eMedicine Specialties > Infectious Diseases > Cardiovascular and Intravascular Infections

Myocardial Abscess

Author: Vibhuti N Singh, MD, MPH, FACC, FSCAI, Director, Suncoast Cardiovascular Center; Chair, Cardiology Division and Cath Labs, Department of Medicine, Bayfront Medical Center; Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine
Coauthor(s): Kul Aggarwal, MD, FACC, Professor of Clinical Medicine, Department of Internal Medicine, Division of Cardiology, University of Missouri School of Medicine; Chief, Cardiology Section, Harry S Truman Veterans Hospital; Rakesh K Sharma, MD, FACC, Adjunct Associate Professor of Medicine and Cardiology; University of Arkansas for Medical Sciences, Medical Center of South Arkansas; Jamshid Shirani, MD, FACC, FAHA, Consulting Staff, Director of Cardiovascular Fellowship Program, Department of Medicine, Division of Cardiology, Geisinger Medical Center; Joel A Strom, MD, ME, Professor of Internal Medicine, Chemical and Biomedical Engineering, and Honors College, University of South Florida; Mingquan Suksanong, MD, Clinical Assistant Professor, Department of Medicine, Division of Infectious Diseases and Tropical Medicine, University of South Florida School of Medicine; Consulting Staff, Department of Medicine, Bayfront Medical Center
Contributor Information and Disclosures

Updated: Aug 27, 2009

Introduction

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

Currently, the most common clinical setting for myocardial abscess is endocarditis of 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

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.3

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.4

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.5

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]5 ), with a catastrophic outcome.

Other clinical settings

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

  • Trauma
  • Deep penetrating wounds
  • Deep burns
  • Infected pseudoaneurysms
  • Suppurative pericardial effusions
  • Infected transplanted hearts
  • Extension from sternal abscess
  • HIV-associated myocarditis and suppuration
  • Parasitic infections
  • Infection of a left ventricular aneurysm or tumor

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.3 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

  • S aureus
  • Haemophilus species
  • Enterococci
  • E coli
  • Beta-hemolytic streptococci
  • S pneumoniae
  • Bacteroides species
  • Parasitic organisms
  • Hydatid cysts, ie, from echinococci
  • Miscellaneous

Pathogenesis

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

  • Vascular endothelium
  • Hemostatic mechanisms
  • Host immune system
  • Gross anatomic abnormalities in the heart
  • Surface properties of microorganisms
  • Extracardiac events that introduce bacteremia

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.

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.6

The incidence of infective endocarditis remained relatively stable from 1950-1987, at approximately 4.2 cases per 100,000 patient-years.7 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.8

  • Infection involving mechanical prostheses often extends into the annulus and 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.9
  • Ben Ismail et al (1987) found annulus infection and valve dehiscence in 38 of 41 (82%) infected mechanical valves examined at surgery or autopsy.10

Mortality/Morbidity

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

  • The mortality rate associated with S aureus infection is 42% overall. If treated with antibiotics only, the mortality rate is 75%. If treated with antibiotics and surgery, the mortality rate falls 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. 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.7 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).

Clinical

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:
    • Significant clinical deterioration, including worsening CHF, worsening heart sounds and murmurs, and new-onset valvular regurgitation (100% of cases)11
    • Poor response to antibiotics
    • Development of conduction defects or progression of heart block, such as bundle-branch block and atrioventricular block (45%)2
    • Sudden onset of complete heart block or Mobitz type II block (highly specific)
    • Type of valve involvement, eg, aortic valve endocarditis (40%-85% incidence)
    • Severe recurrent ventricular arrhythmias
    • Pericarditis (uncommon)
    • Infection of the prosthetic valves (bioprosthetic or metallic)
    • Right-sided endocarditis in patients with congenital heart disease
  • The duration of symptoms is short.
  • Fever is protracted despite adequate antibiotic coverage.
  • The infecting organism is Pneumococcus or Staphylococcus species.
  • Acute MI occurs in the setting of septicemia.
  • Sepsis may be present in patients with 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:
    • Anorexia
    • Weight loss
    • Malaise
    • Dyspnea
    • Cough
    • Stroke
    • Headache
    • Nausea/vomiting
    • Myalgia
    • Arthralgia
    • Chest pain
    • Abdominal pain
    • Back pain
    • Confusion
    • Sweats

