Myocardial Abscess

Back

Background

Myocardial abscess is a suppurative (pus-containing) infection of the myocardium, endocardium, native or prosthetic valves or perivalvular structures, or the cardiac conduction system. In this serious and life-threatening disease, early recognition and institution of appropriate medical and surgical therapy is necessary for patient survival.

In the past, most cases of myocardial abscess were discovered at autopsy. The very first report, published in 1933, was an autopsy report by Cossio and colleagues that involved the finding of a pneumococcal abscess in the region of infarcted myocardial tissue as a complication of bronchopneumonia.[1] Several more such cases were reported later, suggesting that myocardial abscess often occurs in the setting of septicemia and abscesses in other locations. Myocardial abscess can now be detected antemortem using various noninvasive diagnostic modalities.

Infective endocarditis (IE) has become the most common condition underlying myocardial abscesses. This article addresses the presenting features, diagnostic tests, therapeutic interventions, and follow-up strategies for myocardial abscess.

Pathophysiology

Endocarditis

The most common clinical setting for myocardial abscess is as a complication of endocarditis involving either native or prosthetic valves. In a review of 40 cases of infective endocarditis, Gonzalez Vilchez et al (1991) found that 67.5% (27 cases) involved native valves. The most common site was the aortic valve, followed in descending order by the ventricular septa, mitral valves, and papillary muscles. Approximately one third of cases involved the base of the aortic valve. Staphylococcus was the most prevalent species involved, isolated from one third of all cases. Prosthetic valve abscess comprised 34% of cases, and 50% of these were caused by staphylococcal infection.[2] An infected coronary artery stent may be a rare source of multiple myocardial abscesses.[3]

Bacteremia

In the past, the most common setting for myocardial abscess was generalized bacteremia, as described in older autopsy reports. Sanson and colleagues (1963) described 23 cases, 21 of which exhibited multiple abscesses in lungs, kidneys, brain, and myocardium. Myocardial abscesses were small in these patients, and the authors postulated that the patients died too early to develop larger abscesses.[4]

Site of myocardial infarction

Myocardial abscess may develop at the site of a myocardial infarction (MI) but usually develops in the setting of bacteremia. Cossio et al (1933) reported a myocardial abscess at the site of an acute MI.[1] In the case records of the Massachusetts General Hospital, Castleman and McNeely (1970) reported a secondary infection within an inferior wall MI in a patient with Bacteroides bacteremia following genitourinary surgery and placement of an infected indwelling catheter.[5]

In a review of 13 cases of myocardial abscess in acute MI, Weisz and Young (1977) found bronchopneumonia to be the probable source in 4 cases, gastrointestinal and renal sepsis in 2, and no definable source in the others. Organisms included Staphylococcus aureus, Clostridium perfringens, Bacteroides species, Escherichia coli, beta-hemolytic streptococci, and Streptococcus pneumoniae, in order of decreasing frequency.[6]

The propensity of cardiac muscle to develop myocardial abscess in the setting of acute MI and septicemia may be due to the presence of necrosis of the muscular fibers and surrounding inflammatory exudates, decreased or absent perfusion, and lack of cell-mediated immunity secondary to decreased blood flow. Such myocardium also appears to be at a greater risk of rupture than healthy myocardium (7-fold higher per Weisz and Young [1977][6] ), with a catastrophic outcome.

Other clinical settings

Other settings associated with myocardial abscesses that have been reported in the literature include the following:

Microbiology

Usually, a single type of organism acts as the causal agent. However, not uncommonly, these abscesses have a polymicrobial etiology. Sanson and associates (1963) reported that more than 40% of cases involve more than one microbial agent, usually staphylococci or E coli.[4] Whether this reflected a polymicrobial etiology or a single-organism etiology with subsequent polymicrobial overgrowth is unclear. The increase in antibiotic use in general creates a setting in which polymicrobial involvement may become even more common, especially in patients with diabetes mellitus.

Microorganisms

Microorganisms associated with myocardial abscess include the following:

Pathogenesis

Development of infective endocarditis and subsequent myocardial abscess involves interaction of multiple factors, as follows:

Each of these components is in itself complex, affected by many factors, and not fully understood. The rarity of endocarditis despite the relatively high prevalence of transient asymptomatic and symptomatic bacteremia suggests that the intact endothelium is resistant to infection. If the endothelium on the valve surface is damaged, hemostasis is stimulated and the deposition of platelets and fibrin complex begins. This complex, called nonbacterial thrombotic endocarditis (NBTE), is more susceptible to bacterial colonization when bacteremia develops from an extracardiac source that allows the organisms access to the NBTE.

The intracardiac consequences of endocarditis range from trivial, characterized by an infected vegetation with no attendant tissue damage, to catastrophic, when infection is locally destructive or extends beyond the valve leaflet. Distortion or perforation of valve leaflets, rupture of chordae tendineae, and perforations or fistulas may result in progressive congestive heart failure (CHF). Infection, particularly that involving the aortic valve or prosthetic valves, may extend into paravalvular tissue and result in myocardial abscesses and persistent fever due to the infection's unresponsiveness to the antibiotic; disruption of the conduction system, with electrocardiographic conduction abnormalities; and clinically relevant arrhythmias or purulent pericarditis.

Epidemiology

Frequency

United States

Myocardial abscess rarely occurs in the United States.

