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Non Commercial Use Only Clinics and Practice 2017; volume 7:950 Case of acute ST segment elevation myocardial infarction Case Report Correspondence: Ghulam Murtaza, Department of Internal Medicine, East in infective endocarditis- A 56-year-old African American male Tennessee State University, 329 N State of management with intra with history of prostate cancer had under- Franklin Rd, Johnson City, TN, USA 37604. gone open prostatectomy at an outlying hos- Tel.: +14237411863 - Fax: 4239794134. coronary stenting pital, which was followed by a complicated E-mail: [email protected] recovery due to wound dehiscence that ulti- Key words: Endocarditis; myocardial infacr- 1 2 mately led to Enterococcal bacteremia and Ghulam Murtaza, Zia ur Rahman, tion; stent. Puja Sitwala,2 Vatsal Ladia,2 endocarditis. He was started on intravenous Bhavesh Barad,2 Kais Albalbissi,1 gentamicin and ampicillin for 4 weeks Contributions: the authors contributed equally. 2 2 while inpatient and then discharged to com- Timir K. Paul, Vijay Ramu munity nursing home to finish his course of Conflict of interest: the authors declare no 1 Department of Internal Medicine; and antibiotics. One week later he presented to potential conflict of interest. 2Division of Cardiology, East Tennessee our tertiary care center with generalized State University, Johnson City, TN, USA weakness and recurrent falls. Vital signs on Received for publication: 1 February 2017. Revision received: 19 March 2017. admission were blood pressure of 149/78 Accepted for publication: 3 May 2017. mmHg, respiratory rate 17/min, pulse 99 bpm, SaO2 95% on room air. Physical exam This work is licensed under a Creative Abstract showed expiratory wheezing but otherwise Commons Attribution NonCommercial 4.0 unremarkable. Labs were significant for License (CC BY-NC 4.0). Embolic events from infective endo- BUN 41 mg/dL, Cr 5.22 mg/dL, Na 136 ©Copyright G. Murtaza et al., 2017 carditis can cause acute coronary syndrome. meq/L, K4.3meq/L, troponin 0.03 ng/mL, 3 Licensee PAGEPress, Italy Mortality rate is high and optimal manage- WBC count was 14,000/mm , Hb 8.4 g/dL, 3 Clinics and Practice 2017; 7:950 ment might be different from those chosen PLT 505/mm .His baseline creatinine was doi:10.4081/cp.2017.950 in setting of classic atherosclerotic coronary normal. He was found to be in non-oliguric only artery disease. We present a case of 56-year- acute kidney injury likely secondary to gen- old male who had received 5 weeks of tamicin, so ampicillin and gentamicin were antibiotics for aortic valve endocarditis and discontinued and patient was started on dap- Discussion developed acute ST segment elevation tomycin. Electrocardiogram (ECG) showuseed myocardial infarction in hospital settings. normal sinus rhythm without any ST-T Acute ST-segment elevation myocardial Interestingly, patient had recent left heart wave changes. A transthoracic echo was infarction (STEMI) is an uncommon com- catheterization that was normal. This was obtained on which echogenic mass was plication of infective endocarditis with high recognized as embolic event from sterile visualized on aortic valve leaflets measur- mortality rate. In review of 154 patients vegetation. Patient was managed with bal- ing 1.99x1.67 cm with moderate aortic over 6-year period from 1968-1973, coro- regurgitation (Figure 1). Cardiothoracic sur- loon angioplasty and placement of intra- nary embolization was reported in 7% of gery was consulted, they recommended aor- patients with native valve endocarditis.1 In a coronary stent. Following re-vasculariza- tic valve repair once renal function normal- Spanish series of 586 cases of infective tion, patient chest pain and electrocardio- ized. Three days later patient started to com- endocarditis, acute coronary syndrome gram normalized and he improved in short plain of left sided chest pain radiating down (ACS) was found in 14 cases (2.9%). Half term. However due to multiple comorbidi- the left arm and left jaw. Stat ECG was of these patients with ACS had prosthetic ties he had to be intubated and placed on obtainedcommercial that showed ST segment elevation valve endocarditis, 1.5% of cases of ACS dialysis. in I, aVL and V3-V6 leads consistent with occurred with native valves, and embolism anterolateral STEMI (Figure 2). Emergent was the cause in only 3 (0.51%) of 586 coronary angiogram showed 99% left ante- patients.2 In a Russian series 11 out of 104 Nonri or descending artery occlusion (Figure 3). (10.6%) had infarction as result of septic Introduction Due to the presence of persistent symptoms embolism.3 Mostly coronary embolization and ECG changes, a bare metal stent was occurs in left anterior descending artery Systemic embolization is common com- placed. This acute coronary event was because the take