Physical

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

  • Fever
  • Tachycardia
  • Murmur, especially changing or new murmur
  • Neurological abnormalities
  • Embolic event
  • Splenomegaly
  • Clubbing
  • Peripheral manifestations
  • Osler nodes
  • Splinter hemorrhages
  • Petechiae
  • Janeway lesions
  • Retinal lesions (Roth spots)
  • Widening pulse pressure, especially with involvement of the aortic valve and progression of aortic regurgitation

Causes

Causes of myocardial abscess may include the following:

  • Associated with endocarditis
    • Native valve endocarditis
    • Prosthetic valve endocarditis - Bioprosthesis, mechanical prosthesis
    • Myocardial (muscle) infection - Ventricular septal wall, left ventricular posterior wall
  • Associated with septicemia
    • Bronchopneumonias
    • Genitourinary infections
    • Other infections
  • Miscellaneous
    • Complications of acute MI
    • Trauma and deep penetrating wounds
    • Mechanical interventions - Catheterization, angioplasty, stent
    • Infection associated with left ventricular aneurysm
    • Infection associated with atrial myxoma (exceedingly rare)
    • Myocarditis and suppuration associated with HIV
    • Transplanted heart infection
    • Asymptomatic
    • Other

More on Myocardial Abscess

Overview: Myocardial Abscess
Differential Diagnoses & Workup: Myocardial Abscess
Treatment & Medication: Myocardial Abscess
Follow-up: Myocardial Abscess
Multimedia: Myocardial Abscess
References
Further Reading
[ CLOSE WINDOW ]

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Keywords

myocardial abscess, myocardial sepsis, cardiac abscess, bacterial endocarditis, infective endocarditis, IE, endocardial abscess, suppurative endocarditis, infectious myocarditis, heart infection, heart valve infection, valve infection, prosthetic valve infection, perivalvular infection, cardiac conduction system infection

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Contributor Information and Disclosures

Author

Vibhuti N Singh, MD, MPH, FACC, FSCAI, Director, Suncoast Cardiovascular Center; Chair, Cardiology Division and Cath Labs, Department of Medicine, Bayfront Medical Center; Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine
Vibhuti N Singh, MD, MPH, FACC, FSCAI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Florida Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Kul Aggarwal, MD, FACC, Professor of Clinical Medicine, Department of Internal Medicine, Division of Cardiology, University of Missouri School of Medicine; Chief, Cardiology Section, Harry S Truman Veterans Hospital
Kul Aggarwal, MD, FACC is a member of the following medical societies: American College of Cardiology and American College of Physicians
Disclosure: Nothing to disclose.

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

Jamshid Shirani, MD, FACC, FAHA, Consulting Staff, Director of Cardiovascular Fellowship Program, Department of Medicine, Division of Cardiology, Geisinger Medical Center
Jamshid Shirani, MD, FACC, FAHA is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Echocardiography, and Association of Subspecialty Professors
Disclosure: Nothing to disclose.

Joel A Strom, MD, ME, Professor of Internal Medicine, Chemical and Biomedical Engineering, and Honors College, University of South Florida
Joel A Strom, MD, ME is a member of the following medical societies: American College of Cardiology, American Heart Association, American Society of Echocardiography, and Sigma Xi
Disclosure: Merck, Inc. Own stock None; Abbott Labs, Inc. own stock None; Medtronic own stock None; General Electric own stock None

Mingquan Suksanong, MD, Clinical Assistant Professor, Department of Medicine, Division of Infectious Diseases and Tropical Medicine, University of South Florida School of Medicine; Consulting Staff, Department of Medicine, Bayfront Medical Center
Disclosure: Nothing to disclose.

Medical Editor

Craig T Basson, MD, PhD, FAHA, FACC, Gladys and Roland Harriman Professor of Medicine, Weill Cornell Medical College; Director, Cardiovascular Research, Greenberg Division of Cardiology, Department of Medicine, The New York Presbyterian Hospital
Craig T Basson, MD, PhD, FAHA, FACC is a member of the following medical societies: American College of Cardiology and American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance
John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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