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
figure 1

Electrocardiogram at admission

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Fig. 2
figure 2

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
figure 3

Electrocardiogram at discharge

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Fig. 4
figure 4

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.