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A case of acute myocardial infarction and infective endocarditis presented with hemoptysis Rui Tian, MD; Yan Li, MD;Wei Jin, MD;Ruilan Wang, MD Department of critical care medicine, Shanghai First People’s Hospital, Shanghai JiaoTong University, Shanghai, China Corresponding author: Ruilan Wang [email protected] Abstract: Backgroud: Introduce a case needing the differential diagnosis between catastrophic anti-phospholipid syndrome and myocardial infarction. Materials and methods: A 54 year-old male presented in the emergency department with sudden onset of cough, hemoptysis and chest pain, and presented multiple organ dysfunction in 3 days without specific symptoms or signs. Firstly, he was suspected the diagnosis of catastrophic anti-phospholipid syndrome and given the accordingly treatments, his condition was getting better. After further examinations and treatments, he was diagnosed as acute myocardial infarction, infective endocarditis. Then the patient received surgery and PTCA, he recovered well and was discharged 80 days after the onset. Key words: hemoptysis; catastrophic anti-phospholipid syndrome; acute myocardial infarction; infective endocarditis; rupture of the posterior leaflet of mitral valve; Guillain-Barre syndrome Introduction A 54 year-old Caucasian male presented in the emergency department at local hospital on March.8th 2014 with sudden onset of cough, hemoptysis and chest pain in the past 2 hours. At presentation, his oxygen saturation was 91% on breathing mask. His cardiac exam was normal. Lung exam showed rasping breath sound and rales. Emergency EKG showed mild ST suppression on leads AVL,AVF,II,III,V2-V6. Echocardiography showed mild-moderate mitral regurgitation with preserved left ventricular function. Chest CT showed bilateral diffuse pulmonary hemorrhage with infection and triple-vessel coronary atherosclerosis(figure 1a). The patient was admitted to intensive care unit immediately. His condition worsened on March. 10th with oxygen saturation decreasing to 75%. He also developed hypotensive shock, acute renal insufficiency, and was intubated and ventilated immediately. He was also put on CRRT(continuous renal replacement therapy) and received anti-shock treatment. Emergency bronchoscopy showed bilateral diffuse pulmonary bloody frothy sputum. Multiple follow-up EKG showed sinus rhythm, nonspecific ST-T change. Multiple regurgitation, repeated mild echocardiography tricuspid showed regurgitation and mild-moderate mild mitral pulmonary hypertension(36-38mmHg). Mycoplasma antibody, Legionella antibody, Rickettsia antibody, RSV(respiratory syncytial virus) antibody, influenza antibody and tuberculosis antibody were all negative. Influenza type A detection with the colloidal gold method was negative. Blood culture was negative. Anti-glomerular basement membrane antibody(IgG, IgA, IgM) was negative. Anti phospholipid antibody titer was 24.36 RU/ml. The patient was treated with antibiotics and intravenous methylprednisone at the dose of 240mg per day. Methylprednisone dose was then tapered off gradually after 3 days of initiating dose and was discontinued on March. 21st. The patient was given a maintaining dose of methylprednisone again at 40mg per day later on March. 26th. His oxygen saturation started to improve on March. 12th. Bronchoscopy on March. 20th showed large amount of dark red bloody crust in the trachea and bilateral bronchus, on March. 22th, bronchoscopy was done again and most of the bloody crust disappeared, so the patients was weaning the same day. The urinary volume was increasing at the same time and on March. 27th, it reached 1700ml per day. But from March. 21th, the patient began to suffer from muscle strength decreasing in all extremities. The patient was transferred to our intensive care unit on March. 28th 2014. At admission, the patient had normal vitals, normal temperature, regular rhythm. 2-3/6 holosystolic murmur was auscultated at apex. Levido reticularis was observed on the abdomen and proximal thigh. Muscle strength was decreased in all extremities. Proximal muscle was more affected compared with distal muscle. Muscle strength of left upper extremity was II-III-IV. Muscle strength of right upper extremity was I-III-IV. Electromyogram showed diffuse damage of peripheral nerve mainly affecting motor nerve with more evident proximal motor nerve damage and disappearance of F wave. EKG showed sinus rhythm and diffuse ST-T change. Chest CT showed inflammation of the lung. Patient was then given ceftriaxone, moxifloxacin, 40mg per day of methylprednisone and 5-day intra venus immunoglobulin(IVIG) treatment. Echocardiography of our hospital on April. 1st showed dilated left ventricle, prolapse of the posterior leaflet of mitral valve(partial rupture of chordae tendineae), vegetation of mitral valve with severe mitral regurgitation(figure 1b). The patient was continued on conservative medical treatment due to unclear definitive diagnosis. Repeated anti-phospholipid antibody showed IgM 27.9, IgA<12, IgG 7.9 and negative anti-β2-glycoprotein 1 antibody. Anti-glomerular basement membrane antibody was negative. ANCA was negative. Anti-ss DNA antibody was <20 and anti-ds DNA antibody was <100. The immunoglobulin(A,E,G,M), complement(C3,C4,C50) were all negative. ANA+ENA were all negative. Multiple blood culture had negative result. Vessel Doppler was normal. Since April. 