Calculators, Algorithms, Drug Interaction CheckersTools
Back To Search Results

Interventricular Septum Abscess

Author: Mohamed H. Alahmadi Editor: Sara A. Collier Updated: 8/17/2026 2:02:41 AM

Introduction

Interventricular septal abscess is a rare but life-threatening complication of infective endocarditis, characterized by a pocket of infection within the septal wall separating the ventricles. This condition most often results from extension of severe valvular infection (native or prosthetic) into the septum, particularly from aortic valve endocarditis, given the close anatomical proximity. Clinically, a septal abscess may manifest with new atrioventricular conduction blocks (due to involvement of the proximal conduction system) or signs of heart failure if valve function is compromised.

This condition carries a poor prognosis: the presence of an aortic root abscess significantly increases surgical mortality compared to endocarditis without abscess.[1] An intracardiac abscess carries a high level of morbidity and mortality. The abscess may be located within the myocardium, endocardium, or valves (native, prosthetic, or mechanical). Infective endocarditis is an infection of the heart valves, which, if not promptly treated, can progress to a cardiac abscess in 20% to 30% of cases.[2] 

An abscess anywhere in the myocardium can present as an interventricular abscess in rare cases. The interventricular septum is a thick, muscular wall that separates the ventricles. However, the proximal portion of the septum is thin and membranous, and the distal part is thick and muscular.

The proximity of the interventricular septum to the valves makes it highly susceptible to abscess formation.[3][4] An interventricular abscess usually arises as an extension of infective endocarditis from cardiac valves, most commonly the aortic valve.[5] Due to the progression of endocarditis into a paravalvular abscess, it can present as conduction blocks and/or congestive heart failure. Even with optimal treatment, the inpatient mortality of aortic valve endocarditis has been reported as high as 40% to 79%, depending on patient age, comorbidity, and the type of organism.[6] 

There are several risk factors for developing infective endocarditis. These include rheumatic, congenital, and degenerative valve lesions, intracardiac prosthetic devices, intravenous drug use, and use of access devices (eg, indwelling catheters, hemodialysis, pacemakers, among others).[7] In addition, modern interventions have introduced new at-risk populations; for example, endocarditis after transcatheter aortic valve replacements (TAVR) now occurs at rates comparable to surgical prosthetic valve infections.[8]

Staphylococcus aureus is the most common cause of infective endocarditis. Data from more than 70 million hospitalizations in the United States between 1999 and 2008 suggest an increase in the incidence of Staphylococcus aureus infections compared with other microorganisms. In another study on endocarditis, staphylococci accounted for 57.5% of cases, followed by streptococci and enterococci at 33.3%.[9] Bacterial colonization and systemic infection can occur via intravascular catheters, surgical wounds, prosthetic devices, and hemodialysis.[10][11] Recent studies report 30-day mortality rates on the order of 20% to 40% for aortic valve endocarditis complicated by abscess.[12]

Etiology

Register For Free And Read The Full Article
Get the answers you need instantly with the StatPearls Clinical Decision Support tool. StatPearls spent the last decade developing the largest and most updated Point-of Care resource ever developed. Earn CME/CE by searching and reading articles.
  • Dropdown arrow Search engine and full access to all medical articles
  • Dropdown arrow 10 free questions in your specialty
  • Dropdown arrow Free CME/CE Activities
  • Dropdown arrow Free daily question in your email
  • Dropdown arrow Save favorite articles to your dashboard
  • Dropdown arrow Emails offering discounts

Learn more about a Subscription to StatPearls Point-of-Care

Etiology

An interventricular septal abscess most commonly arises from the progression of infective endocarditis in a native or prosthetic valve to the interventricular septum. A perivalvular abscess due to infective endocarditis can also extend and become an interventricular abscess. In both native valve endocarditis and prosthetic valve endocarditis, unchecked infection can erode through the valve annulus and create a periannular abscess, which may track into the septum (especially around the aortic valve annulus, which lies just above the membranous septum).[13] 

The primary etiology of interventricular septal abscess is disseminated bacteremia, extension from an infective source, or local infection.[14][15] The factors leading to an interventricular abscess are similar to infective endocarditis, including degenerative valves, mechanical valves, prosthetic valves, and intravenous illicit drug use. Transcatheter heart valves (eg, TAVR) have also emerged as a new substrate for infection, now comprising a notable subset of prosthetic valve endocarditis cases. Other predisposing factors known to lead to the formation of the abscess in the literature are:

  • Trauma
  • Deep penetrating wounds of the cardiac tissue
  • Infected coronary stents
  • Infected sternal incisions
  • Infected transplanted hearts
  • Deep burns
  • Immunocompromised patients
  • HIV
  • Parasitic infections
  • Pseudoaneurysms
  • Suppurative pericarditis

Epidemiology

Interventricular septal abscesses are uncommon, occurring as a complication in a minority of cases of infective endocarditis (historically, around 20% to 30% of cases of severe endocarditis had some form of cardiac abscess).[16] This condition is more prevalent in developing countries, where patients may not have access to antibiotics for simple bacteremic infections that seed the cardiac structures and later lead to infective endocarditis. In the United States and Europe, patients often have predisposing medical conditions or devices that increase the risk of infection.

Among microbiological etiologies, staphylococci are the leading cause of infective endocarditis, which can produce a septal abscess. The incidence of infective endocarditis in the United States increased from 11 per 100,000 to 15 per 100,000 individuals between 2000 and 2011.[17] Estimating the precise incidence of interventricular abscess is challenging because the criteria for diagnosing infective endocarditis continue to evolve. The variability of risk factors, predisposing medical conditions, microbiological agents, valvular pathologies, intravenous illicit drug use, and socioeconomic factors are also possible causes of an increasing incidence of interventricular abscess with infective endocarditis. 

The most common infectious organisms causing interventricular abscesses include:

  • Staphylococcus aureus
  • Haemophilus species
  • Enterococci 
  • Escherichia coli
  • Beta-hemolytic streptococci
  • Streptococcus pneumoniae
  • Bacteroides species
  • Parasitic organisms
  • Hydatid cysts
  • Listeria monocytogenes
  • HIV
  • Immunocompromised states
  • Miscellaneous

In microbiology, Staphylococcus aureus remains the leading cause of endocarditis-associated myocardial abscesses (consistent with its predominance in acute endocarditis).[18] Streptococcal species (such as the Streptococcus viridans group) and enterococci are also common causes of endocarditis (especially in subacute cases) and can lead to abscess formation. Gram-negative organisms and fungi are less frequent etiologies but are seen in specific contexts (eg, HACEK organisms in culture-negative endocarditis, Candida in intravenous drug users or immunosuppressed patients).

The list of organisms causing septal abscesses generally mirrors that of endocarditis, with S aureus at the top, followed by various streptococci, enterococci, and, in some cases, unusual pathogens (including fastidious organisms such as Bartonella or Coxiella burnetii in culture-negative cases). Significantly, the 2023 updates to diagnostic criteria have expanded the recognized spectrum of “typical” infective endocarditis-causing microorganisms to include some less common pathogens, particularly in the context of prosthetic devices.

Pathophysiology

The damaged cardiac endothelium in the diseased valve serves as a nidus for bacterial colonization, either through direct trauma or inflammation. The exposed subendothelial tissue produces extracellular matrix proteins and tissue factor, and fibrin and platelets are deposited. This then leads to the formation of sterile vegetations that become colonized by bacteria, thus resulting in infective endocarditis.[7]

Staphylococcus aureus, with the help of its cell-wall adherence proteins, attaches to the extracellular matrix proteins, fibrin, and platelets. This series of events culminates in the subsequent invasion of the endothelial cell and ongoing inflammation.[19] Other organisms associated with infective endocarditis (streptococci, enterococci, Candida species, and Pseudomonas) produce biofilms that embed in the extracellular matrix with cell-to-cell communications and gene expression leading to their proliferation. These biofilms protect bacteria from the host immune response and prevent the entry of antimicrobial agents.[20] Complicated infective endocarditis can spread to surrounding tissues, leading to an interventricular septal abscess.

