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Acute myocardial infarction and transient elevated anticardiolipin antibody in a young adult with possible familial hypercholesterolemia: a case report

BMC Cardiovascular Disordersvolume 19, Article number: 156 (2019) | Download Citation

Abstract

Background

Familial hypercholesterolemia (FH) can lead to premature coronary heart disease. Anticardiolipin antibody may be a contributor for thrombosis. Here, we report an adult with possible FH suffered from premature myocardial infarction that may be triggered by transient increased anticardiolipin antibody.

Case presentation

A 29-year-old male had presented with a history of 2-h chest pain and numbness of left upper arm before 5 days. The electrocardiogram (ECG) had demonstrated inferior wall myocardial infarction (MI). Five days later he was admitted to our hospital and diagnosed as acute MI and possible FH (premature coronary heart disease, low density lipoprotein cholesterol of 5.90 mmol/L) with increased anticardiolipin antibody (up to 120 RU/ml). Other auto-antibodies including β2-glicoprotein antibodies IgM, IgA, IgG, lupus anticoagulant (LA), antinuclear antibodies, anti-myocardial antibody were normal. Coronary artery angiography (CAG) showed right coronary artery was total occlusion from the middle segment. Then he underwent percutaneous coronary intervention with a stent. Four days later, he was discharged with complete recovery. CAG showed intra-stent restenosis and anticardiolipin antibody level was normal and the patient had no any symptoms at 6-month follow-up.

Conclusions

Transient elevated anticardiolipin antibody may be a trigger or biomarker of cardiac thrombotic events in younger atherosclerotic patients.

Open Peer Review reports

Background

It is well known that the incidence of premature cardiovascular disease (CVD) is low. Previous studies have revealed that patients aged less than 40 years old only account for 1.2% of all patients with MI [1, 2]. Numerous studies have reported that multiple risk factors relate to ST segment elevated MI (STEMI) including male, smoking state, family history of CVD, dyslipidemia, hypertension, and diabetes mellitus (DM) in patients aged < 40 years [3,4,5,6,7]. Familial hypercholesterolemia (FH) as a type of dyslipidemia is one of the most common risk factors in patients with premature atherosclerotic cardiovascular disease (ASCVD) [8, 9]. In addition, previous evidence has proved that the presence of antiphospholipid antibodies (aPL) increases the thrombotic risk and the decreased titers or the disappearance of aPL closely relates to better prognosis [10,11,12,13]. Thus, a transient increase of anticardiolipin antibody induced by bacteria or viruses infection may contribute to the risk of thrombosis in patient with possible FH [14, 15].

Case presentation

A 29-year-old male patient had presented with a history of 2-h chest pain and numbness of left upper arm before 5 days. The electrocardiogram (ECG) indicated acute inferior wall myocardial infarction (MI) and he refused any treatment at that time. Five days later he was admitted to our hospital for further examination. Physical examination showed no abnormal including arcus corneae and xanthelasma in eyelid, extensor tendon and achilles tendons. He had no histories of diabetes mellitus, hyperthyroidism, heart disease, hepatic or renal disease and no family history of FH. The ECG showed deep Q wave and inverted T wave in leads II, III and aVF (Fig. 1) and the echocardiogram revealed the diastolic dysfunction of left ventricular with a decreased LV ejection fraction (EF, 48%). The lower extremities ultrasound revealed atherosclerotic plaque in the posterior wall of right common femoral artery. Blood tests showed CK-MB of 21.4 U/L, lactate dehydrogenase of 452 U/L, hs-CRP of 71.2 ng/L, triglyceride (TG) (Triglyceride Kit method) of 0.88 mmol/L, total cholesterol (TC) of 6.87 mmol/L (Cholesterol Kitmethod), low density lipoprotein cholesterol (LDL-C) of 5.90 mmol/L and high density lipoprotein cholesterol (HDL-C) of 1.09 mmol/L (Direct Method-Surfactant Clearance Method).Further laboratory tests revealed highly elevated anticardiolipin antibody (ELISA method) of more than 120RU/ml (0-12RU/ml) and no other abnormal auto-antibodies, including β2-glicoprotein antibodies IgM, IgA, IgG, lupus anticoagulant (LA). DNA analysis for antiphospholipid antibody syndrome (APS) was not performed. Coronary artery angiography (CAG) demonstrated predominant right coronary artery (RCA) and diffuse lesions in the middle and distal segments of the left anterior descending (LAD) artery with the stenosis up to 40~50% (Fig. 2a) and total occlusive RCA from the middle segment (Fig. 2b) with LAD-RCA collateral circulation. With the treatments of anticoagulation (heparin), double antiplatelets (aspirin and ticagrelor) and lipid-modulating (rosuvastatin), he was implanted a stent at the middle segment of the RCA (Fig. 2c). Four days later, he was discharged without any complication. The ECG at discharge showed that the inverted T waves were deeper than those at admission in leads II, III and aVF (Fig. 3). At 6-month follow-up, the laboratory test showed the level of anticardiolipin antibody (ELISA method) was less than 2.0 RU/ml (0-12RU/ml). Lipid profile revealed TG of 0.98 mmol/L, TC of 6.22 mmol/L, LDL-C of 5.53 mmol/L and HDL-C of 0.99 mmol/L.CAG showed 70% in-stent restenosis of the RCA. ECG revealed deep Q waves and inverted T waves (Fig. 4). The patient looked good without any activity restriction and discomfort. At 8-month follow-up, the level of anticardiolipin antibody is less than 2.0 RU/ml and the lipid profile showed TG 0.64 mmol/L, TC 4.15 mmol/L, LDL-C 3.47 mmol/L and HDL-C 1.01 mmol/L.

