies with the age and size of the patient, and it is of lesser importance than the physiologic consequences of the degree of shunting through the defect (1). Atrial arrhythmias, such as supraventricular tachycardia (SVT), atrial flutter, or atrial fibrillation, may also occur. The presence of an atrial shunt, even if predominantly left-to-right, may be associated with a paradoxical embolus due to a transient right-to-left shunt. Ultimately, the increase in the pulmonary artery pressure and vascular resistance may result in a bidirectional atrial shunt with cyanosis (Eisenmenger syndrome) during mid to late adulthood (most commonly over the age of 40).

• #10 Ostium Secundum Atrial Septal Defects: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/890991-overview

  A secundum atrial septal defect can result from inadequate formation of the septum secundum so that it does not completely cover the ostium secundum. More often, the ostium secundum is excessively large because of increased resorption so that septum secundum cannot cover it. […] Although heart failure from secundum ASD rarely occurs in children, this complication can often occur in adults. Adults also demonstrate a propensity for atrial dysrhythmias, including atrial flutter and fibrillation, presumably caused by chronic right atrial dilation. These complications may not be reversible if closure is delayed. […] The presence of this phenomenon has been identified as a potential risk factor for stroke due to embolization into the systemic arterial circulation. […] Isolated secundum atrial septal defect occasionally demonstrates familial inheritance in an autosomal dominant pattern, particularly when associated with prolonged atrioventricular conduction (ie, prolonged PR interval on ECG). Familial secundum ASD also occurs in Holt-Oram Syndrome.

• #11 Atrial Septal Defect: Symptoms, Types & Treatment

  https://my.clevelandclinic.org/health/diseases/11622-atrial-septal-defect-asd

  An atrial septal defect (ASD) is a congenital heart defect. Its a hole in the atrial septum, the muscular wall between the two upper chambers (atria) of your heart. An atrial septal defect, or hole between your two atria, allows abnormal blood flow between them. An atrial septal defect (ASD) is a hole in the atrial septum, which is the wall that separates your hearts two upper chambers (atria). It happens when the septum doesnt form properly. An atrial septal defect creates an abnormal route for blood. Some blood from your left atrium flows in the wrong direction, into your right atrium. The bigger the ASD, the more likely it is to cause symptoms and need treatment. The exact cause of atrial septal defects isnt fully known. But genetic changes that happen before birth often cause congenital heart defects. Some genetic variations associated with atrial septal defect affect the NKX2.5/CSX, GATA4 and TBX5 genes. A larger one can strain the right side of your heart. Problems with large atrial septal defects include: Right heart enlargement. This can lead to heart failure if left uncorrected for a very long time. Abnormal heart rhythm (arrhythmia). At least half of adults over age 40 with an ASD heart have an arrhythmia like atrial fibrillation or atrial flutter. Atrial septal defect repair is essential.

• #12 Atrial Septal Defect – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535440/

  Atrial septal defect (ASD) is one of the most common types of congenital heart defects, occurring in about 25% of children. An ASD occurs when the communication between the right and left atria fails to close. ASD encompasses defects in the true septal membrane and other abnormalities that permit communication between the atria. […] ASDs occur as singular defects but are associated with Mendelian inheritance, aneuploidy, transcription errors, mutations, and maternal exposures. ASDs are noted in patients with syndromes such as Down, Treacher-Collins, thrombocytopenia-absent radii, Turner, and Noonan. These conditions occur as a result of Mendelian inheritance. Maternal exposure to rubella and drugs like cocaine and alcohol may also predispose the unborn fetus to developing an ASD. […] Atrial septation begins during the 4th week of gestation and involves a complex series of developmental events. The process starts with the growth of the primary atrial septum, or septum primum, from the roof of the primitive atrium toward the endocardial cushions. The caudal end of the septum primum becomes covered by mesenchymal cells derived from the embryonic endocardium, forming the mesenchymal cap.

• #13 Atrial Septal Defects | Nationwide Children’s Hospital

  https://www.nationwidechildrens.org/conditions/atrial-septal-defect

  In order to minimize the detrimental long-term complications related to ASD (volume and pressure overload, serious arrhythmias) and to prevent embolic events, ASD closure is usually recommended for children and adults. […] A family history/pedigree showing relatives from different generations with ASD raises strong suspicion of a genetic etiology. ASD is heterogeneous (caused by more than one gene). ASD occurs in individuals with a variety of syndromic and genetic disorders including Down syndrome (trisomy 21) and the following Mendelian genetic mutations:

• #14 Atrial Septal Defect – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535440/

  Atrial septal defect (ASD) is one of the most common types of congenital heart defects, occurring in about 25% of children. An ASD occurs when the communication between the right and left atria fails to close. ASD encompasses defects in the true septal membrane and other abnormalities that permit communication between the atria. […] ASDs occur as singular defects but are associated with Mendelian inheritance, aneuploidy, transcription errors, mutations, and maternal exposures. ASDs are noted in patients with syndromes such as Down, Treacher-Collins, thrombocytopenia-absent radii, Turner, and Noonan. These conditions occur as a result of Mendelian inheritance. Maternal exposure to rubella and drugs like cocaine and alcohol may also predispose the unborn fetus to developing an ASD. […] Atrial septation begins during the 4th week of gestation and involves a complex series of developmental events. The process starts with the growth of the primary atrial septum, or septum primum, from the roof of the primitive atrium toward the endocardial cushions. The caudal end of the septum primum becomes covered by mesenchymal cells derived from the embryonic endocardium, forming the mesenchymal cap.