International

Murdoch et al (2009) published a contemporary report on the presentation, etiology, and outcome of infective endocarditis in a large patient cohort from multiple locations worldwide. They analyzed a prospective cohort study of 2781 adults (median age 57.9 y) with definite infective endocarditis (72.1% of the native valve) who were admitted to 58 hospitals in 25 countries over a 5-year period. Seventy-seven percent of the patients presented early in the disease course (ie, within the first month), with few of the classic clinical hallmarks of infective endocarditis. Recent health care exposure was found in one quarter of the patients.

S aureus was the most common pathogen found (31.2% of patients). The mitral valve was found to be infected in 41.1% of cases and the aortic valve in 37.6%. The common complications included stroke (16.9%), embolization other than stroke (22.6%), heart failure (32.3%), and intracardiac abscess (14.4%). Surgical therapy was performed in 48.2% of the patients, and in-hospital mortality rates were high (17.7%).

Several factors portended a high fatality risk, including prosthetic valve involvement (odds ratio [OR], 1.47), increasing age (OR, 1.30), pulmonary edema (OR, 1.79), S aureus infection (OR, 1.54), coagulase-negative staphylococcal infection (OR, 1.50), mitral valve vegetation (OR, 1.34), and paravalvular complications (OR, 2.25). Streptococcus viridans infection (OR, 0.52) and surgery (OR, 0.61) were associated with a decreased fatality risk. In summary, in the early 21st century, infective endocarditis continues to be more often an acute disease, characterized by a high rate of S aureus infection and an unacceptably high mortality rate.[7]

The incidence of infective endocarditis remained relatively stable from 1950-1987, at approximately 4.2 cases per 100,000 patient-years.[8] During the early 1980s, the yearly incidence of infective endocarditis was 2 cases per 100,000 population in the United Kingdom and Wales and 1.9 cases per 100,000 population in the Netherlands. A higher incidence was noted from 1984-1990; 5.9 and 11.6 episodes per 100,000 population were reported from Sweden and metropolitan Philadelphia, respectively.[9]

Infections involving prosthetic valves, especially mechanical prostheses, in which the infection is entirely periannular, often extend into the adjacent myocardium, resulting in paravalvular abscess formation and partial dehiscence of the prosthetic valve with paravalvular regurgitation.

Among 85 patients with endocarditis involving a mechanical prosthesis, annulus invasion and myocardial abscess were noted in 42% and 14% of patients, respectively.[10]

Ben Ismail et al (1987) found annulus infection and valve dehiscence in 38 of 41 (82%) infected mechanical valves examined at surgery or autopsy.[11]

Mortality/Morbidity

Myocardial abscess formation profoundly worsens the prognosis in patients with infective endocarditis.

The mortality rate associated with S aureus infective endocarditis is 42% overall. If treated with antibiotics only, the mortality rate is 75%, while a regimen that combines antibiotics and surgery reduces the mortality rate to 25%.

The presence of an intracardiac abscess or complications increases the mortality rate 13.7-fold.

Race

Myocardial abscess has no substantial racial predilection. However, the condition may be more prevalent in African Americans in urban settings.

Sex

The relative risk ranges from 3.5-8.2. Because mitral valve prolapse (MVP) is more common in women than in men, myocardial abscess is also more common in women than in men.

Among persons who abuse intravenous drugs, myocardial abscess is more prevalent in men (65%-80%).

In adults, MVP has emerged as a prominent predisposing structural abnormality that may account for 7%-30% of cases of nonvalvular endocarditis (NVE). However, myocardial abscess developing in such cases is exceedingly rare.

Age

Involvement of cardiac structures with endocarditis and myocardial abscess mainly depends on the incidence of various underlying structural heart conditions among different age groups.

The incidence of infective endocarditis among hospitalized children ranges from 1 case in 4500 to 1 case in 1280. In the Netherlands, incidences of 1.7 cases per 100,000 persons in boys and 1.2 cases per 100,000 persons in girls have been noted.[8] In neonates, the rate has been increasing because of contaminated intravenous lines and the increased use of right-sided heart catheters. Infective endocarditis usually involves the tricuspid valve and is caused primarily by S aureus. Congenital heart defects are predisposing conditions in toddlers and older children.

In adults, MVP is the most common structural heart abnormality associated with infectious endocarditis, found in as many as 7%-30% of patients with NVE, and the risk increases in patients older than 45 years.

Those who abuse intravenous drugs are increasingly susceptible (2%-5% per patient-year).

Prognosis

With early diagnosis and prompt surgical treatment, patients improve rapidly.

Without surgical intervention, the prognosis worsens very significantly.

Patient Education

Educate patients regarding their condition, and emphasize the importance of prophylaxis.

For excellent patient education resources, visit eMedicineHealth's Infections Center and Heart Health Center. Also, see eMedicineHealth's patient education articles Skin Abscess and Antibiotics.

History

Physicians must maintain a high index of suspicion to diagnose patients who have myocardial abscess. Many of the clinical features of this condition reflect the symptoms and signs of the clinical setting that predisposes to development of the abscess.

Infective endocarditis is associated with the following:

The duration of symptoms is short.

The infecting organism is a Pneumococcus or Staphylococcus species.

Acute MI occurs in the setting of septicemia.

Sepsis may complicate a penetrating chest injury.

Myocardial abscess is more prevalent in the period following mechanical interventions or surgery and in patients with HIV/AIDS-related myocarditis.

Most cases of myocardial abscess occur in the setting of infective endocarditis. Symptoms and signs mainly reflect the presence of infective endocarditis. The clinical features persist or worsen upon development of a complicating myocardial abscess.

Myocardial abscess must be considered in patients who have longstanding persistent bacteremia and who do not respond to antibiotic therapy.

