Abstract
Acute myocardial infarction (MI) in the setting of infective endocarditis (IE) of mechanical cardiac valve is a rare phenomenon. The most challenging aspect is the recognition between septic embolus versus thromboembolism from prosthesis in the setting of sub-therapeutic INR especially when the coronary vasculature is normal and etiology is not clear. We are presenting a case of 56-year-old patient who developed ST elevation MI during treatment of IE of mechanical aortic valve. Cardiac catheterization showed a very subtle blockade at most distal end of LAD therefore percutaneous coronary intervention (PCI) could not be carried out. Given the lack of clear etiology between septic embolus versus prosthesis associated thromboembolism, we opted for a successful conservative approach.
Highlights
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There is limited reporting on ST elevation myocardial infarction (STEMI) secondary to infective endocarditis (IE) of prosthetic cardiac valve.
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We are presenting an interesting case of STEMI where etiology was unclear about septic embolism versus thromboembolism due to prosthesis in the setting of sub therapeutic INR.
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A Successful conservative approach was adopted for the management. This case provided us the opportunity to review the different management strategies in such scenario. Fifteen case reports from literature search are summarized with focus on management and outcomes.
1
Introduction
Acute myocardial infarction as a result of septic embolization from an infected cardiac valve is a rare phenomenon . Similarly, thromboembolism leading to STEMI with prosthetic heart valves in the setting of sub therapeutic INR is also less frequently reported. Acute coronary syndrome (ACS) in the setting of both described situations poses a difficulty in the management. We are presenting a case of 56-year-old female with whom we faced similar situation and her own unique clinical circumstances led us to formulate a management plan. We have also reviewed previous reports with focus on management strategies.
2
Case presentation
A 56-year-old female patient with medical history of mechanical mitral and aortic valves secondary to pneumococcal endocarditis in 2004, moderately severe COPD, hypertension, history of multiple episodes of gastrointestinal bleeding, chronic systolic heart failure and obstructive sleep apnea was admitted with worsening dyspnea on exertion in the setting of acute anemia secondary to gastrointestinal bleeding. Her cardiorespiratory examination was unremarkable. Her hemoglobin (Hgb) was 4 g/dL at the time of presentation. She was transfused with packed red blood cell products to reach the target goal of Hgb 8 g/dL. The source of her gastrointestinal bleeding was arteriovenous malformations in jejunum which were found via enteroscopy and were subsequently treated with argon beam photocoagulation. During the admission, given her known history of mechanical cardiac valves, a transthoracic echocardiogram (TTE) was done to assess status of valves to rule out another potential cause of her shortness of breath. It showed that her aortic valve gradients had dramatically increased from mean and peak gradients of 19 mmHg and 33 mmHg to 61 mmHg and 99 mmHg in 10 months. This had prompted a transesophageal echocardiogram (TEE) which had shown a tiny 26 mm echogenic freely mobile structure on aortic side of prosthesis ( Fig. 1 ). It was unclear initially whether this structure represented a thrombus or vegetation. Blood cultures were drawn and came back positive for oxacillin resistant Staphylococcus epidermidis suffice to suggest she was suffering from infective endocarditis of prosthetic aortic valve. She was started on Vancomycin, Gentamycin and Rifampin. The vegetation was felt to be odontogenic in origin given her poor dentition and peri-apical abscesses involving multiple teeth. They were extracted two days later. Peripherally inserted central catheter (PICC) line was placed and she was discharged with close follow up with infection disease department. Her labs were stable on day of discharge with Hgb of 9.7 g/dL and serum creatinine 1.2 mg/dL.
She was re admitted for acute kidney injury with serum creatinine of 4.4 mg/dL. By now she had completed 3/6 weeks of antibiotics. The most likely etiology was considered to be medication induced renal injury. Nephrology was consulted and they recommended conservative management with intravenous fluids and limiting nephrotoxic medications including Gentamycin. Urine microscopic analysis showed granular casts suggestive of acute tubular necrosis. Vancomycin random levels were noted to be 35.5 at time of presentation therefore it was held initially with serial monitoring of levels. She was continued on Rifampicin. Her renal function started to improve slowly in response to conservative treatment with IV fluids. Vancomycin was resumed when its random level fell below 15. INR was difficult to maintain in therapeutic range due to drug interaction of Rifampicin with Warfarin. Warfarin dosing was cautiously managed given she had history of GI bleeding.
