Left ventricular to right atrial (LV-RA) shunts, also known as Gerbode defects, represent a relatively uncommon yet clinically significant form of cardiac communication. While traditionally associated with congenital anomalies, the incidence of acquired LV-RA shunts has seen a notable rise in recent years, necessitating a comprehensive understanding of their etiology, presentation, diagnosis, and management. This review aims to provide a detailed overview of both congenital and acquired LV-RA shunts, focusing on their pathophysiology, clinical implications, and current treatment strategies.
I. Congenital Left Ventricular to Right Atrial Shunt (Gerbode Defect):
Congenital LV-RA shunts are rare cardiac malformations, typically resulting from incomplete closure of the atrioventricular septum during fetal development. The precise incidence remains unclear due to the infrequent nature of the defect and the challenges in its early diagnosis. These shunts are usually small, and their clinical presentation often remains asymptomatic during childhood and even into adulthood. However, larger shunts can lead to significant hemodynamic consequences, including volume overload of the right heart, pulmonary hypertension, and right heart failure.
The diagnosis of congenital LV-RA shunts often relies on echocardiography, which can visualize the abnormal communication between the left ventricle and the right atrium. Cardiac catheterization may be necessary for precise assessment of shunt size and hemodynamic parameters. Surgical closure is generally recommended for symptomatic patients or those with large shunts, aiming to alleviate right heart strain and prevent long-term complications. The surgical approach typically involves direct closure of the defect using sutures or patches. The surgical outcome is generally favorable, with excellent long-term survival rates reported in the literature.
II. Acquired Left Ventricular–Right Atrium Shunts:
In contrast to their congenital counterparts, acquired LV-RA shunts are increasingly recognized as a clinically significant entity. Their incidence is rising, potentially due to improved diagnostic imaging techniques and increased survival rates of patients with underlying cardiac conditions. Several factors contribute to the development of acquired LV-RA shunts:
* Mitral Valve Disease: This is arguably the most common cause. Severe mitral regurgitation (MR), particularly when associated with left ventricular dilation and dysfunction, can lead to the formation of a shunt through various mechanisms. These include perforation of the mitral valve annulus, stretching and thinning of the interventricular septum, or the development of a fistulous tract between the left ventricle and the right atrium. The increased left ventricular pressure associated with severe MR can exacerbate the risk of shunt formation.
* Myocardial Infarction: Acute myocardial infarction (AMI) can damage the interventricular septum, potentially creating a pathway for blood to flow from the left ventricle to the right atrium. This is more likely to occur in cases of extensive septal infarction, leading to septal rupture or pseudoaneurysm formation. The resulting LV-RA shunt can manifest acutely or develop gradually over time.
* Infective Endocarditis: Bacterial endocarditis can cause destruction of the cardiac valves and surrounding tissues, leading to the formation of fistulas, including those between the left ventricle and the right atrium. This complication is particularly serious, as it can be associated with significant morbidity and mortality.
* Traumatic Injury: Penetrating or blunt trauma to the chest can cause damage to the interventricular septum or mitral valve apparatus, resulting in the formation of an LV-RA shunt.
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