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Thrombus or vegetation: A mystery causing ST elevation myocardial infarction with infective endocarditis of mechanical aortic valve
Cardiovascular Revascularization Medicine xxx (2017) xxx–xxx
Contents lists available at ScienceDirect
Cardiovascular Revascularization Medicine
Thrombus or vegetation: A mystery causing ST elevation myocardial infarction with infective endocarditis of mechanical aortic valve☆ Safi U Khan ⁎, Ahmad N Lone, Charumathi Raghu Subramanian, Michael DePersis, Daniel Sporn Guthrie Clinic/Robert Packer Hospital, Sayre, PA, 18850
a r t i c l e
i n f o
Article history: Received 27 January 2017 Received in revised form 24 February 2017 Accepted 1 March 2017 Available online xxxx Keywords: STEMI, infective endocarditis Septic embolism Prosthetic cardiac valves
a b s t r a c t 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. © 2017 Elsevier Inc. All rights reserved.
1. Introduction Acute myocardial infarction as a result of septic embolization from an infected cardiac valve is a rare phenomenon [1]. 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 Abbreviations: ACS, Acute coronary syndrome; AIVR, Accelerated idioventricular rhythm; CCU, Cardiac care unit; COPD, Chronic obstructive pulmonary disease; IE, Infective Endocarditis; LAD, Left anterior descending artery; MI, Myocardial Infarction; PCI, Percutaneous coronary intervention; PICC, Peripherally inserted central catheter; STEMI, ST segment elevation myocardial infarction; LAD, left anterior descending artery; RCA, right coronary artery; LCX, left circumflex artery; PDA, posterior descending artery; CABG, coronary artery bypass grafting; AVR, aortic valve replacement; MVR, mitral valve replacement; TPA, tissue plasminogen activator. ☆ Conflict of interests: none. ⁎ Corresponding author at: Guthrie Clinic/Robert Packer Hospital, Department of Medicine, One Guthrie Square, Sayre, PA. Tel.: +1 570 867 3444. E-mail address: safi[email protected] (S.U. Khan).
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 periapical 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
http://dx.doi.org/10.1016/j.carrev.2017.03.005 1553-8389/© 2017 Elsevier Inc. All rights reserved.
Please cite this article as: Khan SU, et al, Thrombus or vegetation: A mystery causing ST elevation myocardial infarction with infective endocarditis of mechanical aortic valv..., Cardiovasc Revasc Med (2017), http://dx.doi.org/10.1016/j.carrev.2017.03.005
2
S.U. Khan et al. / Cardiovascular Revascularization Medicine xxx (2017) xxx–xxx
Fig. 1. Transesophageal echocardiogram showing echogenic structure on prosthetic aortic valve.
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
Fig. 2. Electrocardiogram showing ST elevations in leads V2-V6.
Please cite this article as: Khan SU, et al, Thrombus or vegetation: A mystery causing ST elevation myocardial infarction with infective endocarditis of mechanical aortic valv..., Cardiovasc Revasc Med (2017), http://dx.doi.org/10.1016/j.carrev.2017.03.005
S.U. Khan et al. / Cardiovascular Revascularization Medicine xxx (2017) xxx–xxx
Fig. 3. Cardiac catheterization showing subtle cutoff at distal portion of Left anterior descending artery.
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.
3
A case series of 40 patients with ACS from the data base of 15,878 showed 60% of them had aortic prosthetic valve, 22.5% patients had mitral valve prosthesis and 17.5% carried both [7]. The main dilemma in our case was optimal treatment strategy for the patient. There is lack of definite evidence for best treatment option in AMI with IE [8]. Thrombolytics are relatively contraindicated as they pose higher risk of cerebral bleeding due to mycotic aneurysms or silent cerebral micro infarctions [9]. Percutaneous coronary intervention (PCI) also carries its own risks. There is always a substantial risk of distal embolization of vegetation or stent infection if later is deployed in infected site. Balloon angioplasty is also difficult as the vessel wall does generally have native atherosclerosis making it very compliant and prone to reocclusion [10,11]. Aspiration thrombectomy has thus far been believed to be the safest option though data is very limited [11,12]. On the other hand, AMI due to embolization in the setting of prosthetic valves is treated with anticoagulation with heparin, thrombolytics and PCI [13]. Table 1 provides a brief summary of different management strategies employed in STEMI with IE due to septic embolism. We adhered to more conservative approach due to limited treatment options. Anticoagulation with heparin in addition to aspirin was employed. Fortunately, her ST elevation was resolved within 1 h with complete resolution of chest pain (Fig. 4). Heparin was continued and higher doses of Warfarin were employed to reach target therapeutic INR more aggressively. Her infected prosthetic aortic valve was successfully replaced and she was clinically stable on day of discharge.