• #15 Atrial Septal Defect

  https://www.uspharmacist.com/article/atrial-septal-defect

  Atrial septal defect (ASD) is a congenital cardiac disorder. It is caused by the spontaneous malformation of the interatrial septum resulting in one or more openings, commonly referred to as holes in the heart. ASD produces a left-to-right shunt, a diversion of the blood flow through an anomalous opening from the left side of the heart to the right side from the systemic to the pulmonary circulation. Factors such as the size of the defect and extent of the shunt and associated anomalies create a spectrum of disease from insignificant cardiac sequelae to right-sided volume overload, pulmonary arterial hypertension, and even atrial arrhythmias and stroke. ASD occurs with a female-to-male ratio of approximately 2 to 1. While most cases of ASD are isolated and sporadic, genetically ASD may be a familial trait, due to a chromosomal mutation, or an autosomal recessive disorder. Rubella infection and the use of certain medications, alcohol, or drugs (e.g., cocaine) during pregnancy interfere with the developing fetus and can increase the risk of a heart defect. ASDs produce a left-to-right shunt, allowing oxygen-rich blood from the left atrium to mix with oxygen-poor blood from the right atrium. Other hemodynamic changes also occur, such as pulmonary blood flow up to two to four times normal. While most isolated ASDs are well tolerated, some neonates may be vulnerable to profound congestive heart failure. Patients with ASD are at an increased risk for complications, which develop over many years and include pulmonary hypertension, heart failure, atrial fibrillation, and stroke. Atrial fibrillation or atrial flutter occurs in approximately 20% of adults who have an unrepaired ASD, with atrial fibrillation predominating in the majority of patients; incidence of these conditions increases with age. Mortality in patients with ASD is low. In general, postoperative survival is comparable to that of the general population. ASD is characterized by a defect in the interatrial septum producing a left-to-right shunt and is one of the more commonly recognized congenital cardiac anomalies presenting in adulthood. Patients with ASD are at an increased risk for developing complications including pulmonary arterial hypertension, heart failure, atrial fibrillation, and stroke.

• #16 What is Atrial Septal Defect (ASD)? – Baptist Health

  https://www.baptisthealth.com/blog/heart-care/what-is-atrial-septal-defect-asd

  Atrial septal defect (ASD) is a hole in the septum, or muscular tissue, between the left and right atria, the upper valves of the heart. […] An ASD occurs when this partition remains incomplete, leaving a hole in the heart wall. […] Like most congenital heart defects, ASDs are caused by a combination of factors including family history. A mothers condition during pregnancy, such as alcohol/drug abuse, as well as diabetes, lupus and rubella can also be contributing factors.

• #17 Atrial Septal Defect – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535440/

  The septum secundum begins to form to the right of the septum primum, growing caudally from the atrial roof and partially covering the ostium secundum. The space between the septum primum and septum secundum forms the foramen ovale. In the fetus, the foramen ovale enables oxygen-rich blood to bypass the lungs by flowing directly from the right atrium to the left atrium. After birth, pulmonary vascular resistance decreases, leading to a reduction in right atrial pressure. This pressure change causes the septum primum to close the foramen ovale, completing the separation of the atria. […] Normally, the pressure in the right atrium is significantly lower than in its left counterpart, causing blood to flow from the left atrium to the right atrium, resulting in a left-to-right shunt. The size of the defect determines the significance of the shunt. Significant shunts have a pulmonary (Qp) to systemic (Qs) flow ratio greater than 1.5:1 (Qp/Qs 1.5). Chronic volume overload from high pulmonary blood flow leads to remodeling of the pulmonary vasculature.

• #18 Atrial Septal Defect: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/162914-overview

  An atrial septal defect (ASD) is one of the more commonly recognized congenital cardiac anomalies presenting in adults. It is characterized by an abnormal connection between the upper chambers of the heart, allowing for mixing of oxygenated and deoxygenated bloodthus, a defect or hole in the interatrial septum allows pulmonary venous return (oxygenated blood) from the left atrium to pass directly to the right atrium (left-to-right shunt). […] The magnitude of the left-to-right shunt across the atrial septal defect (ASD) depends on the defect size, the relative compliance of the ventricles (ie, determinates of left atrial [LA] and right atrial [RA] pressures), and the relative resistance of the ventricles (ie, in both the pulmonary and systemic circulation. […] A chronic, significant left-to-right shunt can permanently alter the PVR, leading to pulmonary arterial hypertension and, eventually, reversal of shunt (now becoming right to left), also known as Eisenmenger syndrome.

• #19 Pathophysiology and natural history of atrial septal defect

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6174151/

  The objective of this contemporary review is to focus on the pathophysiologic mechanisms underlying the interatrial shunt. The natural history of an isolated atrial septal defect will also be addressed, as it may impact survival, exercise capacity, and favor heart failure, pulmonary hypertension and arrhythmias. […] Usually, atrial septal defects result in a left-to-right shunt. […] Both direction and magnitude of blood flow through a small atrial communication are determined by the size of the defect and by the relative atrial pressures, which relate to the compliances of the left and right ventricles. In large atrial septal defects, both atrial pressures are equalized and the shunt only depends on the ratio of the ventricular compliances. […] Therefore, any condition modifying ventricular compliances may impact the degree and direction of the interatrial shunt.

