Coronary artery anomalies (or malformation of coronary vessels) are congenital abnormalities in the coronary anatomy of the heart. By definition, these abnormalities are variants of anatomy occurring in less than 1% of the general population. They are often found in combination with other congenital heart defects. Many coronary anomalies don't cause symptoms and are recognized only at the time of autopsy.

They can be associated with sudden death. The real risk of death or the best way to treat these patients is not yet known. The Congenital Heart Surgeons' Society has started a long-term ongoing study called anomalous aortic origin of a coronary artery (AAOCA) to identify the best way to treat this defect.

The annulus of the valve is still in the normal position. The valve leaflets, however, are to a varying degree, attached to the walls and septum of the right ventricle. A subsequent 'atrialization' of a portion of the morphologic right ventricle (which is then contiguous with the right atrium) is seen. This causes the right atrium to be large and the anatomic right ventricle to be small in size.

- S3 heart sound

- S4 heart sound

- Triple or quadruple gallop due to widely split S1 and S2 sounds plus a loud S3 and/or S4

- Systolic murmur of tricuspid regurgitation = Holosystolic or early systolic murmur along the lower left sternal border depending on the severity of the regurgitation

- Right atrial hypertrophy

- Right ventricular conduction defects

- Wolff-Parkinson-White syndrome often accompanies

An enlargement of the aorta may occur; an increased risk of abnormality is seen in babies of women taking lithium during the first trimester of pregnancy (though some have questioned this) and in those with Wolff-Parkinson-White syndrome.

In many cases, a bicuspid aortic valve will cause no problems. People with BAV may become tired more easily than those with normal valvular function and have difficulty maintaining stamina for cardio-intensive activities due to poor heart performance.

BAV frequently leads to significant complications in over one-third of affected individuals which often lead to significant morbidity and mortality. Notable complications of BAV include narrowing of the aortic valve opening, backward blood flow at the aortic valve, dilation of the ascending aorta, and infection of the heart valve.

There have been seven described variations of the quadricuspid aortic valve. They are classified on a scale from A to G and describe the variations in size of the four cusps. The most common variation is that of B – three equal-sized cusps and one smaller cusp. There is no correlation between the anatomy and functional status of the aortic cusps.

Anomalous aortic origin of a coronary artery (AAOCA) from the inappropriate sinus of Valsalva with an interarterial, intraconal, or intramural course is a rare heart defect associated with an increased risk of sudden death in children.

In 2009, The Congenital Heart Surgeons' Society (CHSS) established a North American Registry in order to study a large multi-institutional cohort of patients with AAOCA. This initiative is intended to generate new knowledge concerning the natural history of AAOCA, to describe the outcomes of surgical intervention versus observation in children and young adults with AAOCA, and to generate evidence to support risk stratification among patients with AAOCA and eventually suggest evidence-based guidelines for management.

This type of aneurysm is typically congenital and may be associated with heart defects. It is sometimes associated with Marfan syndrome or Loeys–Dietz syndrome, but may also result from Ehlers–Danlos syndrome, bicuspid aortic valve, atherosclerosis, hypoplastic left heart syndrome, syphilis, cystic medial necrosis, chest injury, or infective endocarditis.

A quadricuspid aortic valve (QAV) is a rare congenital heart defect characterized by the presence of four cusps, instead of the usual three found normally in the aortic valve. It is a defect that occurs during embryological development of the aortic trunk during gestation. There is an increased risk of developing post-natal aortic regurgitations and other heart-related diseases; therefore patients with the condition should be carefully monitored.

If unruptured, this type of aneurysm may be asymptomatic and therefore go undetected until symptoms appear or medical imaging is performed for other reasons. A ruptured aneurysm typically leads to an aortocardiac shunt and progressively worsening heart failure.

An aneurysm of the aortic sinus may rupture due to infective endocarditis involving the aortic wall and tertiary-stage syphilis.

The manifestations appear depending on the site where the sinus has ruptured. For example, if the sinus ruptures in a low pressure area like the right atrium or right ventricle then a continuous type of murmur is heard. The murmur is located in the left parasternal region mainly confined to the lower sternum. It is also accompanied by a superficial thrill. A ruptured Sinus of Valsalva abscess represents a surgical emergency.

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.

