A cardiac abscess is a suppurative infection of the myocardium, endocardium, native or prosthetic valve tissue. Similar to other abscesses, it develops either by dissemination from a distant source such as bacteremia or sepsis or by direct extension of a pre-existing 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 and management of patients. A single organism causes cardiac abscesses, usually Staphylococcus aureus or Escherichia coli. Less typically, polymicrobial abscesses have been noted. ,,
Important complications of a cardiac abscess, whether alone or with valve tissue, are conduction abnormalities on electrocardiogram (ECG). The incidence of perivalvular abscess among patients with infective endocarditis is between 30% to 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 presents as frequent sequelae.
Perivalvular abscesses are also more common 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 compression, or disruption, leading to an acute coronary syndrome. Thus far, only aortic valve involvement and current IV drug use 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. 
Cardiac abscesses are most commonly thought to occur primarily by the extent of a pre-existing cardiac infection, as it is with the case of infective endocarditis (IE). Secondary causes of cardiac abscess are believed to be due to bacteremia (persistent or transient) without a known cardiac source, as well as 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 site, pseudoaneurysm, HIV, or parasitic infections. 
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, etiology and estimated the patient incidence of infective endocarditis at about 15%. In regards to prosthetic tissue or prosthetic valves, the infection tends to be entirely peri-annular, extends to the myocardium, and results in paravalvular abscesses from dehiscence of the valve. 
The following are organisms noted to be involved in cardiac abscess formation:
The number one predisposing factor for a cardiac abscess is current or prior infective endocarditis. The most common sites involved are the aortic valve, followed by the ventricular septa, mitral valves, and papillary muscles. S. aureus, the most commonly involved causative agent, is present in up to one-third of all cases and has even higher incidence in patients with prosthetic valves.
Secondly, bacteremia becomes of significant importance although abscesses due to bacteremia alone tend not to be large enough to cause death and have been reported as an incidental postmortem finding in most papers.
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 known prior infection undergoing an acute coronary syndrome or acquiring the infection soon following an MI. It is also suspected that the presence of necrosis of muscle fibers post-MI, in addition to inflammatory state and decreased perfusion with lack of blood flow, increases myocardium susceptibility to this complication. 
Depending on the acuity of presentation (acute versus subacute IE), as well as the location of cardiac abscess and the overall state of a patient with bacteremia, the following are possible history and physical exam findings.
Highly variable, vague symptoms are common. An acute presentation is more toxic; whereas, a subacute patient presents with a more indolent complaint. Depending on conduction abnormality, symptoms related to heart block of any degree may be present.
The possible complications of the most common causative etiology of IE, as well as complications of a cardiac abscess alone. One must keep in mind that the absence of these findings does not rule out IE as the findings are not sufficiently sensitive or specific for this disease process.
Tests to consider include:
Always keep in mind that it is in the realm of possibility to obtain negative cultures and still have a cardiac abscess. For example, a patient whose initial evaluation demonstrated bacteremia with, initially, no physical signs of IE or cardiac conduction deficit may receive intravenous (IV) antibiotics before a further workup, and therefore, cultures may not be reliable. Additionally, if cultures are not drawn properly, the likelihood of positive results decreases significantly.
Intravenous antibiotics should be administered in a timely fashion once a patient is suspected of IE or a cardiac abscess. Empiric broad-spectrum antibiotics until further characterization of infective species should be monitored for at least 6 weeks of therapy in this patient population. 
Surgery consult and the time of surgical intervention is of high importance when approaching a patient with a cardiac abscess. There is increased morbidity and mortality in patients in whom surgery is delayed. Thus early surgery is recommended. Surgery for these patients aims toward the eradication of the infection and correction of hemodynamic abnormalities.
However, some patients with periannular extension of infection or myocardial abscess could potentially be treated without surgical intervention. These patients include:
It is 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.
Prophylaxis against infective endocarditis
Prophylaxis remains a longstanding subject in the matter of prevention of IE or cardiac abscess. Thus far, prophylaxis is mostly based on observational studies and, in fact, places such as the United Kingdom no longer endorse antibiotic prophylaxis for dental procedures to prevent IE, the leading source of the cardiac abscess.
One point against prophylaxis is the fact that tooth brushing has been proven to cause bacteremia and, therefore, makes it difficult to assess the rare versus high magnitude transient bacteremia and its effect on IE and its sequelae. For this reason, the United States and European countries have agreed that the use of prophylaxis is reserved only for those at "highest risk."
On that same matter, the widespread use of antibiotics for the prevention and treatment of IE and abscesses could potentially create a setting where there will be an increased 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 major concern. These adverse effects require close monitoring and an expert team in the management of IE and its complications; these are, unfortunately, not widely available.