• #20 Pathophysiology and natural history of atrial septal defect

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6174151/

  The objective of this contemporary review is to focus on the pathophysiologic mechanisms underlying the interatrial shunt. The natural history of an isolated atrial septal defect will also be addressed, as it may impact survival, exercise capacity, and favor heart failure, pulmonary hypertension and arrhythmias. […] Usually, atrial septal defects result in a left-to-right shunt. […] Both direction and magnitude of blood flow through a small atrial communication are determined by the size of the defect and by the relative atrial pressures, which relate to the compliances of the left and right ventricles. In large atrial septal defects, both atrial pressures are equalized and the shunt only depends on the ratio of the ventricular compliances. […] Therefore, any condition modifying ventricular compliances may impact the degree and direction of the interatrial shunt.

• #21 Atrial Septal Defect: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/162914-overview

  An atrial septal defect (ASD) is one of the more commonly recognized congenital cardiac anomalies presenting in adults. It is characterized by an abnormal connection between the upper chambers of the heart, allowing for mixing of oxygenated and deoxygenated bloodthus, a defect or hole in the interatrial septum allows pulmonary venous return (oxygenated blood) from the left atrium to pass directly to the right atrium (left-to-right shunt). […] The magnitude of the left-to-right shunt across the atrial septal defect (ASD) depends on the defect size, the relative compliance of the ventricles (ie, determinates of left atrial [LA] and right atrial [RA] pressures), and the relative resistance of the ventricles (ie, in both the pulmonary and systemic circulation. […] A chronic, significant left-to-right shunt can permanently alter the PVR, leading to pulmonary arterial hypertension and, eventually, reversal of shunt (now becoming right to left), also known as Eisenmenger syndrome.

• #22 Pathophysiology and natural history of atrial septal defect – Gloan – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/19688/html

  Usually, atrial septal defects result in a left-to-right shunt. Both direction and magnitude of blood flow through a small atrial communication are determined by the size of the defect and by the relative atrial pressures, which relate to the compliances of the left and right ventricles. In large atrial septal defects, both atrial pressures are equalized and the shunt only depends on the ratio of the ventricular compliances. As demonstrated previously, the defect dimensions, measured by means of transthoracic echocardiography, appear to be well correlated with the pulmonary-to-systemic blood flow ratio evaluated by right heart catheterisation. […] However, right ventricular compliance is destined to change over time. At birth, pulmonary vascular resistance is high, while right ventricular compliance is low, changing gradually to a high compliance-low resistance circulation. That explains why, left-to-right shunt increases gradually during the first months of life. Therefore, any condition modifying ventricular compliances may impact the degree and direction of the interatrial shunt. Reduction in left ventricular compliance or any condition with elevation of left ventricular filling pressures (e.g., hypertension, ischemic heart disease, cardiomyopathy, aortic and mitral valve disease) will increase the left-to-right shunt. In case of a large defect, systemic venous congestion can occur. Conversely, any condition reducing right ventricular compliance (e.g., pulmonic stenosis, pulmonary hypertension, right ventricular fibrosing process) or tricuspid valve disease may decrease the left-to-right shunt and eventually cause shunt reversal, resulting in cyanosis.

• #23 Atrial Septal Defect – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535440/

  The septum secundum begins to form to the right of the septum primum, growing caudally from the atrial roof and partially covering the ostium secundum. The space between the septum primum and septum secundum forms the foramen ovale. In the fetus, the foramen ovale enables oxygen-rich blood to bypass the lungs by flowing directly from the right atrium to the left atrium. After birth, pulmonary vascular resistance decreases, leading to a reduction in right atrial pressure. This pressure change causes the septum primum to close the foramen ovale, completing the separation of the atria. […] Normally, the pressure in the right atrium is significantly lower than in its left counterpart, causing blood to flow from the left atrium to the right atrium, resulting in a left-to-right shunt. The size of the defect determines the significance of the shunt. Significant shunts have a pulmonary (Qp) to systemic (Qs) flow ratio greater than 1.5:1 (Qp/Qs 1.5). Chronic volume overload from high pulmonary blood flow leads to remodeling of the pulmonary vasculature.

• #24 Atrial Septal Defect: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/162914-overview

  Atrial septal defects (ASDs) are a congenital cardiac disorder caused by the spontaneous malformation of the interatrial septum. […] The chronic left-to-right shunt results in diastolic volume loading of the right ventricle (RV) and increased pulmonary blood flow. Over time, this chronically increased blood flow will affect the pulmonary vascular resistance (PVR) and filling/geometry of the RV and interventricular septum (IVS). […] The investigators noted that dysregulation of these genes during heart septum morphogenesis may lead to cell cycle as the dominant pathway among downregulated genes, with the potential for the decreased expression of the proteins included in the cell cycle then disturbing cardiomyocyte growth and differentiation during atrial septum formation.

