Symptoms related to aortic stenosis depend on the degree of stenosis. Most people with mild to moderate aortic stenosis do not have symptoms. Symptoms usually present in individuals with severe aortic stenosis, though they may occur in those with mild to moderate aortic stenosis as well. The three main symptoms of aortic stenosis are loss of consciousness, anginal chest pain and shortness of breath with activity or other symptoms of heart failure such as shortness of breath while lying flat, episodes of shortness of breath at night, or swollen legs and feet. It may also be accompanied by the characteristic "Dresden china" appearance of pallor with a light flush.

Angina in setting of heart failure also increases the risk of death. In people with angina, the 5-year mortality rate is 50% if the aortic valve is not replaced.

Angina in the setting of AS occurs due to left ventricular hypertrophy (LVH) that is caused by the constant production of increased pressure required to overcome the pressure gradient caused by the AS. While the muscular layer of the left ventricle thickens, the arteries that supply the muscle do not get significantly longer or bigger, so the muscle may not receive enough blood supply to meet its oxygen requirement. This ischemia may first be evident during exercise when the heart muscle requires increased blood supply to compensate for the increased workload. The individual may complain of anginal chest pain with exertion. At this stage, a cardiac stress test with imaging may be suggestive of ischemia.

Eventually, however, the heart muscle will require more blood supply at rest than can be supplied by the coronary artery branches. At this point there may be signs of "ventricular strain pattern" (ST segment depression and T wave inversion) on the EKG, suggesting subendocardial ischemia. The subendocardium is the region that is most susceptible to ischemia because it is the most distant from the epicardial coronary arteries.

Symptoms of aortic insufficiency are similar to those of heart failure and include the following:

- Dyspnea on exertion

- Orthopnea

- Paroxysmal nocturnal dyspnea

- Palpitations

- Angina pectoris

- Cyanosis (in acute cases)

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.

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.

In mild cases, children may show no signs or symptoms at first and their condition may not be diagnosed until later in life. Some children born with coarctation of the aorta have other heart defects too, such as aortic stenosis, ventricular septal defect, patent ductus arteriosus or mitral valve abnormalities.

Coarctation is about twice as common in boys as it is in girls. It is common in girls who have Turner syndrome.

Symptoms may be absent with mild narrowings (coarctation). When present, they include: difficulty breathing, poor appetite or trouble feeding, failure to thrive. Later on, children may develop symptoms related to problems with blood flow and an enlarged heart. They may experience dizziness or shortness of breath, faint or near-fainting episodes, chest pain, abnormal tiredness or fatigue, headaches, or nosebleeds. They have cold legs and feet or have pain in their legs with exercise (intermittent claudication).

In more severe cases, where severe coarctations, babies may develop serious problems soon after birth because not enough blood can get through the aorta to the rest of their body.

Arterial hypertension in the arms with low blood pressure in the lower extremities is classic. In the lower extremities, weak pulses in the femoral arteries and arteries of the feet are found.

The coarctation typically occurs after the left subclavian artery. However, if situated before it, blood flow to the left arm is compromised and asynchronous or radial pulses of different "strength" may be detected (normal on the right arm, weak or delayed on the left), termed "radio-radial delay". In these cases, a difference between the normal radial pulse in the right arm and the delayed femoral pulse in the legs (either side) may be apparent, whilst no such delay would be appreciated with palpation of both delayed left arm and either femoral pulses. On the other hand, a coarctation occurring after the left subclavian artery will produce synchronous radial pulses, but "radio-femoral delay" will be present under palpation in either arm (both arm pulses are normal compared to the delayed leg pulses).

Pulmonary and tricuspid valve diseases are right heart diseases. Pulmonary valve diseases are the least common heart valve disease in adults.

Pulmonary valve stenosis is often the result of congenital malformations and is observed in isolation or as part of a larger pathologic process, as in Tetralogy of Fallot, Noonan syndrome, and congenital rubella syndrome . Unless the degree of stenosis is severe individuals with pulmonary stenosis usually have excellent outcomes and treatment options. Often patients do not require intervention until later in adulthood as a consequence of calcification that occurs with aging.

Pulmonary valve insufficiency occurs commonly in healthy individuals to a very mild extent and does not require intervention. More appreciable insufficiency it is typically the result of damage to the valve due to cardiac catheterization, aortic balloon pump insertion, or other surgical manipulations. Additionally, insufficiency may be the result of carcinoid syndrome, inflammatory processes such a rheumatoid disease or endocarditis, or congenital malformations. It may also be secondary to severe pulmonary hypertension.

Tricuspid valve stenosis without co-occurrent regurgitation is highly uncommon and typically the result of rheumatic disease. It may also be the result of congenital abnormalities, carcinoid syndrome, obstructive right atrial tumors (typically lipomas or myxomas), or hypereosinophilic syndromes.

