1. AbstractJuvenile idiopathic arthritis (JIA) is the most common chronic inflammatory arthritis under 16 years of age but unlike rheumatoid arthritis, the risk of cardiovascular diseases including Myocardial Infarction (MI) in adulthood with JIA is not yet proven. This young lady with a background of JIA that progressed to adulthood wasradiating to her left arm. The pain was associated with nausea, vomiting and profuse sweating. Serial ECGs were done that showed evolving ST elevation up to 5 mm in limb leads II, III and aVF (Figure 1). She was admitted to CCU with Acute Inferior wall myocardial infarction. This young lady was previously diagnosed with juvenile idiopathic arthritis at the age of 12 years but was not on any regular treatment. For the last 1 year she was started on tapering dose of oral steroids as her arthritis got worsened. Besides that she had no significant past medical or surgical history. Her family history is also unremarkable. On examination of the patient, she had developed cushingoid facies. Vitally she was stable with a BP of 130/80 mm Hg and pulse of 68 bpm. She was maintaining saturation of 96% at room air. There were no visible joint deformities and no signs of acute inflammation. Baseline investigations showed a raised troponin level of 25 ng/ml (Normal: 0.6 ng/ml), raised ESR of 50 mm/1st hr. (Normal: 0-20 mm/1st hr.) and raised quantitative C - reactive protein (CRP) to 53.06 mg/L (Normal: 5.0 mg/L). Quantitative rheumatoid factor (RF) was 16 IU/ml (Normal: 14 IU/ml). Fasting Lipid profile, blood glucose level and liver and kidney function tests were all normal. 2D echocardiogram was obtained the report of which is given in (Figure 2). She was loaded with 300 mg of aspirin and 300 mg clopidogrel per oral. 60 mg of low molecular weight heparin (LMWH) was given subcutaneously. After informed consent she was thrombolysed with 1.5 million IU of streptokinase (SK) diluted in 100 ml normalg adults to cardiovascular diseases, the case presented below is like a spark in the dark as this young lady had an MI without any known risk factors for MI.
3. Case HistoryThis is a story of 24 years old girl who presented to CCU in the evening with 3 hours history of severe crushing central chest painradiating to her left arm. The pain was associated with nausea, vomiting and profuse sweating. Serial ECGs were done that showed evolving ST elevation up to 5 mm in limb leads II, III and aVF (Figure 1). She was admitted to CCU with Acute Inferior wall myocardial infarction. This young lady was previously diagnosed with juvenile idiopathic arthritis at the age of 12 years but was not on any regular treatment. For the last 1 year she was started on tapering dose of oral steroids as her arthritis got worsened. Besides that she had no significant past medical or surgical history. Her family history is also unremarkable. On examination of the patient, she had developed cushingoid facies. Vitally she was stable with a BP of 130/80 mm Hg and pulse of 68 bpm. She was maintaining saturation of 96% at room air. There were no visible joint deformities and no signs of acute inflammation. Baseline investigations showed a raised troponin level of 25 ng/ml (Normal: 0.6 ng/ml), raised ESR of 50 mm/1st hr. (Normal: 0-20 mm/1st hr.) and raised quantitative C - reactive protein (CRP) to 53.06 mg/L (Normal: 5.0 mg/L). Quantitative rheumatoid factor (RF) was 16 IU/ml (Normal: 14 IU/ml). Fasting Lipid profile, blood glucose level and liver and kidney function tests were all normal. 2D echocardiogram was obtained the report of which is given in (Figure 2). She was loaded with 300 mg of aspirin and 300 mg clopidogrel per oral. 60 mg of low molecular weight heparin (LMWH) was given subcutaneously. After informed consent she was thrombolysed with 1.5 million IU of streptokinase (SK) diluted in 100 ml normal
4. DiscussionThe risk of MI in adulthood with JIA is the same as in general population [1]. This case is presented here because no cases has been reported till date to show increased risk of MI in patients with JIA who have no known cardiovascular risk factor. Multicenter studies have been conducted to see the relation which has remained statistically insignificant. Researchers are very keen to uncover this relationship between MI and JIA which offers a lot of work to be done in this area of medicine.
References1. Jason H. Anderson, Katelyn R. Anderson, Hanne A. Aulie, et al. Juvenile Idiopathic Arthritis and Future Risk For Cardiovascular Disease: A Multicenter Study. Scand J Rheumatol. 2016 Jul; 45(4): 299-303.
2. Selvaag AM, Aulie HA, Lilleby V, Flato B. Disease progression into adulthood and predictors of long-term active disease in juvenile idiopathic arthritis. Ann Rheum Dis. 2016 Jan; 75(1): 190-5.
3. Avina-Zubieta JA, Thomas J, Sadatsafavi M, Lehman AJ, Lacaille D. Risk of incident of cardiovascular events in patients with rheumatoid arthritis: a meta-analysis of observational studies. Ann Rheum Dis. 2012; 71(9): 1524-9.
4. Coulson EJ, Ng WF, Goff I, Foster HE. Cardiovascular risk in juvenile idiopathic arthritis. Rheumatology (Oxford). 2013; 52(7): 1163- 71.
Akhtar S .Myocardial Infarction on the Background of Juvenile Idiopathic Arthritis . Annals of Clinical and Medical Case Reports 2021