Signs and symptoms of mitral stenosis include the following:

- Heart failure symptoms, such as dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea (PND)

- Palpitations

- Chest pain

- Hemoptysis

- Thromboembolism in later stages when the left atrial volume is increased (i.e., dilation). The latter leads to increase risk of atrial fibrillation, which increases the risk of blood stasis (motionless). This increases the risk of coagulation.

- Ascites and edema and hepatomegaly (if right-side heart failure develops)

Fatigue and weakness increase with exercise and pregnancy.

The ostium secundum atrial septal defect is the most common type of atrial septal defect, and comprises 6–10% of all congenital heart diseases.

The secundum atrial septal defect usually arises from an enlarged foramen ovale, inadequate growth of the septum secundum, or excessive absorption of the septum primum. About 10 to 20% of individuals with ostium secundum ASDs also have mitral valve prolapse.

An ostium secundum ASD accompanied by an acquired mitral valve stenosis is called Lutembacher's syndrome.

Most individuals with an uncorrected secundum ASD do not have significant symptoms through early adulthood. More than 70% develop symptoms by about 40 years of age. Symptoms are typically decreased exercise tolerance, easy fatigability, palpitations, and syncope.

Complications of an uncorrected secundum ASD include pulmonary hypertension, right-sided heart failure, atrial fibrillation or flutter, stroke, and Eisenmenger's syndrome.

While pulmonary hypertension is unusual before 20 years of age, it is seen in 50% of individuals above the age of 40. Progression to Eisenmenger's syndrome occurs in 5 to 10% of individuals late in the disease process.

At birth, the ductus arteriosus is still open, and there is higher than normal resistance to blood flow in the lungs. This allows for adequate oxygenation via mixing between the atria and a normal appearance at birth. When the ductus begins to close and pulmonary vascular resistance decreases, blood flow through the ductus is restricted and flow to the lungs is increased, reducing oxygen delivery to the systemic circulation. This results in cyanosis and respiratory distress which can progress to cardiogenic shock. The first symptoms are cyanosis that does not respond to oxygen administration or poor feeding. Peripheral pulses may be weak and extremities cool to the touch.

HLHS often co-occurs with low birth weight and premature birth.

In neonates with a small atrial septal defect, termed "restrictive", there is inadequate mixing of oxygenated and deoxygenated blood. These neonates quickly decompensate and develop acidosis and cyanosis.

On EKG, right axis deviation and right ventricular hypertrophy are common, but not indicative of HLHS. Chest x-ray may show a large heart (cardiomegaly) or increased pulmonary vasculature. Neonates with HLHS do not typically have a heart murmur, but in some cases, a pulmonary flow murmur or tricuspid regurgitation murmur may be audible.

Co-occurring tricuspid regurgitation or right ventricular dysfunction can cause hepatomegaly to develop.

d vessels can present a large variety of , and/or . The effects may range from a change in blood pressure to an interruption in circulation, depending on the nature and degree of the misplacement and which vessels are involved.

Although "transposed" literally means "swapped", many types of TGV involve vessels that are in abnormal positions, while not actually being swapped with each other. The terms TGV and TGA are most commonly used in reference to dextro-TGA – in which the arteries "are" in swapped positions; however, both terms are also commonly used, though to a slightly lesser extent, in reference to levo-TGA – in which both the arteries and the ventricles are swapped; while other defects in this category are almost never referred to by either of these terms.

In dextro-Transposition of the great arteries (dextro-TGA) deoxygenated blood from the right heart is pumped immediately through the aorta and circulated to the body and the heart itself, bypassing the lungs altogether, while the left heart pumps oxygenated blood continuously back into the lungs through the pulmonary artery. In effect, two separate "circular" (parallel) circulatory systems are created. It is called a cyanotic congenital heart defect (CHD) because the newborn infant turns blue from lack of oxygen.

Mitral stenosis is a valvular heart disease characterized by the narrowing of the orifice of the mitral valve of the heart.

Isomerism of the bronchial tree is not typically damaging and presents no significant clinical complications. Pulmonary valve stenosis results in issues of blood flow to the lungs.

Abdominal organs, including the liver, stomach, intestinal tract, and spleen may be randomly arranged throughout the left-right axis of the body. Distribution of these organs largely dictates treatment, clinical outcomes, and further evaluation.

The liver is typically symmetrical across the left-right axis in patients with situs ambiguous, which is abnormal. A majority of left atrial isomeric patients have defects throughout the biliary tree, which is responsible for bile production, even when the gall bladder is functional and morphologically normal. This biliary atresia can lead to acute problems such as nutrient malabsorption, pale stools, dark urine, and abdominal swelling. If this condition continues without proper treatment, cirrhosis and liver failure become a major concern. Biliary atresia is not usually observed in patients with right atrial isomerism.