off and downward course is plication that usually occurs in patient with thought to be an embolic --phenomenon more favorable for emboli to lodge com- left sided endocarditis. These emboli can given the fact that he had just had a normal pared to right coronary and left circumflex involve virtually any organ system in body coronary angiogram 3 months prior. artery which have perpendicular take offs.4 with the most common being cerebral circu- Unfortunately, patient’s condition gradually The proposed mechanisms of myocar- lation. Coronary artery embolization is well deteriorated with worsening respiratory and dial infarction in patients with endocarditis known complication of infective endocardi- renal function requiring mechanical ventila- include coronary embolization, complete tis that can rarely present with transmural tion and hemodialysis. Patient was on ven- occlusion of coronary ostia by vegetation myocarditis infarction. This can happen as tilator support for a few days. He continued on aortic cusp or extrinsic compression of initial clinical presentation or even many dialysis through temporary dialysis coronaries from periannular abscesses and weeks after treatment with antimicrobial catheter. His respiratory status improved aneursyms. Occasionally in patients with therapy. Therefore, endocarditis should be gradually and he was extubated. Patient underlying atherosclerotic coronary artery kept as potential cause of ST segment renal functions improved slowly as well and disease, insufficient coronary flow would myocardial infarction in these settings. got discharged to rehabilitation facility He lead to myocardial ischemia from is being followed in cardiology office and decreased perfusion pressure even in the continues to be stable. absence of full blown obstruction. [page 78] [Clinics and Practice 2017; 7:950] Case Report Perriannular aortic complications and ic tissue and possible valve replacement.8 In our case, patient has already been resultant coronary compression is the most In presently described case, patient treated with iv antibiotics for 4 weeks and common mechanism responsible for ACS developed anterior wall Myocardial infarc- his repeat blood cultures were negative. that was found to be the cause in 8 out of 14 tion 5 weeks after starting antibiotics. Acute hemodynamic instability in setting of cases in series of 586 patients with infec- Patient had left heart catheterization done 6 MI obviated the need for urgent coronary tive endocarditis.2 weeks before diagnosis of infective endo- angiography. Balloon angioplasty alone was The presence of aortic valve vegetation carditis that did not show any coronary not successful to sustain patency at site of is an ongoing risk for future development artery disease. His 2-D echocardiogram occlusion so we proceeded with placement of ACS. It depends upon the size of vegeta- clearly demonstrated aortic valve vegeta- of intracoronary stent. There have been five tion, its location and virulence of underly- tion so we did not pursue transesophageal previously reported cases of embolic MI ing organism involved. Depending upon echocardiogram and he was being managed from infective endocarditis managed suc- those risk factors, ACS might be the initial conservatively with outpatient antibiotics. cessfully with intracoronary stenting in manifestation of infection. Usually it Given his recent normal LHC, embolic acute settings. In four of these case, patient occurs early during treatment of infective occlusion of LAD from aortic valve vegeta- survived following PCI and outcomes were endocarditis but may occur even after fin- tion was considered the mechanism respon- favorable.9-12 while in one case patient suc- 11 ishing antibiotic treatment. Clinical presen- sible for MI. cumbed to death. Still there are no con- tation of patients with ACS in setting of infective endocarditis is like those seen in individuals with atherosclerotic coronary artery disease. Majority of cases present with anterior and anterolateral STEMI. Fulminant heart failure and cardiogenic shock might be seen in some cases because of severe left ventricular dysfunction. Treatment of ACS in infective endo- only carditis is the unique therapeutic challenge. Many of these patients have emboli at other sites such brain, spleen and kidneys. Therefore, they are high risk for hemor- rhagic complications and fatal outcomes use with use of traditional antiplatlets, antico- agulants and fibrinolytics.5 Coronary angiography is relatively safer approach but there is always risk of fragmentation of vegetation by the catheter encountering vegetation on valve surface and resultant dislodgement in distal coronary circulation. Therefore, in patients who are hemodynam- ically stable and do not have active ongoing ischemia,
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