Leptin affects the inflammatory response after STEMI.

Leptin is an adipose tissue-derived hormone primarily involved in the regulation of food intake. Leptine has been shown to have a much broader role than just regulating body weight and appetite in response to food intake: among the others, it has been associated with increased ROS production and inflammation, factors involved in the restoration of an effective myocardial reperfusion after myocardial revascularization. Our study, to our best knowledge, is the first showing a direct relationship between leptin serum levels, inflammatory mediators of the ischemia reperfusion damage and effective myocardial reperfusion in patients with ST elevation myocardial infarction undergoing primary percutaneous coronary intervention. Our findings suggest that leptin serum levels are directly associated with the inflammatory response during an acute myocardial infarction and may have a role in risk stratification in this clinical setting.

Risk factors for primary ventricular fibrillation during a first myocardial infarction: Clinical findings from PREDESTINATION (PRimary vEntricular fibrillation and suDden dEath during firST myocardIal iNfArcTION).

BACKGROUND: Few studies prospectively assessed risk factors for ventricular fibrillation (VF) during a first myocardial infarction (MI). We designed a nation-wide study aiming to identify clinical and genetic characteristics associated with primary VF; and report here about clinical features. METHODS: PREDESTINATION (PRimary vEntricular fibrillation and suDden dEath during a firST myocardIal iNfArcTION) is an Italian case-control, prospective multicentre study. Cases are patients aged 18-80 years with a first MI and at least one VF episodes occurring within 24 h of symptoms onset, before reperfusion. Cases and controls are paired 1: 2 by gender and age (±5 years). RESULTS: Among 1026 patients enrolled between 2007 and 2017, 970 entered the primary analysis: 375 cases and 595 controls (mean age 59 years, 85% males). Multivariable analysis identified 5 independent predictors of primary VF: systolic blood pressure (OR 0.982, 95% CI: 0.98-0.99 for each mm Hg) and K+ levels <3.5 mEq/L at presentation (OR 2.28, 95% CI: 1.6-3.3), family history of sudden death (OR 1.80, 95% CI: 1.1-3.0), physical inactivity (OR 1.73, 95% CI: 1.1-2.8) and anterior MI (OR 1.52, 95% CI: 1.1-2.1). Excluding K+ levels obtained after VF, the OR associated with K+ levels <3.5 mEq/L was1.99 (95 CI 1.22-3.21). CONCLUSIONS: The present study identified 5 independent predictors of primary VF: familiarity, anterior MI, low systolic blood pressure, physical inactivity and hypokalaemia. Importantly, the last two risk factors are modifiable and, especially in the presence of a family history of sudden death, they should be avoided as much as possible.

Elevated serum uric acid affects myocardial reperfusion and infarct size in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

AIMS: Elevated serum uric acid (eSUA) was associated with unfavorable outcome in patients with ST-segment elevation myocardial infarction (STEMI). However, the effect of eSUA on myocardial reperfusion injury and infarct size has been poorly investigated. Our aim was to correlate eSUA with infarct size, infarct size shrinkage, myocardial reperfusion grade and long-term mortality in STEMI patients undergoing primary percutaneous coronary intervention. METHODS: We performed a post-hoc patients-level analysis of two randomized controlled trials, testing strategies for myocardial ischemia/reperfusion injury protection. Each patient underwent acute (3-5 days) and follow-up (4-6 months) cardiac magnetic resonance. Infarct size and infarct size shrinkage were outcomes of interest. We assessed T2-weighted edema, myocardial blush grade (MBG), corrected Thrombolysis in myocardial infarction Frame Count, ST-segment resolution and long-term all-cause mortality. RESULTS: A total of 101 (86.1% anterior) STEMI patients were included; eSUA was found in 16 (15.8%) patients. Infarct size was larger in eSUA compared with non-eSUA patients (42.3 ±â€Š22 vs. 29.1 ±â€Š15 ml, P = 0.008). After adjusting for covariates, infarct size was 10.3 ml (95% confidence interval 1.2-19.3 ml, P = 0.001) larger in eSUA. Among patients with anterior myocardial infarction the difference in delayed enhancement between groups was maintained (respectively, 42.3 ±â€Š22.4 vs. 29.9 ±â€Š15.4 ml, P = 0.015). Infarct size shrinkage was similar between the groups. Compared with non-eSUA, eSUA patients had larger T2-weighted edema (53.8 vs. 41.2 ml, P = 0.031) and less favorable MBG (MBG < 2: 44.4 vs. 13.6%, P = 0.045). Corrected Thrombolysis in myocardial infarction Frame Count and ST-segment resolution did not significantly differ between the groups. At a median follow-up of 7.3 years, all-cause mortality was higher in the eSUA group (18.8 vs. 2.4%, P = 0.028). CONCLUSION: eSUA may affect myocardial reperfusion in patients with STEMI undergoing percutaneous coronary intervention and is associated with larger infarct size and higher long-term mortality.