Histopathology

Biopsy and histological assessments are usually not performed as part of the diagnostic workup for septal abscesses. However, gross and microscopic findings can be obtained from surgically removed diseased valves or tissue obtained during an autopsy. In the setting of native or prosthetic valves, infective endocarditis can lead to a myocardial abscess. 

This abscess is caused by the spread of infection beyond the extent of the valve ring into the annulus, periannular tissue, chordae tendinae, and the fibrous tissue surrounding the mitral and aortic valves. Invasion into the ring and septum can lead to prosthetic valve dehiscence and hemodynamically significant paravalvular regurgitation. Histological inspection of a myocardial abscess will often show a polymorphonuclear predominance with damaged cardiac tissue and collagen degradation.[21]

History and Physical

The history and physical examination findings of the interventricular abscess will vary depending on the acuity of presentation, the extent of myocardial involvement, damage to conduction pathways, and cardiac valve patency. There should be a high index of suspicion for an interventricular abscess in patients with arrhythmias, heart block, and extension of the abscess into the annulus.[21]

History

In the setting of an acute infection, a classical presentation of acute hemodynamic distress is more likely.[21][22][23] The history should focus on the area affected by an interventricular abscess, risk factors, the degree of conduction block, and the degree of contraction/anatomical abnormality. An interventricular abscess can present with the following symptoms in history:

  • Dizziness
  • Dyspnea
  • Chest pain is likely due to myocardial infarction or angina symptoms.
  • Paroxysmal nocturnal dyspnea
  • Cyanosis
  • Orthopnea
  • Syncope or near syncope
  • Joint pain
  • Cough
  • Skin rashes
  • Recent surgery or trauma to the heart
  • Travel to endemic areas
  • Exposure to an animal
  • Exposure to an infection risk factor

Physical Exam

The signs and symptoms of an interventricular septal abscess may reflect the presence of infective endocarditis.[22][21][23] The clinical features can persist depending on the antibiotic response to bacteria. No pertinent physical examination findings can mark the diagnosis of an interventricular abscess, but helpful examination findings include:

  • Bradycardia
  • Heart failure signs and symptoms include S3, inspiratory basal crackles in the lungs, jugular venous distention, and bilateral leg edema, abdominal ascites.
  • Aortic regurgitation or dilated aortic root findings, including decrescendo murmur, soft middiastolic rumble heard at the apical area (Austin Flint murmur), Corrigan pulse, De Musset sign, Quincke sign, Muller sign, Hill sign, and Duroziez sign
  • A ventricular septal defect (VSD) may present as a systolic murmur at the left lower sternal border, cyanosis, and heart failure.
  • Pulmonary hypertension signs include a loud P2 component of the second heart sound.
  • Mitral regurgitation findings include a holosystolic apical murmur and pulmonary edema.
  • Diffuse multiorgan involvement features due to systemic emboli from an abscess.
  • Back tenderness due to osteomyelitis
  • Petechia
  • Sublingual or splinter hemorrhages
  • Osler nodes
  • Janeway lesions
  • Roth spots
  • Splenomegaly

Evaluation

The Duke criteria (initially formulated in 1994 and modified in 2000) have been the standard for diagnosing infective endocarditis; fulfilling these criteria is a prerequisite for diagnosing an interventricular septal abscess. In 2023, these criteria were updated by an international collaboration (Duke-ISCVID), incorporating advances in diagnostics.[8][24] The diagnosis of infective endocarditis is crucial for establishing the presence of an interventricular septal abscess.

This diagnosis is based on a set of clinical criteria, which include both major and minor criteria. The criteria can be met by demonstrating 2 major and 1 minor, 1 major and 3 minors, or 5 minor criteria. A simplified approach to diagnosing an interventricular abscess includes identifying infective endocarditis, conduction block, and imaging demonstrating a visible interventricular abscess(see Image. Diagnostic Evaluation of Interventricular Septal Abscess in Infective Endocarditis).[21] Furthermore, the diagnostic evaluation of the interventricular abscess includes:

  • Routine blood tests
    • In acute cases, regular blood work includes a complete blood profile, which may reveal an elevated white blood cell count with a left shift, normocytic anemia, and thrombocytopenia. In the subacute case, the white blood cell count can be normal.[25]
  • Infectious/ inflammatory tests
    • Tests such as acute-phase reactants and inflammatory markers can aid in diagnosing infective endocarditis and interventricular abscess. These tests include erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), ferritin, and other inflammatory markers. An absence of elevated ESR and CRP helps rule out an active acute or chronic infection.[25]
  • Blood cultures
    • Three blood cultures from different sites are a cornerstone of the diagnosis of infective endocarditis and an interventricular abscess. Three blood cultures can detect up to 98% of bacteremia.[25] Although valve culture can be useful for cases that meet the Duke criteria, many patients have negative blood cultures.[26]
    • Valvular cultures should be avoided if a patient does not meet the Duke criteria, as it can lead to false-positive findings. In a study by Munoz et al, 1030 valves were cultured after surgical removal in patients with infective endocarditis; the results showed a 39% positive valvular culture rate among cases meeting the Duke criteria and a 28% positive culture rate among cases not meeting the Duke criteria.[26]
  • Urinalysis
    • Urine workup may show proteinuria and microscopic hematuria. Urine findings can be due to immune-complex deposits from infection or to septic emboli to the kidney from an interventricular abscess or infective endocarditis.[25]
  • Electrocardiogram (EKG)
    • This is a beneficial test for the interventricular abscess. EKG may show various conduction blocks.[27] Conduction blocks can present as first-, second-, or third-degree atrioventricular block, or bundle branch or fascicular blocks.[22][28][29] The development of heart block in infective endocarditis is a good indicator of an extension of infective endocarditis to the myocardial/interventricular septum.[30] The appearance of a new atrioventricular block on an EKG has an 88% positive predictive value but a low sensitivity of 45% for detecting an abscess.[31]

Imaging

Echocardiography is the primary imaging modality for diagnosing infective endocarditis and interventricular abscess. Other helpful imaging studies may include the following: 