One week into this admission she had sudden onset sub-sternal chest pressure associated with diaphoresis and shortness of breath. A STAT EKG showed ST-elevation (STEMI) in anterior leads (V2-V6) ( Fig. 2 ). Given her underlying renal injury she was a risk for contrast induced nephropathy contemplating dialysis. A discussion was carried with the patient and with her consent a target directed cardiac catheterization in the territory of Left main artery distribution was done. It showed a subtle cut-off at the most distal part of the left ascending artery (LAD) ( Fig. 3 ). Her left circumflex and left main arteries were clear of any disease. Given the distal occlusion percutaneous coronary intervention (PCI) could not be carried out. The most likely explanation of this STEMI was either septic embolism of infected aortic valve or embolisms from mechanical valves in the setting of sub therapeutic INR (1.73). She was placed on heparin infusion and was managed closely in CCU. She had an episode of accelerated idioventricular rhythm (AIVR) which was suggestive of reperfusion. Given the complexity of the disease process, she was transferred to a higher center where she eventually underwent surgical aortic valve replacement. Patient was ultimately discharged to short term rehabilitation center.
2
Case presentation
A 56-year-old female patient with medical history of mechanical mitral and aortic valves secondary to pneumococcal endocarditis in 2004, moderately severe COPD, hypertension, history of multiple episodes of gastrointestinal bleeding, chronic systolic heart failure and obstructive sleep apnea was admitted with worsening dyspnea on exertion in the setting of acute anemia secondary to gastrointestinal bleeding. Her cardiorespiratory examination was unremarkable. Her hemoglobin (Hgb) was 4 g/dL at the time of presentation. She was transfused with packed red blood cell products to reach the target goal of Hgb 8 g/dL. The source of her gastrointestinal bleeding was arteriovenous malformations in jejunum which were found via enteroscopy and were subsequently treated with argon beam photocoagulation. During the admission, given her known history of mechanical cardiac valves, a transthoracic echocardiogram (TTE) was done to assess status of valves to rule out another potential cause of her shortness of breath. It showed that her aortic valve gradients had dramatically increased from mean and peak gradients of 19 mmHg and 33 mmHg to 61 mmHg and 99 mmHg in 10 months. This had prompted a transesophageal echocardiogram (TEE) which had shown a tiny 26 mm echogenic freely mobile structure on aortic side of prosthesis ( Fig. 1 ). It was unclear initially whether this structure represented a thrombus or vegetation. Blood cultures were drawn and came back positive for oxacillin resistant Staphylococcus epidermidis suffice to suggest she was suffering from infective endocarditis of prosthetic aortic valve. She was started on Vancomycin, Gentamycin and Rifampin. The vegetation was felt to be odontogenic in origin given her poor dentition and peri-apical abscesses involving multiple teeth. They were extracted two days later. Peripherally inserted central catheter (PICC) line was placed and she was discharged with close follow up with infection disease department. Her labs were stable on day of discharge with Hgb of 9.7 g/dL and serum creatinine 1.2 mg/dL.
She was re admitted for acute kidney injury with serum creatinine of 4.4 mg/dL. By now she had completed 3/6 weeks of antibiotics. The most likely etiology was considered to be medication induced renal injury. Nephrology was consulted and they recommended conservative management with intravenous fluids and limiting nephrotoxic medications including Gentamycin. Urine microscopic analysis showed granular casts suggestive of acute tubular necrosis. Vancomycin random levels were noted to be 35.5 at time of presentation therefore it was held initially with serial monitoring of levels. She was continued on Rifampicin. Her renal function started to improve slowly in response to conservative treatment with IV fluids. Vancomycin was resumed when its random level fell below 15. INR was difficult to maintain in therapeutic range due to drug interaction of Rifampicin with Warfarin. Warfarin dosing was cautiously managed given she had history of GI bleeding.
One week into this admission she had sudden onset sub-sternal chest pressure associated with diaphoresis and shortness of breath. A STAT EKG showed ST-elevation (STEMI) in anterior leads (V2-V6) ( Fig. 2 ). Given her underlying renal injury she was a risk for contrast induced nephropathy contemplating dialysis. A discussion was carried with the patient and with her consent a target directed cardiac catheterization in the territory of Left main artery distribution was done. It showed a subtle cut-off at the most distal part of the left ascending artery (LAD) ( Fig. 3 ). Her left circumflex and left main arteries were clear of any disease. Given the distal occlusion percutaneous coronary intervention (PCI) could not be carried out. The most likely explanation of this STEMI was either septic embolism of infected aortic valve or embolisms from mechanical valves in the setting of sub therapeutic INR (1.73). She was placed on heparin infusion and was managed closely in CCU. She had an episode of accelerated idioventricular rhythm (AIVR) which was suggestive of reperfusion. Given the complexity of the disease process, she was transferred to a higher center where she eventually underwent surgical aortic valve replacement. Patient was ultimately discharged to short term rehabilitation center.