• #25 Pathophysiology and natural history of atrial septal defect – Gloan – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/19688/html

  Interestingly, old hemodynamic studies have demonstrated that the left-to-right shunt mostly occurs over an interval encompassing late ventricular systole and early diastole, when both venous systems, both atria, and both ventricles are in free communication. The shunt also increases during atrial contraction. Respiration influences the shunt, as during periods with increased intrathoracic pressures, the left-to-right gradient increases and during periods with decreased intrathoracic pressures, there is a fall in the left-to-right gradient. […] In normal conditions, high right ventricular compliance explains that atrial septal defects result more often in a left-to-right shunt through the defect. The left-to-right shunt is responsible for right ventricular volume overload and pulmonary overcirculation. Relevant ventricular volume overload is usually observed when the size of the defect is greater than 10 mm. Smaller defects, although responsible for a certain degree of shunting, do not result in significant right ventricular volume overload. For larger shunts, right volume overload gives rise to enlargement of right-sided cavities. This results in altered left ventricular geometry, with the reverse Bernheims effect, proposed by Dexter et al., in which the septum bulges into and encroaches on the left ventricular cavity.

• #26 Pathophysiology and natural history of atrial septal defect – Gloan – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/19688/html

  Therefore, the interventricular interdependence gets impaired, and the left ventricle ultimately underfilled and less distensible (compressed by the dilated right ventricle), with a redirection of left atrial flow to the right atrium through the atrial septal defect, and eventually a reduction in cardiac output. Indeed, diminished left ventricular filling capacity has been suggested by the fact that left ventricular end-diastolic pressure is often comparable to or greater than that of normal subjects despite reduced left ventricular end-diastolic volume because of the atrial left-to-right shunt. […] A longstanding haemodynamically significant shunt leads to chronic right-sided cavities volume overload, and then to myocardial injury, as demonstrated by higher highly sensitive cardiac troponin I values in patients with atrial septal defects compared to matched controls. Right-sided cavities enlargement increases the myocardial oxygen demand, which results in relative hypoperfusion of the myocardium. Higher levels of angiotensine II and catecholamines, inducing necrosis and apoptosis of myocardial cells, may play a role in myocardial injury.

• #27 Pathophysiology and natural history of atrial septal defect – Gloan – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/19688/html

  Therefore, the interventricular interdependence gets impaired, and the left ventricle ultimately underfilled and less distensible (compressed by the dilated right ventricle), with a redirection of left atrial flow to the right atrium through the atrial septal defect, and eventually a reduction in cardiac output. Indeed, diminished left ventricular filling capacity has been suggested by the fact that left ventricular end-diastolic pressure is often comparable to or greater than that of normal subjects despite reduced left ventricular end-diastolic volume because of the atrial left-to-right shunt. […] A longstanding haemodynamically significant shunt leads to chronic right-sided cavities volume overload, and then to myocardial injury, as demonstrated by higher highly sensitive cardiac troponin I values in patients with atrial septal defects compared to matched controls. Right-sided cavities enlargement increases the myocardial oxygen demand, which results in relative hypoperfusion of the myocardium. Higher levels of angiotensine II and catecholamines, inducing necrosis and apoptosis of myocardial cells, may play a role in myocardial injury.

• #28 Pathophysiology and natural history of atrial septal defect – Gloan – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/19688/html

  Therefore, the interventricular interdependence gets impaired, and the left ventricle ultimately underfilled and less distensible (compressed by the dilated right ventricle), with a redirection of left atrial flow to the right atrium through the atrial septal defect, and eventually a reduction in cardiac output. Indeed, diminished left ventricular filling capacity has been suggested by the fact that left ventricular end-diastolic pressure is often comparable to or greater than that of normal subjects despite reduced left ventricular end-diastolic volume because of the atrial left-to-right shunt. […] A longstanding haemodynamically significant shunt leads to chronic right-sided cavities volume overload, and then to myocardial injury, as demonstrated by higher highly sensitive cardiac troponin I values in patients with atrial septal defects compared to matched controls. Right-sided cavities enlargement increases the myocardial oxygen demand, which results in relative hypoperfusion of the myocardium. Higher levels of angiotensine II and catecholamines, inducing necrosis and apoptosis of myocardial cells, may play a role in myocardial injury.

• #29 Pathophysiology and natural history of atrial septal defect – Gloan – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/19688/html

  Therefore, the interventricular interdependence gets impaired, and the left ventricle ultimately underfilled and less distensible (compressed by the dilated right ventricle), with a redirection of left atrial flow to the right atrium through the atrial septal defect, and eventually a reduction in cardiac output. Indeed, diminished left ventricular filling capacity has been suggested by the fact that left ventricular end-diastolic pressure is often comparable to or greater than that of normal subjects despite reduced left ventricular end-diastolic volume because of the atrial left-to-right shunt. […] A longstanding haemodynamically significant shunt leads to chronic right-sided cavities volume overload, and then to myocardial injury, as demonstrated by higher highly sensitive cardiac troponin I values in patients with atrial septal defects compared to matched controls. Right-sided cavities enlargement increases the myocardial oxygen demand, which results in relative hypoperfusion of the myocardium. Higher levels of angiotensine II and catecholamines, inducing necrosis and apoptosis of myocardial cells, may play a role in myocardial injury.