  • Echocardiography
    • Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) aid in the early diagnosis of the interventricular abscess and infective endocarditis. TTE is the first echocardiographic imaging modality used for diagnosis and management guidance. TTE has a low sensitivity of 23% and a very high specificity of 98.6% for diagnosing the myocardial abscess. According to a study by Ellis et al, there are specific echocardiographic criteria for detecting myocardial abscess.[32] These criteria include the following:
      • Evidence of the prosthetic valve rocking
      • Aneurysmal dilatation of the Valsalva sinus
      • Posterior aortic root thickness exceeding 10 mm
      • A higher than 14 mm of perivalvular density in the septum
      • A relatively uncommon but highly specific finding of "echo-free space"
      • M-mode and 2-dimensional (2D) echocardiography can play a significant role in diagnosing a ventricular septal abscess.[5] Real-time 3D TTE is more useful than 2D TTE for confirming the diagnosis of a myocardial abscess, delineating its boundaries, and helping in identifying extension into adjacent structures.[33]
    • TEE has higher sensitivity for detecting myocardial/interventricular abscesses than TTE.[34] In a study by Daniel et al, 43 patients had a documented perivalvular abscess at surgery or autopsy, with TTE sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of 87%, 95%, 91%, and 92%, respectively.[35]
  • Computed tomography (CT)
    • This modality has lower sensitivity than other imaging modalities. 
  • Magnetic resonance imaging (MRI)
    • MRI is an excellent imaging modality that provides functional, morphologic, and prognostic information in a single examination.[36] However, compared with echocardiography, it is less portable and offers lower resolution. 
  • Scintigraphy
    • In areas where TTE is limited in visualizing the myocardial abscess, indium-111 leukocyte scintigraphy is employed. This modality is primarily used for prosthetic valve endocarditis and may allow earlier identification of myocardial abscesses than other imaging modalities.[37] The technique involves using a few milliliters of venous blood mixed with an anticoagulant solution.
    • After centrifugation, the white blood cells are separated and labeled with a radioactive isotope; the cells are resuspended in isotonic sodium chloride solution and reinjected into the patient. Then, using a gamma-ray camera, images are obtained within 16 to 24 hours. Viable radioactive leukocytes accumulate in areas of inflammation or abscesses. If TEE is available, indium-111 scintigraphy is seldom needed. 

Treatment / Management

Medical Therapy

Management of an interventricular septal abscess requires both aggressive antimicrobial therapy and often surgical intervention. Upon diagnosis (or strong suspicion) of endocarditis with abscess, empiric broad-spectrum intravenous antibiotics should be started promptly after obtaining blood cultures. Empiric regimens are chosen to cover Staphylococcus aureus, both methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible Staphylococcus aureus (MSSA), streptococci, and enterococci.

For example, a common empiric regimen is vancomycin plus ceftriaxone, or vancomycin plus an antipseudomonal beta-lactam if healthcare-associated infection is suspected.[38][39] This provides coverage for MRSA, MSSA, viridans strep, and Enterococcus while cultures are pending. Once the causative organism is identified, therapy is narrowed and tailored to susceptibilities.(B2)

For MSSA endocarditis, a beta-lactam (oxacillin or cefazolin) is preferred; for MRSA, vancomycin or high-dose daptomycin is indicated.[40] Notably, current guidelines no longer recommend routine aminoglycoside use for native-valve S aureus endocarditis due to a lack of benefit and increased nephrotoxicity. Gentamicin may still be used for synergy in certain situations, such as short-term use in prosthetic valve staph endocarditis or for resistant Enterococcus, but its role has been minimized. Rifampin is reserved for cases involving prosthetic material (eg, prosthetic valve endocarditis with abscess), as it can help penetrate biofilms; it should not be used in native-valve infection due to the risk of resistance and the lack of proven benefit.(B3)

The duration of antibiotic therapy is prolonged—typically, at least 6 weeks of intravenous bactericidal treatment are required for an abscess, counted from the first day of negative cultures. In many cases of myocardial abscess, even 6 to 8 weeks of intravenous antibiotics may be needed to ensure eradication. The 2023 European Society of Cardiology (ESC) guidelines allow for a portion of this course to be completed with oral antibiotics in stable patients, but only after an initial phase of at least 2 weeks of intravenous therapy and confirmation (usually by TEE) that there is no uncontrolled local infection. 

In practice, this “oral switch” strategy (validated by recent trials) can be considered for patients who have stabilized, to facilitate outpatient completion of therapy.[41] Throughout treatment, close collaboration with an infectious disease specialist is important to optimize the antibiotic regimen and monitor for toxicity. Supportive care is also crucial: management of heart failure (with diuretics, vasodilators if needed), and use of temporary pacing if high-degree atrioventricular block is present due to the abscess.(B3)

Surgery

Open surgical incision and drainage or needle drainage is often part of the management of an interventricular abscess.[42] In the presence of a severe complication, such as a ruptured interventricular abscess, causing a VSD, surgery is often required. Indications for urgent surgical intervention include any signs of uncontrolled infection (eg, a growing abscess, fistula formation, persistent bacteremia) or hemodynamic compromise (such as severe valve regurgitation causing heart failure). In particular, the development of a new conduction block in endocarditis (suggesting septal abscess) or an abscess seen on imaging is considered an urgent surgical indication before the infection ruptures or causes irreversible damage.[41] (B3)

Surgical treatment involves radical debridement of all infected tissue (resecting the abscess cavity and any necrotic septal tissue) and repair of the resulting defect. In cases of aortic root abscess, aortic root replacement or patch repair is often required in conjunction with valve replacement. If the abscess has already ruptured into the septum, causing a VSD, or into adjacent chambers, open-heart surgery to close these communications is required on an emergency basis. The timing of surgery depends on patient stability: truly emergent surgery (within 24 hours) is done for cardiogenic shock or refractory pulmonary edema, whereas urgent surgery (within a few days) is advised for abscesses, even if the patient is hemodynamically stable, to prevent progression. Preoperative management may include placing a temporary pacemaker if complete heart block is present (and ESC guidelines advise considering permanent pacemaker placement early in such cases, especially if the block persists postoperatively or is associated with large abscesses).[21][42](B3)

During the operation, surgeons will drain the abscess cavity (incision and drainage) and reconstruct the affected septum and valve annulus. For example, an abscess near the aortic valve often requires removal of the infected valve and insertion of an aortic graft conduit or patch (the Bentall procedure if the root is involved). If the abscess extends to the mitral or tricuspid area, valve repair or replacement is performed as needed.

Postoperatively, antibiotics must be continued to sterilize any residual infection (the 6-week antibiotic course usually restarts after surgery if an abscess is resected). Close hemodynamic monitoring and support in an intensive care unit (ICU) setting are necessary, as these patients are high-risk. In summary, the management of an interventricular septal abscess is a multimodal approach: prompt initiation of appropriate antibiotics, early involvement of cardiac surgeons, and careful supportive therapy for complications such as heart block or heart failure. This approach, ideally executed by an experienced endocarditis team, offers the best chance of recovery.[1]

Differential Diagnosis

The interventricular septal abscess is a rare and uncommon complication of infective endocarditis.[21] This condition generally presents with vague signs and symptoms and can mimic many other medical disorders, including:

