Infective Endocarditis: Complications and Prognosis


complications of endocarditis

Patients with infective endocarditis can develop the following complications:

  • Myocardial infarction - This complication can occur as a result of the microthrombi forming within the left ventricle, getting dislodged, entering the aorta, and then getting into the coronary arteries. Not only do these emboli (thrombus which was dislodged is called an embolus) block the blood flow within the heart, they also contain a vast amount of bacteria, which can further complicate the condition of the patient.
  • Pericarditis - Spread of the inflammation can cause the pericardium to be involved in the inflammatory processes leading to pericarditis. Clinical presentation of pericarditis and myocardial infarction are quite similar, however there are a number of distinctions. The pain caused by pericarditis usually radiates to the lower portion of scapula on the back, or it doesn’t radiate at all. The pain doesn’t change with exertion. Pain gets worse when the patient is lying down or when takes a large breath in.
  • Cardiac arrhythmia - Inflammation caused by infective endocarditis can damage the electrical conduction system of the heart often leading to atrioventricular blocks. This complication can often lead to the need for installing a pacemaker.
  • Cardiac valvular insufficiency - Infective endocarditis, overtime, leads to the destruction of heart valves preventing them from fully closing and creating a backward flow of blood which creates a major strain on the heart. Overtime, this leads to congestive heart failure as the heart is no longer able to handle the added strain.
  • Congestive heart failure due to valvular (especially aortic) insufficiency - the most common complications of subacute endocarditis. It develops usually after months if the endocarditis is left untreated. Sometimes, however, it can appear a full year after the disease was treated using antibiotics.
  • Stroke and organ damage - Infective endocarditis triggers the formation of parietal blood clots. These thrombi contain a large number of bacteria which can sometimes break loose and travel to the brain, lungs, kidneys, abdominal organs (mesenteric and splenic abscesses or infarct) and extremities. This can result in stroke or formation of abscesses in the affected organs and tissues. Moreover, if the infective endocarditis was caused by fungi, this can result in severe consequences since fungi are more resistant to therapy than bacteria.  Due to the use of antibiotics, the emboli are usually sterile, causing a lot less damage than in the pre-antibiotic era. If the patient has an acute form of infective endocarditis caused by S. aureus, multiple abscesses can quickly form throughout the body damaging the kidneys, the heart and the brain.
  • Aortic root or myocardial abscesses - These abscesses form as a result of spreading infection throughout the blood stream and are usually the result of an acute infective endocarditis.
  • Glomerulonephritis and acute renal failure - Glomerulonephritis happens as a result of the damage caused by immune complex deposition, emboli causing renal infarction, thrombotic microangiopathy and direct invasion of the parenchyma by microorganisms. All these factors can lead to acute renal failure which immediately calls for hemodialysis until the patient is stabilized.


Prognosis of infective endocarditis largely depends on whether complications develop or not. If it is left untreated, this disease is usually fatal. Early detection and proper treatment can be lifesaving. Overall the mortality rate of infective endocarditis is 14.5%; however the numbers vary largely depending on the microbial pathogen that has caused the disease. For example, acute endocarditis caused by S. aureus is the most dangerous with 30-40% mortality rate.

Cure rates depending on the type of infection that caused infective endocarditis:

  • Streptococcus viridans and bovis – 98%
  • Enterococci and Staphylococcus aureus in people who abuse intravenous drugs – 90%
  • Community-acquired Staphylococcus aureus in people who do not abuse intravenous drugs – 60-70%
  • Aerobic gram-negative organisms – 40-60%
  • Fungal organisms – less than 50%.



To learn more about Cardiology, we recommend the following websites: