Cardiac fibroma is a slow-growing tumor that can cause heart electrical transmission defects and arrhythmias. Some features may be seen in the ventricle wall separating the right and left lower chambers or the ventricle muscle. This tumor is rarely seen in atrial locations. Cardiac fibromas are mostly single and well-circumscribed and the average size of the tumor is circular and is 5 cm. Sometimes signs and symptoms are difficult to find in 35% of individuals. Situations like this, the tumor is incidentally diagnosed during a health checkup for other medical conditions. An individual may have abnormal heart sounds, such as a heart murmur.

In 65% of individuals, signs and symptoms are more obvious due to the large size of the tumor. Also, there is blood flow obstruction, especially into or out of the valves. The valves function becomes affected, which leads to heart failure. An individual might experience bluish skin (cyanosis), severe arrhythmias, dizziness, fainting, and other obstructive symptoms may be present.

Symptoms associated with cardiac myxomas are typically due to the effect of the mass of the tumor obstructing the normal flow of blood within the chambers of the heart. Because pedunculated myxomas are somewhat mobile, symptoms may only occur when the patient is in a particular position.

Some symptoms of myxoma may be associated with the release of interleukin 6 (IL-6) by the myxoma. High levels of IL-6 may be associated with a higher risk of embolism of the myxoma.

Symptoms of a cardiac myxoma include:

- Dyspnea on exertion

- Paroxysmal nocturnal dyspnea

- Fever

- Weight loss (see cachexia)

- Lightheadedness or syncope (Loss of consciousness)

- Hemoptysis

- Sudden death

- Tachycardia or milder heartrate, i.e. 75 - 100 cycl/min

Cardiac fibroma, also known as cardiac fibromatosis, is a rare benign tumor of the heart that occurs primarily in infants and children. Benign tumors are typically a solitary, firm grey-white, non-encapsulated tumor that is composed of fibrous and dense connective tissue. It is most commonly located in the interventricular septum or left ventricular wall. Symptoms depend on the size of the tumor, its location relative to the conduction system, and whether it obstructs blood flow. Two-thirds of children with this tumor are asymptomatic, showing no signs and symptoms. Symptomatic cardiac fibromas may be treated by surgical resection. It is associated with Gorlin syndrome. Benign cardiac tumors are rare, 75% are histologically benign. Cardiac fibromas only occur 4-6%, which is less common compared to myxomas (75%) and rhabdomymoas (5-10%).

The diagnosis of these tumors require physical checkups, imaging studies on the heart, and specialized tests to evaluate the heart. Cardiac fibroma is considered a congenital tumor where an ultrasound prenatal scan may help detect during fetal stage. Surgery is the best treatment for an individual with cardiac fibroma. During this surgery, the tumor is completely removed by the surgeon. The overall prognosis is very good with a surgical removal. There have been 200 cases of cardiac fibroma recorded in the medical literature. Risk factors are still unidentified, but 1 in 30 individuals with Gorlin syndrome are known to be present with cardiac fibroma.

1.SMA, smooth muscle actin. 2.MSA, muscle-specific actin. 3.EMA, epithelial membrane antigen.

A rhabdomyoma is a benign tumor of striated muscle. Rhabdomyomas may be either "cardiac" or "extra cardiac" (occurring outside the heart). Extracardiac forms of rhabdomyoma are sub classified into three distinct types: adult type, fetal type, and genital type.

Cardiac rhabdomyomas are the most common primary tumor of the heart in infants and children. It has an association with tuberous sclerosis. In those with tuberous sclerosis, the tumor may regress and disappear completely, or remain consistent in size.

It is most commonly associated with the tongue, and heart, but can also occur in other locations, such as the vagina.

Malignant skeletal muscle tumors are referred to as rhabdomyosarcoma. Only rare cases of possible malignant change have been reported in fetal rhabdomyoma. The differential diagnosis in the tongue includes ectomesenchymal chondromyxoid tumor.

Most heart tumors begin with myxomas, fibromas, rhabdomyomas, and hamartomas, although malignant sarcomas (such as angiosarcoma or cardiac sarcoma) have been known to occur. In a study of 12,487 autopsies performed in Hong Kong seven cardiac tumors were found, most of which were benign. According to Mayo Clinic: "At Mayo Clinic, on average only one case of heart cancer is seen each year." In a study conducted in the Hospital of the Medical University of Vienna 113 primary cardiac tumour cases were identified in a time period of 15 years with 11 being malignant. The mean survival in the latter group of patients was found to be .