  • Infective/paravalvular complications and fistulous lesions
    • Perivalvular/aortic-root abscess and mitral–aortic intervalvular fibrosa (MAIVF) pseudoaneurysm
      • Common extensions of infective endocarditis may track into the septum or appear as a cystic/paraseptal cavity.
      • Major echo criteria for infective endocarditis include abscess or pseudoaneurysm.
      • CT is helpful for paravalvular disease when echocardiography is limited.[6][43]
    • Infected left ventricle pseudoaneurysm
      • Evolving from an extravalvular abscess (eg, at MAIVF).[44]
    • Gerbode defect (left ventricle to right atrium shunt)
      • This can arise from infective endocarditis with septal destruction and be misread as a septal cavity; Doppler jet direction is the key separator.[45]
  • Ischemic/iatrogenic/septal injury
    • Intramyocardial (dissecting) septal hematoma
      • Postmyocardial infarction, after percutaneous coronary intervention of chronic total occlusions (PCI/CTO) work, postsurgery, or trauma, appears as anechoic/heterogeneous intraseptal cavitation with or without flow; a classic mimic.[46]
    • Postinfarction VSD/rupture
      • May present with shock and a new murmur; color Doppler shows a high-velocity left ventricle to right ventricle (left ventricle-to-right ventricle) jet across the septum rather than a walled-off cavity.[47]
  • Congenital/anatomic septal outpouchings
    • Membranous ventricular septal aneurysm (VSA/IVMS aneurysm)
      • Often incidental or associated with VSD closure; can appear as a cystic septal space; key pitfall is confusing it with a sinus of Valsalva aneurysm (SOVA) or abscess.[48]
    • SOVA, ruptured or unruptured
      • Originates above the annulus, often shows the “windsock” sign, and may protrude toward the right ventricular outflow tract (RVOT), mimicking a septal lesion.
      • CT/TEE can distinguish this lesion from a membranous septal aneurysm.[49]
    • VSD
      • Perimembranous or muscular; the cavity is actually a shunt; color Doppler defines the defect.[50]
  • Tumors of the septum 
    • These solid masses that can mimic an “abscess cavity” when necrotic/heterogeneous:
      • Cardiac fibroma
        • Classically intramural, echogenic, often calcified; frequently involves the septum or left ventricular wall.[51]
      • Cardiac rhabdomyoma
        • This can be in the adult or pediatric populations, often with tuberous sclerosis.
        • Septal or left ventricular outflow tract (LVOT) masses; usually multiple in tuberous sclerosis, but can persist solitarily.[52]
      • Lipomatous hypertrophy/mass of the interventricular septum
        • Rare but reported; homogeneous fat signal on CT/MRI.[53]
  • Parasitic & granulomatous infections (cystic or mass-like)
    • Hydatid (Echinococcus) cyst of the interventricular septum
      • Cystic lesion with daughter cysts/laminated membrane; numerous septal cases reported.[54]
    • Cardiac cysticercosis
      • This condition can present as a cystic septal mass with conduction disease.[55]
    • Tuberculous myocardial tuberculoma/abscess of the septum
      • There are both historic and contemporary reports of this condition. 
      • This can cause conduction block or outflow obstruction.[56]
  • Inflammatory cardiomyopathies/infiltrative mimics
    • Cardiac sarcoidosis
      • Septal granulomatous involvement, causing atrioventricular block or arrhythmia; cardiac magnetic resonance (CMR) late gadolinium enhancement (LGE) patterns (midwall/subepicardial, basal septum scarring producing a “hook sign”) and positron emission tomography (PET) uptake help distinguish inflammatory disease from abscess.[57]
  • Septal hypertrophy (clinical mimics when presentation is fever-negative)
    • Hypertrophic cardiomyopathy / basal septal bulge
      • Asymmetric septal thickening may be mistaken for a mass on limited windows but lacks cavitation or central necrosis.[58]

Prognosis

The morbidity and mortality rates of patients with complicated infective endocarditis are high. The severity of the disease varies depending on the source of infection and preexisting comorbidities. The biomarkers of acute infection and indicators of illness severity (scores and multiple organ failure) are independent risk factors for mortality.

Surgical intervention for abscesses is an independent predictor of poorer 30-day outcomes.[59] Although patients who require surgical management have a high mortality rate, patients who do recover often will have an excellent long-term outcome with a low rate of reinfection.[60] In young and otherwise healthy individuals, the prognosis is generally favorable. Other significant prognostic factors affecting the mortality rate include a Charlson score of less than 3, the diagnosis of endocarditis before ICU admission, the use of aminoglycosides, and septic pulmonary embolism.[61]

Complications

An interventricular septal abscess is associated with severe morbidity and mortality. The following complications can occur in a patient during the disease course:

  • Myocardial wall perforation
  • New-onset congestive heart failure
  • The onset of new murmurs
  • New-onset valvular regurgitation 
  • Poor response to antibiotics
  • Acute respiratory distress syndrome
  • Multiorgan failure
  • Stroke
  • Development of conduction defects or progression to bundle-branch block and atrioventricular block
  • Miscellaneous (severe recurrent ventricular arrhythmias, pericarditis, among others)
  • Significant rapid clinical deterioration leading to death [21]

Postoperative and Rehabilitation Care

A successful treatment outcome depends on the patient's underlying health, prompt diagnosis and treatment, and rehabilitation. Medical treatment for these patients often requires 6 to 8 weeks of parenteral antibiotic therapy with close monitoring of hemodynamics. Serial echocardiograms are needed to ensure healing is occurring. The patient must be on a cardiac monitor to detect arrhythmias or heart block.

Even after surgery, complications are common, and close follow-up is required. A patient who has had surgical intervention is still susceptible to developing postoperative complications, including pneumonia, urinary tract infection, and deep vein thrombosis. Adequate nutrition, attention to deep venous thrombosis, and stress ulcer prophylaxis are essential. Physiotherapy to prevent muscle atrophy and an individualized rehabilitation plan for each patient potentially impact both morbidity and mortality.   

Consultations

The management of interventricular abscess requires an interprofessional team of consultants, including gastroenterologists, cardiologists, cardiac surgeons, intensivists, pulmonologists, pathologists, infectious disease specialists, and cardiac rehabilitation specialists.

Deterrence and Patient Education

Interventricular septal abscess is a rare but life-threatening complication of infective endocarditis, most often arising from S aureus or other Streptococcal infections involving the aortic or mitral valves. Because outcomes are closely tied to early recognition and prevention, awareness and education about infective endocarditis are critical. The National Institute for Health and Care Excellence (NICE) guidelines emphasize a prevention-based approach that includes identifying patients at increased cardiac risk, maintaining optimal oral hygiene, understanding the benefits and limitations of antibiotic prophylaxis, and knowing when to seek medical evaluation. Patients at elevated risk, such as those with prosthetic heart valves, congenital heart disease, or a prior history of infective endocarditis, should also be counseled on the infectious risks associated with skin piercings, tattoos, or intravenous drug use.[62] These preventive measures align with the broader goal of minimizing bacteremia-related events that can lead to endocardial infection and subsequent abscess formation.

Education should also focus on the early recognition of infective endocarditis and its complications. Patients should be informed to promptly report symptoms such as persistent fever, malaise, new or changing cardiac murmurs, and signs of heart failure. For those already diagnosed with infective endocarditis, strict adherence to a complete course of intravenous antibiotics and close follow-up with serial echocardiography are essential to detect perivalvular extension or developing abscesses early. Clinicians should reinforce the importance of immediate medical attention if new conduction abnormalities, chest pain, or worsening hemodynamic instability occur, as these may indicate interventricular septal involvement.

Once an interventricular septal abscess is diagnosed, patients and families should understand that surgical intervention is often necessary to eradicate infection, prevent rupture or complete heart block, and restore cardiac function. Education regarding the potential need for pacemaker placement, postoperative antibiotic compliance, and long-term surveillance for reinfection or prosthetic valve dysfunction should be emphasized. In addition, pharmacists, nurses, and primary care clinicians play a key role in ensuring ongoing adherence to medical regimens and reinforcing education about risk factor modification, such as smoking cessation and substance use treatment.

Long-term deterrence focuses on controlling chronic diseases, such as diabetes, hypertension, and hyperlipidemia, to reduce susceptibility to infection, and maintaining lifelong vigilance in patients with prosthetic cardiac material or structural abnormalities. Through continuous interprofessional education, patient counseling, and preventive strategies guided by the NICE and American Heart Association (AHA) recommendations, healthcare professionals can significantly decrease the risk of infective endocarditis and its devastating complication, interventricular septal abscess.

Pearls and Other Issues

Preventing infective endocarditis and interventricular septal abscesses poses various challenges in the healthcare setting due to the heterogeneous etiology, clinical features, and course of these conditions.[63] The differing steps for its diagnosis and management stem from the lack of high-quality randomized controlled studies. Because infective endocarditis is the most common cause of interventricular septal abscess, it is possible to argue that prevention efforts will have a much greater impact.