4. Conclusion 3. Discussion Acute myocardial infarction (AMI) is a rare complication of infective endocarditis [1]. The literature reports only 0.3% coronary embolization rate in infective endocarditis (IE) [2]. Manzano et al. has reported the incidence and mortality rates of ACS with IE to be 2.9% and 64% respectively. The LAD was the most commonly affected vessel in coronary circulation and coronary embolization was most frequently associated with aortic valve endocarditis [3]. The other possible explanation in our patient was systemic embolization due to mechanical valves with inadequate INR. AMI in the setting of mechanical valves (aortic and mitral) and sub therapeutic INR have been reported in several cases [4–6].
This case demonstrates the necessity of always having septic embolism high in differential diagnosis for acute myocardial infarction when the patient is already being treated for IE. Antibiotics along with other medications have well known interactions with Warfarin and they tend to affect the INR values. In a patient with mechanical cardiac valves, INR should always be placed in therapeutic range and cautious dose adjustments of Warfarin to keep INR in restricted range to avoid cerebral bleeding due to possible mycotic aneurysm. Therefore, daily neurological assessment is important. Given the rarity of this phenomenon, thus far there is no consensus as regards optimal management strategy and each patient must be dealt on a case by case basis.
Table 1 Summary of previously reported cases of ST elevation MI secondary to infective endocarditis with treatment strategies and outcomes. Study
Age Sex
Vessel
Organism
Treatment strategy
Outcome
Beldner et al. [14] DeKam et al. [15] DiSalvo et al. [16] Glazier et al. [17]
31 85 49 37
Female Male Male Male
LAD Diagonal LAD LAD
Lactobacillus Coagulase negative Staphylococcus Streptococcus viridians Streptococcus bovis
PCI with stenting and MVR Aspiration thrombectomy TPA PCI with stenting and AVR
Gultekin et al. [18] Herzog et al. [10] Hibbert et al. [19]
40 38 53
Male Male Male
LAD LAD LAD
Coagulase negative Staphylococcus Nutritionally variant strep Staphylococcus aureus
Hohmann et al. [20] Okai et al. [21] Perera et al. [22]
16 53 54
Female LAD Male LAD Female LCX
Roxas and Weekes et al. [23] Roxas and Weekes et al. [23] Singh et al. [8] Winkler et al. [24]
39
Female LAD
Streptococcus mitis Streptococcus sangius Staphylococcus aureus and Enterococcus fecalis Staphylococcus (unspecified)
PCI and conservative Balloon angioplasty Aspiration thrombectomy and PCI with stenting PCI with stenting CABG+MVR TPA
Alive Alive Died Not reported Died Alive Died
56
Male
LAD and PDA
70 67
Male Male
70
Male
RCA LAD and first diagonal LCX
Wojciuk et al. [25]
Alive Alive Died
TPA and MVR
Alive
Streptococcus bovis
CABG and AVR
MRSA Gamella
PCI with stenting PCI and conservative
Not reported Died Died
Β hemolytic Streptococcus group G
Aspiration thrombectomy
Alive
LAD = left anterior descending artery; RCA = right coronary artery; LCX = left circumflex artery; PDA = posterior descending artery; CABG = coronary artery bypass grafting; AVR = aortic valve replacement; MVR = mitral valve replacement; TPA = tissue plasminogen activator.
Please cite this article as: Khan SU, et al, Thrombus or vegetation: A mystery causing ST elevation myocardial infarction with infective endocarditis of mechanical aortic valv..., Cardiovasc Revasc Med (2017), http://dx.doi.org/10.1016/j.carrev.2017.03.005
4
S.U. Khan et al. / Cardiovascular Revascularization Medicine xxx (2017) xxx–xxx
Fig. 4. Electrocardiogram showing resolution of ST elevations.
