The Tumor Plop: A Vanishing Art in Cardiac Auscultation

The Tumor Plop: A Vanishing Art in Cardiac Auscultation

Auscultating the Rare but Diagnostic Sound of Atrial Myxoma

Dr Neeraj Manikath , claude.ai

Abstract

Cardiac auscultation remains a cornerstone of clinical examination despite advances in imaging technology. Among the rarest and most diagnostically significant auscultatory findings is the "tumor plop"—a characteristic sound associated with atrial myxomas. This low-pitched, early diastolic sound, notable for its positional variability, represents the acoustic signature of a pedunculated cardiac tumor prolapsing through an atrioventricular valve. This review explores the pathophysiology, clinical presentation, auscultatory technique, differential diagnosis, and management of this fascinating clinical finding. We emphasize the importance of recognizing this sign in the modern era, where clinical examination skills are increasingly supplemented—but should never be supplanted—by imaging modalities.

Keywords: Atrial myxoma, tumor plop, cardiac auscultation, diastolic sounds, clinical examination


Introduction

In an era dominated by echocardiography and advanced cardiac imaging, the art of cardiac auscultation risks becoming a lost skill among trainees. Yet certain auscultatory findings remain pathognomonic, offering immediate diagnostic direction that can be lifesaving. The "tumor plop" is one such finding—a rare but unmistakable acoustic phenomenon that should prompt immediate investigation and intervention.

Atrial myxomas account for approximately 50% of all primary cardiac tumors and 75% of benign cardiac tumors, with an incidence of 0.5 to 1.0 per million population per year.^1,2^ While rare, their clinical significance is profound: they can cause valvular obstruction, systemic embolization, and sudden death. The tumor plop, when recognized, provides a pre-imaging diagnosis that demands urgent action.

This review aims to equip the modern internist with the knowledge and technical skills necessary to identify this diagnostic pearl, understand its pathophysiologic basis, and differentiate it from other diastolic sounds.


Pathophysiology of the Tumor Plop

The Acoustic Genesis

The tumor plop is generated by the mechanical impact of a mobile, pedunculated tumor striking the ventricular wall or valve apparatus during diastole. In the majority of cases (75%), atrial myxomas arise from the left atrium, typically attached to the interatrial septum near the fossa ovalis by a fibrovascular pedicle.^3^ This attachment allows the tumor to swing freely within the cardiac chamber, responding to blood flow dynamics and gravitational forces.

During ventricular diastole, as the atrioventricular valve opens, the tumor prolapses into the ventricular cavity. The sudden deceleration and impact of the tumor mass against the ventricular wall or valve structures generates a low-frequency sound wave—the tumor plop. This is analogous to the opening snap of rheumatic mitral stenosis, but with crucial differences in timing, pitch, and positional variability.^4^

Hemodynamic Consequences

Beyond its acoustic signature, the myxoma creates hemodynamic disturbances that explain associated clinical findings. The tumor can:

  1. Obstruct valve orifice: Creating intermittent or positional symptoms mimicking valvular stenosis
  2. Interfere with valve closure: Leading to regurgitation
  3. Fragment and embolize: Causing systemic (left atrium) or pulmonary (right atrium) emboli
  4. Trigger arrhythmias: Through mechanical irritation of conducting tissue

The variability of symptoms—often positional—mirrors the mobile nature of the tumor and provides critical diagnostic clues.^5^


Clinical Presentation: The Diagnostic Triad

Atrial myxoma classically presents with a triad of symptoms, though the complete triad is present in fewer than 50% of cases:^6^

1. Obstructive Symptoms (Mimicking Valvular Disease)

  • Dyspnea on exertion or with position changes
  • Orthopnea and paroxysmal nocturnal dyspnea
  • Syncope or presyncope (particularly positional)
  • Sudden death (rare but reported)

Pearl: Positional dyspnea or syncope—symptoms that worsen when lying on one side or standing suddenly—should raise suspicion for an obstructive cardiac mass.

2. Embolic Phenomena

  • Stroke or transient ischemic attacks (most common presentation in 25-30% of cases)^7^
  • Peripheral arterial emboli (digital, renal, splenic, coronary)
  • Pulmonary emboli (right atrial myxomas)
  • Retinal emboli visible on fundoscopy

Oyster: In young patients with stroke and no obvious risk factors, consider paradoxical embolism or, less commonly, left atrial myxoma. The tumor itself can fragment, or thrombus on the tumor surface can embolize.