Random positioning of the stomach is often one of the first signals of situs ambiguous upon examination. Malrotation of the entire intestinal tract, or improper folding and bulging of the stomach and intestines, results in bowel obstruction. This impairment leads to vomiting, abdominal distention, mucus and blood in the stool. Patients may also experience abdominal pain. Intestinal malrotation is more commonly identified in patients with right atrial isomerism than in those with left atrial isomerism.

Isomeric patients often experience disruptions to splenic development during embryogenesis, resulting in an overall lack a spleen (asplenia) or development of many spleens (polysplenia). Asplenia is most often observed in patients with right atrial isomerism. Polysplenia results in 90% of patients with left atrial isomerism. Although they have many spleens, each is usually ineffective resulting in functional asplenia. Rarely, left atrial isomeric patients have a single, normal, functional spleen. Patients lacking a functional spleen are in danger of sepsis and must be monitored.

Hypoplastic left heart syndrome (HLHS) is a rare congenital heart defect in which the left side of the heart is severely underdeveloped. It may affect the left ventricle, aorta, aortic valve, or mitral valve.

A sinus venosus atrial septal defect is a type of atrial septal defect primarily associated with the sinus venosus.

They represent 5% of atrial septal defects.

They can occur near the superior vena cava or inferior vena cava, but the former are more common.

They can be associated with anomalous pulmonary venous connection.

Cor triatriatum (or triatrial heart) is a congenital heart defect where the left atrium (cor triatriatum sinistrum) or right atrium (cor triatriatum dextrum) is subdivided by a thin membrane, resulting in three atrial chambers (hence the name).

Cor triatriatum represents 0.1% of all congenital cardiac malformations and may be associated with other cardiac defects in as many as 50% of cases. The membrane may be complete or may contain one or more fenestrations of varying size.

Cor triatrium sinistrum is more common. In this defect there is typically a proximal chamber that receives the pulmonic veins and a distal (true) chamber located more anteriorly where it empties into the mitral valve. The membrane that separates the atrium into two parts varies significantly in size and shape. It may appear similar to a diaphragm or be funnel-shaped, bandlike, entirely intact (imperforate) or contain one or more openings (fenestrations) ranging from small, restrictive-type to large and widely open.

In the pediatric population, this anomaly may be associated with major congenital cardiac lesions such as tetralogy of Fallot, double outlet right ventricle, coarctation of the aorta, partial anomalous pulmonary venous connection, persistent left superior vena cava with unroofed coronary sinus, ventricular septal defect, atrioventricular septal (endocardial cushion) defect, and common atrioventricular canal. Rarely, asplenia or polysplenia has been reported in these patients.

In the adult, cor triatriatum is frequently an isolated finding.

Cor triatriatum dextrum is extremely rare and results from the complete persistence of the right sinus valve of the embryonic heart. The membrane divides the right atrium into a proximal (upper) and a distal (lower) chamber. The upper chamber receives the venous blood from both vena cavae and the lower chamber is in contact with the tricuspid valve and the right atrial appendage.

The natural history of this defect depends on the size of the communicating orifice between the upper and lower atrial chambers. If the communicating orifice is small, the patient is critically ill and may succumb at a young age (usually during infancy) to congestive heart failure and pulmonary edema. If the connection is larger, patients may present in childhood or young adulthood with a clinical picture similar to that of mitral stenosis. Cor triatriatum may also be an incidental finding when it is nonobstructive.

The disorder can be treated surgically by removing the membrane dividing the atrium.

Hypoplastic right heart syndrome is a congenital heart defect in which the right atrium and right ventricle are underdeveloped. This defect causes inadequate blood flow to the lungs and thus, a blue or cyanotic infant.[3]

Common symptoms include a grayish-blue (cyanosis) coloration to the skin, lips, fingernails and other parts of the body. Other pronounced symptoms can be rapid/difficulty breathing, poor feeding, cold hands or feet, or being inactive and drowsy. "In a baby with hypoplastic left heart syndrome, if the natural connections between the heart's left and right sides (foramen oval and ductus arteriosus) are allowed to close, he or she may go into shock." Signs of shock can include cool or clammy skin, a weak or rapid pulse, and dilated pupils.

In PLSVC, the left brachiocephalic vein does not develop fully and the left upper limb and head & neck drain into the right atrium via the coronary sinus.

The variation, in isolation, is considered benign, but is very frequently associated with cardiac abnormalities (e.g. ventricular septal defect, atrioventricular septal defect) that have a significant mortality and morbidity. It is more frequent in patients with congenital heart defects.