In 1909, Thomas Horder recognized the mouth as a significant source of bacteremia.[64] Dental procedures are the leading cause of infective endocarditis due to the high frequency of bacteremia induced by procedures such as deep cleaning and tooth extraction. At present, the emphasis has shifted from antibiotic prophylaxis before dental procedures to better oral hygiene maintenance. Toothbrushing has also been studied as a source of bacteremia, prompting revisions to prophylaxis guidelines in the United States and Europe. The use of antibiotic prophylaxis has been restricted to high-risk patients, thereby increasing the focus on educating the general population about proper oral hygiene.[65]

The risks associated with prolonged parenteral antibiotic therapy include nephrotoxicity, ototoxicity, and vestibular effects. Clinicians dedicated to managing infective endocarditis can play a vital role in monitoring and managing these complications. Unfortunately, such services are not readily available everywhere.

Enhancing Healthcare Team Outcomes

Interventricular septal abscess is a life-threatening complication of infective endocarditis that requires rapid diagnosis, coordinated decision-making, and timely intervention by an experienced interprofessional team to reduce morbidity and mortality. Patients frequently present with multiple comorbidities, including substance use disorders, depression, hepatitis C, and HIV infection, making comprehensive, patient-centered care essential.[66] Cardiologists play a central role in recognizing clinical and echocardiographic features of septal extension, monitoring for conduction abnormalities, heart failure, stroke, and other complications, and coordinating diagnostic evaluation.

Cardiothoracic surgeons are critical in determining the timing and necessity of surgical debridement, abscess drainage, valve repair or replacement, and reconstruction of affected cardiac structures. Infectious disease specialists direct pathogen-specific antimicrobial therapy based on blood culture and susceptibility results. At the same time, intensivists, pulmonologists, and nephrologists manage hemodynamic instability, respiratory failure, renal dysfunction, and other manifestations of multiorgan involvement.

Pathologists and clinical microbiology laboratory personnel facilitate organism identification and antimicrobial susceptibility testing, allowing timely optimization of targeted therapy. Structured, evidence-based protocols for early diagnosis, multidisciplinary consultation, and treatment, including appropriate pharmacologic and nonpharmacologic management of coexisting mental health disorders, are essential to improving clinical outcomes.[66] Effective interprofessional communication is equally important throughout hospitalization and postoperative recovery.

Nurses provide continuous assessment of hemodynamic status, cardiac rhythm, neurologic function, and signs of heart failure or sepsis while administering prolonged intravenous antimicrobial therapy, monitoring for adverse drug reactions, reinforcing patient and family education, and promptly communicating changes in clinical status to the healthcare team. Cardiovascular specialty nurses are particularly valuable in recognizing early conduction disturbances or postoperative complications requiring urgent intervention. Clinical pharmacists, especially those specializing in cardiology or infectious diseases, optimize antimicrobial selection, perform therapeutic drug monitoring for agents such as vancomycin and aminoglycosides, adjust dosing based on renal function, and minimize drug interactions and medication-related toxicity.

Dietitians support nutritional optimization during prolonged hospitalization, physical therapists facilitate early mobilization and functional recovery, and psychiatrists or behavioral health specialists address coexisting psychiatric illness, substance use disorders, and adherence to long-term treatment plans.[67] Coordinated communication among all team members, regular multidisciplinary case reviews, and shared decision-making with patients and families promote patient safety, enhance team performance, facilitate timely surgical intervention when indicated, and improve both short- and long-term outcomes in patients with interventricular septal abscess.

Media


(Click Image to Enlarge)
<p>Diagnostic Evaluation of Interventricular Septal Abscess in Infective Endocarditis

Diagnostic Evaluation of Interventricular Septal Abscess in Infective Endocarditis. This figure summarizes the diagnostic approach to interventricular septal abscess complicating infective endocarditis. It highlights the Modified Duke Criteria for establishing the diagnosis of infective endocarditis, characteristic electrocardiographic findings suggestive of conduction system involvement, and key transthoracic and transesophageal echocardiographic features—including vegetations, abscess formation, pseudoaneurysm, valve perforation, and perivalvular extension—that facilitate early diagnosis and guide surgical management.

Contributed by Y Sattar, MD

References

[1]

Degife E, Morrison A, Mahmood SBU, Ragnarsson S, Amabile A, Assi R, Vallabjoyshula P, Geirsson A. Surgical treatment and outcomes in aortic valve endocarditis and perivalvular abscesses. Scientific reports. 2024 Nov 26:14(1):29373. doi: 10.1038/s41598-024-79256-8. Epub 2024 Nov 26     [PubMed PMID: 39592664]

[2]

Toyoda N, Chikwe J, Itagaki S, Gelijns AC, Adams DH, Egorova NN. Trends in Infective Endocarditis in California and New York State, 1998-2013. JAMA. 2017 Apr 25:317(16):1652-1660. doi: 10.1001/jama.2017.4287. Epub     [PubMed PMID: 28444279]

[3]

Becher H, Hanrath P, Bleifeld W, Bleese N. Correlation of echocardiographic and surgical findings in acute bacterial endocarditis. European heart journal. 1984 Oct:5 Suppl C():67-70     [PubMed PMID: 6519089]

[4]

Arnett EN, Roberts WC. Prosthetic valve endocarditis: clinicopathologic analysis of 22 necropsy patients with comparison observations in 74 necropsy patients with active infective endocarditis involving natural left-sided cardiac valves. The American journal of cardiology. 1976 Sep:38(3):281-92     [PubMed PMID: 989258]

[5]

Incarvito J, Yang SS, Papa L, Fernandez J, Chang KS. Fungal endocarditis complicated by mycotic aneurysm of sinus of Valsalva, interventricular septal abscess, and infectious pericarditis: unique M-mode and two-dimensional echocardiographic findings. Clinical cardiology. 1981 Jan:4(1):34-8     [PubMed PMID: 6894413]

Level 3 (low-level) evidence

[6]

Habib G, Lancellotti P, Antunes MJ, Bongiorni MG, Casalta JP, Del Zotti F, Dulgheru R, El Khoury G, Erba PA, Iung B, Miro JM, Mulder BJ, Plonska-Gosciniak E, Price S, Roos-Hesselink J, Snygg-Martin U, Thuny F, Tornos Mas P, Vilacosta I, Zamorano JL, ESC Scientific Document Group. 2015 ESC Guidelines for the management of infective endocarditis: The Task Force for the Management of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by: European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM). European heart journal. 2015 Nov 21:36(44):3075-3128. doi: 10.1093/eurheartj/ehv319. Epub 2015 Aug 29     [PubMed PMID: 26320109]

[7]

Moreillon P, Que YA. Infective endocarditis. Lancet (London, England). 2004 Jan 10:363(9403):139-49     [PubMed PMID: 14726169]

[8]

Fowler VG, Durack DT, Selton-Suty C, Athan E, Bayer AS, Chamis AL, Dahl A, DiBernardo L, Durante-Mangoni E, Duval X, Fortes CQ, Fosbøl E, Hannan MM, Hasse B, Hoen B, Karchmer AW, Mestres CA, Petti CA, Pizzi MN, Preston SD, Roque A, Vandenesch F, van der Meer JTM, van der Vaart TW, Miro JM. The 2023 Duke-International Society for Cardiovascular Infectious Diseases Criteria for Infective Endocarditis: Updating the Modified Duke Criteria. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2023 Aug 22:77(4):518-526. doi: 10.1093/cid/ciad271. Epub     [PubMed PMID: 37138445]

[9]