3. Constitutional Symptoms

  • Fever and night sweats
  • Weight loss
  • Arthralgia and myalgia
  • Elevated inflammatory markers (ESR, CRP)
  • Anemia
  • Elevated immunoglobulins

These constitutional symptoms, resulting from interleukin-6 production by the tumor, can mimic infectious endocarditis, vasculitis, or malignancy—leading to delayed diagnosis.^8^


The Art of Auscultation: Technical Mastery

Patient Positioning: The Critical Variable

The hallmark of the tumor plop is its positional variability—a feature that distinguishes it from fixed cardiac sounds. Optimal auscultation requires:

  1. Left lateral decubitus position: The patient lies on their left side, bringing the cardiac apex closer to the chest wall. This position causes the tumor to fall anteriorly and laterally with gravity, potentially accentuating the prolapse and the sound.

  2. Alternative positions:

    • Supine position
    • Right lateral decubitus (may diminish or eliminate the sound)
    • Standing suddenly from sitting (may provoke symptoms and sounds)

Hack: Have the patient change positions during auscultation. A sound that appears, disappears, or changes timing with position is suspicious for a mobile mass. Document the position in which the sound is best heard.

Stethoscope Selection and Placement

  • Use the bell: The tumor plop is a low-frequency sound (20-100 Hz), best appreciated with the bell applied lightly to the skin
  • Location: Apex (5th intercostal space, midclavicular line)
  • Minimal pressure: Excessive pressure converts the bell into a diaphragm, filtering out low frequencies

Teaching Tip: Remind students that the bell is for listening to low-frequency sounds, while the diaphragm filters them out.

Acoustic Characteristics

The tumor plop has distinctive features:

  • Timing: Early to mid-diastole, 80-120 milliseconds after S2 (later than an opening snap but earlier than an S3)^9^
  • Pitch: Low-frequency, dull, "thud-like" quality
  • Quality: Brief, non-musical
  • Intensity: Variable, may be loud enough to be palpable as a "thrill"
  • Location: Best heard at apex with left atrial myxomas; tricuspid area with right atrial myxomas

The Position Test: Ask the patient to turn from left lateral to supine to right lateral while you listen continuously. The tumor plop may:

  • Change in timing relative to S2
  • Increase or decrease in intensity
  • Disappear entirely in certain positions

This positional variability is the diagnostic signature that separates the tumor plop from fixed cardiac sounds.


Differential Diagnosis: The Art of Distinction

The tumor plop must be differentiated from other diastolic sounds—a skill that requires both technical proficiency and pattern recognition.

Third Heart Sound (S3)

Characteristics:

  • Timing: Early diastole, immediately after S2 (0.12-0.18 seconds)
  • Pitch: Low frequency (same as tumor plop)
  • Quality: "Ken-tuc-KY" rhythm when combined with S1 and S2
  • Position: Fixed timing, intensity may vary with position
  • Mechanism: Rapid ventricular filling with reduced compliance

Key Differentiator: An S3 maintains fixed timing after S2 regardless of position, while a tumor plop varies in timing.^10^

Clinical Context: S3 occurs in volume overload states (heart failure, valvular regurgitation) or physiologically in young patients and athletes. A myxoma patient may have both an S3 (from heart failure) and a tumor plop.

Opening Snap (OS)

Characteristics:

  • Timing: Early diastole, 0.04-0.12 seconds after S2 (earlier than tumor plop)
  • Pitch: Higher frequency, "sharp," "clicking" quality
  • Quality: Crisp, brief
  • Position: Fixed timing, heard best at apex with radiation to left sternal border
  • Mechanism: Sudden tensing of stenotic mitral valve leaflets during opening

Key Differentiator: The opening snap is sharper, higher-pitched, occurs earlier after S2, and has fixed timing regardless of position.^11^

Pearl: The A2-OS interval narrows with increasing severity of mitral stenosis. This relationship does not apply to the tumor plop.