Primary malignant cardiac tumors (PMCTs) are even more rare. A study using the Surveillance, Epidemiology and End-Results (SEER) Cancer Registry from 1973–2011 found 551 cases of PMCTs, with an incidence of 34 cases per million persons. The study also found that the incidence has doubled over the past four decades. The associated mortality was very high, with only 46% of patients alive after one year. Sarcomas and mesotheliomas had the worst survival, while lymphomas had better survival. When compared with extracardiac tumors, PMCTs had worse survival.

People with TIC most often present with symptoms of congestive heart failure and/or symptoms related to their irregular heart rhythm. Symptoms of congestive heart failure can include shortness of breath, ankle swelling, fatigue, and weight gain. Symptoms of an irregular heart rhythm can include palpitations and chest discomfort.

The timecourse of TIC is most well-studied in experiments on animals. Researchers have found that animals began to exhibit abnormal changes in blood flow after just one day of an artificially generated fast heart rate (designed to simulate a tachyarrythmia). As their TIC progresses, these animals will have worsening heart function (e.g.: reduced cardiac output and reduced ejection fraction) for 3–5 weeks. The worsened heart function then persists at a stable state until the heart rate is returned to normal. With normal heart rates, these animals begin to demonstrate improving heart function at 1–2 days, and even complete recovery of ejection fraction at 1 month.

Human studies of the timecourse of TIC are not as robust as animal studies, though current studies suggest that the majority of people with TIC will recover a significant degree of heart function over months to years.

Heart cancer is an extremely rare form of cancer that is divided into primary tumors of the heart and secondary tumors of the heart.

In individuals with eccentric hypertrophy there may be little or no indication that hypertrophy has occurred as it is generally a healthy response to increased demands on the heart. Conversely, concentric hypertrophy can make itself known in a variety of ways. Most commonly, chest pain, either with or without exertion is present, along with shortness of breath with exertion, general fatigue, syncope, and palpitations. Overt signs of heart failure, such as edema, or shortness of breath without exertion are uncommon.

Hemopericardium refers to blood in the pericardial sac of the heart. It is clinically similar to a pericardial effusion, and, depending on the volume and rapidity with which it develops, may cause cardiac tamponade.

The condition can be caused by full-thickness necrosis (death) of the myocardium (heart muscle) after myocardial infarction, chest trauma, and by over-prescription of anticoagulants. Other causes include ruptured aneurysm of sinus of Valsalva and other aneurysms of the aortic arch.

Hemopericardium can be diagnosed with a chest X-ray or a chest ultrasound, and is most commonly treated with pericardiocentesis. While hemopericardium itself is not deadly, it can lead to cardiac tamponade, a condition that is fatal if left untreated.

The clinical course of HCM is variable. Many people with HCM are asymptomatic or mildly symptomatic, and many of those carrying disease genes for HCM do not have clinically detectable disease. The symptoms and signs of HCM include shortness of breath due to stiffening and decreased blood filling of the ventricles, exertional chest pain (sometimes known as angina) due to reduced blood flow to the coronary arteries, uncomfortable awareness of the heart beat (palpitations), as well as disruption of the electrical system running through the abnormal heart muscle, lightheadedness, weakness, fainting and sudden cardiac death.

Dyspnea is largely due to increased stiffness of the left ventricle (LV), which impairs filling of the ventricles, but also leads to elevated pressure in the left ventricle and left atrium, causing back pressure and interstitial congestion in the lungs. Symptoms are not closely related to the presence or severity of an outflow tract gradient. Often, symptoms mimic those of congestive heart failure (esp. activity intolerance and dyspnea), but treatment of each is different. Beta blockers are used in both cases, but treatment with diuretics, a mainstay of CHF treatment, will exacerbate symptoms in hypertrophic obstructive cardiomyopathy by decreasing ventricular preload volume and thereby increasing outflow resistance (less blood to push aside the thickened obstructing tissue).