• #30 Pathophysiology and Management of Arrhythmias Associated with Atrial Septal Defect and Patent Foramen Ovale | AER Journal

  https://www.aerjournal.com/articles/pathophysiology-and-management-arrhythmias-associated-atrial-septal-defect-and-patent?language_content_entity=en

  Atrial septal defects (ASDs) are among the most common of congenital heart defects and are frequently associated with atrial arrhythmias. Atrial and ventricular geometrical remodelling secondary to the intracardiac shunt promotes evolution of the electrical substrate, predisposing the patient to atrial fibrillation and other arrhythmias. […] The left-to-right shunt enabled by the presence of an ASD results in cardiac remodelling secondary to long-standing haemodynamic overload. It is this geometrical remodelling that plays an important role in the pathogenesis of AAs. Changes in atrial tissue properties, including interstitial fibrosis, increased myocyte size and alterations in ultracellular structure have been described and predispose to AF in particular. […] Electrical remodelling has also been widely described, even in the absence of AA. The P-wave duration and dispersion is increased, with lengthened sinus node recovery time and conduction delay across the crista terminalis, which is likely to play a key role in the arrhythmogenesis of AFL. […] In summary, remodelling of both the right and left atrium contributes to arrhythmogenesis and the heterogeneity of that remodelling process between atria may contribute to the propensity for native arrhythmias in this patient group.

• #31 Pathophysiology and Management of Arrhythmias Associated with Atrial Septal Defect and Patent Foramen Ovale | AER Journal

  https://www.aerjournal.com/articles/pathophysiology-and-management-arrhythmias-associated-atrial-septal-defect-and-patent?language_content_entity=en

  Atrial septal defects (ASDs) are among the most common of congenital heart defects and are frequently associated with atrial arrhythmias. Atrial and ventricular geometrical remodelling secondary to the intracardiac shunt promotes evolution of the electrical substrate, predisposing the patient to atrial fibrillation and other arrhythmias. […] The left-to-right shunt enabled by the presence of an ASD results in cardiac remodelling secondary to long-standing haemodynamic overload. It is this geometrical remodelling that plays an important role in the pathogenesis of AAs. Changes in atrial tissue properties, including interstitial fibrosis, increased myocyte size and alterations in ultracellular structure have been described and predispose to AF in particular. […] Electrical remodelling has also been widely described, even in the absence of AA. The P-wave duration and dispersion is increased, with lengthened sinus node recovery time and conduction delay across the crista terminalis, which is likely to play a key role in the arrhythmogenesis of AFL. […] In summary, remodelling of both the right and left atrium contributes to arrhythmogenesis and the heterogeneity of that remodelling process between atria may contribute to the propensity for native arrhythmias in this patient group.

• #32 Pathophysiology and Management of Arrhythmias Associated with Atrial Septal Defect and Patent Foramen Ovale | AER Journal

  https://www.aerjournal.com/articles/pathophysiology-and-management-arrhythmias-associated-atrial-septal-defect-and-patent?language_content_entity=en

  Atrial septal defects (ASDs) are among the most common of congenital heart defects and are frequently associated with atrial arrhythmias. Atrial and ventricular geometrical remodelling secondary to the intracardiac shunt promotes evolution of the electrical substrate, predisposing the patient to atrial fibrillation and other arrhythmias. […] The left-to-right shunt enabled by the presence of an ASD results in cardiac remodelling secondary to long-standing haemodynamic overload. It is this geometrical remodelling that plays an important role in the pathogenesis of AAs. Changes in atrial tissue properties, including interstitial fibrosis, increased myocyte size and alterations in ultracellular structure have been described and predispose to AF in particular. […] Electrical remodelling has also been widely described, even in the absence of AA. The P-wave duration and dispersion is increased, with lengthened sinus node recovery time and conduction delay across the crista terminalis, which is likely to play a key role in the arrhythmogenesis of AFL. […] In summary, remodelling of both the right and left atrium contributes to arrhythmogenesis and the heterogeneity of that remodelling process between atria may contribute to the propensity for native arrhythmias in this patient group.

• #33 Pathophysiology and Management of Arrhythmias Associated with Atrial Septal Defect and Patent Foramen Ovale | AER Journal

  https://www.aerjournal.com/articles/pathophysiology-and-management-arrhythmias-associated-atrial-septal-defect-and-patent?language_content_entity=en

  Atrial septal defects (ASDs) are among the most common of congenital heart defects and are frequently associated with atrial arrhythmias. Atrial and ventricular geometrical remodelling secondary to the intracardiac shunt promotes evolution of the electrical substrate, predisposing the patient to atrial fibrillation and other arrhythmias. […] The left-to-right shunt enabled by the presence of an ASD results in cardiac remodelling secondary to long-standing haemodynamic overload. It is this geometrical remodelling that plays an important role in the pathogenesis of AAs. Changes in atrial tissue properties, including interstitial fibrosis, increased myocyte size and alterations in ultracellular structure have been described and predispose to AF in particular. […] Electrical remodelling has also been widely described, even in the absence of AA. The P-wave duration and dispersion is increased, with lengthened sinus node recovery time and conduction delay across the crista terminalis, which is likely to play a key role in the arrhythmogenesis of AFL. […] In summary, remodelling of both the right and left atrium contributes to arrhythmogenesis and the heterogeneity of that remodelling process between atria may contribute to the propensity for native arrhythmias in this patient group.