Minor tricuspid insufficiency is common in healthy individuals. In more severe cases it is a consequence of dilation of the right ventricle, leading to displacement of the papillary muscles which control the valve's ability to close. Dilation of the right ventricle occurs secondary to ventricular septal defects, right to left shunting of blood, eisenmenger syndrome, hyperthyroidism, and pulmonary stenosis. Tricuspid insufficiency may also be the result of congenital defects of the tricuspid valve, such as Ebstein's anomaly.

The symptoms associated with MI are dependent on which phase of the disease process the individual is in. Individuals with acute MI are typically severely symptomatic and will have the signs and symptoms of acute decompensated congestive heart failure (i.e. shortness of breath, pulmonary edema, orthopnea, and paroxysmal nocturnal dyspnea), as well as symptoms of cardiogenic shock (i.e., shortness of breath at rest). Cardiovascular collapse with shock (cardiogenic shock) may be seen in individuals with acute MI due to papillary muscle rupture, rupture of a chorda tendinea or infective endocarditis of the mitral valve.

Individuals with chronic compensated MI may be asymptomatic for long periods of time, with a normal exercise tolerance and no evidence of heart failure. Over time, however, there may be decompensation and patients can develop volume overload (congestive heart failure). Symptoms of entry into a decompensated phase may include fatigue, shortness of breath particularly on exertion, and leg swelling. Also there may be development of an irregular heart rhythm known as atrial fibrillation.

Findings on clinical examination depend on the severity and duration of MI. The mitral component of the first heart sound is usually soft and with a laterally displaced apex beat, often with heave. The first heart sound is followed by a high-pitched holosystolic murmur at the apex, radiating to the back or clavicular area. Its duration is, as the name suggests, the whole of systole. The loudness of the murmur does not correlate well with the severity of regurgitation. It may be followed by a loud, palpable P, heard best when lying on the left side. A third heart sound is commonly heard.

In acute cases, the murmur and tachycardia may be the only distinctive signs.

Patients with mitral valve prolapse may have a holosystolic murmur or often a mid-to-late systolic click and a late systolic murmur. Cases with a late systolic regurgitant murmur may still be associated with significant hemodynamic consequences.

Bicuspid aortic valves may assume three different types of configuration:

1. "Real" bicuspid valves with two symmetric leaflets

2. A tricuspid architecture with a fusion of two leaflets

3. A tricuspid architecture with a fusion of three leaflets

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.

Among some of the symptoms consistent with pulmonary valve stenosis are the following:

- Heart murmur

- Cyanosis

- Dyspnea

- Dizziness

- Upper thorax pain

- Developmental disorders

Major symptoms of Lutembacher's syndrome as a result of ASD and MS can range from heart failure to pulmonary congestion.

- Right ventricular overload and Right-sided heart failure: Both are caused by a large ASD and MS (moderate to severe).

- Palpitations: This is caused by blood flowing from left atrium to the right atrium causing a higher left atrial pressure and leading to mitral stenosis. Both atria will be dilated (stretched or open)leading to future atrial arrhythmias or atrial fibrillation (Riaz).

- Pulmonary congestion: When blood or fluid pools within the lungs; this is usually a symptom of mitral stenosis and a small ASD.

- Loud mitral S1 and wide fixed split of pulmonary S2: The loud sound of the mitral S1 and the wide fixed split of pulmonary S2 is a symptoms of mitral stenosis. The sounds often are caused by a reduced pressure gradient in the mitral area that was caused from decompression of the left atrium from the ASD and a displacement (moving from normal position) of the left ventricular lower portion of the heart to the a large right ventricle. The second heart sound (S2) split is caused by the increase right heart blood flow through the ASD causing a late closing of the pulmonary component of the S2 as well as decreased left ventricular and aortic blood flow.

- III/IV mid diastolic murmur, early systolic murmur: This heart murmur is caused by an increase blood flow through the tricuspid valve due to ASD; it is heard best in the left lower sternal area or the bottom of the heart (apex).

There are three types of aortic coarctations:

1. Preductal coarctation: The narrowing is proximal to the ductus arteriosus. Blood flow to the aorta that is distal to the narrowing is dependent on the ductus arteriosus; therefore severe coarctation can be life-threatening. Preductal coarctation results when an intracardiac anomaly during fetal life decreases blood flow through the left side of the heart, leading to hypoplastic development of the aorta. This is the type seen in approximately 5% of infants with Turner syndrome.

2. Ductal coarctation: The narrowing occurs at the insertion of the ductus arteriosus. This kind usually appears when the ductus arteriosus closes.