Funding This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. Acknowledgment None. References [1] Brunson JG. Coronary embolism in bacterial endocarditis. Am J Pathol 1953;29(4):689–701. [2] Fabri Jr J, Issa VS, Pomerantzeff PM, Grinberg M, Barretto AC, Mansur AJ. Timerelated distribution, risk factors and prognostic influence of embolism in patients with left-sided infective endocarditis. Int J Cardiol 2006;110(3):334–9. [3] Manzano MC, Vilacosta I, San Roman JA, Aragoncillo P, Sarria C, Lopez D, et al. Acute coronary syndrome in infective endocarditis. Rev Esp Cardiol 2007;60(1):24–31. [4] Sial JA, Ferman MT, Saghir T, Rasool SI. Coronary embolism causing acute myocardial infarction in a patient with mitral valve prosthesis: successful management with angioplasty. J Pak Med Assoc 2009;59(6):409–11. [5] Nakazone MA, Tavares BG, Machado MN, Maia LN. Acute myocardial infarction due to coronary artery embolism in a patient with mechanical aortic valve prosthesis. Case Rep Med 2010;2010:751857. [6] Levis JT, Schultz G, Lee PC. Acute myocardial infarction due to coronary artery embolism in a patient with a tissue aortic valve replacement. Perm J 2011;15(3):82–6. [7] Iakobishvili Z, Eisen A, Porter A, Cohen N, Abramson E, Mager A, et al. Acute coronary syndromes in patients with prosthetic heart valves-a case-series. Acute Card Care 2008;10(3):148–51. [8] Singh M, Mishra A, Kaluski E. Acute ST-elevation myocardial infarction due to septic embolism: a case report and review of management options. Catheter Cardiovasc Interv 2015;85(6):E166–71. [9] Hunter AJ, Girard DE. Thrombolytics in infectious endocarditis associated myocardial infarction. J Emerg Med 2001;21(4):401–6. [10] Herzog CA, Henry TD, Zimmer SD. Bacterial endocarditis presenting as acute myocardial infarction: a cautionary note for the era of reperfusion. Am J Med 1991;90(3):392–7.
[11] Overend L, Rose E. Uncertainties in managing myocardial infarction associated with infective endocarditis. Exp Clin Cardiol 2012;17(3):144–5. [12] Baek MJ, Kim HK, Yu CW, Na CY. Mitral valve surgery with surgical embolectomy for mitral valve endocarditis complicated by septic coronary embolism. Eur J Cardiothorac Surg 2008;33(1):116–8. [13] Atas H, Sari I, Delil K, Ileri C, Samadov F. Acute inferior myocardial infarction in a patient with a prosthetic aortic valve and high international normalized ratio. Postepy Kardiol Interwencyjnej 2014;10(1):63–5. [14] Beldner S, Bajwa A, Kaplan B, Rosen S, Steinberg B, Cacciabaudo J. Septic coronary embolism. J Interv Cardiol 2002;15(4):301–4. [15] Dekam MJ, Depta JP, Lincoff AM. A rare complication of infective endocarditis. Cleve Clin J Med 2010;77(5):296–7. [16] Di Salvo TG, Tatter SB, O'Gara PT, Nielsen GP, DeSanctis RW. Fatal intracerebral hemorrhage following thrombolytic therapy of embolic myocardial infarction in unsuspected infective endocarditis. Clin Cardiol 1994;17(6):340–4. [17] Glazier JJ, McGinnity JG, Spears JR. Coronary embolism complicating aortic valve endocarditis: treatment with placement of an intracoronary stent. Clin Cardiol 1997; 20(10):885–8. [18] Gultekin N, Kucukates E, Bulut G. A coronary septic embolism in double prosthetic valve endocarditis presenting as acute Anteroseptal ST-segment-elevation myocardial infarction. Balkan Med J 2012;29(3):328–30. [19] Hibbert B, Kazmi M, Veinot JP, O'Brien ER, Glover C. Infective endocarditis presenting as ST-elevation myocardial infarction: an angiographic diagnosis. Can J Cardiol 2012; 28(4):515.e15–7. [20] Hohmann D, Bertram H, Schieffer B, Wessel A. Acute myocardial infarction in a 16year-old girl caused by infective endocarditis of a bicuspid aortic valve. Pediatr Cardiol 2011;32(4):534–5. [21] Okai I, Inoue K, Yamaguchi N, Makinae H, Maruyama S, Komatsu K, et al. Infective endocarditis associated with acute myocardial infarction caused by septic emboli. J Cardiol Cases 2010;1(1):e28–32. [22] Perera R, Noack S, Dong W. Acute myocardial infarction due to septic coronary embolism. N Engl J Med 2000;342(13):977–8. [23] Roxas CJ, Weekes AJ. Acute myocardial infarction caused by coronary embolism from infective endocarditis. J Emerg Med 2011;40(5):509–14. [24] Winkler J, Chaudhry SP, Stockwell PH. Gemella endocarditis presenting as an STsegment-elevation myocardial infarction. Tex Heart Inst J 2016;43(3):258–60. [25] Wojciuk J, Goode GK, More RS. Unusual presentation of endocarditis as inferior STEMI. Eur Heart J 2012;33(19):2499.
