Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sogand Goudarzi, MD [2]Maria Fernanda Villarreal, M.D. [3]Cafer Zorkun, M.D., Ph.D. [4]Ahmad Al Maradni, M.D. [5]

A myxoma (Myxo- = Latin for mucus) is the most common primary tumor of the heart. Cardiac myxoma was first described in 1845. In 1951, Prichard described a kind of microscopic endocardial structure of the atrial septum, which was suggested to be associated with cardiac myxoma. Clarence Crafoord, a Swedish cardiovascular surgeon successfully removed a cardiac myxoma for the first time in 1954. Before 1951, cardiac myxoma diagnosis was made only at post-mortem examination. In 1959, the first M-mode echocardiogram of a left atrial myxoma was reported. Cardiac myxomas are classified by the WHO histological classification of tumors of the heart “Benign tumors and tumor-like lesions” and categorized into a type of pluripotent mesenchymal tumor. Cardiac myxoma arises from remnants of subendocardial vasoformative reserve cells, which are primitive mesenchymal cells that are normally involved in the supportive structure of the endocardium. Myxomas are usually located in the fossa ovalis and endocardium of the atrial septum. Some symptoms of myxoma may be associated with the release of interleukin 6 (IL-6). On gross pathology, a gelatinous, irregular surface that fills the left atrium is the characteristic finding of myxoma. A common histopathological finding is the Gamna-Gandy Bodies that consist of fibrosis and deposition of iron pigments. The main cause of cardiac myxoma remains unknown. However, in some cases like inherited myxomatosis, there is a strong relation with genetic mutations of PRKAR1A gene. Cardiac myxoma should be differentiated from other benign and malignant primary heart tumors including papillary fibroelastoma, lipoma, rhabdomyoma, and cardiac metastasis. Cardiac myxomas are the most common primary cardiac tumor in adults, with a reported prevalence of 0.03% in general population. The incidence of cardiac myxoma is about 1/ 100,000 per year. The majority of patients with cardiac myxoma are diagnosed between 30 to 60 years; children are rarely affected. Females are more commonly affected with cardiac myxoma than men. The female-to-male ratio is approximately 1.8 to 1. Cardiac myxomas represent 78% of heart tumors. Common risk factors in the development of myxoma are female gender and genetic predisposition. In some cases, right atrial myxoma has been associated with tricuspid stenosis and atrial fibrillation. If left untreated, cardiac myxoma progression occurs slowly. The overlap of various phenomena such as thrombosis, hemorrhage, or fragmentation may influence tumor growth, detachment, and consequently embolism. Constitutional symptoms, such as: weight loss, fatigue, weakness are often the initial clinical onset of cardiac myxoma, and may resemble those from endocarditis. Metastases are uncommon in cardiac myxoma. Since the majority of the cardiac myxomas are left-sided, it may progress to develop mitral valve obstruction or systemic embolic events, such as stroke. Whereas, right atrial myxomas may obstruct the tricuspid valve and can present as right sided heart failure. Approximately 20% of patients with cardiac myxoma are asymptomatic. Overall, clinical features of cardiac myxoma are associated with the size of the tumor, location, size, and mobility. There is no single diagnostic study of choice for myxoma. Myxoma may be diagnosed based on clinical presentation and detecting the cardiac mass. Symptoms associated with cardiac myxomas are typically due to the effect of the mass of the tumor obstructing the normal blood flow within the heart chambers. Left atrial myxoma symptoms may mimic mitral stenosis, while right atrial myxomas rarely produce symptoms until they have grown to be at least 13 cm wide. General symptoms may also mimic those of infective endocarditis. Cardiac myxoma symptoms may occur at any time, but most often they tend to occur with changes in body position. Common symptoms include: chest pain, palpitation, dizziness, syncope and dyspnea on exertion. There are no specific physical findings for cardiac myxoma. The auscultatory presence of a “tumor plop” (which is caused by the obstruction of the mitral valve orifice by the tumor) on physical examination is highly suggestive of cardiac myxoma. Common physical examination findings of cardiac myxoma include systolic or diastolic murmurs (depending on size, mobility, and location of the tumor). Laboratory findings consistent with cardiac myxoma are generally non-specific, results often demonstrate anemia, leukocytosis and elevated erythrocyte sedimentation rate. On chest x-ray, cardiac myxoma is characterized by normal results and in some cases a calcification overlying the heart. On CT scan, cardiac myxoma is characterized by low attenuation and areas of dystrophic calcification in cardiac chambers. CT scan may be helpful in the diagnosis of cardiac myxoma because it provides better soft-tissue contrast than echocardiography, and it can also differentiate calcification and fat, and may allow tissue diagnosis of some masses such as lipomas. On Magnetic Resonance Imaging (MRI) or Cardiac Magnetic Resonance (CMR), cardiac myxoma is characterized by a soft tissue mass within the cardiac chambers isointense to skeletal muscle. This imaging modality plays an important role in the evaluation of cardiac masses and is of great value when echocardiographic findings are suboptimal or when the lesion has an atypical location or appearance. The echocardiogram is the initial modality and most useful diagnostic imaging study in cardiac myxoma. On cardiac ultrasound, cardiac myxoma is characterized by the presence of a heterogeneous pedunculated mass that is commonly located in the left atrium. Echocardiography allows for evaluation assessment of tumor mobility, as it often protrudes through valve flaps. As a testing modality, two-dimensional echocardiography is often coupled with other modalities (such as, Doppler echocardiography) to detect vascular abnormalities that frequently occur in cardiac myxomas. Another diagnostic study for cardiac myxoma is cardiac angiography, which often demonstrates contrast media-enhanced tumor vasculature. There is no known medical therapy for cardiac myxomas. Surgery is the mainstay of treatment for cardiac myxoma. The feasibility of surgery depends on the patient hemodynamic stability at diagnosis. Cardiac myxoma surgery has operative mortality around 0 to 3%, depending on risk factors or mechanical damage to a heart valve, as well as adhesion of the tumor to valve leaflets. The short and long-term prognosis is generally regarded as excellent.