Pericardial Knock

Characteristics:

  • Timing: Early diastole, similar to tumor plop
  • Pitch: Higher frequency than tumor plop or S3
  • Quality: Sharp, high-pitched "knock"
  • Position: Fixed, best heard at left sternal border
  • Mechanism: Abrupt cessation of ventricular filling in constrictive pericarditis

Key Differentiator: The pericardial knock is higher-pitched and fixed in timing. Clinical context (prior pericarditis, tuberculosis, radiation) and other signs of constriction (Kussmaul sign, prominent y descent) aid diagnosis.

Prosthetic Valve Sounds

Characteristics:

  • Timing: Variable depending on valve type and position
  • Quality: Often louder, clicking, metallic
  • History: Known valve replacement

Hack: Always check for a median sternotomy scar! Bioprosthetic valve sounds can be subtler than mechanical valves.


Associated Physical Examination Findings

A thorough cardiovascular examination may reveal additional clues:

Auscultatory Findings

  • Diastolic murmur: Mid-to-late diastolic rumble at apex (mimicking mitral stenosis)
  • Systolic murmur: If tumor interferes with valve closure (regurgitation) or causes outflow obstruction
  • Variable intensity: Murmurs and sounds change with position
  • Absence of opening snap: When tumor obstructs valve, the opening snap of stenosis may be absent

Hemodynamic Signs

  • Pulse irregularity: Atrial fibrillation (10-15% of cases)^12^
  • Blood pressure: May be normal or show signs of low output
  • Jugular venous pressure: Elevated if right-sided heart failure or right atrial myxoma

Embolic Stigmata

  • Digital examination: Splinter hemorrhages, digital ischemia, Osler nodes (mimicking endocarditis)
  • Neurologic examination: Focal deficits from prior stroke
  • Fundoscopy: Retinal emboli (Hollenhorst plaques)
  • Abdominal examination: Renal or splenic infarction tenderness

Oyster: The combination of cardiac symptoms, fever, elevated inflammatory markers, and embolic phenomena can lead to misdiagnosis as infective endocarditis. However, blood cultures remain negative (hence "culture-negative endocarditis" in the differential).


Diagnostic Approach: From Bedside to Operating Room

Immediate Actions

When a tumor plop is suspected based on clinical examination:

  1. Continuous cardiac monitoring: Risk of arrhythmias and hemodynamic compromise
  2. Activity restriction: Prevent positional changes that might precipitate obstruction or embolization
  3. STAT transthoracic echocardiography (TTE): First-line imaging modality

Hack: In a patient with suspected atrial myxoma, avoid unnecessary maneuvers that increase transvalvular flow or change position abruptly—theoretically, these could precipitate tumor fragmentation or acute obstruction.

Echocardiographic Evaluation

Transthoracic Echocardiography (TTE):

  • Sensitivity: 90-95% for left atrial myxomas^13^
  • Findings:
    • Pedunculated mobile mass attached to interatrial septum
    • Movement across mitral valve in diastole
    • Valve obstruction or regurgitation
    • Left atrial enlargement
    • Chamber thrombus (differential consideration)

Transesophageal Echocardiography (TEE):

  • Superior imaging of left atrium and tumor attachment
  • Essential for surgical planning
  • Identifies tumor characteristics (size, attachment site, surface characteristics)
  • Rules out additional tumors (5% of cases are multifocal)^14^

Cardiac MRI:

  • Excellent tissue characterization
  • Differentiates myxoma from thrombus, other tumors
  • Identifies tumor vascularity and attachment
  • Useful when echocardiography is inconclusive

Laboratory Investigations

No specific biomarkers diagnose myxoma, but typical findings include:

  • Elevated ESR and CRP (inflammatory response)
  • Normocytic anemia
  • Thrombocytopenia or thrombocytosis
  • Elevated immunoglobulins (especially IgG)
  • Normal or negative blood cultures

Management: A Surgical Emergency

Definitive Treatment

Surgical Excision: The only definitive treatment, typically performed urgently once diagnosis is confirmed.^15^

Surgical Approach:

  • Median sternotomy with cardiopulmonary bypass
  • Biatrial approach for optimal exposure
  • Wide excision of tumor with portion of interatrial septum to prevent recurrence
  • Primary septum repair or patch closure
  • Careful tumor handling to prevent intraoperative embolization