One must bear in mind certain constellations of symptoms that may raise the suggestion of myocardial abscess. For example, fever is the most common symptom, presenting in 80%-85% of patients. It is absent in some patients who are elderly; those who have CHF, severe debility, or chronic renal failure; and in patients with coagulase-negative staphylococcal infection and abscess. Another characteristic symptom is chills, which occurs in 42%-75% of cases.

Other signs and symptoms include the following:

Physical

Physical examination findings commonly encountered in myocardial abscess are mainly due to the underlying infective endocarditis. These include the following:

Causes

Causes of myocardial abscess associated with endocarditis may include the following:

Causes of myocardial abscess associated with septicemia may include the following:

Miscellaneous causes of myocardial abscess may include the following:

Complications

The following are potential complications of myocardial abscess:

Laboratory Studies

Routine blood tests

Complete blood cell count findings (ie, hematological parameters) commonly are abnormal.

Anemia with normochromic normocytic red cell indices is present. A low serum iron level is also observed. A low serum iron-binding capacity is observed in 70-90% of patients.

Anemia worsens with increased duration of illness.

In subacute endocarditis, the white blood cell count is usually normal. In contrast, a leukocytosis with increased segmented granulocytes is common in acute endocarditis and myocardial abscess.

Thrombocytopenia occurs only rarely.

Perform a metabolic chemistry panel.

Erythrocyte sedimentation rate

The erythrocyte sedimentation rate (ESR) is elevated (on average approximately 55 mm/h) in almost all patients with endocarditis and myocardial abscess; the exceptions are those with CHF, renal failure, or disseminated intravascular coagulation.

Although the results are nonspecific, the absence of an increased ESR, other than in the selected circumstances already mentioned, is evidence against a diagnosis of endocardial or myocardial infection or abscess.

Blood cultures

Blood cultures are the crucial laboratory tests for confirming the diagnosis of the underlying endocarditis.

Urinalysis

Urinalysis results are often abnormal, even when renal function remains normal.

Proteinuria and microscopic hematuria are noted in 50% of patients.

Urinalysis also plays a standard role in the evaluation of azotemia, which is frequently associated with myocardial abscess.

Other tests

Perform these as needed for the assessment of the primary source of bacteremia.

Imaging Studies

In the past, most cases of myocardial abscess were found during autopsy; however, detection of myocardial abscess can now be achieved antemortem using multiple noninvasive imaging modalities, including transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE), indium In 111 radionuclide scintigraphy, computed tomography (CT) scan, and magnetic resonance imaging (MRI).

Chest radiography

Perform chest radiography to look for associated pulmonary infection.

Chest radiographic findings help assess for CHF.

Transthoracic echocardiography

TTE helps evaluate patients in whom endocarditis or myocardial abscess is suggested clinically. Findings frequently allow the morphologic confirmation of infection and increasingly aid in making decisions regarding management.

One must perform an echocardiographic evaluation in all patients suspected of having an intracardiac or pericardial infection, including those with negative blood culture findings.

TTE has a sensitivity of 23% and specificity of 98.6%.

According to Ellis et al (1985), the following 5 criteria are 86% sensitive and 88% specific for myocardial abscess:[13]

Walker et al report a rare case of a myocardial abscess in valvular endocarditis that was difficult to assess with 2-dimensional TTE; however, real-time 3-dimensional contrast TTE allowed visualization of the full extent of the defect and its precise anatomical location, prior to successful surgical resection.[14]

Transesophageal echocardiography

Although many patients with NVE involving the aortic or mitral valve can be adequately assessed using TTE, TEE with color flow and continuous pulsed Doppler is the state-of-the-art technique. Doppler and color-flow Doppler or contrast 2-dimensional echocardiography helps optimally define fistulas and abscess pockets and extensions. See the image below.



View Image

Myocardial abscess. Color Doppler imaging showing flow into the aortic root abscess.

TEE has a sensitivity of 87% and specificity of 94.6%. Patients in whom an abscess is suggested but has not been detected using TEE should undergo MRI, including magnetic resonance angiography. See the images below.



View Image

Myocardial abscess. Transesophageal echocardiogram exhibiting aortic valvular endocarditis and aortic root abscess.



View Image

Myocardial abscess. Aortic valvular ring abscess seen by transesophageal echocardiography.

Scintigraphy

Indium In 111 leukocyte scintigraphy is especially useful in prosthetic valve endocarditis, in which echocardiography shows too much scatter.

A few milliliters of venous blood is drawn and mixed with an anticoagulant solution. The white blood cells are separated and labeled with radioactive isotope111 In, centrifuged, resuspended in isotonic sodium chloride solution, and reinjected into the patient. Images are then obtained with a gamma-ray camera within 16-24 hours. The viable radioactive leukocytes potentially accumulate in the areas of inflammation or abscess. Obtain oblique views to avoid overshadowing by sternal accumulation.

The need for111 In scintigraphy is very low if TEE is used.

MRI

This is a good modality for helping delineate myocardial abscess. However, the portability and excellent resolution of echocardiography make it more practical than MRI.

CT scan

Only anecdotal reports of diagnosis are available. It is not very sensitive.

Intraoperative echocardiography

Although invasive, small abscesses can be detected in the operating room by means of intraoperative echocardiography, which may enable the operating surgeon to drain the abscess effectively.

Other Tests

Electrocardiography

New-onset and persistent electrocardiographic conduction abnormalities may be observed. Gradual PR prolongation may be observed, and it may suggest development of valve ring abscess.

Although not a sensitive indicator of perivalvular infection or abscess (28%), these findings are relatively specific (85-90%). See the image below.