Cardiac myxoma was first described in 1845. In 1951, Prichard described a kind of microscopic endocardial structure of the atrial septum, which was suggested to be associated with cardiac myxoma. Clarence Crafoord, a Swedish cardiovascular surgeon successfully removed a cardiac myxoma for the first time in 1954. Before 1951, cardiac myxoma diagnosis was made only at post-mortem examination. In 1959, the first M-mode echocardiogram of a left atrial myxoma was reported.

Cardiac myxomas are classified by the WHO histological classification of tumors of the heart “Benign tumors and tumor-like lesions” and categorized into a type of pluripotent mesenchymal tumor.

Cardiac myxoma arises from remnants of subendocardial vasoformative reserve cells, which are primitive mesenchymal cells that are normally involved in the supportive structure of the endocardium. Myxomas are usually located in the fossa ovalis and endocardium of the atrial septum

Some symptoms of myxoma may be associated with the release of interleukin 6 (IL-6). On gross pathology, a gelatinous, irregular surface that fills the left atrium is the characteristic finding of myxoma. A common histopathological finding is the Gamna-Gandy Bodies that consist of fibrosis and deposition of iron pigments.

The main cause of cardiac myxoma remains unknown. However, in some cases like inherited myxomatosis, there is a strong relation with genetic mutations of PRKAR1A gene.

Cardiac myxoma should be differentiated from other benign and malignant primary heart tumors including papillary fibroelastoma, lipoma, rhabdomyoma, and cardiac metastasis.

Cardiac myxomas are the most common primary cardiac tumor in adults, with a reported prevalence of 0.03% in general population. The incidence of cardiac myxoma is about 1/ 100,000 per year. The majority of patients with cardiac myxoma are diagnosed between 30 to 60 years; children are rarely affected. Females are more commonly affected with cardiac myxoma than men. The female-to-male ratio is approximately 1.8 to 1. Cardiac myxomas represent 78% of heart tumors.

Common risk factors in the development of myxoma are female gender and genetic predisposition. In some cases, right atrial myxoma has been associated with tricuspid stenosis and atrial fibrillation.

If left untreated, cardiac myxoma progression occurs slowly. The overlap of various phenomena such as thrombosis, hemorrhage, or fragmentation may influence tumor growth, detachment, and consequently embolism. Constitutional symptoms, such as: weight loss, fatigue, weakness are often the initial clinical onset of cardiac myxoma, and may resemble those from endocarditis. Metastases are uncommon in cardiac myxoma.