In anatomy, a persistent left superior vena cava (PLSVC) is the most common variation of the thoracic venous system, is prevalent in 0.3% of the population, and an embryologic remnant that results from a failure to involute.

Congenital stenosis of vena cava is a congenital anomaly in which the superior vena cava or inferior vena cava has an aberrant interruption or coarctation.

In some cases, it can be asymptomatic, and in other cases it can lead to fluid accumulation and cardiopulmonary collapse.

The anomalous venous return forms a curved shadow on chest x-ray such that it resembles a scimitar. This is called the Scimitar Sign. Associated abnormalities include right lung hypoplasia with associated dextroposition of the heart, pulmonary artery hypoplasia and pulmonary sequestration.Incidence is around 1 per 100,000 births.

Anomalous pulmonary venous connection (or anomalous pulmonary venous drainage or anomalous pulmonary venous return) is a congenital defect of the pulmonary veins.

Scimitar syndrome, or congenital pulmonary venolobar syndrome, is a rare congenital heart defect characterized by anomalous venous return from the right lung (to the systemic venous drainage, rather than directly to the left atrium). This anomalous pulmonary venous return can be either partial (PAPVR) or total (TAPVR). The syndrome associated with PAPVR is more commonly known as "Scimitar syndrome" after the curvilinear pattern created on a chest radiograph by the pulmonary veins that drain to the inferior vena cava. This radiographic density often has the shape of a scimitar, a type of curved sword. The syndrome was first described by Catherine Neill in 1960.

"Total anomalous pulmonary venous connection", also known as "total anomalous pulmonary venous drainage" and "total anomalous pulmonary venous return", is a rare cyanotic congenital heart defect in which all four pulmonary veins are malpositioned and make anomalous connections to the systemic venous circulation. (Normally, pulmonary veins return oxygenated blood from the lungs to the left atrium where it can then be pumped to the rest of the body). A patent foramen ovale, patent ductui arteriosa or an atrial septal defect "must" be present, or else the condition is fatal due to a lack of systemic blood flow.

In some cases, it can be detected prenatally.

There are four variants: Supracardiac (50%): blood drains to one of the innominate veins (brachiocephalic veins) or the superior vena cava; Cardiac (20%), where blood drains into coronary sinus or directly into right atrium; Infradiaphragmatic (20%), where blood drains into portal or hepatic veins; and a mixed (10%) variant.

TAPVC can occur with "obstruction", which occurs when the anomalous vein enters a vessel at an acute angle and can cause pulmonary venous hypertension and cyanosis because blood cannot enter the new vein as easily.

IVCS presents with a wide variety of signs and symptoms, making it difficult to diagnose clinically.

- Edema of the lower extremities (peripheral edema), caused by an increase in the blood pressure in the veins.

- Tachycardia. This is caused by the decreased preload, causing the heart to increase its frequency.

- In pregnant women, signs of fetal hypoxia and distress may be seen in the cardiotocography. This is caused by decreased perfusion of the uterus, resulting in hypoxemia of the fetus.

- Supine hypotensive syndrome

Left atrial enlargement (LAE) or left atrial dilation refers to enlargement of the left atrium (LA) of the heart, and is a form of cardiomegaly.

Inferior vena cava syndrome (IVCS) is a result of obstruction of the inferior vena cava. It can be caused by invasion or compression by a pathological process or by thrombosis in the vein itself. It can also occur during pregnancy.Pregnancy can lead to problems with blood return due to high venous pressure in the lower limbs, failure of blood return to the heart, decreased cardiac output due to obstructions in inferior vena cava, sudden rise in venous pressure which can lead to placental separation, and a decrease in renal function. All of these issues can arise from lying in the supine position during late pregnancy which can cause compression of the inferior vena cava. Symptoms of late pregnancy inferior vena cava syndrome consist of intense pain in the right hand side, muscle twitching, drop of blood pressure, and fluid retention.

In the general population, obesity appears to be the most important risk factor for LAE. LAE has been found to be correlated to body size, independent of obesity, meaning that LAE is more common in people with a naturally large body size. Also, a study found that LAE can occur as a consequence of atrial fibrillation (AF), although another study found that AF by itself does not cause LAE. The latter study also showed that the persistent type of AF was associated with LAE, but the number of years that a subject had AF was not.

Obstructive sleep apnea (OSA) may be a cause of LAE in some cases. When an OSA event occurs, an attempt is made to breathe with an obstructed airway and the pressure inside the chest is suddenly lowered. The negative intrathoracic pressure may cause the left atrium to expand and stretch its walls during each OSA event. Over time, the repetitive stretching of the left atrium may result in a persistent left atrial enlargement.