View Image

Myocardial abscess. Complete heart block seen on a 12-lead electrocardiogram in a patient with myocardial abscess involving the prosthetic aortic valv....

Tests of immune system stimulation

Tests results may show disease activity, but the tests are costly and not very efficient for diagnosis or monitoring response to therapy

These may include testing of circulating immune complexes, rheumatoid factor, quantitative immune globulin, cryoglobulins, and C-reactive protein.

Serologic tests

Serological test findings are used to evaluate cardiac sepsis in which blood culture findings are negative.

Tests to detect antibodies to ribitol teichoic acids from staphylococci may help distinguish uncomplicated S aureus bacteremia from that associated with cardiac involvement.

These tests have not been used in clinical applications because of their lack of adequate specificity or predictive value.

Procedures

Cardiac catheterization may add very little to the imaging studies and is not recommended unless coronary angiography is needed for patients undergoing valve surgery who also may have significant coronary artery disease.

Histologic Findings

Biopsy and histologic assessment is not a part of the diagnostic workup of myocardial abscess. However, surgically removed valves and autopsy findings from fatal cases reveal certain gross and microscopic features. See the images below.



View Image

Myocardial abscess (gross).



View Image

Myocardial abscess (opened).

The infection in native valves and mechanical prostheses that leads to development of myocardial abscess tends to extend beyond the valve ring into the annulus and periannular tissue and into the mitral-aortic intravalvular fibrosa, resulting in ring abscesses, septal abscesses, fistulous tracts, and dehiscence of the prosthesis with hemodynamically significant paravalvular regurgitation.

In autopsy experience with 74 patients, annular invasion was noted in 85%, myocardial abscess formation in 32%, valve obstruction by vegetation overgrowth in 19%, and erosion through the aortic annulus to cause pericarditis in 5%. In another series of 85 patients, the findings were annulus invasion in 42%, myocardial abscess in 14%, valve obstruction in 4%, and pericarditis in 2%. The intracardiac pathology of bioprosthetic valve infective endocarditis is more heterogeneous and includes invasive disease and leaflet destruction.

Myocardial abscess histology findings demonstrate damaged cardiac tissue with degraded collagen and polymorphonuclear predominance.

Medical Care

Medical treatment includes the following:

Supportive treatment includes the following:

Surgical Care

Once the diagnosis of myocardial abscess is made, the treatment of choice is surgical in nature. Appropriate procedures include the following:

Consultations

Myocardial abscess usually develops in patients who are generally very ill, with multiorgan system involvement and unremitting infective endocarditis. The expertise of several subspecialists is needed:

Diet

Patients with myocardial abscess are often critically ill. Supplementation of nutritive food, either by the enteral or parenteral route, is very important.

Patients must be maintained without oral intake until a decision regarding surgical intervention has been made and surgery has been performed.

Postoperatively, gradual advancement in the diet is recommended.

Activity

Critically ill patients with myocardial abscess and infective endocarditis are usually bedridden, with minimal activity.

Frequently, such patients must receive prophylaxis to prevent development of deep venous thrombosis (DVT) and pulmonary embolization (PE).

Gradual increase in ambulation is recommended following surgical intervention.

Prevention

Prompt and effective treatment of infective endocarditis is required.

A high index of suspicion and early recognition of the changes that suggest development of myocardial abscess are necessary.

Regular prophylaxis for subacute bacterial endocarditis, with preoperative antibiotics according to the recommendations of the American Heart Association, is necessary.

Critically ill patients with myocardial abscess and infective endocarditis are usually bedridden, with minimal activity. Frequently, such patients must receive prophylaxis to prevent development of DVT and PE.

Further Outpatient Care

Further outpatient care may include the following:

Further Inpatient Care

Aggressive postoperative supportive therapy in patients with myocardial abscess includes the following:

Continuation of antibiotic therapy may be necessary. Patients may still require a prolonged 6-week course of antibiotic therapy.

Inpatient & Outpatient Medications

These include the following:

Transfer

Patients with infective endocarditis usually exhibit rapid deterioration, and they may require transfer to a tertiary care facility for a diagnostic workup and open heart surgery. Such patients must be transported via an Advanced Cardiac Life Support ambulance staffed with well-trained and experienced paramedics.

Medication Summary

Even though the main mode of treatment is surgical, patients with myocardial abscess still require antibiotics and adjunct agents for stabilization of hemodynamic status (ie, pressors).

Vancomycin (Lyphocin, Vancoled, Vancocin)

Clinical Context:  Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have not responded to penicillins and cephalosporins or those who have infections with resistant staphylococci. For abdominal penetrating injuries, combine with an agent active against enteric flora and/or anaerobes. To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use CrCl to adjust dose in patients diagnosed with renal impairment. Used in conjunction with gentamicin for prophylaxis in patients allergic to penicillin who are undergoing GI or GU procedures.

Gatifloxacin (Tequin)

Clinical Context:  Fluoroquinolone with antimicrobial activity based on ability to inhibit bacterial DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Fluoroquinolones have broad activity against gram-positive and gram-negative aerobic organisms. Differences in chemical structure between quinolones have resulted in altered levels of activity against different bacteria. Altered chemistry in quinolones results in toxicity differences.

Gentamicin (Garamycin)

Clinical Context:  Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes.

Not DOC. Consider if penicillins or other less-toxic drugs are contraindicated, when clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms.

Dosing regimens are numerous; adjust dose based on CrCl and changes in volume of distribution. May be given IV/IM.