Since the majority of the cardiac myxomas are left-sided, it may progress to develop mitral valve obstruction or systemic embolic events, such as stroke. Whereas, right atrial myxomas may obstruct the tricuspid valve and can present as right sided heart failure. Approximately 20% of patients with cardiac myxoma are asymptomatic. Overall, clinical features of cardiac myxoma are associated with the size of the tumor, location, size, and mobility.

There is no single diagnostic study of choice for myxoma. Myxoma may be diagnosed based on clinical presentation and detecting the cardiac mass.

Symptoms associated with cardiac myxomas are typically due to the effect of the mass of the tumor obstructing the normal blood flow within the heart chambers. Left atrial myxoma symptoms may mimic mitral stenosis, while right atrial myxomas rarely produce symptoms until they have grown to be at least 13 cm wide. General symptoms may also mimic those of infective endocarditis. Cardiac myxoma symptoms may occur at any time, but most often they tend to occur with changes in body position. Common symptoms include: chest pain, palpitation, dizziness, syncope and dyspnea on exertion.

There are no specific physical findings for cardiac myxoma. The auscultatory presence of a “tumor plop” (which is caused by the obstruction of the mitral valve orifice by the tumor) on physical examination is highly suggestive of cardiac myxoma. Common physical examination findings of cardiac myxoma include systolic or diastolic murmurs (depending on size, mobility, and location of the tumor).

Laboratory findings consistent with cardiac myxoma are generally non-specific, results often demonstrate anemia, leukocytosis and elevated erythrocyte sedimentation rate.

On chest x-ray, cardiac myxoma is characterized by normal results and in some cases a calcification overlying the heart.

On CT scan, cardiac myxoma is characterized by low attenuation and areas of dystrophic calcification in cardiac chambers. CT scan may be helpful in the diagnosis of cardiac myxoma because it provides better soft-tissue contrast than echocardiography, and it can also differentiate calcification and fat, and may allow tissue diagnosis of some masses such as lipomas.

On Magnetic Resonance Imaging (MRI) or Cardiac Magnetic Resonance (CMR), cardiac myxoma is characterized by a soft tissue mass within the cardiac chambers isointense to skeletal muscle. This imaging modality plays an important role in the evaluation of cardiac masses and is of great value when echocardiographic findings are suboptimal or when the lesion has an atypical location or appearance.

The echocardiogram is the initial modality and most useful diagnostic imaging study in cardiac myxoma. On cardiac ultrasound, cardiac myxoma is characterized by the presence of a heterogeneous pedunculated mass that is commonly located in the left atrium. Echocardiography allows for evaluation assessment of tumor mobility, as it often protrudes through valve flaps. As a testing modality, two-dimensional echocardiography is often coupled with other modalities (such as, Doppler echocardiography) to detect vascular abnormalities that frequently occur in cardiac myxomas.

Another diagnostic study for cardiac myxoma is cardiac angiography, which often demonstrates contrast media-enhanced tumor vasculature.

There is no known medical therapy for cardiac myxomas.

Surgery is the mainstay of treatment for cardiac myxoma. The feasibility of surgery depends on the patient hemodynamic stability at diagnosis. Cardiac myxoma surgery has operative mortality around 0 to 3%, depending on risk factors or mechanical damage to a heart valve, as well as adhesion of the tumor to valve leaflets. The short and long-term prognosis is generally regarded as excellent.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sogand Goudarzi, MD [2] Maria Fernanda Villarreal, M.D. [3]

Cardiac myxoma was first described in 1845. In 1951, Prichard described a kind of microscopic endocardial structure of the atrial septum, which was suggested to be associated with cardiac myxoma. Clarence Crafoord, a Swedish cardiovascular surgeon successfully removed a cardiac myxoma for the first time in 1954. Before 1951, cardiac myxoma diagnosis was made only at post-mortem examination.

