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Cardiac Abscess

Editor: Mark A. Law Updated: 10/6/2024 7:28:50 PM

Introduction

A cardiac abscess is a suppurative infection of the myocardium, endocardium, and native or prosthetic valve tissue. Like other abscesses, it develops either by dissemination from a distant source such as bacteremia or sepsis or by direct extension of a preexisting cardiac infective focus. Infective endocarditis has long been identified as the main cause of the latter. Although the incidence of cardiac abscesses continues to be investigated, it is presumably higher than noted postmortem and is of great importance when deciding the prognosis of and therapeutic strategy for patients. Cardiac abscesses are typically monomicrobial; the most common etiologic agents are Staphylococcus aureus or Escherichia coli. Polymicrobial cardiac abscesses are less typical but do occur.[1][2][3] Myocardial abscesses may also form in regions of the heart that have experienced prior damage, such as those affected by recent infarction.[4]

Significant complications of a cardiac abscess, whether alone or with valve tissue, are conduction abnormalities. The incidence of perivalvular abscess among patients with infective endocarditis is between 30% and 40%, with the aortic valve having a higher predisposition than the mitral valve and annulus. Native aortic valve endocarditis, usually located in a weak part of the annulus near the atrioventricular node (AV), clearly demonstrates the anatomic predisposition and exemplifies why abscesses and heart block present as frequent sequelae.

Perivalvular abscesses are also more familiar with prosthetic valves. In this case, the annulus, instead of the leaflet, is usually the primary site of infection. The degree of conduction disruption, therefore, depends on the extent of the involvement of the conduction system and is more commonly seen in perivalvular aortic abscesses. Additionally, the severe extension of perivalvular infection can also result in extrinsic coronary arterial compression or disruption, leading to acute coronary syndrome. Thus far, only aortic valve involvement and current intravenous drug use (IVDU) have been prospectively identified as independent risk factors for a perivalvular abscess. Any patient with a cardiac abscess, regardless of all other factors, has an increased risk of embolization, morbidity, and mortality.[5] Right-sided infective endocarditis represents 5% to 10% of all cases and is frequently linked to IVDU, intracardiac devices, and central venous catheters. The prevalence of these factors has increased in the United States over the last 2 decades.[6]

Etiology

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Etiology

Cardiac abscesses are most commonly thought to occur primarily via extension of a preexisting cardiac infection, as in the case of infective endocarditis. Secondary causes of cardiac abscess are believed to be due to bacteremia (persistent or transient) without a known cardiac source, susceptible heart tissue soon after myocardial infarction (MI), or prosthetic valve disease, usually in the setting of bacteremia. Other less common predisposing factors may be trauma, penetrating wounds, deep burns, infected transplanted hearts, infected sternal incision sites, pseudoaneurysm, HIV, or parasitic infections.[7]

Epidemiology

Cardiac abscesses are rare in the United States. Staphylococcus aureus is the most common pathogen when the disease is present. The mitral valve is most commonly implicated in patients with native valves and heart tissue. A 2009 study by Murdoch et al looked at the presentation and etiology and estimated the patient incidence of infective endocarditis at approximately 15%. Regarding prosthetic tissue or valves, the infection tends to be entirely periannular, extends to the myocardium, and results in paravalvular abscesses from the dehiscence of the valve.[8][9]

The following are organisms noted to be involved in cardiac abscess formation:

  • Staphylococcus aureus
  • Haemophilus species
  • Enterococci 
  • Escherichia coli
  • ß-hemolytic streptococci 
  • Streptococcus pneumoniae 
  • Bacteroides species
  • Parasitic organisms
  • Hydatid cysts
  • Miscellaneous

Pathophysiology

Current or prior infective endocarditis is the primary predisposing factor for a cardiac abscess. The most common sites involved are the aortic valve, the ventricular septa, the mitral valves, and the papillary muscles. S aureus, the most commonly involved causative agent, is present in up to one-third of all cases and has an even higher incidence in patients with prosthetic valves.

Secondly, bacteremia may become a significant pathophysiologic mechanism, although abscesses due to bacteremia alone tend not to be large enough to cause death. Most studies report this as an incidental postmortem finding. Moreover, the site of prior MI has also been documented as a predisposing risk factor for the development of a cardiac abscess in patients in whom bacteremia is of concern. Such a scenario is plausible in a patient with a known prior infection undergoing an acute coronary syndrome or acquiring the infection soon following an MI. Necrosis of muscle fibers post-MI, in addition to an inflammatory state and decreased perfusion with lack of blood flow, is also suspected to increase myocardium susceptibility to this complication.[10]

History and Physical

Depending on the acuity of presentation (ie, acute versus subacute infective endocarditis), the location of the cardiac abscess, and the overall state of a patient with bacteremia, several clinical features may be observed during clinical assessment.

