The advent of highly active antiretroviral therapy (HAART) has led to a marked decrease in morbidity and mortality among patients with human immunodeficiency virus (HIV) infection,1–4 and a consequent increase in their life expectancy and in the prevalence of chronic diseases not previously associated with HIV. These include cardiovascular and liver disease and cancer,5–7 the treatment of which is becoming increasingly important in these patients.

There is in fact a well-documented higher risk of coronary artery disease (CAD) in HIV patients compared to the general population.3,8,9 In a study carried out by the Antiretroviral Therapy Cohort Collaboration,6 which included 39272 patients from 13 cohorts of patients receiving HAART between 1996 and 2006 in Europe and the USA, mortality attributed to cardiovascular disease in HIV patients was 7.9% (40% of which was due to CAD or myocardial infarction [MI] and 18% to stroke). The D:A:D study,7 which was completed later and included 49731 patients followed between 1999 and 2011 in clinics in Europe, the USA and Australia, reported mortality of 11% due to cardiovascular disease.

There are few data on the risk of adverse cardiovascular events in HIV-infected patients undergoing percutaneous coronary intervention (PCI) with drug-eluting stents in the context of acute coronary syndrome (ACS). Some studies10–12 have reported similar rates for infected and non-infected patients.

We report the case of an HIV patient with diabetes who presented acute thrombosis of drug-eluting stents in two different coronary arteries four hours after hospital discharge, which manifested as ST-elevation MI.

An unusual case of acute stent thrombosis in an HIV patient is presented, together with a literature review and discussion of possible explanations for this atypical presentation.

A 57-year-old man, black, born in Guinea and resident in Portugal since 1982, an astrologer, had a personal history of co-infection with HIV-2 and hepatitis B virus (HBV). HIV-2 was diagnosed in 1997 (19 years before this hospitalization), when HAART was begun. The patient's CD4+ T cell count before therapy is unknown. He was regularly monitored and complied with therapy, which included the antiretrovirals lamivudine, stavudine, indinavir and abacavir.

The patient's viral load and CD4+ T cell count were generally under control from the time of diagnosis, except for a period of one year approximately two years before this admission, when he presented an increased viral load (maximum 4500 copies/ml, although his CD4+ T cell count was controlled throughout this period).

At admission, the patient was under combined HAART, namely tenofovir and emtricitabine 300 mg/200 mg once daily; darunavir in combination with ritonavir 600 mg/100 mg twice daily and raltegravir 400 mg twice daily. He presented adequate CD4+ T cell counts and negative viral load. HBV infection was diagnosed in 2010 (six years before this hospitalization), and regular monitoring continued to show negative viral load under tenofovir therapy.

He had a history of insulin-treated type 2 diabetes, diagnosed 17 years prior to this admission, with no known microvascular complications, and mixed dyslipidemia (predominantly hypertriglyceridemia), diagnosed 10 years previously. Laboratory tests at the time of diagnosis showed total cholesterol 205 mg/dl, high density lipoprotein (HDL) cholesterol 21 mg/dl, low density lipoprotein (LDL) cholesterol 90 mg/dl, and triglycerides 265 mg/dl. Therapy with fenofibrate 145 mg/daily was begun, which the patient had continued ever since. Persistently high total and LDL cholesterol levels during follow-up led to atorvastatin 20 mg being added around four years previously.

The patient had no other risk factors, including smoking, cocaine use, hypertension, obesity or family history of sudden death.

Besides HAART, he was thus being medicated as an outpatient with atorvastatin 20 mg, fenofibrate 145 mg, pantoprazole 20 mg, linagliptin 5 mg and insulin (Insulatard®).

The patient went to the emergency department (ED) due to right chest pain radiating to the neck that had begun that morning as soon as he arose, not associated with effort and with no aggravating or alleviating factors. He reported no respiratory or gastrointestinal problems, fever or history of trauma.

Physical examination on admission to the ED revealed no significant alterations. Diagnostic exams included an ECG, which showed sinus rhythm and right bundle branch block (RBBB), but no ST-segment changes. Laboratory tests revealed hemoglobin 11.5 g/dl, sodium 134 mmol/l, potassium 4.6 mmol/l, chloride 100 mmol/l, urea 56 mg/dl, creatinine 1.46 mg/dl (estimated glomerular filtration rate 61 ml/min/1.73 m2 according to the Chronic Kidney Disease Epidemiology Collaboration equation), and increased myocardial necrosis markers (high-sensitivity troponin I 348.5 μg/l at first assessment and 392.2 μg/l at second assessment, a rise of 13%).