• #34 Atrial Septal Defect – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535440/

  The smooth muscle layer in the vascular wall thickens as the pulmonary vessels remodel. This increase in muscle mass raises the resistance to flow in the pulmonary circuit. Pulmonary hypertension develops due to the rise in vascular resistance and, subsequently, pulmonary pressures. When pulmonary pressures equal systemic pressures, the shunt across the ASD reverses, allowing deoxygenated blood to flow into the left atrium and, ultimately, the systemic circulation. This reversal of the shunt due to pulmonary hypertension leads to Eisenmenger syndrome.

• #35 Atrial Septal Defect – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535440/

  The smooth muscle layer in the vascular wall thickens as the pulmonary vessels remodel. This increase in muscle mass raises the resistance to flow in the pulmonary circuit. Pulmonary hypertension develops due to the rise in vascular resistance and, subsequently, pulmonary pressures. When pulmonary pressures equal systemic pressures, the shunt across the ASD reverses, allowing deoxygenated blood to flow into the left atrium and, ultimately, the systemic circulation. This reversal of the shunt due to pulmonary hypertension leads to Eisenmenger syndrome.

• #36 Atrial Septal Defect (ASD) | University of Michigan Health

  https://www.uofmhealth.org/conditions-treatments/ped-heart/conditions/atrial-septal-defect

  Possible long term effects of moderate and large atrial defects include pulmonary artery hypertension, congestive heart failure, and abnormal heart rhythms (arrhythmias). The size of the defect determines how much blood returns to the right heart and to the lungs. Large defects allow up to 2 to 3 times the ordinary amount of blood to circulate through the heart’s right side. Over time this results in enlargement of the right atrium and the right ventricle due to the extra workload. In response to the extra blood flow, the wall of the pulmonary arteries becomes thick and stiff leading to a condition called pulmonary vascular obstructive disease. Long term effects of moderate to large atrial septal defects can include abnormal heart rhythms, most often atrial flutter or atrial fibrillation. This problem is related to stretching of the atrial chamber from the extra blood flow.

• #37 Atrial Septal Defect – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535440/

  The smooth muscle layer in the vascular wall thickens as the pulmonary vessels remodel. This increase in muscle mass raises the resistance to flow in the pulmonary circuit. Pulmonary hypertension develops due to the rise in vascular resistance and, subsequently, pulmonary pressures. When pulmonary pressures equal systemic pressures, the shunt across the ASD reverses, allowing deoxygenated blood to flow into the left atrium and, ultimately, the systemic circulation. This reversal of the shunt due to pulmonary hypertension leads to Eisenmenger syndrome.

• #38 Atrial septal defect – Wikipedia

  https://en.wikipedia.org/wiki/Atrial_septal_defect

  A patent foramen ovale (PFO) is a remnant opening of the fetal foramen ovale, which often closes after a person’s birth. This remnant opening is caused by the incomplete fusion of the septum primum and the septum secundum; in healthy hearts, this fusion forms the fossa ovalis, a portion of the interatrial septum which corresponds to the location of the foramen ovale in the fetus. […] The mechanism by which a PFO may play a role in stroke is called paradoxical embolism. In the case of PFO, a blood clot from the venous circulatory system is able to pass from the right atrium directly into the left atrium via the PFO, rather than being filtered by the lungs, and thereupon into systemic circulation toward the brain. […] If the ASD is left uncorrected, the pulmonary hypertension progresses and the pressure in the right side of the heart becomes greater than the left side of the heart. This reversal of the pressure gradient across the ASD causes the shunt to reverse a right-to-left shunt. This phenomenon is known as Eisenmenger’s syndrome. Once right-to-left shunting occurs, a portion of the oxygen-poor blood gets shunted to the left side of the heart and ejected to the peripheral vascular system. This causes signs of cyanosis.

• #39 Atrial septal defect pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Atrial_septal_defect_pathophysiology

  If left uncorrected, the pressure in the right side of the heart will be greater than the left side of the heart. This will cause the pressure in the right atrium to be higher than the pressure in the left atrium. This will reverse the pressure gradient across the ASD, and the shunt will reverse; a right-to-left shunt will exist. This phenomenon is known as Eisenmenger’s syndrome. Once right-to-left shunting occurs, a portion of the oxygen-poor blood will get shunted to the left side of the heart and ejected to the peripheral vascular system. This will cause signs of cyanosis. once Eisenmenger’s syndrome develops, the patient can no longer benefit from surgery to correct the defect.

• #40 Atrial septal defect pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Atrial_septal_defect_pathophysiology

  If left uncorrected, the pressure in the right side of the heart will be greater than the left side of the heart. This will cause the pressure in the right atrium to be higher than the pressure in the left atrium. This will reverse the pressure gradient across the ASD, and the shunt will reverse; a right-to-left shunt will exist. This phenomenon is known as Eisenmenger’s syndrome. Once right-to-left shunting occurs, a portion of the oxygen-poor blood will get shunted to the left side of the heart and ejected to the peripheral vascular system. This will cause signs of cyanosis. once Eisenmenger’s syndrome develops, the patient can no longer benefit from surgery to correct the defect.