Clinical History

Highly variable, vague symptoms are common. An acute presentation is more toxic, whereas a subacute patient presents more indolently. Depending on the conduction abnormality, symptoms of any degree of heart block may be present. Other symptoms may include:

  • Fever, subjective or objective
  • Anorexia
  • Myalgias
  • Headache
  • Dyspnea
  • Joint pain
  • Rashes
  • Cough
  • Chest pain

Physical Examination

Findings associated with cardiac abscesses frequently manifest due to infective endocarditis or cardiac abscess complications that develop. Clinicians must remember that the absence of these findings does not exclude infective endocarditis, as clinical features are not sufficiently sensitive or specific for this disease process. Findings that can be indicative of cardiac abscess include:

  • Fever
  • Signs and symptoms of heart failure (eg, S3 heart sounds, jugular venous distention, and pulmonary crackles)
  • Signs and symptoms of valvular insufficiency (usually systolic murmurs related to the tricuspid, mitral, or aortic valves or diastolic murmurs, more common in patients with prosthetic valve endocarditis and perivalvular leak or disease)
  • Focal neurologic complaints due to emboli
  • Back pain associated with osteomyelitis
  • Petechiae, nonspecific
  • Subungal or splinter hemorrhages
  • Osler nodes (painful subcutaneous nodules most commonly on hands)
  • Janeway lesions (nontender lesions of palms or soles)
  • Roth spots (retinal hemorrhages visible during fundoscopy)
  • Splenomegaly

Evaluation

All patients with a suspected cardiac abscess require an electrocardiogram (ECG). Continuous electrocardiographic monitoring is preferred; a new atrioventricular block has a positive predictive value of 88% for abscess formation but a low sensitivity of 45%.

Laboratory Studies

Various laboratory tests are recommended when evaluating a patient with a suspected cardiac abscess, including blood and urine studies and blood cultures. These studies help evaluate the differential diagnoses that should be considered based on the clinical features present. A cardiac abscess in the setting of negative blood cultures is possible. For example, a patient whose initial evaluation demonstrated bacteremia with no physical signs of infective endocarditis or cardiac conduction deficit may receive intravenous (IV) antibiotics before a further workup. Therefore, cultures may not be reliable. Additionally, if cultures are not drawn correctly, the likelihood of positive results decreases significantly.

Imaging Studies

Echocardiography is an important component of the evaluation of a patient with a suspected cardiac abscess. Transesophageal echocardiography (TEE) is the recommended imaging study in the initial assessment of a patient with a suspected cardiac abscess. If TEE is unavailable, transthoracic echocardiography (TTE) should be performed. TEE is more sensitive and specific for cardiac abscess than TTE.

Electrocardiogram-gated cardiac computed tomography (CT) offers multiplanar cine reconstructions that complement the information obtained from echocardiography. While TEE is more sensitive for detecting small vegetation (<4 mm), CT is superior in assessing the anatomical extent of the disease. Additionally, cardiac CT is useful for preoperative assessment of the risks associated with sternal reentry. When evaluating coronary anatomy, CT may be favored over invasive angiography to reduce the potential risk of infectious embolization into the coronary arteries.[11]

The role of cardiac magnetic resonance imaging (MRI) in diagnosing suspected infective endocarditis remains undefined, with image quality often impacted by artifacts from prosthetic materials. However, cardiac MRI excels in tissue characterization, detecting myocardial inflammation or fibrosis using T2-weighted sequences and post-gadolinium delayed enhancement sequences. Long inversion time imaging (around 600 ms) can distinguish vegetations from other intracardiac masses like thrombi. Additionally, MRI with gadolinium-based contrast is considered a safer alternative in patients with renal impairment, where iodine-based contrast for CT might pose a risk.[12]

Positron emission tomography CT (PET-CT) is widely recognized for its effectiveness in assessing prosthetic valve endocarditis and infections of vascular grafts. Research has demonstrated increased sensitivity in detecting endocarditis, though this may come with a reduction in specificity. A significant limitation of PET-CT is its difficulty in distinguishing endocarditis from other inflammatory processes, particularly in patients recovering from recent cardiac surgery where tissue healing may be ongoing.[11][13]

Treatment / Management

Intravenous antibiotics should be administered promptly once infective endocarditis or a cardiac abscess is suspected. Empiric broad-spectrum antibiotics, until further characterization of infective species, should be monitored for at least 6 weeks of therapy in this patient population.[14]

When approaching a patient with a cardiac abscess, the surgery consult and the time of surgical intervention are of high importance. Patients in whom surgery is delayed experience increased morbidity and mortality. Thus, early surgery is recommended. Surgery for these patients aims to eradicate the infection and correct hemodynamic abnormalities.

