Elevated uric acid/albumin ratio as a predictor of poor coronary collateral circulation development in patients with non-ST segment elevation myocardial infarction.

BACKGROUND: Uric acid/albumin ratio (UAR) is a novel composite biomarker with superior predictive value for cardiovascular disease. OBJECTIVE: To investigate the relationship between UAR and coronary collateral circulation (CCC) in patients with non-ST segment elevation myocardial infarction (NSTEMI). METHODS: A total of 205 NSTEMI patients who underwent coronary arteriography with at least one major coronary stenosis, 95% were included. Patients were divided into two groups according to CCC development: poorly-developed CCC group (Rentrop 0-1) and well-developed CCC (Rentrop 2-3). Univariate analysis and logistic regression analysis were utilized to investigate the factors influencing adverse CCC formation in NSTEMI patients. The receiver operating characteristic (ROC) curve was plotted to evaluate the predictive value of UAR, C-reactive protein (CRP), uric acid, and albumin for patients with poorly developed CCC, and the area under the curve (AUC) was compared. RESULTS: The UAR values of NSTEMI patients were significantly higher in the poorly developed CCC group than those in the well-developed CCC group (10.19 [8.80-11.74] vs. 7.79 [6.28-9.55], p < .001). In the multiple logistic regression tests, UAR (odds ratio [OR]: 1.365, 95% confidence interval [CI]: 1.195-1.560, p < .001), CRP (OR: 1.149, 95% CI: 1.072-1.231, p < .001), and diabetes (OR: 2.924, 95% CI: 1.444-5.920, p = .003) were independent predictors of poorly developed CCC. The ROC curve analysis showed that the optimal cut-off value of UAR was 8.78 in predicting poorly developed CCC with a sensitivity of 76.8% and specificity of 62.4%, with the AUC of 0.737 (95% Cl: 0.668-0.805, p < .001). CONCLUSION: Elevated UAR may be an independent and effective biomarker for predicting poorly-developed CCC development in NSTEMI patients.

Essential thrombocythemia with non-ST-segment elevation myocardial infarction as the first manifestation: A case report.

BACKGROUND: We report a case of essential thrombocythemia (ET) in a 44-year-old male who exhibited non-ST-segment-elevation myocardial infarction (NSTEMI) as the first manifestation without known cardiovascular risk factors (CVRFs). For the first time, we reported a left main trifurcation lesion in NSTEMI caused by ET, including continuous stenosis lesions from the left main to the ostial left anterior descending (LAD) artery and an obvious thrombotic lesion in the ostial and proximal left circumflex (LCX) artery. There was 60% diffuse stenosis in the left main (LM) that extended to the ostial LAD, thrombosis of the ostial LAD and proximal LCX, and 90% stenosis in the proximal LCX. During the operation, thrombus aspiration was performed, but no obvious thrombus was aspirated. Performing the kissing balloon technique (KBT) in the LCX and LM unexpectedly increased the narrowness of the LAD. Then, the single-stent crossover technique, final kissing balloon technique and proximal optimization technique (POT) were performed. On the second day after percutaneous coronary intervention (PCI), the number of platelets (PLTs) still increased significantly to as high as 696 × 109/L. The bone marrow biopsy done later, together with JAK2 (exon 14) V617F mutation, confirms the diagnosis of ET. Hydroxyurea was administered to inhibit bone marrow proliferation to control the number of PLTs. CASE SUMMARY: A 44-year-old male patient went to a local hospital for treatment for intermittent chest pain occurring over 8 h. The examination at the local hospital revealed elevated cTnI and significantly elevated platelet. Then, he was diagnosed with acute myocardial infarction and transferred to our hospital for emergency interventional treatment by ambulance. During the operation, thrombus aspiration, the single-stent crossover technique, final kissing balloon technique and POT were performed. Dual antiplatelet therapy comprising aspirin and ticagrelor was used after PCI. Evidence of mutated JAK2 V617F and bone marrow biopsy shown the onset of ET. Together with JAK2 (exon 14) V617F mutation, ET was diagnosed according to the World Health Organization (WHO) diagnostic criteria, and the patient was placed on hydroxyurea. During the one-year postoperative period, repeated examinations showed a slight increase in PLTs, but the patient no longer had chest tightness, chest pain or bleeding or developed new thromboembolisms. CONCLUSION: Routine physical examinations and screenings are conducive to the early detection of ET, and the risk for thrombosis should be assessed. Then, active antiplatelet therapy and myelosuppression therapy should be used for high-risk ET patients.