"Myocardial infarction" is because of this rheumatism, 90% of doctors have never seen it!

*Only for medical professionals to read and refer to the little "heart" of everything! Summary of the previous situation: A 39-year-old male patient with chest pain after exertion, which seems to be an "unremarkable" acute coronary syndrome (ACS), has many twists and turns during the diagnosis and treatment process
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Chasing the culprit in many ways: Who is the initiator of a seemingly simple illness? Medical history: A 39-year-old man developed orthopnea and severe left pleural pain after exertion.
The symptoms worsened when lying down and improved when he leaned forward
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At the same time, it was accompanied by multiple joint pains, bilateral scleritis and oral ulcers
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He recently took apixaban for unprovoked bilateral pulmonary embolism
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Previous auxiliary examination data: antinuclear antibody (ANA) positive, titer 1:60; rheumatoid factor (RF) negative, anti-cyclic citrullinated peptide (CCP) antibody and anti-extractable nuclear antigen antibody (ENA) were all negative
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After re-examination, the RF was slightly elevated (18 IU/ml), and the anti-CCP antibody was negative, and methotrexate + glucocorticoid therapy was taken (the specific diagnosis is unknown)
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Have a history of myocardial infarction
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 Physical examination: heart rate 105 beats/min, no abnormality in other vital signs, distant heart sounds, and subcutaneous nodules on bilateral forearms
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 Auxiliary examination: The first ECG showed PR segment depression and ST segment elevation (I, II, V2-V6) in multiple leads, suggesting acute myopericarditis, and pathological Q wave and T wave inversion in the inferior leads, suggesting that He had a history of myocardial infarction (Figure 1), and the patient's electrocardiogram a year earlier showed normal sinus rhythm without pathological Q-wave or T-wave inversion
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 Figure 1 PR segment depression in the red circle and ST segment elevation in the blue circle, all suggest that the patients with acute pericarditis have troponin I (TNI) 8.
98 μg/L, C-reactive protein (CRP) 51.
4 mg/L, and erythrocyte sedimentation rate (ESR) 36 mm/h, slightly elevated liver enzymes, microscopic hematuria and subclinical proteinuria (protein/creatinine ratio 0.
90), normal blood urea nitrogen and creatinine
.

Chest X-ray showed enlarged heart
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Angiographic CT (CTA) showed no evidence of thrombotic disease
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Echocardiography (TTE) showed normal left ventricular function, no wall abnormalities, and mild pericardial effusion
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Repeat TTE showed increased pericardial effusion (Figure 2)
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Combined with the performance of the patient's ACS, elective coronary angiography is planned
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  Figure 2 TTE showed a pericardial exudation of about 2.
47 cm (red scale).
At the same time, the physical examination showed an anomalous pulse, suggesting cardiac tamponade
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Although the white blood cell count (WBC) of the patient's blood routine was normal, the doctor performed an emergency pericardiocentesis and sent for cytology based on the medical history data and the re-examination of TTE results
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At this time, the patient's acute symptoms and pericardial effusion have no reasonable cause, but the most important thing is to relieve the patient's acute disease, and other things have no time to consider
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  Preliminary diagnosis: Combined with symptoms and medical history, the doctor considered that the patient was most likely to have ACS or even myocardial infarction, but the electrocardiogram showed acute myopericarditis, but TTE did not show myocardial abnormality
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Combined with the elevated inflammatory markers in the patient, the doctor wanted to perform further cardiac MRI to see if it was in line with the diagnosis of myopericarditis, but the metal in the patient disrupted this arrangement
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In addition, physicians had considered the patient to have post-myocardial infarction syndrome, but the patient's clinical evidence did not seem to fully support this diagnosis
.

 Diagnosis and treatment experience: 6 days after admission, the patient's chest pain suddenly worsened.
Unlike pleural or orthostatic pain on admission, the electrocardiogram showed mild ST segment changes in the inferior leads (Figure 3), and TNI after pericarditis-related treatment was given.
on a downward trend
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At this time, doctors worried that the patient had a new pulmonary embolism, or that he had a dangerous primary disease such as aortic dissection, but the subsequent CTA also ruled out this possibility
.

 Figure 3 ECG before coronary angiography showed T wave inversion in leads I (red circle) mild ST segment abnormalities in leads II, III and avF (basket circle) Repeat TTE showed new wall motion in the descending branch of the right coronary artery (RCA) Abnormal, the ejection fraction (EF) dropped to 40%
.

Coronary CT showed complete occlusion of the RCA, thickening of the mid-segment wall of the left anterior descending artery (LAD), considered to be associated with vasculitis, and dilated aneurysm in the area of ​​the left main bifurcation to the LAD and left circumflex artery (Figure 4)
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 Figure 4 CTA showing RCA occlusion (red arrow) Subsequently, the patient underwent emergency percutaneous coronary intervention (PCI), which revealed complete proximal RCA occlusion (Figure 5)
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  Figure 5 The left is the RCA that was completely occluded before stent placement, and the right was the RCA that was not occluded after stent placement.
The cause of the attack
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Considering the patient's positive history of ANA, the doctor further carried out immunological examination on the patient, and the results showed: ANA positive (titer>1:2560), anti-double-stranded DNA (dsDNA) antibody positive (titer 1:320) and complement C3 decreased, while complement C4 and angiotensin-converting enzyme (ACE) were normal
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HIV and hepatitis C virus negative
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At the same time, human leukocyte antigen (HLA) B51, anti-neutrophil cytoplasmic antibody (ANCA), anti-Smith antibody (anti-Sm antibody), anti-ribonucleoprotein antibody (anti-RNP antibody), anti-Scl-70 antibody, anti-SSA antibody , anti-SSB antibody, anti-Jo-1 antibody, anti-liver-kidney microsomal antibody, anti-smooth muscle antibody (SMA) and anti-mitochondrial antibody were all negative
.

Anticardiolipin IgG and anticardiolipin IgM were normal on antiphospholipid antibody (APLA) tests
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Anti-β2-glycoprotein IgG, anti-β2-glycoprotein IgM, and lupus anticoagulant were all negative
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The patient's diagnosis and treatment ideas have gradually become clear, and it is most likely caused by an autoimmune disease, and the cytological examination results of the pericardial puncture fluid previously submitted for examination point to: there may be lupus cells in the puncture fluid
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This also suggests that the patient may have had an acute ischemic event before the onset of symptoms
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 Figure 6 A is an example of a high-resolution image of lupus erythematosus cells, characterized by nuclei that have been phagocytosed and digested by mature multinucleated WBCs; B and C are suspected lupus cells (red circles) in the patient's pericardiocentesis fluid after a series of diagnostic measures , Through a relatively comprehensive autoantibody spectrum examination, the doctor was diagnosed with systemic lupus erythematosus (SLE) based on pericardiocentesis fluid cytology, positive ANA and anti-dsDNA antibodies, and decreased complement C3
.

Experience time: SLE patients should also be more "heart"! During the treatment period of unclear etiology, the patient's pleural pain has not been completely relieved, but the symptoms gradually decreased
.

When physicians evaluate patients for risk factors for acute myocardial infarction, and early TTE does not even reveal wall abnormalities, it is easy to attribute this chest pain entirely to myopericarditis
.

Until CTA and PCI show that the RCA is completely occluded, it can be seen that "seeing" is not necessarily completely true
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At the same time, the patient belongs to the high-risk patients of APLA syndrome, but the APLA examination results cannot make a definite diagnosis, and further re-examination is required
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In addition, patients with acute myocardial infarction due to acute plaque rupture typical of ACS or thrombosis of APLA still need to be diagnosed
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At present, there are few case studies on myopericarditis in patients with SLE, so there is no sufficient clinical evidence to identify and diagnose it at the first time
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In SLE patients, myocardial infarction is a relatively rare first-diagnostic manifestation, but clinicians and researchers have paid attention to it
.