Federspiel JJ, Stearns SC, Peppercorn AF, Chu VH, Fowler VG Jr. Increasing US rates of endocarditis with Staphylococcus aureus: 1999-2008. Archives of internal medicine. 2012 Feb 27:172(4):363-5. doi: 10.1001/archinternmed.2011.1027. Epub     [PubMed PMID: 22371926]

Level 3 (low-level) evidence

[10]

Murdoch DR, Corey GR, Hoen B, Miró JM, Fowler VG Jr, Bayer AS, Karchmer AW, Olaison L, Pappas PA, Moreillon P, Chambers ST, Chu VH, Falcó V, Holland DJ, Jones P, Klein JL, Raymond NJ, Read KM, Tripodi MF, Utili R, Wang A, Woods CW, Cabell CH, International Collaboration on Endocarditis-Prospective Cohort Study (ICE-PCS) Investigators. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Archives of internal medicine. 2009 Mar 9:169(5):463-73. doi: 10.1001/archinternmed.2008.603. Epub     [PubMed PMID: 19273776]

[11]

Benito N, Miró JM, de Lazzari E, Cabell CH, del Río A, Altclas J, Commerford P, Delahaye F, Dragulescu S, Giamarellou H, Habib G, Kamarulzaman A, Kumar AS, Nacinovich FM, Suter F, Tribouilloy C, Venugopal K, Moreno A, Fowler VG Jr, ICE-PCS (International Collaboration on Endocarditis Prospective Cohort Study) Investigators. Health care-associated native valve endocarditis: importance of non-nosocomial acquisition. Annals of internal medicine. 2009 May 5:150(9):586-94     [PubMed PMID: 19414837]

[12]

Haidari Z, Knipp S, Turaev I, El Gabry M. Aortic Valve Infective Endocarditis with Root Abscess: Root Repair Versus Root Replacement. Pathogens (Basel, Switzerland). 2025 Jun 23:14(7):. doi: 10.3390/pathogens14070626. Epub 2025 Jun 23     [PubMed PMID: 40732674]

[13]

González Vílchez FJ, Martín Durán R, Delgado Ramis C, Vázquez de Prada Tiffe JA, Ochoteco Azcárate A, Zarauza Navarro J, Sánchez González A. [Active infective endocarditis complicated by paravalvular abscess. Review of 40 cases]. Revista espanola de cardiologia. 1991 May:44(5):306-12     [PubMed PMID: 1852959]

Level 2 (mid-level) evidence

[14]

Nand N, Singla SK, Magu S. Cardiac Abscess with Ventricular Aneurysm Secondary to Old Myocardial Infarction. The Journal of the Association of Physicians of India. 2017 May:65(5):95-96     [PubMed PMID: 28598059]

[15]

Gnann JW, Dismukes WE. Prosthetic valve endocarditis: an overview. Herz. 1983 Dec:8(6):320-31     [PubMed PMID: 6363238]

Level 3 (low-level) evidence

[16]

Thomas D, Desruennes M, Jault F, Isnard R, Gandjbakhch I. [Cardiac and extracardiac abscesses in bacterial endocarditis]. Archives des maladies du coeur et des vaisseaux. 1993 Dec:86(12 Suppl):1825-35     [PubMed PMID: 8024388]

[17]

Pant S, Patel NJ, Deshmukh A, Golwala H, Patel N, Badheka A, Hirsch GA, Mehta JL. Trends in infective endocarditis incidence, microbiology, and valve replacement in the United States from 2000 to 2011. Journal of the American College of Cardiology. 2015 May 19:65(19):2070-6. doi: 10.1016/j.jacc.2015.03.518. Epub     [PubMed PMID: 25975469]

[18]

Shmueli H, Thomas F, Flint N, Setia G, Janjic A, Siegel RJ. Right-Sided Infective Endocarditis 2020: Challenges and Updates in Diagnosis and Treatment. Journal of the American Heart Association. 2020 Aug 4:9(15):e017293. doi: 10.1161/JAHA.120.017293. Epub 2020 Jul 23     [PubMed PMID: 32700630]

[19]

Que YA, Haefliger JA, Piroth L, François P, Widmer E, Entenza JM, Sinha B, Herrmann M, Francioli P, Vaudaux P, Moreillon P. Fibrinogen and fibronectin binding cooperate for valve infection and invasion in Staphylococcus aureus experimental endocarditis. The Journal of experimental medicine. 2005 May 16:201(10):1627-35     [PubMed PMID: 15897276]

Level 3 (low-level) evidence

[20]

Elgharably H, Hussain ST, Shrestha NK, Blackstone EH, Pettersson GB. Current Hypotheses in Cardiac Surgery: Biofilm in Infective Endocarditis. Seminars in thoracic and cardiovascular surgery. 2016 Spring:28(1):56-9. doi: 10.1053/j.semtcvs.2015.12.005. Epub 2015 Dec 11     [PubMed PMID: 27568136]

[21]

Mildvan D, Goldberg E, Berger M, Altchek MR, Lukban SB. Diagnosis and successful management of septal myocardial abscess: a complication of bacterial endocarditis. The American journal of the medical sciences. 1977 Nov-Dec:274(3):311-6     [PubMed PMID: 610417]

Level 3 (low-level) evidence

[22]

Arnett EN, Roberts WC. Valve ring abscess in active infective endocarditis. Frequency, location, and clues to clinical diagnosis from the study of 95 necropsy patients. Circulation. 1976 Jul:54(1):140-5     [PubMed PMID: 1277418]

[23]

Atik FA, Campos VG, da Cunha CR, de Oliveira FB, Otto ME, Monte GU. Unusual mechanism of myocardial infarction in prosthetic valve endocarditis. International medical case reports journal. 2015:8():111-6. doi: 10.2147/IMCRJ.S61348. Epub 2015 May 25     [PubMed PMID: 26045678]

Level 3 (low-level) evidence

[24]

Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. The American journal of medicine. 1994 Mar:96(3):200-9     [PubMed PMID: 8154507]

Level 3 (low-level) evidence

[25]

Cahill TJ, Prendergast BD. Infective endocarditis. Lancet (London, England). 2016 Feb 27:387(10021):882-93. doi: 10.1016/S0140-6736(15)00067-7. Epub 2015 Sep 1     [PubMed PMID: 26341945]

[26]

Muñoz P, Bouza E, Marín M, Alcalá L, Rodríguez Créixems M, Valerio M, Pinto A, Group for the Management of Infective Endocarditis of the Gregorio Marañón Hospital. Heart valves should not be routinely cultured. Journal of clinical microbiology. 2008 Sep:46(9):2897-901. doi: 10.1128/JCM.02173-07. Epub 2008 Jul 16     [PubMed PMID: 18632908]

[27]

Meine TJ, Nettles RE, Anderson DJ, Cabell CH, Corey GR, Sexton DJ, Wang A. Cardiac conduction abnormalities in endocarditis defined by the Duke criteria. American heart journal. 2001 Aug:142(2):280-5     [PubMed PMID: 11479467]

Level 2 (mid-level) evidence

[28]

Daniell JE, Nelson BS, Ferry D. ED identification of cardiac septal abscess using conduction block on ECG. The American journal of emergency medicine. 2000 Oct:18(6):730-4     [PubMed PMID: 11043631]

Level 3 (low-level) evidence

[29]

Fouchard J, Ponsonaille J, Mujica J, Paraiso N, Guerinon J, Iris L, Vial F. [Atrio-ventricular block due to septal abscess]. Coeur et medecine interne. 1973 Oct:12(4):679-87     [PubMed PMID: 4802091]

[30]