• In 1845, the first description of a left atrial myxoma was reported by King.^[1]

• In 1951, Prichard described a kind of microscopic endocardial structure of the atrial septum, which was suggested to be related to cardiac myxoma.^[2]
• In 1951, intracardiac myxoma was recognized by angiography for the first time. Before 1951, cardiac myxoma diagnosis was made only at autopsy.^[3]

• In 1959, the first M-mode echocardiogram was used to diagnose a left atrial myxoma.^[4]

• In 2000, gene mutation PRKAR1A was first identified in the pathogenesis of cardiac myxoma syndromes, such as; LAMB (lentigines, atrial myxoma, mucocutaneous myxomas and blue nevi), NAME (nevi, atrial myxoma, mucinosis of the skin, and endocrine overactivity), and Carney complex (myxomas, spotty skin pigmentation and endocrine overactivity).^[5][6].

• In 1954, Clarence Crafoord (1899 – 1984), a Swedish cardiovascular surgeon, successfully removed a cardiac myxoma for the first time. This case also represents the first extirpation of a cardiac tumor on cardiopulmonary support.^[7][8]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sogand Goudarzi, MD [2] Maria Fernanda Villarreal, M.D. [3]

Cardiac myxomas are classified by the World Health Organization (WHO) histological classification of tumors of the heart, as “Benign tumors and tumor-like lesions” and categorized into a type of pluripotent mesenchymal tumor.

• Based on the location and biological behavior of symptoms, cardiac myxomas may be classified into two groups: typical and atypical.^[1]
• Typical:
  • In typical cases, cardiac myxomas are almost always single, and there is a striking predilection for the left atrium, with approximately 75-86% occurring there.^[2][3][4]
• atypical.
  • In atypical cases, presentation is usually early and multicentricity is more common. They are more frequently located on the right side of the heart (38%), or in the left ventricle (5%). There is also recurrence after surgical excision (12%–22%) and an association with other conditions, such as the Carney complex.^[2]
• Cardiac myxomas are anatomically distributed, as following:^[2]
  • Atria (95%)
    • Left (75%)
    • Right (20%)
  • Ventricles (5%)

• There is no established histological differentiation between both type of cardiac myxomas (typical and atypical).^[5]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sogand Goudarzi, MD [2] Maria Fernanda Villarreal, M.D. [3]Cafer Zorkun, M.D., Ph.D. [4]Ahmad Al Maradni, M.D. [5]

Cardiac myxoma is a benign intracavitary endocardial mass that represents the most common primary tumor of the heart. Myxoma cells are characterized by undifferentiated mesenchymal cells, which potentially differentiate into many tissues such as blood vessels, glandular structures, and bones. The primary distribution of cardiac myxoma is the left atrium (75%) of the heart; regularly, they tend to be located in the fossa ovalis and endocardium of the atrial septum.

• Cardiac myxoma arises from remnants of subendocardial vasoformative reserve cells, which are primitive mesenchymal cells that are normally involved in the supportive structure of the endocardium.^{[1][2][3][4][5]}
• The exact pathogenesis of cardiac myxoma is not fully understood.^[5]
• It is thought that cardiac myxoma is produced by the neoplastic theory, dysembryoplastic theory, histopathogenesis of glandular cells in myxoma or the thrombotic theory.^[6][7]
• The site of tumor attachment, normally the foramen ovale, is considered to be consistent with an origin from multipotent mesenchymal cells or from embryonic rests.^[8]

• Sporadic cardiac myxomas and familial forms are related with several chromosome and gene alterations which involve cardiac development.^[9]
• Inherited myxomas are usually present in Carney complex.^[9]
• The development of Carney complex is a result of PRKAR1A gene inactivation mutation that is associated with chromosome 17q24.2-q24.3.^[9]
• The gene 17q24.2-q24.3 plays an important role in cardiac development and myxomagenesis. The expression of PRKAR1A causes myxomatous changes in the endocardium.^[9]
• The encoded protein of PRKAR1A is a type 1A regulatory subunit of protein kinase A.Inactivating germline mutations of this gene are found in 70% of people with Carney complex.^[10]
• Less commonly, the molecular pathogenesis of Carney complex is a variety of genetic changes at chromosome 2p16.^[11]
• Both types of Carney complex are autosomal dominant.
• Despite dissimilar genetics, there appears to be no phenotypic difference between PRKAR1A and chromosome 2p16 mutations.^[12]

• The Carney complex is characterized by myxomatous neoplasms (cardiac, endocrine, cutaneous, and neural), and a host of pigmented lesions of the skin and mucosae, including the rarely occurring epitheloid blue nevus.^[13][14][15]
• Approximately 7% of all cardiac myxomas are associated with Carney complex.^[16]