• #41 Pathophysiology and natural history of atrial septal defect

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6174151/

  The objective of this contemporary review is to focus on the pathophysiologic mechanisms underlying the interatrial shunt. The natural history of an isolated atrial septal defect will also be addressed, as it may impact survival, exercise capacity, and favor heart failure, pulmonary hypertension and arrhythmias. […] Usually, atrial septal defects result in a left-to-right shunt. […] Both direction and magnitude of blood flow through a small atrial communication are determined by the size of the defect and by the relative atrial pressures, which relate to the compliances of the left and right ventricles. In large atrial septal defects, both atrial pressures are equalized and the shunt only depends on the ratio of the ventricular compliances. […] Therefore, any condition modifying ventricular compliances may impact the degree and direction of the interatrial shunt.

• #42 Pathophysiology and natural history of atrial septal defect – Gloan – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/19688/html

  Usually, atrial septal defects result in a left-to-right shunt. Both direction and magnitude of blood flow through a small atrial communication are determined by the size of the defect and by the relative atrial pressures, which relate to the compliances of the left and right ventricles. In large atrial septal defects, both atrial pressures are equalized and the shunt only depends on the ratio of the ventricular compliances. As demonstrated previously, the defect dimensions, measured by means of transthoracic echocardiography, appear to be well correlated with the pulmonary-to-systemic blood flow ratio evaluated by right heart catheterisation. […] However, right ventricular compliance is destined to change over time. At birth, pulmonary vascular resistance is high, while right ventricular compliance is low, changing gradually to a high compliance-low resistance circulation. That explains why, left-to-right shunt increases gradually during the first months of life. Therefore, any condition modifying ventricular compliances may impact the degree and direction of the interatrial shunt. Reduction in left ventricular compliance or any condition with elevation of left ventricular filling pressures (e.g., hypertension, ischemic heart disease, cardiomyopathy, aortic and mitral valve disease) will increase the left-to-right shunt. In case of a large defect, systemic venous congestion can occur. Conversely, any condition reducing right ventricular compliance (e.g., pulmonic stenosis, pulmonary hypertension, right ventricular fibrosing process) or tricuspid valve disease may decrease the left-to-right shunt and eventually cause shunt reversal, resulting in cyanosis.

• #43 Pathophysiology and natural history of atrial septal defect – Gloan – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/19688/html

  Usually, atrial septal defects result in a left-to-right shunt. Both direction and magnitude of blood flow through a small atrial communication are determined by the size of the defect and by the relative atrial pressures, which relate to the compliances of the left and right ventricles. In large atrial septal defects, both atrial pressures are equalized and the shunt only depends on the ratio of the ventricular compliances. As demonstrated previously, the defect dimensions, measured by means of transthoracic echocardiography, appear to be well correlated with the pulmonary-to-systemic blood flow ratio evaluated by right heart catheterisation. […] However, right ventricular compliance is destined to change over time. At birth, pulmonary vascular resistance is high, while right ventricular compliance is low, changing gradually to a high compliance-low resistance circulation. That explains why, left-to-right shunt increases gradually during the first months of life. Therefore, any condition modifying ventricular compliances may impact the degree and direction of the interatrial shunt. Reduction in left ventricular compliance or any condition with elevation of left ventricular filling pressures (e.g., hypertension, ischemic heart disease, cardiomyopathy, aortic and mitral valve disease) will increase the left-to-right shunt. In case of a large defect, systemic venous congestion can occur. Conversely, any condition reducing right ventricular compliance (e.g., pulmonic stenosis, pulmonary hypertension, right ventricular fibrosing process) or tricuspid valve disease may decrease the left-to-right shunt and eventually cause shunt reversal, resulting in cyanosis.

• #44 Pathophysiology and natural history of atrial septal defect – Gloan – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/19688/html

  Interestingly, old hemodynamic studies have demonstrated that the left-to-right shunt mostly occurs over an interval encompassing late ventricular systole and early diastole, when both venous systems, both atria, and both ventricles are in free communication. The shunt also increases during atrial contraction. Respiration influences the shunt, as during periods with increased intrathoracic pressures, the left-to-right gradient increases and during periods with decreased intrathoracic pressures, there is a fall in the left-to-right gradient. […] In normal conditions, high right ventricular compliance explains that atrial septal defects result more often in a left-to-right shunt through the defect. The left-to-right shunt is responsible for right ventricular volume overload and pulmonary overcirculation. Relevant ventricular volume overload is usually observed when the size of the defect is greater than 10 mm. Smaller defects, although responsible for a certain degree of shunting, do not result in significant right ventricular volume overload. For larger shunts, right volume overload gives rise to enlargement of right-sided cavities. This results in altered left ventricular geometry, with the reverse Bernheims effect, proposed by Dexter et al., in which the septum bulges into and encroaches on the left ventricular cavity.