Major risk factors for sudden death in individuals with HCM include prior history of cardiac arrest or ventricular fibrillation, spontaneous sustained ventricular tachycardia, family history of premature sudden death, unexplained syncope, LV thickness greater than or equal to 30 mm, abnormal exercise blood pressure and nonsustained ventricular tachycardia.

Symptoms can be as follows. They are periodic, and occur only during an "episode", usually after eating.

- Sinus bradycardia

- Difficulty inhaling

- Angina pectoris

- Left ventricular discomfort

- Fatigue

- Anxiety

- Uncomfortable breathing

- Poor perfusion

- Muscle pain (crampiness)

- Burst or sustained vertigo or dizziness

- Sleep disturbance (particularly when sleeping within a few hours of eating, or lying on the left side)

- Extrasystoles

- Hot flashes

Cardiac fibrosis may refer to an abnormal thickening of the heart valves due to inappropriate proliferation of cardiac fibroblasts but more commonly refers to the excess deposition of extracellular matrix in the cardiac muscle. Fibrotic cardiac muscle is stiffer and less compliant and is seen in the progression to heart failure. The description below focuses on a specific mechanism of valvular pathology but there are other causes of valve pathology and fibrosis of the cardiac muscle.

Fibrocyte cells normally secrete collagen, and function to provide structural support for the heart. When over-activated this process causes thickening and fibrosis of the valve, with white tissue building up primarily on the tricuspid valve, but also occurring on the pulmonary valve. The thickening and loss of flexibility eventually may lead to valvular dysfunction and right-sided heart failure.

Tachycardia-induced cardiomyopathy (TIC) is a disease where prolonged tachycardia (a fast heart rate) or arrhythmia (an irregular heart rhythm) cause an impairment of the myocardium (heart muscle), which can result in heart failure. People with TIC may have symptoms associated with heart failure (e.g. shortness of breath or ankle swelling) and/or symptoms related to the tachycardia or arrhythmia (e.g. palpitations). Though atrial fibrillation is the most common cause of TIC, several tachycardias and arrhythmias have been associated with the disease.

There are no formal diagnostic criteria for TIC. Thus, TIC is typically diagnosed when (1) tests have excluded other causes of cardiomyopathy and (2) there is improvement in myocardial function after treatment of the tachycardia or arrhythmia. Treatment of TIC can involve treating the heart failure as well as the tachycardia or arrhythmia. TIC has a good prognosis with treatment, with most people recovering some to all of their heart function.

The number of cases that occur is unclear. TIC has been reported in all age groups.

Roemheld syndrome (RS), also known as Roemheld-Techlenburg-Ceconi-Syndrome or gastric-cardia, is a complex of gastrocardiac symptoms first described by Ludwig von Roemheld (1871–1938). It is a syndrome where maladies in the gastrointestinal tract or abdomen are found to be associated with cardiac symptoms like arrhythmias and benign palpitations. There is rarely a traceable cardiac source to the symptoms which may lead to a lengthy period of misdiagnosis.

Dilated cardiomyopathy develops insidiously, and may not initially cause symptoms significant enough to impact on quality of life. Nevertheless, many people experience significant symptoms. These might include:

- Shortness of breath

- Syncope (fainting)

- Angina, but only in the presence of ischemic heart disease

A person suffering from dilated cardiomyopathy may have an enlarged heart, with pulmonary edema and an elevated jugular venous pressure and a low pulse pressure. Signs of mitral and tricuspid regurgitation may be present.

Cardiac arrest is preceded by no warning symptoms in approximately 50% of people. For those who do, they have non specific symptoms such as, new or worsening chest pain, fatigue, blackouts, dizziness, shortness of breath, weakness, and vomiting.

When the arrest occurs, the most obvious sign of its occurrence will be the lack of a palpable pulse in the person experiencing it (since the heart has ceased to contract, the usual indications of its contraction such as a pulse will no longer be detectable). Certain types of prompt intervention can often reverse a cardiac arrest, but without such intervention the event will almost always lead to death. In certain cases, it is an expected outcome of a serious illness where death is expected.