A myocardial abscess is a life-threatening disorder of the endocardium, and early recognition and initiation of treatment are necessary for patient survival. In the majority of cases, a myocardial abscess is a complication of endocarditis that either involves native or prosthetic valves. However, a myocardial abscess can also occur in many other settings including infective endocarditis, trauma, suppurative pericarditis, infected transplanted heart, HIV, and parasitic infections. The condition carries a very high mortality ranging from 30% to 75% without treatment. To reduce the morbidity and mortality of this disorder, it is imperative that a structured approach is developed to make an early diagnosis and begin treatment. Myocardial abscess tends to occur in critically ill patients with multiorgan involvement in the face of a severe case of infective endocarditis. Thus, the following multidisciplinary team of healthcare professionals is recommended:
Cardiologist to monitor for complications like heart block, septal perforation
Cardiovascular surgeon for debridement, replacement of the valve
Infectious disease specialist to ensure that the patient is on the right antibiotics
Intensive care medicine and pulmonary medicine specialists to monitor the patients
Nephrologist to dialyze the patients when the patient has renal failure
Laboratory technology/pathologist to determine the type of organisms and cause; it is important to note that many patients have negative blood cultures due to prior administration of antibiotics
Nurses to educate the patient and family on hand washing and endocarditis prophylaxis
Physical therapist to improve muscular activity and lessen the risk of deep vein thrombosis
Dietitian to ensure that failure to thrive does not develop; patients are extremely ill and often require food supplementation, either entirely or parenterally
Pharmacist to monitor the antibiotic therapy which may extend for several months; many patients with prosthetic valves may be on oral anticoagulants and need monitoring of their coagulation parameters; these patients may also be on diuretics to treat heart failure and antiarrhythmic drugs
A myocardial abscess is an uncommon, life-threatening disorder. Most patients require immediate treatment, and it is difficult to perform randomized controlled studies; hence, evidence-based guidelines are not yet available. Most of the recommendations have been made indirectly from the care of patients with infective endocarditis. The outcomes usually depend on the comorbidity, location of the abscess, and presence of complications. No matter what approach is taken, the care of these patients should be aggressive and by an interprofessional group of healthcare experts. Even with therapy, mortality rates of 5% to 15% are not uncommon. The only way to improve these abysmal statistics is to identify the condition early and initiate treatment. 
|||Grant R,Page S,Iyer A, Contained myocardial abscess following a myocardial infarction. Journal of cardiac surgery. 2018 Mar [PubMed PMID: 29526056]|
|||Desaint P,Chauvat A,Garaud T,Andremont O,Plantefève G,Mentec H,Contou D, Perivalvular Mitral Abscess Fistulised to the Pericardial Cavity Revealing Staphylococcal Endocarditis. Heart, lung [PubMed PMID: 29133025]|
|||Nand N,Singla SK,Magu S, Cardiac Abscess with Ventricular Aneurysm Secondary to Old Myocardial Infarction. The Journal of the Association of Physicians of India. 2017 May [PubMed PMID: 28598059]|
|||Kong WKF,Choong CC,Sule JA,Poh KK,Kofidis T, Paravalvular root abscess with mycotic pseudoaneurysm. European heart journal. 2018 Jul 17 [PubMed PMID: 30020432]|
|||Kim JS,Kang MK,Cho AJ,Seo YB,Kim KI, Complicated infective endocarditis: a case series. Journal of medical case reports. 2017 May 8 [PubMed PMID: 28482860]|
|||Perrotta S,Aljassim O,Jeppsson A,Bech-Hanssen O,Svensson G, Survival and quality of life after aortic root replacement with homografts in acute endocarditis. The Annals of thoracic surgery. 2010 Dec [PubMed PMID: 21095327]|
|||Subbaraju P,Rai S,Morakhia J,Midha G,Kamath A,Saravu K, Clinical - microbiological characterization and risk factors of mortality in infective endocarditis from a tertiary care academic hospital in Southern India. Indian heart journal. 2018 Mar - Apr [PubMed PMID: 29716704]|
|||Oliveira JLR,Santos MAD,Arnoni RT,Ramos A,Togna DD,Ghorayeb SK,Kroll RTM,Souza LCB, Mortality Predictors in the Surgical Treatment of Active Infective Endocarditis. Brazilian journal of cardiovascular surgery. 2018 Jan-Feb [PubMed PMID: 29617499]|
|||Drissa M,Helali S,Chebbi M,Ezzaouia K,Omri F,Drissa H, Prosthetic valve endocarditis: clinical, bacteriological and therapeutic aspects. La Tunisie medicale. 2017 Jul [PubMed PMID: 29694648]|
|||Fernando RJ,Johnson SD,Augoustides JG,Patel PA,Gutsche JT,Dashiell JM,Feinman JW,Zhou E,Weiss SJ,Goldhammer JE,Panikkath PV,Gerstein NS, Simultaneous Right-Sided and Left-Sided Infective Endocarditis: Management Challenges in a Multidisciplinary Setting. Journal of cardiothoracic and vascular anesthesia. 2018 Apr [PubMed PMID: 29249580]|
|||Hitzeroth J,Beckett N,Ntuli P, An approach to a patient with infective endocarditis. South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde. 2016 Feb [PubMed PMID: 27303769]|
|||Elgalad A,Arafat A,Elshazly T,Elkahwagy M,Fawzy H,Wahby E,Taha AH,Sampaio L,Herregods MC,Peetermans W,Herijgers P, Surgery for Active Infective Endocarditis of the Aortic Valve With Infection Extending Beyond the Leaflets. Heart, lung [PubMed PMID: 30181036]|
|||Meshaal MS,Labib D,Said K,Hosny M,Hassan M,Abd Al Aziz S,Elkholy A,Anani M,Rizk H, Aspergillus endocarditis: Diagnostic criteria and predictors of outcome, A retrospective cohort study. PloS one. 2018 [PubMed PMID: 30092074]|