• #45 Pathophysiology and natural history of atrial septal defect – Gloan – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/19688/html

  Usually, atrial septal defects result in a left-to-right shunt. Both direction and magnitude of blood flow through a small atrial communication are determined by the size of the defect and by the relative atrial pressures, which relate to the compliances of the left and right ventricles. In large atrial septal defects, both atrial pressures are equalized and the shunt only depends on the ratio of the ventricular compliances. As demonstrated previously, the defect dimensions, measured by means of transthoracic echocardiography, appear to be well correlated with the pulmonary-to-systemic blood flow ratio evaluated by right heart catheterisation. […] However, right ventricular compliance is destined to change over time. At birth, pulmonary vascular resistance is high, while right ventricular compliance is low, changing gradually to a high compliance-low resistance circulation. That explains why, left-to-right shunt increases gradually during the first months of life. Therefore, any condition modifying ventricular compliances may impact the degree and direction of the interatrial shunt. Reduction in left ventricular compliance or any condition with elevation of left ventricular filling pressures (e.g., hypertension, ischemic heart disease, cardiomyopathy, aortic and mitral valve disease) will increase the left-to-right shunt. In case of a large defect, systemic venous congestion can occur. Conversely, any condition reducing right ventricular compliance (e.g., pulmonic stenosis, pulmonary hypertension, right ventricular fibrosing process) or tricuspid valve disease may decrease the left-to-right shunt and eventually cause shunt reversal, resulting in cyanosis.

• #46 Atrial septal defect – WikEM

  https://wikem.org/wiki/Atrial_septal_defect

  Many ASDs go undiagnosed in childhood. […] Spontaneous closure in up to 40% of patients within the first 5 years of life. […] LV stiffness increases as a part of normal aging, impairing left heart diastolic filling. […] Increases left to right shunt across ASD. […] Produces RA and RV volume overload. […] May predispose to paradoxical embolus, causing stroke, TIA, acute limb ischemia, mesenteric ischemia, etc. […] Right to left shunt may occur during coughing, for example. […] Pulmonary hypertension produces this shunting pattern even at rest. […] Unlike ventricular septal defects, uncomplicated ASDs are not associated with high risk of bacterial endocarditis (lower turbulence and velocity of blood flow). […] Crochetage pattern on ECG for atrial septal defect. […] An ECG may show the crochetage pattern (92% specific) a notch near the apex of the R wave in inferior limb leads.

• #47 Atrial septal defect – Wikipedia

  https://en.wikipedia.org/wiki/Atrial_septal_defect

  A patent foramen ovale (PFO) is a remnant opening of the fetal foramen ovale, which often closes after a person’s birth. This remnant opening is caused by the incomplete fusion of the septum primum and the septum secundum; in healthy hearts, this fusion forms the fossa ovalis, a portion of the interatrial septum which corresponds to the location of the foramen ovale in the fetus. […] The mechanism by which a PFO may play a role in stroke is called paradoxical embolism. In the case of PFO, a blood clot from the venous circulatory system is able to pass from the right atrium directly into the left atrium via the PFO, rather than being filtered by the lungs, and thereupon into systemic circulation toward the brain. […] If the ASD is left uncorrected, the pulmonary hypertension progresses and the pressure in the right side of the heart becomes greater than the left side of the heart. This reversal of the pressure gradient across the ASD causes the shunt to reverse a right-to-left shunt. This phenomenon is known as Eisenmenger’s syndrome. Once right-to-left shunting occurs, a portion of the oxygen-poor blood gets shunted to the left side of the heart and ejected to the peripheral vascular system. This causes signs of cyanosis.

• #48 Atrial septal defect – WikEM

  https://wikem.org/wiki/Atrial_septal_defect

  Many ASDs go undiagnosed in childhood. […] Spontaneous closure in up to 40% of patients within the first 5 years of life. […] LV stiffness increases as a part of normal aging, impairing left heart diastolic filling. […] Increases left to right shunt across ASD. […] Produces RA and RV volume overload. […] May predispose to paradoxical embolus, causing stroke, TIA, acute limb ischemia, mesenteric ischemia, etc. […] Right to left shunt may occur during coughing, for example. […] Pulmonary hypertension produces this shunting pattern even at rest. […] Unlike ventricular septal defects, uncomplicated ASDs are not associated with high risk of bacterial endocarditis (lower turbulence and velocity of blood flow). […] Crochetage pattern on ECG for atrial septal defect. […] An ECG may show the crochetage pattern (92% specific) a notch near the apex of the R wave in inferior limb leads.

• #49 Pathophysiology and natural history of atrial septal defect

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6174151/

  A longstanding haemodynamically significant shunt leads to chronic right-sided cavities volume overload, and then to myocardial injury, as demonstrated by higher highly sensitive cardiac troponin I values in patients with atrial septal defects compared to matched controls. […] Atrial septal defects allow communication between the systemic and the pulmonary circulations. The nature of the shunt, including direction and magnitude of blood flow, depends on both the size of the defect and the relative atrial pressures, which relate to the compliances of the left and right ventricles. Any hemodynamic condition modifying the ventricular compliances or intracardiac pressures will impact the interatrial shunt. A longstanding significant interatrial shunt will lead to a chronic right-sided cavities overload, and therefore will impact survival and morbidity.

• #50 Pathophysiology and natural history of atrial septal defect – Gloan – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/19688/html

  Atrial septal defects allow communication between the systemic and the pulmonary circulations. The nature of the shunt, including direction and magnitude of blood flow, depends on both the size of the defect and the relative atrial pressures, which relate to the compliances of the left and right ventricles. Any hemodynamic condition modifying the ventricular compliances or intracardiac pressures will impact the interatrial shunt. A longstanding significant interatrial shunt will lead to a chronic right-sided cavities overload, and therefore will impact survival and morbidity. Significant interatrial shunting may decrease exercise capacity, favor atrial arrhythmias, contribute to the development of heart failure and pulmonary hypertension, and ultimately impact survival.

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