Levofloxacin (Levaquin)

Clinical Context:  For pseudomonal infections and infections due to multidrug-resistant gram-negative organisms.

Class Summary

These agents are used to treat susceptible organisms, especially Staphylococcus species, which are the most common organisms in myocardial abscesses.

Dopamine (Intropin)

Clinical Context:  Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect dependent on dose. Lower doses predominantly stimulate dopaminergic receptors, which, in turn, produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation produced by higher doses.

After initiating therapy, increase dose by 1-4 mcg/kg/min q10-30min until optimal response is obtained. More than 50% of patients are maintained satisfactorily on doses < 20 mcg/kg/min.

Class Summary

These agents are used to raise blood pressure and improve tissue perfusion in patients with septic shock or hypotension.

Heparin

Clinical Context:  Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.

Warfarin (Coumadin)

Clinical Context:  Interferes with hepatic synthesis of vitamin K – dependent coagulation factors. Used for prophylaxis and treatment of DVT, PE, and thromboembolic disorders. Tailor dose to maintain INR in range of 2-3.

Class Summary

Antithrombin and anticoagulant agents may be needed for prevention of DVT. Anticoagulants are required for stroke prevention after replacement of cardiac valves with mechanical prostheses.

Author

Vibhuti N Singh, MD, MPH, FACC, FSCAI, Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine; Director, Cardiology Division and Cardiac Catheterization Lab, Chair, Department of Medicine, Bayfront Medical Center, Bayfront Cardiovascular Associates; President, Suncoast Cardiovascular Research

Disclosure: Nothing to disclose.

Coauthor(s)

Jamshid Shirani, MD, Director of Cardiology Fellowship Program, Director of Echocardiography Laboratory, Director of Hypertrophic Cardiomyopathy Clinic, St Luke's University Health Network

Disclosure: Nothing to disclose.

Joel A Strom, MD, ME, Academic Administration, Florida Polytechnic University

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Coramaze<br/>Received own stock from Merck, Inc. for none; Received own stock from Abbott Labs, Inc. for none; Partner received own stock from Medtronic for none; Received own stock from General Electric for none; Received own stock from Pfizer, Inc. for other. for: Stock ownership: Merck Inc; Pfizer Inc; Edwards Lifesciences; Medtronic; .

Kul Aggarwal, MD, FACC, Professor of Clinical Medicine, Department of Internal Medicine, Division of Cardiology, University of Missouri-Columbia School of Medicine; Chief, Cardiology Section, Harry S Truman Veterans Hospital

Disclosure: Nothing to disclose.

Mingquan Suksanong, Clinical Assistant Professor, Department of Medicine, Division of Infectious Diseases and Tropical Medicine, University of South Florida College of Medicine; Consulting Staff, Department of Medicine, Bayfront Medical Center

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

Disclosure: Nothing to disclose.

Chief Editor

Mark R Wallace, MD, FACP, FIDSA, Infectious Disease Physician, Skagit Valley Hospital, Skagit Regional Health

Disclosure: Nothing to disclose.

Additional Contributors

Craig T Basson, MD, PhD, Translational Medicine Head – Cardiovascular, Translational Medicine Head - Diabetes and Metabolism, Novartis Institutes for BioMedical Research

Disclosure: Nothing to disclose.

Acknowledgements

Rakesh K Sharma, MD, FACC Adjunct Associate Professor of Medicine and Cardiology, Medical Center of South Arkansas , University of Arkansas for Medical Sciences

Rakesh K Sharma, MD, FACC is a member of the following medical societies: American College of Cardiology, American College of International Physicians, American College of Physicians, American Heart Association, and American Medical Association

Disclosure: Nothing to disclose.