One study[1] divided 850 patients with SLE and myocardial infarction under the age of 35 years from 1975 to 2006 into three subgroups according to etiology: normal coronary artery or thrombosis (group I), coronary aneurysm or arteritis (group I).
Group II) and coronary atherosclerosis (Group III), and found that the lag time between SLE diagnosis and myocardial infarction onset was the longest in group III and the smallest in group
I.

Many studies have also shown that cardiovascular disease is one of the main causes of death in SLE patients and significantly reduces the life expectancy of patients.
At the same time, the increased risk of coronary artery disease in SLE patients cannot be explained by traditional cardiovascular concepts [2]
.

The mortality rate of SLE with cardiovascular disease as the cause of death is bimodal, and it can shorten the lifespan of patients by up to 20 years [3]
.

In a retrospective study of cardiovascular outcomes in 263 SLE patients, the relative risk of non-fatal myocardial infarction was 10.
1 and the relative risk of death from coronary heart disease was 17.
0, suggesting a significantly increased risk of coronary heart disease in patients with SLE, whereas traditional risk factors cannot fully explain this [4]
.

Studies have shown that risk factors include traditional risk factors (age, male gender, family history of coronary heart disease, obesity, hypertension, diabetes, dyslipidemia, metabolic syndrome, hyperhomocysteinemia, and smoking) and disease-specific risk Factors (disease activity, cumulative damage, disease duration, antiphospholipid and dsDNA antibodies, high-sensitivity CRP, renal disease, neuropsychiatric disease, hormones, and use of immunosuppressive agents), and recommended for SLE with one or more typical high cardiovascular risk of patients are screened for APLA syndrome, and the carotid artery is evaluated by ultrasound [5]
.

Currently, the evidence for monitoring and prevention of coronary vascular events in SLE is limited
.

Our patient's SLE was unclear at the onset of cardiac symptoms, which led physicians not to initially consider the association between inflammation and coronary heart disease
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From this example, we can know that whether or not the patient has other risk factors for cardiovascular disease, such as age, requires careful evaluation
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It also suggests that there is still a gap between the risk stratification method and practice of acute coronary events for doctors, and it should not be careless
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Conclusion Patients with SLE should be carefully evaluated for potential cardiovascular disease risk, regardless of age or other traditional risk factors.
Conversely, it should be recognized that patients with SLE may have an increased incidence of ACS, which is important for early clinical diagnosis and coronary revascularization.
critical
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On the one hand, in young SLE patients presenting with chest pain, physicians should be vigilant about myocardial infarction and be cautious in differential diagnosis; on the other hand, APLA examination should be considered in any SLE patient with evidence of thrombosis, and timely Initiate appropriate anticoagulation therapy
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Although APLA was negative in this patient, primary prevention of APLA thrombosis included the use of low-dose aspirin, warfarin, and hydroxychloroquine
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Direct oral anticoagulants lack evidence of efficacy in APLA, so warfarin is the anticoagulant of choice in such patients
.

