Effects of remote ischemic preconditioning on contrast induced nephropathy after percutaneous coronary intervention in patients with acute coronary syndrome.

OBJECTIVE: The aim of this study was to explore the clinical effects of remote ischemic preconditioning (RIPC) on contrast-induced nephropathy after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS). PATIENTS AND METHODS: The study was a single-center, prospective, randomized, controlled study. A total of 161 patients with ACS and the rate of estimate glomerular filtration (eGFR) 15 to 70 mL/min/1.73 m2 undergoing PCI were randomly assigned to RIPC group (induced by 4 times of 5-minute inflations of a blood pressure cuff to 200 mmHg around the upper arm, followed by 5-min intervals of reperfusion at 1 hour before PCI therapy) or control group (an uninflated cuff around the arm). Successful completion of the PCI eventually included 107 cases of patients, including 50 cases in the RIPC group and 57 cases in the control group. The level of serum creatinine (Scr), CystatinC (CysC), blood neutrophil gelatinase-associated lipocalin (NGAL), eGFR were measured in all patients at 6 AM before the day of PCI, and 4-hour NGAL, 24-hour CysC, 72-hour Scr, and eGFR after PCI in the 2 groups. The incidence of major adverse events in the kidney (including the incidence of CIN, the need for dialysis, or renal replacement therapy after using contrast agent) and the composite endpoint of cardiovascular events were recorded at 6 months after PCI. RESULTS: There were no statistically significant differences in baseline indicators between the 2 groups. Scr, CysC, and blood NGAL levels and the incidence of CIN in patients with RIPC group were significantly lower than those form the control group after PCI (P < .05), but there were no significant differences between the average value of eGFR and occurrence of Major cardiovascular events in the postoperative 6 months (P > .05). CONCLUSIONS: RIPC can reduce PCI-related CIN and protect renal function in patients with ACS. The benefits of these patients by RIPC may be related to the reduction of the NGAL and CysC.

Apelin­13 promotes cell proliferation in the H9c2 cardiomyoblast cell line by triggering extracellular signal­regulated kinase 1/2 and protein kinase B phosphorylation.

Apelin­13 (APL­13), a peptide hormone that serves as a ligand for G­protein coupled receptors, has been demonstrated to be highly expressed in left ventricular hypertrophy rat models. It has been implicated in cardio­protection under pathological states. The present study aimed to assess the physiological proliferation effect of APL­13 in cultured H9c2 cardiomyoblast cells, and to elucidate the underlying mechanisms. Cell proliferation was determined by MTT assay. The extracellular signal­regulated kinase (ERK) 1/2 and protein kinase B (Akt) signaling pathway was identified, and protein expression levels were detected using western blot analysis. The results demonstrated that APL­13 markedly increased cell proliferation. Western blotting results suggested that APL­13 significantly enhanced the expression of phosphoinositide ERK1/2 and Akt activation in a dose­dependent manner. U0126 (10 µM; ERK1/2 inhibitor) and/or 10 µM LY294002 (Akt inhibitor) were used to help to determine the APL­signaling mechanism. As a result, LY294002 and U0126 partially blocked the APL­13 induced H9c2 proliferation. In conclusion, these data suggested that APL­13 has a proliferative effect on myocardium cells via the Akt and ERK1/2 signaling pathways, and provide potential novel pharmaceutical targets for cardiovascular disease.

Effect of prolonged intra-aortic balloon pumping in patients with cardiogenic shock following acute myocardial infarction.

BACKGROUND: To evaluate the efficacy of prolonged intra-aortic balloon pumping (IABP) support in patients with cardiogenic shock following acute myocardial infarction (AMI). MATERIAL/METHODS: Thirty-nine patients with cardiogenic shock after AMI were treated with percutaneous coronary intervention which was supported by IABP. After 72 hours of IABP, the patients who attained the criteria of IABP withdrawal were randomly divided into two groups. The control group ceased IABP whereas the study group continued IABP for additional seven days. RESULTS: After IABP, mean arterial pressure, cardiac index, left ventricle ejection fraction and arterial oxygen saturation were significantly elevated in all patients whereas pulmonary capillary wedge pressure and heart rate were decreased. The improvement of cardiac index, left ventricular ejection fraction and pulmonary capillary wedge pressure in the study group was greater than the control group (P<0.05). After 12-month follow-up, the 6-min walking test and left ventricular ejection fraction in the study group were significantly higher than those of the control group (P<0.05). No significant differences were noted between the two groups in the incidence ventricular aneurysm and mortality rate. CONCLUSIONS: Prolonged use of IABP for up to 10 days offers additional long term benefit in left ventricular function and exercise tolerance.