Infective Endocarditis With Coronary Artery Embolization and Multisystem Involvement in a Patient With a History of IV Drug Use: A Case Report

Abstract

Background

Infective endocarditis (IE) is a rare cause of myocardial infarction (MI). In contrast to other embolic phenomena associated with IE, the incidence of coronary embolism is <1 % with a mortality rate of >65 %. Common risk factors of IE include intravenous drug use (IVDU), hemodialysis and the use of cardiac devices. We present a unique case of multiple coronary artery involvement on 2 separate occasions highlighting the need for increased awareness among healthcare professionals.

Case report

A 38-year-old female with history of IVDU, hepatitis B and C presented with acute chest pain and was found to have NSTEMI and active aortic valve vegetation. Left heart catheterization (LHC) revealed an occlusion of the right coronary artery (RCA), which was treated with stent placement. However, on experiencing ventricular fibrillation on hospital day 2, a repeat cardiac catheterization revealed a re-occlusion of RCA proximal to the stent as well as occlusion of the first obtuse marginal artery (OM1). Subsequent investigations also revealed multiple intraparenchymal hemorrhages and probable renal infarcts. The involvement of multiple systems, as well as the occlusion of multiple coronary arteries on separate occasions distinguishes this case from previously reported cases.

Conclusion

Timely intervention is critical in the management of MI due to septic embolism. A high index of suspicion and immediate action can be lifesaving. Early diagnostic imaging and percutaneous or surgical interventions can improve patient outcomes. Greater awareness of multisystem and multi-coronary artery embolic phenomena is needed.

1. Introduction

Infective endocarditis (IE) is frequently associated with systemic embolization; however, coronary artery embolism resulting in myocardial infarction (MI) is an exceedingly rare event, reported in fewer than 1 % of IE cases and carrying a mortality rate as high as 64 %.1,2 Sudden cardiac death is the first clinical manifestation in nearly 25–40 % of such presentations.4 The incidence of these events has risen in parallel with an expanding at-risk population—namely, individuals with intravenous drug use (IVDU), those receiving hemodialysis, and patients with intracardiac devices.3 Although successful management of septic coronary embolism has been reported, prognosis remains grim, particularly in the setting of active bacteremia.5 (see Figs. 1–3)

Fig. 1.

Coronary angiogram showing haziness (arrow) in the first obtuse marginal (OM1) branch suggestive of septic embolism.

Fig. 2.

Non-contrast CT head showing acute hemorrhages in the right temporal and left parietal lobes, with subarachnoid blood in adjacent sulci.

Fig. 3.

Abdominal CT showing bilateral striated nephrograms and a hypoenhancing area in the right kidney indicating infarction.

Diagnosis often relies on clinical suspicion, electrocardiography, cardiac imaging (e.g., MRI), and positive blood cultures. Cardiac catheterization, while both diagnostic and potentially therapeutic, poses a heightened risk of further embolization—especially when the aortic valve is involved. Adjunct investigations such as brain MRI may be warranted to detect concomitant cerebral emboli or hemorrhage.

This case is unique for RCA infarction secondary to infective endocarditis followed by reinfarction of RCA, along with OM1 involvement and multi-system embolization to the brain and kidneys.

2. Case presentation

A 38-year-old Caucasian female with a history of chronic IVDU (fentanyl) and untreated chronic hepatitis B/C presented with acute-onset chest pain of 24-h duration. Her symptoms included pressure-like, non-radiating pain, diffuse myalgias, and anorexia. She was afebrile and denied fever, chills, dyspnea, nausea, or vomiting. Her vitals were notable for tachycardia (heart rate 108 beats/minute) with otherwise normal hemodynamics. BMI was 26.7. She had no known HIV, psychiatric disorders, or traditional cardiovascular risk factors. Urine toxicology was negative. Given positive blood cultures, a history of IVDU, and absence of autoimmune disease, bacterial endocarditis was favored over Libman-Sacks endocarditis.

On physical exam, she appeared acutely ill and in visible distress. Cardiac auscultation revealed a soft diastolic murmur at the left lower sternal border. Dermatologic exam showed track marks consistent with IVDU, livedo reticularis, and petechiae on her lower limbs. Neurologic evaluation was non-focal. Lungs and abdomen were unremarkable. Serum lactate was within normal limits.

The patient presented with ongoing chest pain. ECG showed deep T-wave inversions in leads II, III, and aVF, with no prior tracings for comparison. Troponin was >10,000 ng/L and CK was 7900 U/L. Given ischemic symptoms and biomarker elevation, emergent coronary angiography was performed. A nitro-glycerine infusion was started, and CTA chest ruled out pulmonary embolism. Chest X-ray was normal.

She was found to be thrombocytopenic (platelets: 50,000/μL). Differential included sepsis-associated coagulopathy and hepatitis-related thrombocytopenia. Workup for cryoglobulinemia, thrombotic microangiopathy, and HIT was negative. Due to moderate HIT risk, bivalirudin was used instead of heparin.

Left heart catheterization with a Judkins left 4 (JL4) catheter revealed 80 % occlusion of the proximal right coronary artery (RCA) due to embolic material, with no angiographic evidence of atherosclerosis. The remaining coronary arteries were patent. A drug-eluting stent was placed in the RCA, restoring thrombolysis in myocardial infarction (TIMI) 3 flow. Left ventriculography was deferred due to concern for additional embolization. The clinical picture raised high suspicion for IE, with the RCA lesion likely representing the first sign of the disease.

