Recombinant human interleukin-1 receptor antagonist provides cardioprotection during myocardial ischemia reperfusion in the mouse.

PURPOSE: Acute myocardial infarction (AMI) drives an intense inflammatory response that contributes to infarct healing and cardiac remodeling. Recently, different studies have identified a role of interleukin-1 (IL-1) in the development of adverse cardiac remodeling. However, in animal models of AMI IL-1 has been shown to be cardioprotective in preconditioning, raising the question of clinical safety of therapeutic IL-1 blockade for autoinflammatory diseases or for the prevention or the treatment of AMI. In this study we proposed to evaluate the effects of pretreatment with recombinant human interleukin-1 receptor antagonist (rhIL-1Ra) on ischemia reperfusion (I/R) injury to the heart. METHODS: RhIL-1Ra was given 4 h or 30 min before the surgical induction of I/R. Left ventricular ejection fraction(LVEF) and infarct size were assessed to determine the effects of the drug pretreatment compared to vehicle treated mice. RESULTS: RhIL-1Ra, given 4 h or 30 min before the onset of the ischemia, showed marked cardioprotection though preservation of the LVEF (no change vs sham operated mice) and the reduction of the infarct size (-40 % vs vehicle-treated mice). No differences were observed between the two groups of rhIL-1Ra treatment. CONCLUSIONS: IL-1 blockade therapies using rhIL-1Ra prior the onset of AMI protects the myocardium and preserves cardiac function.

Large hemopericardium and pericardial tamponade from presumed erosion of a Watchman 2.5 device 1-year postimplantation.

Percutaneous left atrial appendage closure has allowed patients with atrial fibrillation who are at high risk of bleeding to safely discontinue their anticoagulant therapy shortly after device implantation. The procedure, however, comes with a small risk of complications, including pericardial effusion and tamponade. The complications pertaining to pericardial effusion occur mainly perioperatively. We present an 82-year-old man with a 24 mm Watchman 2.5 device who developed hemopericardium resulting in tamponade and shock from presumed erosion of the device into the pericardium 1 year after implantation.

Intravenous Fluid Therapy Is Associated with a Reduced Incidence of Contrast-Induced Nephropathy but not with a Reduced Long-Term Incidence of Renal Dysfunction After Cardiac Catheterization.

BACKGROUND: Intravenous fluid (IVF) administration for the prevention of contrast-induced nephropathy (CIN) is considered standard of care, but the effect of IVF therapy on longer-term outcomes after radiocontrast dye administration is not well known. METHODS AND RESULTS: We studied 4367 patients undergoing coronary and peripheral angiography and intervention at a veterans' administration medical center. 2653 patients (61%) received IVF prior to the procedure and 1714 (39%) did not. Of the 4367 subjects 1962 (45%) had repeat creatinine values at 72 h and 3100 (70%) had repeat creatinine values at 3 months. CIN at 72 h occurred in 68 (6.7%) patients in the IVF group and in 87 patients (9.8%) in the group receiving no IVF (odds ratio [OR] 0.97; 95% confidence interval [CI] 0.94-0.99; p = 0.004). At 3 months, renal dysfunction was seen in 224 (11.5%) patients of the IVF group versus 152 (13.1%) of the group receiving no IVF (OR 0.98, CI 0.96-1.01; p = 0.18). In adjusted analyses using a propensity score, IVF therapy was associated with a significant reduction in CIN occurrence at 72 h (OR = 0.97, (95% CI 0.94-0.99, p = 0.01) but was not associated with a change in the incidence of renal dysfunction at 3 months (OR 0.98, 95% CI 0.96-1.01. p = 0.18). CONCLUSION: In this cohort of US veterans, IVF administration was associated with a decreased incidence of CIN at 72 h but was not associated with a decreased incidence of renal dysfunction at 3 months.

Race, contrast-induced nephropathy and long-term outcomes after coronary and peripheral angiography and intervention.