Brown RE, Chiaco JM, Dillon JL, Catherwood E, Ornvold K. Infective Endocarditis Presenting as Complete Heart Block With an Unexpected Finding of a Cardiac Abscess and Purulent Pericarditis. Journal of clinical medicine research. 2015 Nov:7(11):890-5. doi: 10.14740/jocmr2228w. Epub 2015 Sep 25     [PubMed PMID: 26491503]

[31]

Blumberg EA, Karalis DA, Chandrasekaran K, Wahl JM, Vilaro J, Covalesky VA, Mintz GS. Endocarditis-associated paravalvular abscesses. Do clinical parameters predict the presence of abscess? Chest. 1995 Apr:107(4):898-903     [PubMed PMID: 7705150]

Level 2 (mid-level) evidence

[32]

Ellis SG, Goldstein J, Popp RL. Detection of endocarditis-associated perivalvular abscesses by two-dimensional echocardiography. Journal of the American College of Cardiology. 1985 Mar:5(3):647-53     [PubMed PMID: 3973262]

[33]

Jariwala P, Punjani A, Mirza S, Harikishan B, Madhawar DB. Myocardial abscess secondary to staphylococcal septicemia: diagnosis with 3D echocardiography. Indian heart journal. 2013 Jan-Feb:65(1):124-5. doi: 10.1016/j.ihj.2012.12.005. Epub 2012 Dec 26     [PubMed PMID: 23438629]

Level 3 (low-level) evidence

[34]

Baddour LM, Wilson WR, Bayer AS, Fowler VG Jr, Tleyjeh IM, Rybak MJ, Barsic B, Lockhart PB, Gewitz MH, Levison ME, Bolger AF, Steckelberg JM, Baltimore RS, Fink AM, O'Gara P, Taubert KA, American Heart Association Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young, Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and Stroke Council. Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Scientific Statement for Healthcare Professionals From the American Heart Association. Circulation. 2015 Oct 13:132(15):1435-86. doi: 10.1161/CIR.0000000000000296. Epub 2015 Sep 15     [PubMed PMID: 26373316]

[35]

Daniel WG, Mügge A, Martin RP, Lindert O, Hausmann D, Nonnast-Daniel B, Laas J, Lichtlen PR. Improvement in the diagnosis of abscesses associated with endocarditis by transesophageal echocardiography. The New England journal of medicine. 1991 Mar 21:324(12):795-800     [PubMed PMID: 1997851]

[36]

Murillo H, Restrepo CS, Marmol-Velez JA, Vargas D, Ocazionez D, Martinez-Jimenez S, Reddick RL, Baxi AJ. Infectious Diseases of the Heart: Pathophysiology, Clinical and Imaging Overview. Radiographics : a review publication of the Radiological Society of North America, Inc. 2016 Jul-Aug:36(4):963-83. doi: 10.1148/rg.2016150225. Epub     [PubMed PMID: 27399236]

Level 3 (low-level) evidence

[37]

Cerqueira MD, Jacobson AF. Indium-111 leukocyte scintigraphic detection of myocardial abscess formation in patients with endocarditis. Journal of nuclear medicine : official publication, Society of Nuclear Medicine. 1989 May:30(5):703-6     [PubMed PMID: 2715834]

Level 3 (low-level) evidence

[38]

Shackcloth MJ, Dihmis WC. Contained rupture of a myocardial abscess in the free wall of the left ventricle. The Annals of thoracic surgery. 2001 Aug:72(2):617-9     [PubMed PMID: 11515915]

Level 3 (low-level) evidence

[39]

Yamamoto S, Hosokawa N, Sogi M, Inakaku M, Imoto K, Ohji G, Doi A, Iwabuchi S, Iwata K. Impact of infectious diseases service consultation on diagnosis of infective endocarditis. Scandinavian journal of infectious diseases. 2012 Apr:44(4):270-5. doi: 10.3109/00365548.2011.638317. Epub 2011 Dec 18     [PubMed PMID: 22176644]

Level 2 (mid-level) evidence

[40]

McDonald EG, Aggrey G, Aslan AT, Casias M, Cortes-Penfield N, Dong MQD, Egbert S, Footer B, Isler B, King M, Maximos M, Wuerz TC, Azim AA, Alza-Arcila J, Bai AD, Blyth M, Boyles T, Caceres J, Clark D, Davar K, Denholm JT, Forrest G, Ghanem B, Hagel S, Hanretty A, Hamilton F, Jent P, Kang M, Kludjian G, Lahey T, Lapin J, Lee R, Li T, Mehta D, Moore J, Mowrer C, Ouellet G, Reece R, Ryder JH, Sanctuaire A, Sanders JM, Stoner BJ, So JM, Tessier JF, Tirupathi R, Tong SYC, Wald-Dickler N, Yassin A, Yen C, Spellberg B, Lee TC. Guidelines for Diagnosis and Management of Infective Endocarditis in Adults: A WikiGuidelines Group Consensus Statement. JAMA network open. 2023 Jul 3:6(7):e2326366. doi: 10.1001/jamanetworkopen.2023.26366. Epub 2023 Jul 3     [PubMed PMID: 37523190]

Level 3 (low-level) evidence

[41]

Delgado V, Ajmone Marsan N, de Waha S, Bonaros N, Brida M, Burri H, Caselli S, Doenst T, Ederhy S, Erba PA, Foldager D, Fosbøl EL, Kovac J, Mestres CA, Miller OI, Miro JM, Pazdernik M, Pizzi MN, Quintana E, Rasmussen TB, Ristić AD, Rodés-Cabau J, Sionis A, Zühlke LJ, Borger MA, ESC Scientific Document Group. 2023 ESC Guidelines for the management of endocarditis. European heart journal. 2023 Oct 14:44(39):3948-4042. doi: 10.1093/eurheartj/ehad193. Epub     [PubMed PMID: 37622656]

Level 3 (low-level) evidence

[42]

Arita M, Kusuyama Y, Takatsuji M, Kawazoe K, Masuyama Y. Septal myocardial abscess and infectious pericarditis in a case of bacterial endocarditis. Japanese circulation journal. 1985 Apr:49(4):451-5     [PubMed PMID: 4009931]

Level 3 (low-level) evidence

[43]

Dalebout EM, Hirsch A, Kluin J, Galema TW, Roos-Hesselink JW, Budde RPJ. Computed Tomography in Infectious Endocarditis. Journal of the Society for Cardiovascular Angiography & Interventions. 2024 Mar:3(3Part B):101292. doi: 10.1016/j.jscai.2023.101292. Epub 2024 Mar 26     [PubMed PMID: 39131217]

[44]

Silbiger JJ, Krasner A, Chikwe J, Marino T, Mathewkutty S, Marcali M, Edebohls B, Kamran M. Pseudoaneurysm formation in infective endocarditis. Echocardiography (Mount Kisco, N.Y.). 2013 Nov:30(10):E319-21. doi: 10.1111/echo.12333. Epub 2013 Jul 30     [PubMed PMID: 23906264]

[45]

Saker E, Bahri GN, Montalbano MJ, Johal J, Graham RA, Tardieu GG, Loukas M, Tubbs RS. Gerbode defect: A comprehensive review of its history, anatomy, embryology, pathophysiology, diagnosis, and treatment. Journal of the Saudi Heart Association. 2017 Oct:29(4):283-292. doi: 10.1016/j.jsha.2017.01.006. Epub 2017 Feb 16     [PubMed PMID: 28983172]

[46]

Tanabe J, Okazaki K, Endo A, Tanabe K. Left Ventricular Intramyocardial Dissecting Hematoma. CASE (Philadelphia, Pa.). 2021 Dec:5(6):349-353. doi: 10.1016/j.case.2021.07.016. Epub 2021 Sep 3     [PubMed PMID: 34993361]