Timing: Urgent but not necessarily emergent—within days of diagnosis. Emergent surgery required for:

  • Hemodynamic instability
  • Acute valve obstruction
  • Mobile, highly fragmented tumors with high embolic risk

Outcomes

  • Operative mortality: 0-5% in experienced centers^16^
  • Recurrence rate: 1-5% for sporadic cases, higher (10-20%) for familial/Carney complex cases^17^
  • Long-term prognosis: Excellent after complete resection with regular follow-up

Follow-up Protocol:

  • Echocardiography at 6 months, then annually for 4 years
  • More frequent surveillance for familial cases
  • Lifelong follow-up for Carney complex patients

Special Considerations

Familial Atrial Myxoma and Carney Complex

Approximately 7% of myxomas occur in a familial pattern, often as part of Carney complex—an autosomal dominant syndrome characterized by:^18^

  • Multiple cardiac myxomas (may be recurrent)
  • Cutaneous pigmentation (lentigines, blue nevi)
  • Endocrine tumors (pituitary adenomas, thyroid nodules, testicular tumors)
  • Schwannomas

Pearl: Examine the patient for spotty skin pigmentation. Multiple lentigines or blue nevi in a young patient with atrial myxoma suggest Carney complex and warrant genetic counseling and family screening.

Right Atrial Myxomas

Comprising 15-20% of myxomas:^19^

  • Tumor plop heard at left lower sternal border
  • Symptoms of right heart failure (edema, ascites, hepatomegaly)
  • Pulmonary emboli rather than systemic emboli
  • May present as "unexplained" pulmonary hypertension

Clinical Pearls and Teaching Points

Pearls for Recognition

  1. The Position Test is Diagnostic: A diastolic sound that changes timing or intensity with position is a mobile mass until proven otherwise.

  2. Young Stroke = Think Myxoma: In stroke patients under 50 without traditional risk factors, consider atrial myxoma alongside other causes like dissection, vasculitis, and hypercoagulable states.

  3. Constitutional Symptoms are Common: Don't be misled by fever and elevated inflammatory markers into diagnosing infection or malignancy without considering cardiac myxoma.

  4. Emboli Can Contain Tumor: Pathologic examination of embolic material may reveal myxomatous tissue, providing unexpected diagnosis.

  5. Mitral Stenosis Without Rheumatic History: A diastolic murmur suggestive of mitral stenosis in a patient without rheumatic fever history warrants echocardiography to exclude myxoma.

Oysters for the Astute Clinician

  1. The "Wrecking Ball" Phenomenon: Very large myxomas can cause positional syncope—a dramatic presentation where the patient loses consciousness when changing from supine to upright as the tumor obstructs the valve orifice.

  2. Myxoma Mimicking Everything: Myxomas have been misdiagnosed as endocarditis, vasculitis, pulmonary embolism, multiple sclerosis (from embolic strokes), and even malignancy. Maintain a high index of suspicion.

  3. Coronary Embolization: Myxoma fragments can embolize to coronary arteries, causing myocardial infarction—particularly in young patients without coronary risk factors.

  4. Systemic Embolization Despite Anticoagulation: Patients on anticoagulation for atrial fibrillation can still experience embolic events from myxoma, as the source is tumor fragmentation, not thrombus.

Hacks for Clinical Efficiency

  1. The Dynamic Auscultation Protocol:

    • Listen in left lateral position for 30 seconds
    • Roll patient to supine, listen immediately
    • Continue to right lateral position
    • Document any sound that appears, disappears, or changes
  2. Use Your Phone: Record the cardiac sounds if possible (with patient consent). This allows review, teaching, and documentation of positional variability.

  3. The "Tumor Plop Red Flag Bundle":

    • Positional symptoms (dyspnea, syncope)
    • Young patient with stroke
    • Culture-negative endocarditis picture
    • Diastolic sound with positional variability

    Any three = STAT echocardiogram

  4. Teach With Analogies: Describe the tumor plop to students as "a ball on a string hitting the floor"—the tumor is the ball, the pedicle is the string, and the ventricular wall is the floor.