Fig. 1
figure1

Electrocardiogram at admission

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Fig. 2
figure2

Coronary artery angiography and percutaneous coronary intervention (PCI). a. Left anterior descending artery (LAD); b. Right coronary artery (RCA); c. Implantation of stent in the middle right coronary artery

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Fig. 3
figure3

Electrocardiogram at discharge

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Fig. 4
figure4

Electrocardiogram at 6-month follow-up

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Discussion and conclusions

FH is a risk factor for premature ASCVD [16, 17] and antiphospholipid antibody is a contributor of thrombosis for myocardial infarction [14, 18]. According to the Dutch Lipid Clinic Network (DLCN) Diagnostic criteria (DLCN) [19], the patient was confirmed as possible FH with 5 scores including the premature coronary heart disease (2 points) and LDL-C level of 5.90 mmol/L (3 points). With the International Consensus Statement for Definite APS [20], we could not give a definite diagnosis of APS for this patient. However, the antiphospholipid antibodies can be present in the common population with bacterial or viral infection including HIV, HBV, HCV, herpes virus and parvovirus B19 [15, 21]. Infection-related antibodies will totally disappear once the infection is gone [22]. Although this patient did not have an obvious infectious manifestation before his admission, some occult infections could not be completely excluded. Therefore, transient elevation of anticardiolipin antibody could be a trigger or biomarker for MI in patients with FH [14, 18]; however, the causative effects of transient increased anticardiolipin antibody and MI still need further study.

Limitations

We did not perform the genetic testing about the APS and the test of anticardiolipin antibody at 12-week follow-up.

Availability of data and materials

All the data in this study are included in the manuscript.

Abbreviations

AMI:

Acute myocardial infarction

aPL:

Antiphospholipid antibody

APS:

Antiphospholipid antibody syndrome

ASCVD:

Atherosclerotic cardiovascular disease

CAD:

Coronary artery disease

CK-MB:

Creatine kinase isoenzyme

ECG:

Electrocardiograph

FH:

Familial hypercholesterolemia

HDL-C:

High-density lipoprotein cholesterol

hs-CRP:

High-sensitivity C-reactive protein

LDL-C:

Low-density lipoprotein cholesterol

LDLR:

LDL receptor

TC:

Total cholesterol

TG:

Triglyceride

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Acknowledgements

Not Applicable.

Funding

This work was supported by the National Natural Science Foundation of China (81460072) and CAS “Light of West China” Program where the publication fees are from.

Author information

Affiliations

  1. Department of Cardiology, Gansu Provincial Hospital, Lanzhou University, Lanzhou, 730000, People’s Republic of China

    • Xin Su
    • , Aqian Wang
    • , Hai Zhu
    • , Hongling Su
    • , Yichao Duan
    • , Yan Huang
    •  & Yunshan Cao

  2. School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, People’s Republic of China

    • Xin Su
    • , Aqian Wang
    •  & Shanlian Wu

  3. School of Clinical Medicine, Ningxia Medical University, Lanzhou, 730000, People’s Republic of China

    • Yichao Duan

  4. Department of Pathology, Gansu Provincial Hospital, Lanzhou University, Lanzhou, 730000, People’s Republic of China

    • Min Zhang

  5. Department of Radiology, Gansu Provincial Hospital, Lanzhou University, Lanzhou, 730000, People’s Republic of China

    • Xing Zhou

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Contributions

XS, AQW were involved in the patient management and manuscript writing. HZ, HLS, YCD and SLW collected information and collated pictures of the patient. MZ and YH focused on error correction. XZ and YSC performed interventional therapy for the case and revised the manuscript attentively. All the authors read and approved the final manuscript.

Corresponding authors

Correspondence to Xing Zhou or Yunshan Cao.

Ethics declarations

Ethics approval and consent to participate

The study is approved by Ethics committee of Gansu Provincial Hospital.

Consent for publication

We have obtained written informed consent from the patient for the publication.

Competing interests

The authors have no any conflicts of interests to disclose.

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Keywords

  • Familial hypercholesterolemia
  • Thrombosis
  • Myocardial infarction
  • Anticardiolipin antibody

BMC Cardiovascular Disorders

ISSN: 1471-2261

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