• On gross pathology, external appearance, consistency size, and weight are extremely variable findings of cardiac myxoma.^[17]
• Tumor consistency depends on the quantity and distribution of fibrous tissue and calcification (it can be smooth, lobulated, friable or gelatinous).
• Myxomas are usually described as having a gelatinous, irregular surface.
• Myxomas that have an irregular consistency are more likely to form surface thrombi and embolize.^[18]
• Morphologically, these lesions tend to be attached to the endocardium by a broad-based pedunculated stalk.^[8]
• In some cases, the attachment to the endocardium can also be without a clear stalk, or sessile.^[8]
• Cardiac myxomas are non-invasive tumors, thus there is no infiltration to underlying tissues.^[19]
• Cardiac myxomas are intracavitary tumors.
• The distribution is normally within the interatrial septum or adjacent to foramen ovale (75%).
• However, they can also be found in other cardiac chambers, such as right atrium (15%), ventricles (2%) or cardiac valves (rare).
• Large cardiac myxomas are usually located in fossa ovalis.^[5]
• The size of the tumor varies from 0.6 to 12 cm, with a mean weight of 40 g.
• Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

• On microscopic histopathological analysis, myxoma cells have an ovoid nucleus with large nucleoli, abundant eosinophilic cytoplasm, and indistinct cell borders.^[20]

• They are usually arranged in perivascular ring structures (typically, infiltrated by lymphocytes and macrophages).^[17]

• The Gamna-Bodies which consist of fibrosis and deposition of iron pigments are a characteristic finding of myxoma tumors.^[17]

• Other frequent histological findings, are hemosiderin within the histiocytes, thrombosis, fibrosis and calcifications.^[17]

• In some cases, extramedullary hematopoiesis is present and mucin-producing glands can be also seen in the base of the tumor.^[17]

• The extracellular matrix forms an alcian blue-positive myxoid stroma, composed of variable amounts of proteoglycans, elastin and collagen.^[17]

• Cardiac myxoma cells exhibit immuno-reactivity mainly for calretinin (75–100%) followed by vimentin (>50%), NOTCH1, alpha-1 antichymotrypsin and plakophilin- 2.^[21]

• Calretinin plays an important role in the discrimination of mural thrombi and papillary fibroelastoma.^[21]

• Another immunohistochemical marker, survivin (an apoptosis inhibitor) has been detected to play an important role in the development and growth of cardiac myxomas.^[22]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Sogand Goudarzi, MD [2] Maria Fernanda Villarreal, M.D. [3]

The cause of cardiac myxoma has not been identifie. However, in some cases like inherited myxomatosis there is a strong relation with genetic mutations of PRKAR1A gene.

Disease name] may be caused by [cause1], [cause2], or [cause3].

OR

Common causes of [disease] include [cause1], [cause2], and [cause3].

OR

The most common cause of [disease name] is [cause 1]. Less common causes of [disease name] include [cause 2], [cause 3], and [cause 4].

OR

The cause of [disease name] has not been identified. To review risk factors for the development of [disease name], click here.

• Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of disease name, however complications resulting from untreated disease name is common.
• Life-threatening causes of [symptom/manifestation] include [cause1], [cause2], and [cause3].^[1]

• [Cause] is a life-threatening cause of [disease].

Common causes of [disease name] may include:^[2]

• [Cause1]
• [Cause2]
• [Cause3]

OR

• [Disease name] is caused by an infection with [pathogen name].
• [Pathogen name] is caused by [pathogen name].

Less common causes of [disease name] include:

• [Cause1]
• [Cause2]
• [Cause3]

• [Disease name] is caused by a mutation in the [gene name] gene.

List the causes of the disease in alphabetical order:

• There are no established causes for cardiac myxoma.^[3][4][5][6]
• About 10% of cardiac myxomas are familial.
• Inherited myxomatosis is caused by a mutation in the PRKAR1A gene.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]Cafer Zorkun, M.D., Ph.D. [3] Ahmad Al Maradni, M.D. [4] Maria Fernanda Villarreal, M.D. [5]

Cardiac myxoma should be differentiated from other benign and malignant primary heart tumors including papillary fibroelastoma, lipoma, rhabdomyoma, and cardiac metastasis. Primarily, cardiac myxoma should be differentiated from other diseases that cause mitral valve obstruction and embolic events, such as thrombi or endocarditis.