References

  1. Cossio P, Berconsky I. Abceso parietal del corazon e infarto del myocardio. Seman Med. 1933. 2:1691-8.
  2. Gonzalez Vilchez FJ, Martin Duran R, Delgado Ramis C, et al. [Active infective endocarditis complicated by paravalvular abscess. Review of 40 cases]. Rev Esp Cardiol. 1991 May. 44(5):306-12. [View Abstract]
  3. Elbadawi A, Saad M, Elgendy IY, Zafar A, Chow MY. Multiple myocardial abscesses secondary to late stent infection. Cardiovasc Pathol. 2017 May - Jun. 28:1-2. [View Abstract]
  4. Sanson J, Slodki S, Gruhn JG. Myocardial abscesses. Am Heart J. 1963 Sep. 66:301-8. [View Abstract]
  5. Castleman B, McNeely BU. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 27-1970. N Engl J Med. 1970 Jun 25. 282(26):1477-85. [View Abstract]
  6. Weisz S, Young DG. Myocardial abscess complicating healed myocardial infarction. Can Med Assoc J. 1977 May 21. 116(10):1156-8. [View Abstract]
  7. Murdoch DR, Corey GR, Hoen B, Miró JM, Fowler VG Jr, Bayer AS. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Arch Intern Med. 2009 Mar 9. 169(5):463-73. [View Abstract]
  8. van der Meer JT, Thompson J, Valkenburg HA, Michel MF. Epidemiology of bacterial endocarditis in The Netherlands. II. Antecedent procedures and use of prophylaxis. Arch Intern Med. 1992 Sep. 152(9):1869-73. [View Abstract]
  9. Hogevik H, Olaison L, Andersson R, et al. Epidemiologic aspects of infective endocarditis in an urban population. A 5-year prospective study. Medicine (Baltimore). 1995 Nov. 74(6):324-39. [View Abstract]
  10. Dismukes WE, Karchmer AW, Buckley MJ, et al. Prosthetic valve endocarditis. Analysis of 38 cases. Circulation. 1973 Aug. 48(2):365-77. [View Abstract]
  11. Ben Ismail M, Hannachi N, Abid F, et al. Prosthetic valve endocarditis. A survey. Br Heart J. 1987 Jul. 58(1):72-7. [View Abstract]
  12. 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. [View Abstract]
  13. Ellis SG, Goldstein J, Popp RL. Detection of endocarditis-associated perivalvular abscesses by two- dimensional echocardiography. J Am Coll Cardiol. 1985 Mar. 5(3):647-53. [View Abstract]
  14. Walker N, Bhan A, Desai J, Monaghan MJ. Myocardial abscess: a rare complication of valvular endocarditis demonstrated by 3D contrast echocardiography. Eur J Echocardiogr. 2010 Dec. 11(10):E37. [View Abstract]
  15. Adachi I, Kobayashi J, Nakajima H. Coronary embolism and subsequent myocardial abscess complicating ventricular aneurysm and tachycardia. Ann Thorac Surg. 2005 Dec. 80(6):2366-8. [View Abstract]
  16. Adams BK. Tc-99m leukocyte scintigraphy in infective endocarditis. Clin Nucl Med. 1995 May. 20(5):395-7. [View Abstract]
  17. Aguado JM, Gonzalez-Vilchez F, Martin-Duran R, et al. Perivalvular abscesses associated with endocarditis. Clinical features and diagnostic accuracy of two-dimensional echocardiography. Chest. 1993 Jul. 104(1):88-93. [View Abstract]
  18. Ait Ben Ali S, Hilmani S, Choukri M, et al. [Multiple cerebral hydatic cysts of cardiac origin. A case report]. Neurochirurgie. 1999 Dec. 45(5):426-9. [View Abstract]
  19. Almond DS, Lea BI, Saltissi S, et al. Interventricular septal abscess formation in an HIV-positive man. Int J STD AIDS. 1999 Nov. 10(11):749-50. [View Abstract]
  20. Antonov VA. [Electric alternation of the heart in myocardial abscesses]. Kardiologiia. 1991 Jul. 31(7):49-50. [View Abstract]
  21. Arruabarrena IM, Von Wichmann MA, Iribarren JA, et al. [Favorable evolution of a myocardial abscess using medical treatment in an HIV-positive patient]. Enferm Infecc Microbiol Clin. 1998 Mar. 16(3):156. [View Abstract]
  22. Bajraktari G, Olloni R, Daullxhiu I, Ademaj F, Vela Z, Pajaziti M. MRSA endocarditis of bovine Contegra valved conduit: a case report. Cases J. 2009. 2(1):57. [View Abstract]
  23. Balaguer JM, Soto E, Perry D, Moran JM. Postoperative intramyocardial abscess caused by mucormycosis. Ann Thorac Surg. 1994 Dec. 58(6):1760-2. [View Abstract]
  24. Bayer AS, Bolger AF, Taubert KA, et al. Diagnosis and management of infective endocarditis and its complications. Circulation. 1998 Dec 22-29. 98(25):2936-48. [View Abstract]
  25. Behnam R, Walter S, Hanes V. Myocardial abscess complicating myocardial infarction. J Am Soc Echocardiogr. 1995 May-Jun. 8(3):334-7. [View Abstract]
  26. Berman DA, Burgess JB, Steeper TA. Myocardial abscess due to Fusobacterium following acute myocardial infarction. Clin Cardiol. 1988 Aug. 11(8):575-7. [View Abstract]
  27. Borowski A, Korb H, Voth E, de Vivie ER. Asymptomatic myocardial abscess. Thorac Cardiovasc Surg. 1988 Dec. 36(6):338-40. [View Abstract]
  28. Cerqueira MD, Jacobson AF. Indium-111 leukocyte scintigraphic detection of myocardial abscess formation in patients with endocarditis. J Nucl Med. 1989 May. 30(5):703-6. [View Abstract]
  29. Chakrabarti J. Diagnostic evaluation of myocardial abscesses. A new look at an old problem. Int J Cardiol. 1995 Dec. 52(3):189-96. [View Abstract]
  30. Chang CH, Huang JY, Lai PC, Yang CW. Posterior mediastinal abscess in a hemodialysis patient - a rare but life-threatening complication of Staphylococcus bacteremia. Clin Nephrol. 2009 Jan. 71(1):92-5. [View Abstract]