Level 3 (low-level) evidence

[47]

David TE. Post-infarction ventricular septal rupture. Annals of cardiothoracic surgery. 2022 May:11(3):261-267. doi: 10.21037/acs-2021-ami-111. Epub     [PubMed PMID: 35733715]

[48]

Assaf A, Berry R, Mantha Y, Zughaib M, Saba S. Isolated Ventricular Septal Aneurysm: A Differential Diagnosis for a Right Sinus of Valsalva Aneurysm. The American journal of case reports. 2021 May 23:22():e930930. doi: 10.12659/AJCR.930930. Epub 2021 May 23     [PubMed PMID: 34023848]

Level 3 (low-level) evidence

[49]

Kim HR, Kim SJ, Lim KH, Kim JM, Lee JH, Kim YG, Jung JP, Lee SG. A Case of Perimembranous Ventricular Septal Defect Associated with Sinus of Valsalva Aneurysm Mimicking Membranous Septal Aneurysm. Journal of cardiovascular ultrasound. 2015 Jun:23(2):113-7. doi: 10.4250/jcu.2015.23.2.113. Epub 2015 Jun 26     [PubMed PMID: 26140155]

Level 3 (low-level) evidence

[50]

Minette MS, Sahn DJ. Ventricular septal defects. Circulation. 2006 Nov 14:114(20):2190-7     [PubMed PMID: 17101870]

[51]

Walpot J, Shivalkar B, Bogers JP, Salgado R, Rodrigus I, Van Marck E, Pasteuning WH, Klazen C. A patient with cardiac fibroma and a subvalvular aortic stenosis caused by a subvalvular membrane. Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography. 2007 Jul:20(7):906.e1-4     [PubMed PMID: 17617321]

[52]

Nati-Castillo HA, Quintero JM, Molina OA, Arias-Intriago M, Melgar Muñoz FP, Izquierdo-Condoy JS. Unusual adult-onset cardiac rhabdomyomas in tuberous sclerosis complex: a case report. Frontiers in medicine. 2024:11():1386089. doi: 10.3389/fmed.2024.1386089. Epub 2024 Jul 31     [PubMed PMID: 39144655]

Level 3 (low-level) evidence

[53]

Komoriya Y, Suzuki S, Iwakawa N, Kondo T, Murohara T. A rare case of cardiac tumor of the interventricular septum complicated with atrioventricular block. Journal of cardiology cases. 2022 Dec:26(6):419-422. doi: 10.1016/j.jccase.2022.09.002. Epub 2022 Sep 29     [PubMed PMID: 36506495]

Level 3 (low-level) evidence

[54]

Tefera E, Knapp J, Teodori M. Hydatid cyst of the interventricular septum. Global cardiology science & practice. 2017 Mar 31:2017(1):e201709. doi: 10.21542/gcsp.2017.9. Epub 2017 Mar 31     [PubMed PMID: 28971108]

[55]

Dung LT, Van Sy T, Van NT. Solitary cardiac cysticercosis. Radiology case reports. 2023 Jun:18(6):2103-2106. doi: 10.1016/j.radcr.2023.03.001. Epub 2023 Apr 5     [PubMed PMID: 37089977]

Level 3 (low-level) evidence

[56]

Rawls WJ, Shuford WH, Logan WD, Hurst JW, Schlant RC. Right ventricular outflow tract obstruction produced by a myocardial abscess in a patient with tuberculosis. The American journal of cardiology. 1968 May:21(5):738-45     [PubMed PMID: 4230731]

[57]

Lehtonen J, Uusitalo V, Pöyhönen P, Mäyränpää MI, Kupari M. Cardiac sarcoidosis: phenotypes, diagnosis, treatment, and prognosis. European heart journal. 2023 May 1:44(17):1495-1510. doi: 10.1093/eurheartj/ehad067. Epub     [PubMed PMID: 36924191]

[58]

Canepa M, Pozios I, Vianello PF, Ameri P, Brunelli C, Ferrucci L, Abraham TP. Distinguishing ventricular septal bulge versus hypertrophic cardiomyopathy in the elderly. Heart (British Cardiac Society). 2016 Jul 15:102(14):1087-94. doi: 10.1136/heartjnl-2015-308764. Epub 2016 Apr 27     [PubMed PMID: 27122487]

[59]

Samol A, Kaese S, Bloch J, Görlich D, Peters G, Waltenberger J, Baumgartner H, Reinecke H, Lebiedz P. Infective endocarditis on ICU: risk factors, outcome and long-term follow-up. Infection. 2015 Jun:43(3):287-95. doi: 10.1007/s15010-014-0715-0. Epub 2015 Jan 10     [PubMed PMID: 25575463]

Level 2 (mid-level) evidence

[60]

Mullany CJ, Chua YL, Schaff HV, Steckelberg JM, Ilstrup DM, Orszulak TA, Danielson GK, Puga FJ. Early and late survival after surgical treatment of culture-positive active endocarditis. Mayo Clinic proceedings. 1995 Jun:70(6):517-25     [PubMed PMID: 7776709]

Level 2 (mid-level) evidence

[61]

Georges H, Leroy O, Airapetian N, Lamblin N, Zogheib E, Devos P, Preau S, Hauts de France endocarditis study group. Outcome and prognostic factors of patients with right-sided infective endocarditis requiring intensive care unit admission. BMC infectious diseases. 2018 Feb 21:18(1):85. doi: 10.1186/s12879-018-2989-9. Epub 2018 Feb 21     [PubMed PMID: 29466956]

[62]

Richey R, Wray D, Stokes T, Guideline Development Group. Prophylaxis against infective endocarditis: summary of NICE guidance. BMJ (Clinical research ed.). 2008 Apr 5:336(7647):770-1. doi: 10.1136/bmj.39510.423148.AD. Epub     [PubMed PMID: 18390528]

[63]

Cahill TJ, Baddour LM, Habib G, Hoen B, Salaun E, Pettersson GB, Schäfers HJ, Prendergast BD. Challenges in Infective Endocarditis. Journal of the American College of Cardiology. 2017 Jan 24:69(3):325-344. doi: 10.1016/j.jacc.2016.10.066. Epub     [PubMed PMID: 28104075]

[64]

Bayliss R, Clarke C, Oakley C, Somerville W, Whitfield AG. The teeth and infective endocarditis. British heart journal. 1983 Dec:50(6):506-12     [PubMed PMID: 6360190]

Level 2 (mid-level) evidence

[65]

Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, Bolger A, Cabell CH, Takahashi M, Baltimore RS, Newburger JW, Strom BL, Tani LY, Gerber M, Bonow RO, Pallasch T, Shulman ST, Rowley AH, Burns JC, Ferrieri P, Gardner T, Goff D, Durack DT, American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, American Heart Association Council on Cardiovascular Disease in the Young, American Heart Association Council on Clinical Cardiology, American Heart Association Council on Cardiovascular Surgery and Anesthesia, Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007 Oct 9:116(15):1736-54     [PubMed PMID: 17446442]

Level 2 (mid-level) evidence

[66]

Yanagawa B, Bahji A, Lamba W, Tan DH, Cheema A, Syed I, Verma S. Endocarditis in the setting of IDU: multidisciplinary management. Current opinion in cardiology. 2018 Mar:33(2):140-147. doi: 10.1097/HCO.0000000000000493. Epub     [PubMed PMID: 29232248]

Level 3 (low-level) evidence

[67]

Smith MA, Smith TL, Davidson BT. Managing the infected heart. Critical care nursing clinics of North America. 2007 Mar:19(1):99-106     [PubMed PMID: 17338955]