Management and recommendations for the prevention of contrast-induced acute kidney injury. state of the art in clinical practice

Contrast-induced acute kidney injury (CI-AKI) is defined as an acute kidney failure following iodine-based contrast medium administration determining relevant health and socio-sanitary implications. Knowledge of pathophysiology, early diagnosis, and prevention in patients at risk are critical points in CI-AKI management. Determination of risk and functional kidney evaluation must precede every iodine-based contrast medium (CM) administration in order to eventually introduce medical prophylaxis. Furthermore, early laboratoristic evaluation after iodine-based CM exposure should be performed for a prompt identification of acute kidney injury. Therefore, clinicians must know and strictly follow valid recommendations to minimize the development of complications

Is successful stent implantation protecting myocardium from stunning?

not availabl

Ischemic episodes induced by balloon inflation impair global rather than regional LV function in humans.

not availabl

Regional Left Ventricular contractility during episodes induced by balloon inflations: a transesophageal echocardiographic study.

not availabl

Normalization of impairment of TIMI flow and of hibernating and stunned myocardium after coronary stenting and alpha-adrenergic blockade

not availabl

The a1fa1-adrenergic blocker urapidil improves contractile function in patients 3 months after coronary stenting: A randomized, double-blinded study

Background The recovery of left ventricular function (LVF) after revascularization takes time. -Adrenergic blockade acutely improves coronary blood flow and LVF, whereas the effects of more prolonged -adrenergic blockade on LVF recovery after stenting are unknown. Methods In 32 patients (age 58 12 y) with an 82% 6% stenosis, ejection fraction (EF) and systolic thickening (%Th) were measured by transthoracic echocardiography before and 30 minutes to 2 hours after revascularization. In a double-blinded protocol, either 200 g/kg urapidil or placebo was given intravenously, and LVF was measured 10 minutes later. Two hours later, oral treatment with 30 mg/d drug or placebo was started, and LVF measured again after 24 hours and 3 months. Results Before revascularization, EF was 49.4% 8.5% (SD) and 51.3% 8.8% in the urapidil-treated and the placebo groups, respectively. Thirty minutes to 2 hours after coronary stenting, EF was unchanged. After intravenous drug administration, EF increased to 56.5% 9.7%). At 24 hours and 3 months after revascularization, EF became 59.5% 7.9% and 59.6% 8.2% in the urapidil-treated group, respectively, whereas EF in the placebo group did not change (50.4% 5.7% and 49.7% 4.9%, respectively). Revascularization did not acutely improve %Th. Intravenous urapidil improved %Th from 31.4% 17.6% to 44.2% 11.6%, whereas there was no change in the placebo group. At 3 months, %Th was 49.5% 12.9% in the urapidil-treated group and 39.7% 8.9% in the placebo group. Conclusions These data suggest that long-term -adrenergic blockade might improve LVF at midterm after coronary revascularization

Myocardial ischemia and coronary flow reserve impairment

not availabl