Conclusions

The tumor plop remains one of cardiology's most fascinating and diagnostically valuable auscultatory findings. While echocardiography has revolutionized cardiac diagnosis, the skilled clinician who can recognize this sound at the bedside provides immediate diagnostic direction that can be lifesaving. The tumor plop exemplifies the enduring value of physical examination in modern medicine—not as a replacement for imaging, but as a guide for when and how urgently to proceed with further investigation.

For the medical educator, teaching the tumor plop offers an opportunity to emphasize several fundamental principles: the importance of positional maneuvers during examination, the value of understanding pathophysiology to predict physical findings, and the continued relevance of careful bedside assessment in the era of advanced technology.

For the clinician, recognizing a tumor plop means recognizing a surgical emergency. The combination of clinical suspicion based on history and physical examination, followed by urgent echocardiography and cardiothoracic surgery consultation, exemplifies the integration of clinical skills and technology that defines excellent patient care.

As we train the next generation of physicians, we must ensure that skills like cardiac auscultation—and the recognition of rare but crucial findings like the tumor plop—are not lost to time. These skills save lives, and they embody the art of medicine that technology can support but never fully replace.


References

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  2. Amano J, Kono T, Wada Y, et al. Cardiac myxoma: its origin and tumor characteristics. Ann Thorac Cardiovasc Surg. 2003;9(4):215-221.

  3. Pinede L, Duhaut P, Loire R. Clinical presentation of left atrial cardiac myxoma: a series of 112 consecutive cases. Medicine (Baltimore). 2001;80(3):159-172.

  4. Shah M, Joshi S. Cardiac auscultation: beyond the basics. J Assoc Physicians India. 2007;55:283-286.

  5. Bjessmo S, Ivert T. Cardiac myxoma: 40 years' experience in 63 patients. Ann Thorac Surg. 1997;63(3):697-700.

  6. Pucci A, Gagliardotto P, Zanini C, et al. Histopathologic and clinical characterization of cardiac myxoma: review of 53 cases from a single institution. Am Heart J. 2000;140(1):134-138.

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  8. Mendoza CE, Rosado MF, Bernal L. The role of interleukin-6 in cases of cardiac myxoma: clinical features, immunologic abnormalities, and a possible role in recurrence. Tex Heart Inst J. 2001;28(1):3-7.

  9. Tavel ME. Cardiac auscultation: a glorious past—but does it have a future? Circulation. 1996;93(6):1250-1253.

  10. Drazner MH, Rame JE, Dries DL. Third heart sound and elevated jugular venous pressure as markers of the subsequent development of heart failure in patients with asymptomatic left ventricular dysfunction. Am J Med. 2003;114(6):431-437.

  11. Rothman A, Goldberger AL. Aids to cardiac auscultation. Ann Intern Med. 1983;99(3):346-353.

  12. Ipek G, Erentug V, Bozbuga N, et al. Surgical management of cardiac myxoma. J Card Surg. 2005;20(3):300-304.

  13. Engberding R, Daniel WG, Erbel R, et al. Diagnosis of heart tumours by transoesophageal echocardiography: a multicentre study in 154 patients. Eur Heart J. 1993;14(9):1223-1228.

  14. Hoffmeier A, Sindermann JR, Scheld HH, Martens S. Cardiac tumors—diagnosis and surgical treatment. Dtsch Arztebl Int. 2014;111(12):205-211.

  15. Keeling IM, Oberwalder P, Anelli-Monti M, et al. Cardiac myxomas: 24 years of experience in 49 patients. Eur J Cardiothorac Surg. 2002;22(6):971-977.

  16. Guhathakurta S, Riordan JP. Surgical treatment of right atrial myxoma. Tex Heart Inst J. 2000;27(1):61-63.

  17. Carney JA, Gordon H, Carpenter PC, Shenoy BV, Go VL. The complex of myxomas, spotty pigmentation, and endocrine overactivity. Medicine (Baltimore). 1985;64(4):270-283.

  18. Stratakis CA, Kirschner LS, Carney JA. Clinical and molecular features of the Carney complex: diagnostic criteria and recommendations for patient evaluation. J Clin Endocrinol Metab. 2001;86(9):4041-4046.

  19. Griborio-Guzman AG, Aseyev O, Shah H, Sadreddini M. Right atrial myxoma: case report and review of the literature. Medicine (Baltimore). 2016;95(17):e3474.


Conflict of Interest Statement: The author declares no conflicts of interest.


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