Myocardial Abscess

Updated: Jan 28, 2015
  • Author: Vibhuti N Singh, MD, MPH, FACC, FSCAI; Chief Editor: Mark R Wallace, MD, FACP, FIDSA  more...
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Overview

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.

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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]

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 pericarditis
  • Infected transplanted hearts
  • Extension from sternal abscess
  • HIV-associated myocarditis and suppuration
  • Parasitic infections
  • Infection of a left ventricular aneurysm or tumor
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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.

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Microorganisms

Microorganisms associated with myocardial abscess include the following:

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

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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. [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]

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. [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 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. [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).

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