  31. Chikwe J, Barnard J, Pepper JR. Myocardial abscess. Heart. 2004 Jun. 90(6):597. [View Abstract]
  32. Cowan JC, Patrick D, Reid DS. Aortic root abscess complicating bacterial endocarditis. Demonstration by computed tomography. Br Heart J. 1984 Nov. 52(5):591-3. [View Abstract]
  33. Dajani AS, Taubert KA, Wilson W. Prevention of bacterial endocarditis. Recommendations by the American Heart Association. Available at http://www.americanheart.org/Scientific/statements/1997/079701.html. JAMA. 1997 Jun 11. 277(22):1794-801. [View Abstract]
  34. Daniel WG, Nellessen U, Schroeder E. Trans-esophageal echocardiography as a method of choice for the detection of endocarditis-associated abscess. Circulation. 1986. 74(Supl II):55.
  35. Dean JW, Kuo J, Wood AJ. Myocardial infarction due to coronary artery compression by aortic root abscess. Int J Cardiol. 1993 Sep. 41(2):165-7. [View Abstract]
  36. Egan TM, Maitland A, Sinave C, et al. Myocardial abscess in a patient with AIDS-related complex: pericardial patch repair. Ann Thorac Surg. 1990 Mar. 49(3):481-2. [View Abstract]
  37. Eicher JC, Falcon-Eicher S, Sota FX, et al. Mitral ring abscess caused by bacterial endocarditis on a heavily calcified mitral annulus fibrosus: Diagnosis by multiplane transesophageal echocardiography. Am Heart J. 1996 Apr. 131(4):818-20. [View Abstract]
  38. Fan CC, Andersen BR, Sahgal S. Isolated myocardial abscess causing coronary artery rupture and fatal hemopericardium. Arch Pathol Lab Med. 1994 Oct. 118(10):1023-5. [View Abstract]
  39. Fredenrich A, Jourdan J, Gibelin P, et al. [Ventricular arrhythmias disclosing myocardial abscess in infectious mitro-aortic endocarditis]. Ann Cardiol Angeiol (Paris). 1990 Nov. 39(9):531-3. [View Abstract]
  40. Ghani M, Boughner D. Echocardiographic diagnosis of myocardial abscess complicating myocardial infarction. J Am Soc Echocardiogr. 1994 May-Jun. 7(3 Pt 1):318-20. [View Abstract]
  41. Gladden JR. Myocardial abscess with perforation of the heart following Staphylococcal pyemia. Clin Orthop. 1999. 362:6-11. [View Abstract]
  42. Gunther HU, Strupp G, Volmar J, et al. [Coronary stent implantation: infection and abscess with fatal outcome]. Z Kardiol. 1993 Aug. 82(8):521-5. [View Abstract]
  43. Harris DG, Rossouw GJ. Myocardial abscess with contained rupture: successful repair. Ann Thorac Surg. 2001. 71(4):1360-1. [View Abstract]
  44. Iqbal J, Ahmed I, Baig W. Metastatic myocardial abscess on the posterior wall of the left ventricle: a case report. J Med Case Reports. 2008. 2:258. [View Abstract]
  45. Katz A. Abscess of the myocardium complicating infarction: report of two cases. Can Med Assoc J. 1964 Dec 5. 91:1225-7. [View Abstract]
  46. Khoo DE, Zebro TJ, English TA. Bacterial endocarditis in a transplanted heart. Pathol Res Pract. 1989 Oct. 185(4):445-7. [View Abstract]
  47. Kortleve JW, Duren DR, Becker AE. Cardiac aneurysm complicated by Salmonella abscess. A clinicopathologic correlation in two patients. Am J Med. 1980 Mar. 68(3):395-400. [View Abstract]
  48. Kurland S, Enghoff E, Landelius J, et al. A 10-year retrospective study of infective endocarditis at a university hospital with special regard to the timing of surgical evaluation in S. viridans endocarditis. Scand J Infect Dis. 1999. 31(1):87-91. [View Abstract]
  49. [Guideline] Little J. The American Heart Association's guidelines for the prevention of bacterial endocarditis: a critical review. Gen Dent. 1998 Sep-Oct. 46(5):508-15. [View Abstract]
  50. Lo SS, Ong YE, Sheppard MN, et al. Streptococcal mural endocarditis and myocardial abscess occurring in a left ventricular aneurysm--case report and review. Clin Cardiol. 1998 Jun. 21(6):435-8. [View Abstract]
  51. Massachusetts General Hospital. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 46-1989. A 52-year-old diabetic man with myocardial infarction, pericarditis, and persistent fever. N Engl J Med. 1989 Nov 16. 321(20):1391-402. [View Abstract]
  52. McIlwaine L, Stott S, Hogg D. Fatal unruptured myocardial abscesses. Available at www.heartjnl.com. Heart. 2000 May. 83(5):498. [View Abstract]
  53. Mylonakis E, Calderwood SB. Infective endocarditis in adults. N Engl J Med. 2001 Nov 1. 345(18):1318-30. [View Abstract]
  54. Nandish S, Khardori N. Valvular and myocardial abscesses due to Erysipelothrix rhusiopathiae. Clin Infect Dis. 1999. 29(5):1351-2. [View Abstract]
  55. Persaud H, Pande PN, Easley JM Jr, Downing TP. Myocardial abscess complicating acute myocardial infarction. N Y State J Med. 1988 Jan. 88(1):38-9. [View Abstract]
  56. Prunier L, Lavergne T, Perier P, et al. [Recurrent myocardial abscess during Streptococcus B endocarditis]. Arch Mal Coeur Vaiss. 1988 Jul. 81(7):925-8. [View Abstract]
  57. Recio J, Alegre J, Fernandez de Sevilla T. Myocardial abscess with salmonella infection. Ann Intern Med. 1999 Sep 21. 131(6):477-8. [View Abstract]
  58. Roberts JH, Aponte V, Naidich DP, Bhalla M. Myocardial abscess resulting in a pseudoaneurysm: case report. Cardiovasc Intervent Radiol. 1991 Sep-Oct. 14(5):307-10. [View Abstract]