Please cite this article as: Khan SU, et al, Thrombus or vegetation: A mystery causing ST elevation myocardial infarction with infective endocarditis of mechanical aortic valv..., Cardiovasc Revasc Med (2017), http://dx.doi.org/10.1016/j.carrev.2017.03.005
Contents lists available at ScienceDirect
Cardiovascular Revascularization Medicine
Thrombus or vegetation: A mystery causing ST elevation myocardial infarction with infective endocarditis of mechanical aortic valve☆ Safi U Khan ⁎, Ahmad N Lone, Charumathi Raghu Subramanian, Michael DePersis, Daniel Sporn Guthrie Clinic/Robert Packer Hospital, Sayre, PA, 18850
a r t i c l e
i n f o
Article history: Received 27 January 2017 Received in revised form 24 February 2017 Accepted 1 March 2017 Available online xxxx Keywords: STEMI, infective endocarditis Septic embolism Prosthetic cardiac valves
a b s t r a c t 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. © 2017 Elsevier Inc. All rights reserved.
1. Introduction Acute myocardial infarction as a result of septic embolization from an infected cardiac valve is a rare phenomenon [1]. 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 Abbreviations: ACS, Acute coronary syndrome; AIVR, Accelerated idioventricular rhythm; CCU, Cardiac care unit; COPD, Chronic obstructive pulmonary disease; IE, Infective Endocarditis; LAD, Left anterior descending artery; MI, Myocardial Infarction; PCI, Percutaneous coronary intervention; PICC, Peripherally inserted central catheter; STEMI, ST segment elevation myocardial infarction; LAD, left anterior descending artery; RCA, right coronary artery; LCX, left circumflex artery; PDA, posterior descending artery; CABG, coronary artery bypass grafting; AVR, aortic valve replacement; MVR, mitral valve replacement; TPA, tissue plasminogen activator. ☆ Conflict of interests: none. ⁎ Corresponding author at: Guthrie Clinic/Robert Packer Hospital, Department of Medicine, One Guthrie Square, Sayre, PA. Tel.: +1 570 867 3444. E-mail address: safi[email protected] (S.U. Khan).
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 periapical 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
http://dx.doi.org/10.1016/j.carrev.2017.03.005 1553-8389/© 2017 Elsevier Inc. All rights reserved.
Please cite this article as: Khan SU, et al, Thrombus or vegetation: A mystery causing ST elevation myocardial infarction with infective endocarditis of mechanical aortic valv..., Cardiovasc Revasc Med (2017), http://dx.doi.org/10.1016/j.carrev.2017.03.005
2
S.U. Khan et al. / Cardiovascular Revascularization Medicine xxx (2017) xxx–xxx
Fig. 1. Transesophageal echocardiogram showing echogenic structure on prosthetic aortic valve.
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
Fig. 2. Electrocardiogram showing ST elevations in leads V2-V6.
Please cite this article as: Khan SU, et al, Thrombus or vegetation: A mystery causing ST elevation myocardial infarction with infective endocarditis of mechanical aortic valv..., Cardiovasc Revasc Med (2017), http://dx.doi.org/10.1016/j.carrev.2017.03.005
S.U. Khan et al. / Cardiovascular Revascularization Medicine xxx (2017) xxx–xxx
Fig. 3. Cardiac catheterization showing subtle cutoff at distal portion of Left anterior descending artery.
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.
3
A case series of 40 patients with ACS from the data base of 15,878 showed 60% of them had aortic prosthetic valve, 22.5% patients had mitral valve prosthesis and 17.5% carried both [7]. The main dilemma in our case was optimal treatment strategy for the patient. There is lack of definite evidence for best treatment option in AMI with IE [8]. Thrombolytics are relatively contraindicated as they pose higher risk of cerebral bleeding due to mycotic aneurysms or silent cerebral micro infarctions [9]. Percutaneous coronary intervention (PCI) also carries its own risks. There is always a substantial risk of distal embolization of vegetation or stent infection if later is deployed in infected site. Balloon angioplasty is also difficult as the vessel wall does generally have native atherosclerosis making it very compliant and prone to reocclusion [10,11]. Aspiration thrombectomy has thus far been believed to be the safest option though data is very limited [11,12]. On the other hand, AMI due to embolization in the setting of prosthetic valves is treated with anticoagulation with heparin, thrombolytics and PCI [13]. Table 1 provides a brief summary of different management strategies employed in STEMI with IE due to septic embolism. We adhered to more conservative approach due to limited treatment options. Anticoagulation with heparin in addition to aspirin was employed. Fortunately, her ST elevation was resolved within 1 h with complete resolution of chest pain (Fig. 4). Heparin was continued and higher doses of Warfarin were employed to reach target therapeutic INR more aggressively. Her infected prosthetic aortic valve was successfully replaced and she was clinically stable on day of discharge.