Anomalous left coronary artery from the pulmonary artery (ALCAPA or Bland-White-Garland syndrome or White-Garland syndrome) is a rare congenital anomaly in which the left coronary artery (LCA) branches off the pulmonary artery instead of the aortic sinus. After birth, the pressure in other coronary arteries (namely the RCA) will have a pressure that exceeds the LCA and collateral circulation will increase. This, ultimately, can lead to blood flowing from the RCA into the LCA (retrograde) and into the pulmonary artery, thus forming a left-to-right shunt.

The syndrome is named for Edward Franklin Bland, Paul Dudley White, and Joseph Garland.

Crisscross heart is a type of congenital heart defect where the right atrium is closely associated with the left ventricle in space, and the left atrium is closely associated with the right ventricle.

Although it is classified as a defect, the criss-cross is more of a spatial anomaly than a functional one, and it is possible for the heart to have relatively normal functioning.

Generally, it has a good prognosis. In Kawasaki's disease, untreated, there is a 1–2% death rate, from cardiac causes.

For many people cardiomegaly is asymptomatic. For others, if the enlarged heart begins to affect the body's ability to pump blood effectively, then symptoms associated with congestive heart failure may arise.

- Heart palpitations – irregular beating of the heart, usually associated with a valve issue inside the heart.

- Severe shortness of breath (especially when physically active) – irregularly unable to catch one's breath.

- Chest pain

- Fatigue

- Swelling in legs

- Increased abdominal girth

- Weight gain

- Edema – swelling

- Fainting

Acquired causes include atherosclerosis, Kawasaki disease and coronary catheterization.

It can also be congenital.

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.

Cardiomegaly is a medical condition in which the heart is enlarged. It is more commonly referred to as an enlarged heart. The causes of cardiomegaly may vary. Many times this condition results from high blood pressure (hypertension) or coronary artery disease. An enlarged heart may not pump blood effectively, resulting in congestive heart failure. Cardiomegaly may improve over time, but many people with an enlarged heart need lifelong treatment with medications. Having an immediate family member who has or had cardiomegaly may indicate that a person is more susceptible to getting this condition. Cardiomegaly is not a disease but rather a condition that can result from a host of other diseases such as obesity or coronary artery disease. Recent studies suggest that cardiomegaly is associated with a higher risk of sudden cardiac death (SCD).

Coronary arteriovenous fistula between coronary artery and another cardiac chamber, like, the coronary sinus, right atrium, or right ventricle may cause steal syndrome under conditions like myocardial infarction and possible angina or ventricular arrhythmias, if the shunt is large in magnitude.

It can also be associated with new patterns of blood vessel growth.

Even though many types of sick sinus syndrome produce no symptoms, a person may present with one or more of the following signs and symptoms:

- Stokes-Adams attacks – fainting due to asystole or ventricular fibrillation

- Dizziness or light-headedness

- Palpitations

- Chest pain or angina

- Shortness of breath

- Fatigue

- Headache

- Nausea

Coronary steal (with its symptoms termed coronary steal syndrome or cardiac steal syndrome) is a phenomenon where an alteration of circulation patterns leads to a reduction in the blood directed to the coronary circulation. It is caused when there is narrowing of the coronary arteries and a coronary vasodilator is used – "stealing" blood away from those parts of the heart. This happens as a result of the narrowed coronary arteries being always maximally dilated to compensate for the decreased upstream blood supply. Thus, dilating the resistance vessels in the coronary circulation causes blood to be shunted away from the coronary vessels supplying the ischemic zones, creating more ischemia.

Sick sinus syndrome (SSS), also called sinus dysfunction, or sinoatrial node disease ("SND"), is a group of abnormal heart rhythms (arrhythmias) presumably caused by a malfunction of the sinus node, the heart's primary pacemaker. Tachycardia-bradycardia syndrome is a variant of sick sinus syndrome in which the arrhythmia alternates between slow and fast heart rates. Tachycardia-bradycardia syndrome is often associated with ischemic heart disease and heart valve disease.

Vein of Galen aneurysmal malformations (VGAM) and Vein of Galen aneurysmal dilations (VGAD) are the most frequent arteriovenous malformations in infants and fetuses. VGAM consist of a tangled mass of dilated vessels supplied by an enlarged artery. The malformation increases greatly in size with age, although the mechanism of the increase is unknown. Dilation of the great cerebral vein of Galen is a secondary result of the force of arterial blood either directly from an artery via an arteriovenous fistula or by way of a tributary vein that receives the blood directly from an artery. There is usually a venous anomaly downstream from the draining vein that, together with the high blood flow into the great cerebral vein of Galen causes its dilation. The right sided cardiac chambers and pulmonary arteries also develop mild to severe dilation.