However, some patients with periannular extension of infection or myocardial abscess could potentially be treated without surgical intervention. These patients include:

  • Patients with smaller (<1 cm) abscesses
  • Patients who do not have complications of heart block, an echocardiographic progression of abscess during antibiotic therapy
  • Patients who do not have valvular dehiscence or insufficiency

According to the recent Endocarditis European Society of Cardiology (ESC) Guidelines and data from the European Endocarditis (EURO-ENDO) registry, 11.5% of patients presented with conduction disturbances at diagnosis, primarily 1st-, 2nd-, and 3rd-degree atrioventricular block (AVB). The development of a new AVB due to an abscess indicates urgent cardiac surgery.[15] These recommended that patients who do not undergo surgery are monitored closely with serial TEE repeated at 2, 4, and 8 weeks after completion of antibiotic therapy. (B3)

Differential Diagnosis

Differential diagnoses of cardiac abscess that should be considered during evaluation include:

  • Fever of unknown origin (FUO)
  • First-degree atrioventricular block
  • Heart transplantation
  • Heart-lung transplantation
  • Infections after solid organ transplantations
  • Infective endocarditis
  • Mitral regurgitation
  • Myocardial infarction
  • Penetrating chest trauma
  • Septic shock

Prognosis

Patients can recover quickly if the diagnosis is made early and treatment ensues without delay. Without surgical intervention, the prognosis is usually not favorable.

Complications

Complications of cardiac abscess include:

  • Heart block
  • Arrhythmias
  • Congestive heart failure
  • Stroke
  • Multiple organ failure
  • Acute respiratory distress syndrome
  • Death

Postoperative and Rehabilitation Care

Posttreatment and postsurgical considerations of cardiac abscess management include:

  • These patients often require 6 to 8 weeks of parenteral antibiotic therapy. They also need deep vein thrombosis (DVT) prophylaxis. Those with a prosthetic valve may require oral anticoagulants.
  • Because the patients are critically ill, nutrition is essential.
  • An exercise program is also recommended to help prevent muscle atrophy and DVT.

Consultations

The management of a cardiac abscess may require input from different specialties, including:

  • Cardiologist
  • Cardiac surgeon
  • Physical therapy
  • Dietitian
  • Intensivist
  • Infectious disease

Deterrence and Patient Education

Patient education regarding their illness and emphasis on the significance of prophylaxis is crucial. Prophylaxis remains a longstanding subject in the prevention of infective endocarditis or cardiac abscess. Thus far, prophylaxis is mainly based on observational studies. Places such as the United Kingdom no longer endorse antibiotic prophylaxis for dental procedures to prevent infective endocarditis, the leading source of cardiac abscesses.

One argument against prophylaxis is that tooth brushing has been proven to cause bacteremia. This makes it challenging to assess rare versus high-magnitude transient bacteremia and its effect on infective endocarditis and its sequelae. For this reason, the United States and European countries have agreed that prophylaxis is reserved only for those at the highest risk.

On the same matter, the widespread use of antibiotics to prevent and treat infective endocarditis and abscesses could potentially increase the incidence of polymicrobial infection and antibiotic resistance, especially in immunocompromised patients. Furthermore, the risk of drug-related adverse effects increases with prolonged drug exposure. In the case of antibiotic therapy, vestibular, auditory, and nephrotoxic adverse effects are of significant concern. These adverse effects require close monitoring and an expert team to manage infective endocarditis and its complications; unfortunately, these are not widely available.

Enhancing Healthcare Team Outcomes

Effective management of myocardial abscesses requires coordinated efforts from an interprofessional team to enhance patient-centered care, improve outcomes, and ensure patient safety. Physicians, including cardiologists, cardiovascular surgeons, and infectious disease specialists, must work together to monitor for complications, initiate appropriate antibiotics, and consider surgical interventions when necessary. Advanced practitioners and intensive care specialists oversee the acute management of critically ill patients, monitoring for organ failure and maintaining hemodynamic stability. Nurses play a pivotal role in patient education, infection prevention, and ongoing monitoring of vitals, while pharmacists ensure proper antibiotic dosing, anticoagulation management, and drug safety. Nephrologists and dietitians address comorbidities like renal failure and nutritional needs, while physical therapists promote mobility and prevent complications like deep vein thrombosis.

Effective interprofessional communication and collaboration are essential for timely diagnosis, early intervention, and a structured, aggressive approach to care, which are vital in reducing the high morbidity and mortality associated with myocardial abscesses. This coordinated strategy ensures that each health professional contributes their expertise to optimize both team performance and patient outcomes.

References


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