Cardiac myxoma should be differentiated from other cardiac tumors that present as a cardiac mass. The following are the differentials:^{[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48]}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maria Fernanda Villarreal, M.D. [2]Ahmad Al Maradni, M.D. [3]

Cardiac myxoma is a rare disease with a reported prevalence of 0.03% in general population. The incidence of cardiac myxoma is about 1/ 100,000 per year. The majority of patients with cardiac myxoma are diagnosed between 30 to 60 years; children are rarely affected. Females are more commonly affected with cardiac myxoma than men. The female-to-male ratio is approximately 1.8 to 1. Cardiac myxomas represent 78% of heart tumors.

• The prevalence of cardiac myxoma is reported as 0.03% in general population.^[1][2]

• The incidence of benign cardiac tumor including cardiac myxoma is about 1/100,000 per year.^[1]

• The mean age of patients at diagnosis is 50 years, most patients are between 30-60 age range.^[3]
• Cardiac myxomas are rare in children. However, in the pediatric population cardiac myxomas are more likely to be related with familial forms such as the (Carney complex).^[4]

• Females are more commonly affected with cardiac myxoma than men. The female-to-male ratio is approximately 1.8 to 1.^[5]
• Patients with Carney complex, tend to be younger and male.^[5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sogand Goudarzi, MD [2], Maria Fernanda Villarreal, M.D. [3], Ahmad Al Maradni, M.D. [4]

Common risk factors in the development of myxoma are female gender and genetic predisposition. In some cases, right atrial myxoma has been associated with tricuspid stenosis and atrial fibrillation.

• Common risk factors in the development of myxoma are:^[1]
  • Female gender
  • Genetic predisposition (Carney complex)
  • In some cases, right atrial myxoma has been associated with tricuspid stenosis and atrial fibrillation.
• Risk factors for the embolism in myxoma include the following:^[2]
  • Tumor location
  • Macroscopic appearance
  • Platelet volume
  • High platelet count

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmad Al Maradni, M.D. [2]Maria Fernanda Villarreal, M.D. [3]

If left untreated, cardiac myxoma progression occurs slowly. The overlap of various phenomena such as thrombosis, hemorrhage, or fragmentation may influence tumor growth, detachment, and consequently embolism. Complications that can develop as a result of myxoma are: arrhythmias, pulmonary edema, peripheral emboli, metastasis, blockage of the mitral heart valve. The survival rates after 5-years are 83% for benign heart tumors.

• If left untreated, cardiac myxoma progression occurs slowly. The overlap of various phenomena such as thrombosis, hemorrhage, or fragmentation may influence tumor growth, detachment, and consequently embolism..^[1][2]
• Constitutional symptoms, such as: weight loss, fatigue, and weakness are often the initial clinical presentation of cardiac myxoma patients, and may resemble those from endocarditis.^[3]
• Metastases are very uncommon in cardiac myxoma.^[4]
• Overall, clinical features of cardiac myxoma are associated with the tumor size, location, and mobility.^[5]
• Approximately 20% of patients with cardiac myxoma are asymptomatic.^[6]
• Since the majority of the cardiac myxomas are left sided, it may progress to develop mitral valve obstruction or systemic embolic events, such as stroke.^[7]
• Whereas, right atrial myxomas may obstruct the tricuspid valve and can present as right sided heart failure.^[8]

Complications are common. Some of the complications that may develop as a result of myxoma are:^[9][10][11]

• Peripheral emboli
• Blockage of the mitral heart valve
• Syncope
• Arrhythmias
• Pulmonary edema
• Metastasis
• Sudden death
• Fusiform cerebral aneurysms

Depending on the complications derivated from the cardiac myxoma at the time of diagnosis (embolic event or valve obstruction) the prognosis may vary. However with no complications, the prognosis is generally regarded as favorable after surgery. Recurrence rates (either locally or elsewhere in the heart) reported in 1-3% of cases. In atypical cases the rate is much higher (12-22%). The survival rates after 5-years are 83% for benign heart tumors.^[1]

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