  59. Romero-Menor C, Espanol I, Alcaide F, et al. Myocardial abscess at a distant zone from the active valvular infection. J Cardiovasc Surg (Torino). 1998 Apr. 39(2):227-8. [View Abstract]
  60. Rosen JM, Murthy S, Hain DR. A comparison of indium-111 leukocyte and gallium-67 scintigraphy in a patient with a myocardial abscess. Clin Nucl Med. 1993 Nov. 18(11):997-8. [View Abstract]
  61. Ryon DS, Pastor BH, Myerson RM. Abscess of the myocardium. Am J Med Sci. 1966 Jun. 251(6):698-705. [View Abstract]
  62. Sheppard RC, Chandrasekaran K, Ross J, Mintz GS. An acquired interatrial fistula secondary to para-aortic abscess documented by transesophageal echocardiography. J Am Soc Echocardiogr. 1991 May-Jun. 4(3):271-6. [View Abstract]
  63. Smith RE, Martin JE, Mills PG. Myocardial abscess and sternal osteomyelitis following myocardial infarction and resuscitation. Postgrad Med J. 1989 Aug. 65(766):589-90. [View Abstract]
  64. Sproule MW, Briggs MJ. Salmonellosis complicated by myocardial abscess and cerebral mycotic aneurysms. Br J Clin Pract. 1995 Sep-Oct. 49(5):273-4. [View Abstract]
  65. Tedeschi CG, Stevenson TD Jr, Levenson HM. Abscess formation in myocardial infarction. N Engl J Med. 1950 Dec 28. 243(26):1024-7. [View Abstract]
  66. Tennant R, Parks HW. Myocardial abscesses. A study of pathogenesis with report of a case. Arch Pathol. 1959 Oct. 68:456-60. [View Abstract]
  67. Terry SM, Ryan PE Jr. Penetrating mitral valve annular abscess. J Heart Valve Dis. 1997 Nov. 6(6):621-4. [View Abstract]
  68. Thomas D, Choussat R, Isnard R, et al. [Cardiac abscess in infectious endocarditis. A multicenter study apropos of 233 cases. The Working Group on Valvulopathy of the French Society of Cardiology]. Arch Mal Coeur Vaiss. 1998 Jun. 91(6):745-52. [View Abstract]
  69. Thomas D, Desruennes M, Jault F, et al. [Cardiac and extracardiac abscesses in bacterial endocarditis]. Arch Mal Coeur Vaiss. 1993 Dec. 86(12 Suppl):1825-35. [View Abstract]
  70. Timsit JF, Wolff MA, Bedos JP, et al. Cardiac abscess following percutaneous transluminal coronary angioplasty. Chest. 1993 Feb. 103(2):639-41. [View Abstract]
  71. Valencia ME, Guinea J, Moreno V, González Lahoz JM. [Myocardial abscess without concomitant valve lesion and parenteral drug addiction]. Rev Clin Esp. 1992 Oct. 191(5):289. [View Abstract]
  72. Vinereanu D, Musumeci F, Fraser AG. Diagnosis of Myocardial Abscess After Acute Myocardial Infarction by Transesophageal Echocardiography: Case Report and Short Review of Published Data. Echocardiography. 1999 Aug. 16(6):581-584. [View Abstract]
  73. Völker U, Kraft P. [An unusual cause of myocardial infarct. Bacterial mitral valve endocarditis, valve ring and myocardial abscess with direct coronary lesion]. Z Kardiol. 1993 May. 82(5):287-92. [View Abstract]
  74. Weernink EE, de Boer MJ, Brutel de la Rivière A. Myocardial abscess after silent myocardial infarction. Thorac Cardiovasc Surg. 1989 Apr. 37(2):103-4. [View Abstract]
  75. Weinstein LW, Brusch JL. Infective Endocarditis. New York, NY: Oxford University Press; 1996. 175-7.
  76. Wickline CL, Goli VD, Buell JC. Coronary artery narrowing due to extrinsic compression by myocardial abscess. Cathet Cardiovasc Diagn. 1991 Jun. 23(2):121-3. [View Abstract]
  77. Wilson WR, Karchmer AW, Dajani AS. Antibiotic treatment of adults with infective endocarditis due to streptococci, enterococci, staphylococci, and HACEK microorganisms. American Heart Association. Available at http://www.americanheart.org/Scientific/statements/1995/129501.html. JAMA. 1995 Dec 6. 274(21):1706-13. [View Abstract]
  78. Winek RR, Schwenk NM, Edwards WD. Fatal hemopericardium due to ruptured solitary myocardial abscess unassociated with infective endocarditis. Am J Cardiovasc Pathol. 1988. 2(3):255-7. [View Abstract]
  79. Witham M, Dittmer I, Williams A, et al. Myocardial abscess: an unusual complication of long-term hemodialysis line presence. Clin Nephrol. 1999 Mar. 51(3):193-4. [View Abstract]
  80. Zeineddin M, Stewart JA. Echocardiographic detection of non-valve-ring myocardial abscess complicating aortic valve endocarditis. Am J Med. 1988 Jul. 85(1):97-9. [View Abstract]

Myocardial abscess. Color Doppler imaging showing flow into the aortic root abscess.

Myocardial abscess. Transesophageal echocardiogram exhibiting aortic valvular endocarditis and aortic root abscess.

Myocardial abscess. Aortic valvular ring abscess seen by transesophageal echocardiography.

Myocardial abscess. Complete heart block seen on a 12-lead electrocardiogram in a patient with myocardial abscess involving the prosthetic aortic valve ring.

Myocardial abscess (gross).

Myocardial abscess (opened).

Myocardial abscess. Transesophageal echocardiogram exhibiting aortic valvular endocarditis and aortic root abscess.

Myocardial abscess. Complete heart block seen on a 12-lead electrocardiogram in a patient with myocardial abscess involving the prosthetic aortic valve ring.

Myocardial abscess. Color Doppler imaging showing flow into the aortic root abscess.

Myocardial abscess. Aortic valvular ring abscess seen by transesophageal echocardiography.

Myocardial abscess (gross).

Myocardial abscess (opened).