Reference [1] Korkmaz C, Cansu DU, Kaşifoğlu T.
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Non-ST-elevation myocardial infarction hiding behind myopericarditis in a patient with systemic lupus erythematosus.
BMJ Case Rep.
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Published 2022 Feb 25.
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Novel Insights in Systemic Lupus Erythematosus and Atherosclerosis.
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Traditional Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus.
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gov/11665973/[5]Tselios K, Sheane BJ, Gladman DD, Urowitz MB.
Optimal Monitoring For Coronary Heart Disease Risk in Patients with Systemic Lupus Erythematosus: A Systematic Review.
J Rheumatol.
2016;43(1):54-65.
doi:10.
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https://pubmed.
ncbi.
nlm.
nih.
gov/26568591/ Author of this article: Gui Zhi Review of this article: Chen Xinpeng, Deputy Chief Physician Editor in charge: The copyright of the cassette states that this article is original, if you need to reprint, please contact the authorization - End - Call for manuscripts "Medical Rheumatism Immunity Channel" long-term recruitment of online authors, 1.
Clinical practical skills, misdiagnosed cases, clinical medication, interesting 2.
Interesting diagnosis and treatment stories of rheumatologists; 3.
Significant progress in the field of rheumatology; 4.
Others (contents that rheumatologists are interested in)1002/15290131(200110)44:10<2331::aidart395>3.
0.
co;2i.
https://pubmed.
ncbi.
nlm.
nih.
gov/11665973/[5]Tselios K, Sheane BJ, Gladman DD, Urowitz MB.
Optimal Monitoring For Coronary Heart Disease Risk in Patients with Systemic Lupus Erythematosus: A Systematic Review.
J Rheumatol.
2016;43(1):54-65.
doi:10.
3899/jrheum.
150460.
https://pubmed.
ncbi.
nlm.
nih.
gov/26568591/ Author of this article: Gui Zhi Review of this article: Chen Xinpeng, Deputy Chief Physician Responsible editor: The copyright of the cassette states that this article is original, if you need to reprint, please contact for authorization - End - Call for Papers "Rheumatology and Immunity Channel in the Medical Community" Long-term Recruitment Online Author of the manuscript, 1.
Clinical practical skills, misdiagnosed cases, clinical medication, interesting content of rheumatology and immunology; 2.
Interesting diagnosis and treatment stories of rheumatology immunologists; 3.
Major progress in the field of rheumatology and immunology; content that the doctor is interested in)1002/15290131(200110)44:10<2331::aidart395>3.
0.
co;2i.
https://pubmed.
ncbi.
nlm.
nih.
gov/11665973/[5]Tselios K, Sheane BJ, Gladman DD, Urowitz MB.
Optimal Monitoring For Coronary Heart Disease Risk in Patients with Systemic Lupus Erythematosus: A Systematic Review.
J Rheumatol.
2016;43(1):54-65.
doi:10.
3899/jrheum.
150460.
https://pubmed.
ncbi.
nlm.
nih.
gov/26568591/ Author of this article: Gui Zhi Review of this article: Chen Xinpeng, Deputy Chief Physician Responsible editor: The copyright of the cassette states that this article is original, if you need to reprint, please contact for authorization - End - Call for Papers "Rheumatology and Immunity Channel in the Medical Community" Long-term Recruitment Online Author of the manuscript, 1.
Clinical practical skills, misdiagnosed cases, clinical medication, interesting content of rheumatology and immunology; 2.
Interesting diagnosis and treatment stories of rheumatology immunologists; 3.
Major progress in the field of rheumatology and immunology; content that the doctor is interested in)ncbi.
nlm.
nih.
gov/26568591/ Author of this article: Gui Zhi Review of this article: Deputy Chief Physician Chen Xinpeng Editor in charge: Copyright statement on the cassette Author of online manuscripts, 1.
Clinical practical skills, misdiagnosed cases, clinical medication, and interesting content in rheumatology and immunology; 2.
Interesting diagnosis and treatment stories of rheumatology immunologists; 3.
Major progress in the field of rheumatology and immunology; 4.
Others ( Content of interest to rheumatologists can be)ncbi.
nlm.
nih.
gov/26568591/ Author of this article: Gui Zhi Review of this article: Deputy Chief Physician Chen Xinpeng Editor in charge: Copyright statement on the cassette Author of online manuscripts, 1.
Clinical practical skills, misdiagnosed cases, clinical medication, and interesting content in rheumatology and immunology; 2.
Interesting diagnosis and treatment stories of rheumatology immunologists; 3.
Major progress in the field of rheumatology and immunology; 4.
Others ( Content of interest to rheumatologists can be)
.

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