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Transcript
ATRIAL SEPTAL DEFECT Dr. M. A. Sofi MD; FRCP (London); FRCPEdin; FRCSEdin Atrial septal defect • Atrial septal defect is characterized by a defect in the interatrial septum allowing pulmonary venous return from the left atrium to pass directly to the right atrium. • Depending on the size of the defect, size of the shunt, and associated anomalies, this can result: – No significant cardiac sequelae – Right-sided volume overload – Pulmonary arterial hypertension – Atrial arrhythmias. The subtle physical examination minimal symptoms during the first 2-3 decades contribute to a delay in diagnosis until adulthood Majority (more than 70%) of which is detected by the fifth decade. Atrial septal defect Frequency • The 3 major types of atrial septal defect (ASD) account for 10% of all CHD and as much as 20-40% of congenital heart disease presenting in adulthood • Ostium secundum: Most common accounting for 75% of ASD cases • Ostium primum: Second most common accounting for 15-20% ASDs • Sinus venosus: Least common of the three, accounting for 5-10% ASDs Sex: F- M ratio of approximately 2:1. Age: ASD can be asymptomatic through infancy and childhood • Clinical presentation depends on the degree of left-to-right shunt. • By the age of 40 years, 90% of untreated patients have symptoms of • Exertional dyspnea • Fatigue, palpitation • Sustained arrhythmia • Heart failure CLASSIFICATION — ASDs are classified according to their location and the nature of the embryologic defect: Isolated ASDs include patent foramen ovale (PFO), ASD at the fossa ovalis (secundum ASD), superior sinus venosus defect, inferior sinus venosus defect, and coronary sinus defects • Secundum ASD — Defects in the foramen ovalis are classified as secundum type ASD. This type of ASD can result from poor growth of the secundum septum or excessive absorption of the primum septum • This defect accounts for 70 to 75 percent of all ASDs and is more common in females. • The rare combination of an ASD with mitral stenosis, the result is known as Lutembacher syndrome • Primum ASD — The primum type ASD develops if the primum septum does not fuse with the endocardial cushions, leaving a defect at the base of the interatrial septum that is usually large . • This type of defect accounts for 15 to 20 percent of ASDs. • It has been suggested that both partial and complete AV canal defects are related to maldevelopment of the ventricular septum rather than a decrease in atrial septal tissue Atrial septal defects A. The normal atrial septum B. Secundum ASD is formed by the poor growth of the septum secundum or excessive absorption of the septum primum. C. Primum ASD is formed by the failure of the septum primum to fuse with the endocardial cushions. The fossa ovalis is normal. D. Sinus venosus ASD is caused by the malposition of the insertion of the superior or inferior vena cava and is outside the area of the fossa ovalis. Pathophysiology: Left-to-right shunting occurs primarily in late ventricular systole and early diastole, with some augmentation during atrial systole. Even when the right and left atrial pressures are equal, as occurs with a large defect, left-to-right shunting still occurs because of the greater compliance of the right compared to left ventricle. Clinical presentation • Significant mitral regurgitation is associated with septum primum ASD • Its incidence, extent, and degree of dysfunction increases with age. • Mitral valve insufficiency leads to further increase in left atrial pressure and a higher degree of left-toright shunt. • Most common presenting symptoms include: • Dyspnea • Fatigability • Palpitations • Arrhythmia • Syncope • Stroke • Heart failure PHYSICAL FINDINGS: Classic physical findings of ASD are related to the size and location of the defect, the size of the shunt at atrial level, and the pulmonary arterial pressure. • Precordial palpation — large left-to-right shunts can lead to: • An enlarged right ventricle with right ventricular heave. • It can also cause left precordial bulge. • Enlarged of the pulmonary artery with a palpable pulmonary artery impulse. • This may be more pronounced in patients with pulmonary hypertension. Heart sounds: Characteristic finding is fixed splitting of the second heart sound (S2). Heart murmurs: • Mid systolic pulmonary flow/ ejection murmur loudest over the 2nd left intercostal space • Mitral regurgitation: due to a cleft mitral valve in ostium primum defects and mitral valve prolapse in secundum defects. • A diastolic rumble due to the increased flow across the TV Clinical presentation Atrial arrhythmias: Common manifestation of an ASD. • The risk of atrial arrhythmias increases with increasing age. • Patients with AF are at risk for embolic events. Stroke due to paradoxical embolization: • Patients with a PFO or, much less often, an ASD with a right-to-left shunt are at risk for stroke due to paradoxical embolization (stroke, TIA, or peripheral emboli). • Migraine headache: Evidence is conflicting whether migraine is associated with right to left shunt via PFO or ASD • Pulmonary hypertension and Eisenmenger syndrome: The development of pulmonary vascular injury is related to the degree and duration of right heart volume overload. • Cyanosis — Cyanosis in ASD is either concomitant pulmonary valve stenosis resulting in elevated right heart pressures, and thus right-to-left shunt, or Eisenmenger syndrome Physical examination • Depend on the degree of left-to-right shunt • Hyperdynamic right ventricular impulse due to large stroke volume • Pulsation of the pulmonary artery and an ejection click can be detected • S1 is typically split, and increased in intensity second component • S2 is often widely split and fixed • Systolic ejection murmur in the second intercostal space • Ostium primum defect an apical systolic regurgitant murmur of mitral regurgitation may be present. Laboratory Studies Routine laboratory studies should for ASD include: • CBC/LFT/TFT/BUN/ • Metabolic profile or chemistry • Coagulation studies (prothrombin time [PT] and activated partial thromboplastin time [aPTT]) Electrocardiogram: • The ECG may be normal with an uncomplicated ASD and small shunt. • Atrial arrhythmias often occur beyond the third decade (especially atrial fibrillation but also atrial flutter and supraventricular tachycardia). Echocardiogram — is the imaging modality of choice for ASD diagnosis Imaging Studies CXR may reveal: • Cardiomegaly because of dilatation of the right atrium and right ventricular chamber. • Prominent Pulmonary artery and pulmonary vascular markings • Left atrial enlargement is rare only if clinically significant mitral regurgitation. • Dilatation of the superior vena cava can be seen in sinus venosus defect. • Transthoracic and Transesophageal echocardiography can provide excellent definition of the atrial septum. • TEE is also useful in guiding device placement during catheter ASD occlusion procedures and in providing immediate intra-operative assurance that defect closure is accomplished. ASD with pulmonary arterial hypertension Normal chest radiograph The plain frontal chest radiograph in a patient with a known atrial septal defect demonstrates typical features including an enlarged right atrium and right ventricle with marked prominence of the hilar or proximal pulmonary arterial vasculature (arrows). Treatment • The decision to repair any kind of atrial septal defect (ASD) is based on clinical and echocardiographic information • The size and location of the ASD • Hemodynamic impact of the left-to-right shunt • The presence and degree of pulmonary arterial hypertension • Elective closure is advised for all ASDs with right ventricular overload or with a clinically significant shunt • The widespread use of catheter closure of secundum ASD with lower mortality has raised the question regarding the need to close even small defects Contraindications to surgical repair • Closure of ASD is not recommended in patients with a clinically insignificant shunt • Those who have severe pulmonary arterial hypertension or irreversible pulmonary vascular occlusive disease • Those who have a reversed shunt with atrest arterial oxygen saturations of less than 90%. • In addition to the high surgical mortality and morbidity risk, closure of a defect in the latter situation may worsen the prognosis. • Those patients whose condition is diagnosed well in the sixth decade of life would benefit from surgical closure remains controversial.