BACKGROUND: Contrast-induced nephropathy (CIN) is a complication of diagnostic angiography and percutaneous coronary and endovascular intervention. We investigated the effect of race on the development of CIN. METHODS: We studied 4070 predominantly male patients undergoing peripheral and coronary angiography and percutaneous coronary and endovascular intervention. We analyzed the incidence of CIN at 72 h, of renal dysfunction at 3 months as well as the long-term incidence of hemodialysis and of death. RESULTS: The mean age was 67.2 years. CIN occurred in 92 (7.1%) Caucasian patients and in 42 (6.6%) non-Caucasians at 72 h after the procedure (odds ratio [OR] 1.08, 95% confidence interval [CI] 0.74-1.57; P = 0.69). At 3 months, renal dysfunction was seen in 231 (11.24%) Caucasian patients versus 121 (11.52%) of the non-Caucasian group (OR 0.97, CI 0.77-1.23; P = 0.81). After a follow-up of 5 years, of the 4070 patients, 17 patients (0.64%) of the Caucasian group were placed on dialysis versus 27 (1.88%) of the non-Caucasian group (OR 0.34, 0.18-0.62; P = 0.0004) and 535 (20.28%) of the Caucasian patients had died compared to 293 (20.44%) of the non-Caucasian group (OR = 0.99, 95% CI 0.85-1.17; P = 0.94). CONCLUSIONS: In this cohort of patients, race was not associated with the development of CIN at 72 h, or the development of renal dysfunction at 3 months post angiography or intervention. In the long-term, the rate of initiation of dialysis was significantly lower in the Caucasian patients but mortality was not.

Race and contrast-induced nephropathy in patients undergoing coronary angiography and cardiac catheterization.

Contrast-induced nephropathy (CIN) is an acute worsening of renal function after receiving intravascular contrast during a procedure. Some of the predisposing factors include underlying diabetes, chronic kidney disease, congestive heart failure, periprocedural hypotension, anemia, contrast volume, and osmolality of contrast; however, it remains unclear if risk varies for CIN with race and ethnicity. There is evidence in the literature showing the link between race/ethnicity and the discrepancies in the utilization of preventive care services and the resources related to cardiovascular and renal health. While these disparities continue to exist and affect some of the predictors of CIN, this review will explore the extent to which race and ethnicity directly affect CIN.

Tolerability and Biological Effects of Long-Acting Octreotide in Patients With Continuous Flow Left Ventricular Assist Devices.

Patients with implanted continuous, nonpulsatile, left ventricular assist devices (LVADs) have increased the occurrence of gastrointestinal bleeding (GIB). Although the pathophysiology is multifactorial, there are few treatments beyond supportive care. Octreotide acetate is a somatostatin analog that reduces GIB in various patient populations. However, there are sparse case series that suggest octreotide acetate may reduce GIB in LVAD patients. This 10 patient, 28 week phase I study evaluated the safety and tolerability of octreotide acetate long-acting release (LAR) 20 mg depot injection every 4 weeks until week 16 after LVAD placement. Secondary aims were occurrence of GIB and measurement of vascular endothelial growth factor, fibrinogen, von Willebrand factor, and platelet aggregation across the study period. Ten patients were enrolled, and eight completed the study. The two study dropouts were not related to octreotide. None of the patients experienced side effects or safety concerns related to octreotide nor did GIB occur in the study population. Vascular endothelial growth factor levels were maintained in the reference range throughout the duration of the study. There did appear to be laboratory evidence of acquired von Willebrand syndrome, with mildly low platelet aggregation studies. In conclusion, octreotide acetate LAR 20 mg depot injection was safe and effective in this population.

Myocardial protection from ischemia-reperfusion injury post coronary revascularization.

Effective primary and secondary prevention and advances in cardiac surgery have significantly improved the care and outcomes of patients with myocardial ischemia. While timely reperfusion has proved to be an invaluable tool, ischemia-reperfusion injury represents a mechanism that may limit its effectiveness. Numerous experimental studies have shown effective protection from ischemia-reperfusion injury in animal models, but translation into clinical practice has been less successful. This article summarizes the role of ischemia-reperfusion injury in the pathophysiology of ischemic heart disease and gives an overview of the various modalities that have been developed in order to provide myocardial protection from reperfusion injury in clinical practice.