Asymptomatic hyperuricemia: to treat or not a threat? A clinical and evidence-based approach to the management of hyperuricemia in the context of cardiovascular diseases.

Asymptomatic hyperuricemia is defined by serum uric acid levels above 6.2 mg/dl in women and 7 mg/dl in men. In the presence of monosodium urate crystal formation and articular inflammation, hyperuricemia may become symptomatic (namely nephrolithiasis and gout). Uric acid results from purine catabolism and is at the centre of a complex metabolic interplay that involves oxidative stress, inflammation, renin-angiotensin-aldosterone system (RAAS) activation and insulin resistance. Uric acid levels present a continuous relation with conditions like hypertension and chronic kidney disease (CKD) and are reported to have an impact on risk of cardiovascular events. However, whether elevated uric acid is a causal agent and thus a possible therapeutic target is still uncertain and matter of further investigation. Treating symptomatic hyperuricemia involves lowering uric acid drugs and controlling inflammation. Urate-lowering agents are well tolerated but show minimal impact on cardiovascular events in patients with gout. Use of direct-acting urate-lowering agents in asymptomatic hyperuricemia associated with cardiovascular diseases does not warrant a clear benefit, whereas addressing cardiovascular issues with guideline-recommended therapies lowers uric acid and reduces the occurrence of cardiovascular events. Regular assessment of uric acid and clinical symptoms is advised before starting and renewing a urate-lowering treatment.

A New Frontier for Drug-Coated Balloons: Treatment of "De Novo" Stenosis in Large Vessel Coronary Artery Disease.

Background: Drug-coated balloons (DCB) are a well-established option for treating in-stent restenosis endorsed by European Guidelines on myocardial revascularization. However, in recent years, a strategy of "leaving nothing behind" with DCB in de novo coronary stenosis has emerged as an appealing approach. Methods: We performed a systematic review to evaluate the current literature on the use of drug-coated balloons in the treatment of de novo stenosis in large vessel disease. Results: Observational studies, as well as randomized studies, demonstrated the safety of DCB percutaneous coronary interventions (PCI) in large vessel disease. The rate of major adverse cardiac events is even lower compared to drug-eluting stents in stable coronary artery disease. Conclusions: DCB PCI is feasible in large vessel disease, and future large, randomized studies are ongoing to confirm these results.

Role of perilipin 2 in microvascular obstruction in patients with ST-elevation myocardial infarction.

AIMS: Coronary microvascular obstruction (MVO) occurs frequently in patients with ST-elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI). However, mechanisms are multiple and not yet fully understood. Perilipin 2 (PLIN2) is involved in lipid metabolism of macrophages resident in atherosclerotic plaques, along with a role in enhancing plaque inflammation. We studied the association between PLIN2 and MVO in STEMI patients undergoing primary PCI, and we assessed the role of PLIN2 to predict major adverse cardiovascular events (MACEs). METHODS AND RESULTS: STEMI patients undergoing primary PCI were enrolled. PLIN2 was evaluated in peripheral blood monocytes; MVO was assessed using coronary angiogram. MACEs, as a composite of cardiac death, non-fatal myocardial infarction, re-admission for heart failure, and target vessel revascularization were investigated at follow-up. Among 100 STEMI patients, 33 (33.0%) had MVO. Patients with MVO had higher levels of PLIN2 (1.03 ± 0.28 vs. 0.90 ± 0.16, P = 0.019). Age [odds ratio (OR) (95% confidence interval, CI), 1.045 (1.005-1.087), P = 0.026] and PLIN2 [OR (95% CI), 16.606 (2.027-136.030), P = 0.009] were associated with MVO at univariate analysis, although only PLIN2 [OR (95% CI), 12.325 (1.446-105.039), P = 0.022] was associated with MVO at multivariate analysis. After a mean follow-up of 182.2 ± 126.6 days, 13 MACEs occurred. MVO [hazard ratio (HR) (95% CI), 6.791 (2.053-22.462), P = 0.002], hypercholesterolaemia [HR (95% CI), 3.563 (1.094-11.599), P = 0.035], and PLIN2 [HR (95% CI), 82.991 (9.857-698.746), P < 0.001] were predictors of MACEs at univariate analysis, although only PLIN2 [HR (95% CI), 26.904 (2.461-294.100), P = 0.007] predicted MACEs at multivariate analysis. CONCLUSIONS: In STEMI patients undergoing primary PCI, PLIN2 was independently associated with MVO and was an independent predictor of MACEs at follow-up, suggesting to further explore PLIN2 as a target for future cardioprotection therapies.