3rd, the patient had developed repeated dyspnea, left chest and back pain, recurrent heart failure and hemoptysis. Emergency mitral valve replacement and vegetation removal was performed on the night of April. 9th. During the surgery, we observed enlarged heart (especially left atrium and left ventricle), enlarged mitral annulus, and prolapse of posterior leaflet and rupture of chordae tendineae. There was a 1*1cm soft and loose vegetation on the posterior leaflet. After the surgery, symptoms of heart failure improved with decreased rales compared with pre-operational baseline. The heart murmur and abdominal levido reticularis have disappeared. Patient was extubated on post-operational day 2. Pathology of the vegetation showed coagulative necrosis of myocardium with focal fibrosis. Bacterial culture of vegetation showed Staphylococcus capitis. After the surgery, multiple repeated anti-phospholipid antibody test were negative. Patient was put on daptomycin and ceftazidime, corticosteroid(tapered off gradually) and continued anticoagulation. On April. 20th, the patient developed symptoms of heart failure again with generalized fatigue and segmental akinesis of the left ventricle on echocardiography. EKG still showed diffuse ST-T change. Considered recurrent heart failure, the patient underwent CRRT again to reduce volume load, and meanwhile, too quick tapering off of the corticosteroid was hypothesized to contribute to the exacerbation. Therefore, intravenous methylprednisone was given again at the dose of 80mg per day, with the initiation of oral methylprednisone, then tapered off and gradually discontinued. After the management previously described, the patient was relatively stabilized with intermittent heart failure well controlled by medical treatment. Patient regained normal renal function on May. 9th 2014 and CRRT was discontinued. Coronary angiography on May. 12th showed ulcerative unstable plaque on the proximal LAD(left anterior descending artery) with 75% stenosis. There was also 80% stenosis of the proximal LCX(left circumflex artery) with obliterated middle segment and collateral circulation from RCA on the distal segment. There was 60% stenosis on distal RCA(right coronary artery,figure 1). Patient had PTCA on May. 16th and post-interventional coronary angiography showed no stenosis. Patient recovered well from intervention and had no more heart failure. He had normal renal function and the muscle strength returned to 4/5 in all extremities. Eechocardiography on May. 26th showed segmental akinesis of left ventricle and EF is 53%. The patient was discharged on May. 27th . Discussion The patient presented with acute onset of illness which resulted in multiple organ dysfunction in 3 days without specific symptoms or signs. Therefore, differential diagnosis had always been focused on catastrophic anti-phospholipid syndrome, acute left heart failure and myocardial infarction during the whole process. Catastrophic anti-phospholipid syndrome is a subtype of anti-phospholipid syndrome, manifested with acute onset with multiple organ failure(≥3) and multiple vascular embolism within a few days to a few weeks. It is characterized by diffuse vascular embolism in multiple organs resulting in ischemia and dysfunction of concerned tissue and organs. Classic examples would be renal vascular embolism leading to acute renal dysfunction, pulmonary vascular embolism contributing to ARDS(acute respiratory distress syndrome), cerebral vascular embolism causing cerebral infarction and etc[1]. In this case, our patient developed multiple organ failure (heart, lung and kidney) within 3 days of onset of illness. His manifestations like valve regurgitation, pulmonary hypertension, alveolar hemorrhage, ARDS, rapidly developed neurological deficits and levido reticularis are all classic in the catastrophic anti-phospholipid syndrome[1,2,3]. His twice positive anti-phospholipid antibody and early remission rapidly induced by corticosteroid further enhanced our suspicion of catastrophic anti-phospholipid syndrome. The reason why we couldn’t reach definitive diagnosis was that we didn’t have evidence of vascular embolism(multiple vascular Doppler failed to show thrombosis). Echocardiography at our hospital showed vegetation on mitral valve. However, the patient was afebrile and multiple blood culture turned back negative in the course of disease. This led us to the presumption that this vegetation was thrombotic rather than infective. The diagnosis of catastrophic anti-phospholipid syndrome could be made if histologic evidence of thrombosis had been found[1,4]. Finally, pathologic result of the vegetation confirmed that it was coagulation necrosis of myocardium with focal fibrosis and culture of the vegetation showed the growth of staphylococcus capitis. The anti-phospholipid antibody was negative after surgery. All of these meant the diagnosis of catastrophic anti-phospholipid syndrome was excluded. Diagnosis of acute myocardial infarction was made possible due to recurrent chest pain, elevation of troponin and ST depression on EKG in the course of disease. However, early