What is the diagnosis and cause of death for a patient with a history of intravenous (IV) drug use, presenting with fever, heart murmur, splenomegaly, splinter hemorrhages, and elevated creatine kinase-muscle band (CK-MB), who experiences sudden cardiac arrest with autopsy findings of aortic valve destruction?

Infective Endocarditis in an IV Drug User with Sudden Cardiac Death

This patient has acute bacterial endocarditis caused by Staphylococcus aureus with aortic valve destruction leading to sudden cardiac death from either acute severe aortic regurgitation causing ventricular tachycardia/fibrillation, coronary artery embolism, or myocardial abscess with conduction system disruption.

A. Expected Blood Culture Results

Blood cultures will most likely grow Staphylococcus aureus, which is the predominant pathogen in IV drug users with endocarditis. 1, 2

• S. aureus causes acute endocarditis and can develop on normal valves, particularly in IV drug users 1
• While right-sided (tricuspid) endocarditis is more common in IV drug users (60-70% of cases), this patient has left-sided disease involving the aortic valve 2, 3
• Left-sided endocarditis in IV drug users occurs in 20-30% of cases and carries significantly worse prognosis than right-sided disease 2, 3
• The organism is most commonly methicillin-sensitive S. aureus (MSSA) in most geographic areas, though methicillin-resistant S. aureus (MRSA) occurs in 30-40% of cases 3, 4

Alternative organisms to consider:

• Streptococcal species (less common in acute presentations) 1
• Enterococci 1
• Gram-negative bacilli (rare, worse prognosis) 3
• Polymicrobial infection (2-5% of IV drug user cases) 3

B. Explanation of Splinter Hemorrhages

Splinter hemorrhages are peripheral embolic phenomena resulting from septic microemboli from the infected aortic valve vegetations lodging in the nail bed capillaries. 5

• These represent a minor criterion in the modified Duke criteria for diagnosing infective endocarditis under "immunological phenomena" 5
• They occur alongside other peripheral stigmata including Osler nodes, Janeway lesions, petechiae, and Roth spots 5
• The presence of splinter hemorrhages with fever, new murmur, and splenomegaly strongly suggests the diagnosis of infective endocarditis 5
• Embolic phenomena affect 30% of patients with infective endocarditis and can involve brain, lung, spleen, or peripheral vasculature 5

The splenomegaly in this case represents:

• Septic emboli to the spleen causing infarction and/or abscess formation 1
• Immune complex deposition and chronic antigenic stimulation 5

C. Cause of Death

The sudden cardiac arrest resulted from acute aortic regurgitation secondary to cuspal destruction, which triggered fatal ventricular arrhythmias. 1

Primary Mechanisms of Death in Aortic Valve Endocarditis:

1. Acute Severe Aortic Regurgitation Leading to Ventricular Tachycardia/Fibrillation (Most Likely)

• Endocarditis of the aortic valve causes rapid death due to acute valvular disruption 1
• The acute hemodynamic compromise from acute aortic regurgitation can result in ventricular tachycardia 1
• The elevated CK-MB indicates myocardial injury from either ischemia or direct myocardial involvement 1
• Development of cardiac rhythm disturbances portends poorly in infective endocarditis 1

2. Coronary Artery Embolism

• Emboli to the coronary arteries from aortic valve vegetations cause acute myocardial infarction and sudden death 1
• This would explain the elevated CK-MB 1

3. Perivalvular Abscess with Conduction System Disruption

• Abscesses in the valvular rings or septum can cause complete heart block or ventricular arrhythmias 1
• Abscess formation occurs more often in aortic than mitral valve endocarditis 1
• New-onset heart block in endocarditis is highly specific for abscess 1
• If the abscess erodes into the septum, it disrupts the conduction system causing fatal arrhythmias 1

4. Myocardial Rupture (Less Common but Documented)

• Transmural extension of infection can cause myocardial wall rupture with hemopericardium and tamponade 1, 6
• Endocarditis has been associated with sudden cardiac death related to tamponade secondary to rupture 1

Prognostic Context:

Left-sided endocarditis in IV drug users carries mortality of 20-30% with medical therapy alone and 15-25% even with surgery. 3, 4

• Overall mortality for left-sided S. aureus endocarditis is 38% 4
• CNS complications increase mortality risk 6-fold in native valve endocarditis 4
• Development of multiple complications (cardiac failure, renal failure, CNS events) exponentially increases mortality risk 4
• Untreated endocarditis is almost always fatal 1

Critical factors that made this case fatal:

• Acute presentation with large vegetations causing cuspal destruction 1
• Left-sided (aortic) involvement rather than right-sided disease 2, 3
• Likely S. aureus infection, which has the highest mortality among endocarditis pathogens 4
• Development of acute valvular disruption before surgical intervention could be performed 1