3. Postductal coarctation: The narrowing is distal to the insertion of the ductus arteriosus. Even with an open ductus arteriosus, blood flow to the lower body can be impaired. This type is most common in adults. It is associated with notching of the ribs (because of collateral circulation), hypertension in the upper extremities, and weak pulses in the lower extremities. Postductal coarctation is most likely the result of the extension of a muscular artery (ductus arteriosus) into an elastic artery (aorta) during fetal life, where the contraction and fibrosis of the ductus arteriosus upon birth subsequently narrows the aortic lumen.

Aortic coarctation and aortic stenosis are both forms of aortic narrowing. In terms of word root meanings, the names are not different, but a conventional distinction in their usage allows differentiation of clinical aspects. This spectrum is dichotomized by the idea that aortic coarctation occurs in the aortic arch, at or near the ductus arteriosis, whereas aortic stenosis occurs in the aortic root, at or near the aortic valve. This naturally could present the question of the dividing line between a postvalvular stenosis and a preductal coarctation; nonetheless, the dichotomy has practical use, as most defects are either one or the other.

In regards to the cause of pulmonary valve stenosis a very high percentage are congenital, the right ventricular flow is hindered (or obstructed by this). The cause in turn is divided into: valvular, external and intrinsic (when it is acquired).

Heart valve dysplasia is a congenital heart defect which affects the aortic, pulmonary, mitral, and tricuspid heart valves. Dysplasia of the mitral and tricuspid valves can cause leakage of blood or stenosis.

Dysplasia of the mitral and tricuspid valves - also known as the atrioventricular (AV) valves - can appear as thickened, shortened, or notched valves. The chordae tendinae can be fused or thickened. The papillary muscles can be enlarged or atrophied. The cause is unknown, but genetics play a large role. Dogs and cats with tricuspid valve dysplasia often also have an open foramen ovale, an atrial septal defect, or inflammation of the right atrial epicardium. In dogs, tricuspid valve dysplasia can be similar to Ebstein's anomaly in humans.

Mitral valve stenosis is one of the most common congenital heart defects in cats. In dogs, it is most commonly found in Great Danes, German Shepherd Dogs, Bull Terriers, Golden Retrievers, Newfoundlands, and Mastiffs. Tricuspid valve dysplasia is most common in the Old English Sheepdog, German Shepherd Dog, Weimaraner, Labrador Retriever, Great Pyrenees, and sometimes the Papillon. It is inherited in the Labrador Retriever.

The disease and symptoms are similar to progression of acquired valve disease in older dogs. Valve leakage leads to heart enlargement, arrhythmias, and congestive heart failure. Heart valve dysplasia can be tolerated for years or progress to heart failure in the first year of life. Diagnosis is with an echocardiogram. The prognosis is poor with significant heart enlargement.

Aortic insufficiency (AI), also known as aortic regurgitation (AR), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle. As a consequence, the cardiac muscle is forced to work harder than normal.

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.

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

Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.

VSD is an acyanotic congenital heart defect, aka a left-to-right shunt, so there are no signs of cyanosis in the early stage. However, uncorrected VSD can increase pulmonary resistance leading to the reversal of the shunt and corresponding cyanosis.

- Pansystolic (Holosystolic) murmur along lower left sternal border (depending upon the size of the defect) +/- palpable thrill (palpable turbulence of blood flow). Heart sounds are normal. Larger VSDs may cause a parasternal heave, a displaced apex beat (the palpable heartbeat moves laterally over time, as the heart enlarges). An infant with a large VSD will fail to thrive and become sweaty and tachypnoeic (breathe faster) with feeds.

The restrictive VSDs (smaller defects) are associated with a louder murmur and more palpable thrill (grade IV murmur). Larger defects may eventually be associated with pulmonary hypertension due to the increased blood flow. Over time this may lead to an Eisenmenger's syndrome the original VSD operating with a left-to-right shunt, now becomes a right-to-left shunt because of the increased pressures in the pulmonary vascular bed.

During pregnancy, prenatal ultrasound may reveal the abnormal course of the arch. On chest radiography, a right-sided aortic arch is visualized by the aortic knob (the prominent shadow of the aortic arch) that is located right from the sternum instead of left. Complex lesions are often assessed by MRI or CT.

Canine subvalvular aortic stenosis (SAS) is an abnormal, congenital heart murmur caused by subaortic stenosis (SAS). There is a high incidence of this condition among Rottweiler dogs.

There is very good evidence that it is heritable, passed on from generation to generation genetically. This genetic trait is what is called polygenic, so that the inheritance is complex. An animal might have the genes for SAS, yet have no actual sign of SAS. Also, an animal might have signs of subaortic stenosis, and yet offspring with signs of SAS may not be seen for a couple of generations. Any animal that has subaortic stenosis should not be bred, because they can definitely pass the defect on to future offspring. There is some controversy as to whether the parents of an animal with SAS should be bred again.

Heart murmurs are graded on a scale of 1 to 6, with one being very mild and six being very serious, with some animals dying before they reach this high stage due to a sudden leap in the grade or through long-term slowing down. Murmurs can exist due to a large number of heart problems (infection, trauma, anemia, etc.; some are innocent, with no cardiac pathology. Tests such as chest X-rays, echocardiography, and electrocardiography can be performed to evaluate the severity of the situation

The condition is usually detected during puppy visits to the veterinarian by hearing a heart murmur during physical examination. A heart murmur is the abnormal sound of blood rushing through one of the heart valves. Instead of just the heartbeat, a whistle of blood flow through a narrowed opening is heard. The puppy will most likely appear normal in all other respects. There is a possibility that the murmur may come and go, or it may develop slowly; this can be determined by frequent checks of a puppy's heart during its first few months. The chance for long-term survival of SAS is low.

Puppies and dogs diagnosed with subaortic stenosis can suffer from heart failure and sudden death. If a dog with SAS develops heart failure, medications can be prescribed to alleviate the clinical signs (sudden/strong lethargicism, continuous heavy panting, rise in temperature etc.)

The OFA has established a Congenital Heart Registry whose guidelines were established by veterinary cardiologists. A dog which auscultates normally at 12 months of age is considered to be free of congenital heart disease; upon confirmation of this, the OFA will issue a certificate.

As Lutembacher's syndrome is known for ASD and MS, most of the symptoms experienced will be associated with ASD and MS. For most people, they will remain asymptomatic (experience no symptoms) but when symptoms are shown, they are due mainly to ASD and will vary depending on the size of the hole in the atria. If the patient has a large ASD, pulmonary congestion (blood or fluid buildup in the lungs) will happen later but if the patient has a small ASD, symptoms will appear early in the disorder. In general, unless the ASD and mitral stenosis causing Lutembacher's syndrome is severe, symptoms may not appear until the second and third decade of the patient's life. As many of the symptoms are asymptomic and may not appear until later in life, the duration or frequency of the symptoms varies. For symptoms such as palipitations, ventricular overload, heart failure, and pulmonary congenstion, these symptoms may be sudden and not that frequent as they are very severe symptoms. For symptoms such as loud mitral S1, pulmonary S2, mid-diastolic murmur, fatigue, reduced exercise tolerance, weight gain, ankle edema, and right upper quadrant pain, and ascities, these symptoms may be less frequent and severe; their duration may be only a few seconds, minutes, or even months.

Mitral insufficiency (MI), mitral regurgitation or mitral incompetence is a disorder of the heart in which the mitral valve does not close properly when the heart pumps out blood. It is the abnormal leaking of blood backwards from the left ventricle, through the mitral valve, into the left atrium, when the left ventricle contracts, i.e. there is regurgitation of blood back into the left atrium. MI is the most common form of valvular heart disease.

Valvular heart disease is any disease process involving one or more of the four valves of the heart (the aortic and mitral valves on the left and the pulmonary and tricuspid valves on the right). These conditions occur largely as a consequence of aging, but may also be the result of congenital (inborn) abnormalities or specific disease or physiologic processes including rheumatic heart disease and pregnancy.

Anatomically, the valves are part of the dense connective tissue of the heart known as the cardiac skeleton and are responsible for the regulation of blood flow through the heart and great vessels. Valve failure or dysfunction can result in diminished heart functionality, though the particular consequences are dependent on the type and severity of valvular disease. Treatment of damaged valves may involve medication alone, but often involves surgical valve repair (valvuloplasty) or replacement (insertion of an artificial heart valve).

Left to right shunting heart defects include:

- Ventricular septal defect (VSD) (30% of all congenital heart defects)

- Atrial septal defect (ASD)

- Atrioventricular septal defect (AVSD)

- Patent ductus arteriosus (PDA)

- Previously, Patent ductus arteriosus (PDA) was listed as acyanotic but in actuality it can be cyanotic due to pulmonary hypertension resulting from the high pressure aorta pumping blood into the pulmonary trunk, which then results in damage to the lungs which can then result in pulmonary hypertension as well as shunting of blood back to the right ventricle. This consequently results in less oxygenation of blood due to alveolar damage as well as oxygenated blood shunting back to the right side of the heart, not allowing the oxygenated blood to pass through the pulmonary vein and back to the left atrium.

- (Edit - this is called Eisenmenger's syndrome and can occur with Atrial septal defect and ventricular septal defect as well (actually more common in ASD and VSD) therefore PDA can still be listed as acyanotic as, acutely, it is)

Others:

- levo-Transposition of the great arteries (l-TGA)

Acyanotic heart defects without shunting include:

- Pulmonary stenosis (a narrowing of the pulmonary valve)

- Aortic stenosis

- Coarctation of the aorta