Transthoracic echocardiography (TTE) revealed a suspicious aortic valve vegetation, prompting Transoesophageal echocardiography (TEE), which confirmed a mobile 2.7 cm vegetation on the right coronary cusp of a trileaflet aortic valve. There was no aortic stenosis or regurgitation. Left ventricular ejection fraction (LVEF) was 50–55 %, but the septum was dyskinetic, likely due to right-sided volume overload. The right ventricle was dilated; the left heart was otherwise structurally normal.

On hospital day 2, the patient experienced a ventricular fibrillation arrest requiring one defibrillation and brief CPR. Amiodarone was initiated for rhythm control. Repeat angiography revealed new 95 % occlusion of the proximal OM1 branch with severe haziness (suggestive of embolism) and 50 % in-stent restenosis in the RCA. Percutaneous transluminal coronary angioplasty (PTCA) of the OM1 was performed.

Repeat TEE demonstrated a precipitous decline in LVEF to 10–15 %. CT head showed multiple foci of acute intraparenchymal hemorrhage—the largest being 1.3 cm in the right temporal lobe and 0.9 cm in the left parietal lobe—with associated subarachnoid hemorrhage. No hydrocephalus or mass effect was identified.

She subsequently developed hypothermia, lactic acidosis, and acute kidney injury (creatinine rose from 1.1 to 2.2 mg/dL). Abdominal CT revealed bilateral striated nephrograms and a hypoenhancing lesion in the right renal lower pole—suggestive of infarction—alongside colitis, possibly due to mesenteric ischemia.

Empiric antibiotics (vancomycin and piperacillintazobactam) were initiated upon admission. Blood cultures later grew MRSA. Sodium bicarbonate was given for acidosis. Due to combined septic and cardiogenic shock, vasopressors were started. Continuous renal replacement therapy (CRRT) was initiated with subsequent creatinine improvement (peak 2.7 to 1.5 mg/dL). Anticoagulation was withheld due to intracranial hemorrhage and stent-associated risks. Her hepatitis C viral load was 30,235 IU/mL but was not addressed given her critical status. Despite intensive multidisciplinary care, the patient unfortunately succumbed to multiorgan failure on the 4th day of hospitalization.

3. Discussion

Systemic embolization occurs in 20–50 % of patients with IE.4 Coronary artery embolism is an uncommon but devastating complication, with incidence under 1 % and a high associated mortality.1,2

Large (>10 mm) and mobile vegetations confer increased embolic risk.2,8 Staphylococcus aureus is the most frequently implicated pathogen, responsible for approximately one-third of cases.13,14 Coronary embolism in IE most commonly affects the left anterior descending (LAD) due to its anatomical trajectory,6,7 though mitral vegetations have also been implicated in non-coronary embolic events.11

In this case, the RCA was initially affected—an atypical finding—followed by OM1 embolism and re-occlusion of the RCA within 24 h. Such sequential multi-vessel involvement is rarely documented and underscores the aggressive embolic potential of this infection.

Differential mechanisms of coronary involvement in IE include direct septic embolism, extrinsic compression from periannular abscesses, coronary ostial occlusion by vegetations, and coronary hypoperfusion secondary to valvular dysfunction.2,7 In a Spanish case series (n = 586), the most frequent etiology was extrinsic compression, followed by embolism.2

Diagnosis of septic coronary embolism requires a high index of suspicion. ECG changes, elevated biomarkers, and echocardiographic detection of vegetations support the diagnosis. Angiography, while helpful in differentiating embolic from atherosclerotic lesions, is approached cautiously in aortic valve IE due to embolic risk.6,9

Treatment hinges on IV antibiotics for 4–6 weeks.13 Anticoagulation is generally avoided due to risks of hemorrhage, especially cerebral.4,10 PCI is reserved for ongoing ischemia or hemodynamic instability. Surgery may be warranted for large vegetations or structural valvular compromise.3 In cases of intracranial hemorrhage, surgical intervention is typically deferred. In a Japanese multicenter study (n = 181), early surgery (2–7 days post-stroke) led to neurological deterioration in 44 % of patients, compared to only 2.3 % when surgery was delayed >4 weeks.15

Angioplasty and stenting also pose procedural hazards. Angioplasty may dislodge vegetations, and stenting has been associated with mycotic aneurysm formation.2,12

4. Conclusion

Septic coronary embolism, though rare, can present as acute MI and should be promptly considered in select high-risk patients to guide timely and appropriate intervention. This case illustrates an unusual presentation of rapidly progressive, multi-vessel coronary embolism due to aortic valve endocarditis. The complexity of diagnosis, the evolving nature of embolic events, and therapeutic dilemmas emphasize the need for heightened awareness and a tailored, multidisciplinary management strategy. In young patients with atypical MI presentations and risk factors such as IVDU, septic coronary embolism should always be considered as a differential diagnosis. In conclusion, patients with infective endocarditis and atypical presentations of myocardial infarction, particularly those with risk factors like intravenous drug use, septic coronary embolism should be considered early to guide timely intervention and avoid fatal multisystem complications.