4. Conclusion 3. Discussion Acute myocardial infarction (AMI) is a rare complication of infective endocarditis [1]. The literature reports only 0.3% coronary embolization rate in infective endocarditis (IE) [2]. Manzano et al. has reported the incidence and mortality rates of ACS with IE to be 2.9% and 64% respectively. The LAD was the most commonly affected vessel in coronary circulation and coronary embolization was most frequently associated with aortic valve endocarditis [3]. The other possible explanation in our patient was systemic embolization due to mechanical valves with inadequate INR. AMI in the setting of mechanical valves (aortic and mitral) and sub therapeutic INR have been reported in several cases [4–6].
This case demonstrates the necessity of always having septic embolism high in differential diagnosis for acute myocardial infarction when the patient is already being treated for IE. Antibiotics along with other medications have well known interactions with Warfarin and they tend to affect the INR values. In a patient with mechanical cardiac valves, INR should always be placed in therapeutic range and cautious dose adjustments of Warfarin to keep INR in restricted range to avoid cerebral bleeding due to possible mycotic aneurysm. Therefore, daily neurological assessment is important. Given the rarity of this phenomenon, thus far there is no consensus as regards optimal management strategy and each patient must be dealt on a case by case basis.
Table 1 Summary of previously reported cases of ST elevation MI secondary to infective endocarditis with treatment strategies and outcomes. Study
Age Sex
Vessel
Organism
Treatment strategy
Outcome
Beldner et al. [14] DeKam et al. [15] DiSalvo et al. [16] Glazier et al. [17]
31 85 49 37
Female Male Male Male
LAD Diagonal LAD LAD
Lactobacillus Coagulase negative Staphylococcus Streptococcus viridians Streptococcus bovis
PCI with stenting and MVR Aspiration thrombectomy TPA PCI with stenting and AVR
Gultekin et al. [18] Herzog et al. [10] Hibbert et al. [19]
40 38 53
Male Male Male
LAD LAD LAD
Coagulase negative Staphylococcus Nutritionally variant strep Staphylococcus aureus
Hohmann et al. [20] Okai et al. [21] Perera et al. [22]
16 53 54
Female LAD Male LAD Female LCX
Roxas and Weekes et al. [23] Roxas and Weekes et al. [23] Singh et al. [8] Winkler et al. [24]
39
Female LAD
Streptococcus mitis Streptococcus sangius Staphylococcus aureus and Enterococcus fecalis Staphylococcus (unspecified)
PCI and conservative Balloon angioplasty Aspiration thrombectomy and PCI with stenting PCI with stenting CABG+MVR TPA
Alive Alive Died Not reported Died Alive Died
56
Male
LAD and PDA
70 67
Male Male
70
Male
RCA LAD and first diagonal LCX
Wojciuk et al. [25]
Alive Alive Died
TPA and MVR
Alive
Streptococcus bovis
CABG and AVR
MRSA Gamella
PCI with stenting PCI and conservative
Not reported Died Died
Β hemolytic Streptococcus group G
Aspiration thrombectomy
Alive
LAD = left anterior descending artery; RCA = right coronary artery; LCX = left circumflex artery; PDA = posterior descending artery; CABG = coronary artery bypass grafting; AVR = aortic valve replacement; MVR = mitral valve replacement; TPA = tissue plasminogen activator.
Please cite this article as: Khan SU, et al, Thrombus or vegetation: A mystery causing ST elevation myocardial infarction with infective endocarditis of mechanical aortic valv..., Cardiovasc Revasc Med (2017), http://dx.doi.org/10.1016/j.carrev.2017.03.005
4
S.U. Khan et al. / Cardiovascular Revascularization Medicine xxx (2017) xxx–xxx
Fig. 4. Electrocardiogram showing resolution of ST elevations.
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Please cite this article as: Khan SU, et al, Thrombus or vegetation: A mystery causing ST elevation myocardial infarction with infective endocarditis of mechanical aortic valv..., Cardiovasc Revasc Med (2017), http://dx.doi.org/10.1016/j.carrev.2017.03.005