A diagnosis of non-ST elevation MI was made, a loading dose of dual antiplatelet therapy (aspirin and clopidogrel) was administered and the patient was admitted. He presented no further episodes of chest pain, myocardial necrosis markers fell from 409.9 μg/l (peak) to 78.2 μg/l and there were no new ECG alterations.

Coronary angiography on the fourth day of hospital stay showed two-vessel disease (90% stenosis of the mid segment of the right coronary artery [RCA], and 95% stenosis of the first marginal), and two drug-eluting stents were successfully implanted.

The patient remained hemodynamically stable under dual antiplatelet therapy (aspirin 100 mg/daily and clopidogrel 75 mg/daily) and high-dose statin therapy (atorvastatin 40 mg). Bisoprolol and lisinopril were also started during hospital stay. The patient also received the same antiretroviral therapy he had been receiving as an outpatient.

Laboratory tests during hospitalization showed poor metabolic control, with glycosylated hemoglobin 9.2% (7.0% three months previously) and undetectable HBV and HIV-2 viral loads. The patient's lipid profile at admission was total cholesterol 142 mg/dl, HDL cholesterol 18 mg/dl, LDL cholesterol 52 mg/dl (by direct measurement), and triglycerides 326 mg/dl. Testing for thrombophilia included measurement of protein S, protein C, homocysteine, factor V Leiden, antithrombin and von Willebrand factor, all of which were within the reference range; screening for anti-nuclear antibodies and lupus anticoagulant was also negative.

The patient was discharged on the 11th day of hospitalization, under the medication described above and maintaining the antiretroviral therapy he was receiving at admission. There were no further complications.

He returned to the ED four hours after discharge, due to chest pain radiating to his left arm.

The ECG showed sinus rhythm, RBBB and ST elevation in leads DII, DIII, and aVF and ST depression in leads V1-V3 (Figure 1).

Figure 1.

Admission electrocardiogram on second hospitalization, showing sinus rhythm, right bundle branch block, ST elevation in leads DII, DIII and aVF, and ST depression in leads V1-V3.

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Coronary angiography was performed within an hour of pain onset, and revealed occlusion of both stents (Figure 2a and b). Optical coherence tomography (OCT) of the two arteries was performed to clarify the situation. OCT of the RCA showed good stent apposition, intrastent thrombus and dissection beginning at the distal margin of the stent (Figure 3a-c), while OCT of the first marginal showed good apposition and intrastent thrombi but no dissection (Figure 4a, c-e). Angioplasty of the mid segment of the RCA was then performed, and a stent was implanted after thrombus aspiration (Figure 3d-f), as well as balloon angioplasty of the first marginal after thrombus aspiration (Figure 4b). There was a good final result, TIMI 3 flow being re-established in both arteries. A glycoprotein IIb/IIIa inhibitor (abciximab) was administered, due to the patient's high thrombotic burden.

Figure 2.

(a) Stent thrombosis in the right coronary artery (RCA) (arrow); (b) intraluminal subtraction image suggestive of RCA dissection (arrow); (c) RCA after thrombus aspiration.

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Figure 3.

(a) Right coronary artery (RCA) dissection visible by optical coherence tomography (OCT); (b) and (c) intrastent thrombosis in RCA visible by OCT; (d-f) intrastent view of the RCA by OCT after thrombus aspiration.

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Figure 4.

(a) Stent thrombosis in the first marginal; (b) first marginal after thrombus aspiration and stent placement; (c-e) thrombus in the first marginal documented by optical coherence tomography.

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After the procedure it was decided to replace clopidogrel by ticagrelor. The patient experienced no recurrence of pain or new ECG alterations during the rest of hospital stay. He was discharged medicated with aspirin 100 mg once daily, ticagrelor 90 mg twice daily, bisoprolol 5 mg once daily and lisinopril 20 mg once daily.

At the time this case report was prepared, the patient had undergone cardiological assessment after four months of follow-up, and no further ischemic complications were recorded.

The increased life expectancy of HIV-infected patients following the introduction of HAART has been accompanied by an increased prevalence of metabolic disorders, which raises new problems for their management.

The transformation of HIV infection from a disease with high short-term mortality to a chronic disease has raised new and pressing research questions regarding the cardiovascular risk of this population, given their known risk profile.

The current approach to reducing cardiovascular risk consists of early initiation of HAART and adequate control of conventional risk factors.

However, the case presented highlights the fact that adequate control of HIV infection and conventional risk factors may be insufficient, and raises various questions that require thorough investigation.

Finally, a multidisciplinary approach will help in choosing the most appropriate care for these patients, with emphasis on the role of the cardiologist, infectologist and internist.

The authors have no conflicts of interest to declare.