Also, as a result of inadequate blood flow to the brain (cerebral perfusion), the patient will quickly become unconscious and will have stopped breathing. The main diagnostic criterion to diagnose a cardiac arrest (as opposed to respiratory arrest which shares many of the same features) is lack of circulation; however, there are a number of ways of determining this. Near-death experiences are reported by 10–20% of people who survived cardiac arrest.

Athletic heart syndrome (AHS), also known as athlete's heart, athletic bradycardia, or exercise-induced cardiomegaly is a non-pathological condition commonly seen in sports medicine, in which the human heart is enlarged, and the resting heart rate is lower than normal.

The athlete's heart is associated with physiological remodeling as a consequence of repetitive cardiac loading. Athlete's heart is common in athletes who routinely exercise more than an hour a day, and occurs primarily in endurance athletes, though it can occasionally arise in heavy weight trainers. The condition is generally considered benign, but may occasionally hide a serious medical condition, or may even be mistaken for one.

Athlete's heart most often does not have any physical symptoms, although an indicator would be a consistently low resting heart rate. Athletes with AHS often do not realize they have the condition unless they undergo specific medical tests, because athlete's heart is a normal, physiological adaptation of the body to the stresses of physical conditioning and aerobic exercise. People diagnosed with athlete's heart commonly display three signs that would usually indicate a heart condition when seen in a regular person: bradycardia, cardiomegaly, and cardiac hypertrophy. Bradycardia is a slower than normal heartbeat, at around 40–60 beats per minute. Cardiomegaly is the state of an enlarged heart, and cardiac hypertrophy the thickening of the muscular wall of the heart, specifically the left ventricle, which pumps oxygenated blood to the aorta. Especially during an intensive workout, more blood and oxygen are required to the peripheral tissues of the arms and legs in highly trained athletes' bodies. A larger heart results in higher cardiac output, which also allows it to beat more slowly, as more blood is pumped out with each beat.

Another sign of athlete's heart syndrome is an S3 gallop, which can be heard through a stethoscope. This sound can be heard as the diastolic pressure of the irregularly shaped heart creates a disordered blood flow. However, if an S4 gallop is heard, the patient should be given immediate attention. An S4 gallop is a stronger and louder sound created by the heart, if diseased in any way, and is typically a sign of a serious medical condition.

Ventricular hypertrophy (VH) is thickening of the walls of a ventricle (lower chamber) of the heart. Although left ventricular hypertrophy (LVH) is more common, right ventricular hypertrophy (RVH), as well as concurrent hypertrophy of both ventricles can also occur.

Ventricular hypertrophy can result from a variety of conditions, both adaptive and maladaptive. For example, it occurs in what is regarded as a physiologic, adaptive process in pregnancy in response to increased blood volume; but can also occur as a consequence of ventricular remodeling following a heart attack. Importantly, pathologic and physiologic remodeling engage different cellular pathways in the heart and result in different gross cardiac phenotypes.

Ectopic beat (or cardiac ectopy) is a disturbance of the cardiac rhythm frequently related to the electrical conduction system of the heart, in which beats arise from fibers or group of fibers outside the region in the heart muscle ordinarily responsible for impulse formation ("i.e.", the sinoatrial node). An ectopic beat can be further classified as either a premature ventricular contraction, or a premature atrial contraction.

Some patients describe this experience as a 'flip' or a 'jolt' in the chest, or a 'heart hiccups', while others report dropped or missed beats. Ectopic beats are more common during periods of stress, exercise or debility; they may also be triggered by consumption of some food like alcohol, strong cheese, or chocolate.

It is a form of cardiac arrhythmia in which ectopic foci within either ventricular or atrial , or from finer branches of the electric transduction system, cause additional beats of the heart. Some medications may worsen the phenomenon.

Ectopic beats are considered normal and are not indicative of cardiac pathology. Ectopic beats often remain undetected and occur as part of minor errors in the heart conduction system. They are rarely indicative of cardiac pathology, although may occur more frequently or be more noticeable in those with existing cardiac abnormalities. Ectopic beats are a type of cardiac arrhythmias, which is a variety of cardiac abnormalities relating to rate or rhythm of the cardiac cycle.

Ectopic beats may become more frequent during anxiety, panic attack, and the fight-or-flight response due to the increase in sympathetic nervous activity, stimulating more frequent contractions and increasing stroke volume. The consumption of nicotine, alcohol, epinephrine and caffeine may also increase the incidences of ectopic beats, due to their influence on the action of cardiomyocytes.

Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) occur when the heart abruptly begins to beat in an abnormal or irregular rhythm (arrhythmia). Without organized electrical activity in the heart muscle, there is no consistent contraction of the ventricles, which results in the heart's inability to generate an adequate cardiac output (forward pumping of blood from heart to rest of the body). There are many different types of arrhythmias, but the ones most frequently recorded in SCA and SCD are ventricular tachycardia (VT) or ventricular fibrillation (VF).

Sudden cardiac arrest can result from cardiac and non-cardiac causes including the following:

Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly rather than contracting in a co-ordinated fashion (from the apex of the heart to the outflow of the ventricles), and so the ventricles fail to pump blood around the body - because of this, it is classified as a cardiac arrest rhythm, and patients in V-fib should be treated with cardiopulmonary resuscitation and prompt defibrillation. Left untreated, ventricular fibrillation is rapidly fatal as the vital organs of the body, including the heart, are starved of oxygen, and as a result patients in this rhythm will not be conscious or responsive to stimuli. Prior to cardiac arrest, patients may complain of varying symptoms depending on the underlying cause. Patients may exhibit signs of agonal breathing, which to the layperson can look like normal spontaneous breathing, but it is in fact a sign of hypoperfusion of the brainstem.

It has an appearance on electrocardiography of irregular electrical activity with no discernable pattern. It may be described as 'coarse' or 'fine' depending on its amplitude, or as progressing from coarse to fine V-fib. Coarse V-fib may be more responsive to defibrillation, while fine V-fib can mimic the appearance of asystole on a defibrillator or cardiac monitor set to a low gain. Some clinicians may attempt to defibrillate fine V-fib in the hope that it can be reverted to a cardiac rhythm compatible with life, whereas others will deliver CPR and sometimes drugs as described in the advanced cardiac life support protocols in an attempt to increase its amplitude and the odds of successful defibrillation.

Symptoms of hemopericardium often include difficulty breathing, abnormally rapid breathing, and fatigue, each of which can be a sign of a serious medical condition not limited to hemopericardium. In many cases, patients also report feeling chest pressure and have an abnormally elevated heart rate.

The soft fibroma (fibroma molle) or fibroma with a shaft (acrochordon, skin tag, fibroma pendulans) consist of many loosely connected cells and less fibroid tissue. It mostly appears at the neck, armpits or groin. The photo shows a soft fibroma of the eyelid.

Athlete's heart is usually an incidental finding during a routine screening or during tests for other medical issues. An enlarged heart can be seen at echocardiography or sometimes on a chest X-ray. Similarities at presentation between athlete's heart and clinically relevant cardiac problems may prompt electrocardiography (ECG) and exercise cardiac stress tests. The ECG can detect sinus bradycardia, a resting heart rate of fewer than 60 beats per minute. This is often accompanied by sinus arrhythmia. The pulse of a person with athlete's heart can sometimes be irregular while at rest, but usually returns to normal after exercise begins.

Regarding differential diagnosis, left ventricular hypertrophy is usually indistinguishable from athlete's heart and at ECG, but can usually be discounted in the young and fit.

It is important to distinguish between athlete's heart and hypertrophic cardiomyopathy, a serious cardiovascular disease characterised by thickening of the heart's walls, which produces a similar ECG pattern at rest. This genetic disorder is found in one of 500 Americans and is a leading cause of sudden cardiac death in young athletes (although only about 8% of all cases of sudden death are actually exercise-related). The following table shows some key distinguishing characteristics of the two conditions.

The medical history of the patient (endurance sports) and physical examination (bradycardia, and maybe a third or fourth heart sound), can give important hints.

- ECG - typical findings in resting position are, for example, sinus bradycardia, atrioventricular block (primary and secondary) and right bundle branch block - all those findings normalize during exercise.

- Echocardiography - differentiation between physiological and pathological increases of the heart's size is possible, especially by estimating the mass of the wall (not over 130 g/m) and its end diastolic diameter (not much less 60 mm) of the left ventricle.

- X-ray examination of the chest may show increased heart size (mimicking other possible causes of enlargement).