definitive diagnosis couldn’t be made due to several reasons as followed: First, EKG of this patient didn’t show characteristic pattern and progression of acute myocardial infarction. Second, hypokinesis of ventricle is not observed by multiple echocardiographies early in the course of disease. The acute renal dysfunction precluded the coronary angiography in fear of contrast-induced nephropathy. Two weeks after the the cardiosurgery, patient had recurrent chest pain, acute exacerbation of heart failure again. Repeated echocardiography showed local hypokinesis of ventricle and the diagnosis of myocardial infarction was thus established. With improvement of renal function later, coronary angiography was implemented and further confirmed the diagnosis of myocardial infarction. Combining history and EKG of this patient, diagnosis of non-ST elevation myocardial infarction was made[5]. The infective endocarditis in this case was considered secondary. First, multiple repeated echocardiographies at the local hospital didn’t reveal rupture of chordae tendioniae or vegetation. This signified that the patient hadn’t have infective endocarditis at that time. Second, patient came in with acute myocardial infarction and injury of myocardium was worsened by failure of prompt diagnosis and revascularization. Early corticosteroid use also contributed to the further damage of myocardium which was later complicated with rupture of chordae tendoniae. Vegetation then formed and infective endocarditis developed on the basis of all above[6]. Decreasing muscle strength in all extremities 2 weeks after the onset of the illness was considered Guillan-Barre Syndrome. This is an immune-mediated acute inflammatory peripheral neuropathy. Some components of pathogen (virus, bacteria, etc) share similarity with peripheral myelin which causes activation of auto-immune T cells and production of autoantibodies. The deregulated immune system then respondes to components of peripheral nerves which causes loss of peripheral myelin. Guillain-Barre Syndrome is characterized by acute onset with its peak symptoms at 2 weeks after the onset. It is manifested with fairly symmetric muscle weakness in all extremities and depressed or absent deep tendon reflex caused by polyradiculopathy and peripheral nerve damage. The syndrome may cause flaccid paralysis with superimposed peripheral sensory disturbance[7]. Muscle weakness caused by Guillain-Barre Syndrome usually affects proximal or distal muscle of extremities. Electromyogram may show decreased conduction velocity with prolonged or absent F waves and absent H reflexes. The patient was diagnosed with Gullain-Barre Syndrome according to his clinical presentation and electromyogram results. The diagnosis should be confirmed specifically with albuminocytologic separated in cerebro-spinal fluids. However, this patient had severe onset of illness which precluded the lumbar puncture. After the use of IVIG and corticosteroid, his symptoms improved rapidly, making lumbar puncture unneccesary. Local hospital once considered the diagnosis of critical illness polyneuropathy. Critical illness polyneuropathy usually affects distal muscle of extremities. Electromyogram shows primary axonal damage without abnormal F wave or depressed H wave, reflex which is discordant with this patient’s manifestations. In conclusion, the final diagnosis of the patient are acute myocardial infarction, rupture of the posterior leaflet of mitral valve, infective endocarditis, congestive heart failure(NYHA grade IV), acute renal failure and Guillain-Barre syndrome. Acknowledgement: We thank Jun Liu, MD; Weizhen Wang, MD, Guobing Zhang, MD; Zhiyan He, MD; Jian Liu, MD; Zhongxiang Yuan, MD; Lianhua Chen, MD; Guangzhong Lu, MD; Qing Yu, MD; Qianghua Wei, MD for the consultant and help in treating the patient. Conflicts of interest: The authors report no conflicts of interest. Reference 1、 Saigal R, Kansal A, Mittal M, et al: Antiphospholipid antibody syndrome. J Assoc Physicians India 2010;58:176-184 2、 Koolaee RM, Moran AM, Shahane A: Diffuse alveolar hemorrhage and Libman-Sacks endocarditis as a manifestation of possible primary antiphospholipid syndrome. J Clin Rheumatol 2013;19(2):79-83 3、 Asherson RA, Cervera R, Piette JC, et al: Catastrophic antiphospholipid syndrome. Clinical and laboratory features of 50 patients. Medicine (Baltimore) 1998; 77(3):195-207 4、 Miyakis SL, Lockshin MD, Atsumi T, et al: International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS). J Thromb Haemost 2006; 4(2):295-306 5、 Skinner JS, Smeeth L, Kendall JM, et al: NICE guidance. Chest pain of recent onset: assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin. Heat 2010;96(12):974-978 6、 Habib G, Hoen B, Tornos P, et al: Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009). Eur Heart J 2009; 30(19):2369-2413 7、 Vail Doom PA, Ruts L, Jacobs BC. Clinical features, pathogenesis, and treatment of Guillain-Barre syndrome. Lancet Neurol 2008;7:939-950 Figure legend: Figure 1 (a)Chest CT on day 1 at local hospital:bilateral diffuse bleeding dots with infectious focus. (b)Echocardiography on April 1st 2014:prolapse of the posterior leaflet of mitral valve, formation of vegetation(arrow on the left picture) and severe regurgitation(right picture).