Download A case of acute myocardial infarction and infective endocarditis

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
In this report, we introduce a case with atypical symptom, needing the differential
diagnosis between catastrophic anti-phospholipid syndrome and myocardial
infarction.
Case report
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.
Reference
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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).