Relationship between coronary artery disease and C-reactive protein levels in NSTEMI patients with renal dysfunction: a retrospective study.

BACKGROUND: While chronic renal damage is a condition with low-grade inflammation, the potential role of inflammation in kidney disease as a marker of cardiovascular damage is of current interest. This study analyzed the relationship between renal dysfunction, chronic inflammation, and extension of coronary atherosclerosis in patients with non-ST-segment elevation myocardial infarction (NSTEMI). METHODS: This retrospective study was carried out on consecutive patients presenting with NSTEMI to Maggiore Hospital's emergency department between January 1, 2010 and December 31, 2011. Patients' electronic charts were reviewed to gather information on patients' history, clinical and biochemical variables, with a special focus on inflammatory markers, coronary vessel damage, and drug treatments. RESULTS: Of the 320 individuals in the study population, 138 (43.1%) had an admission GFR <60 mL/min/1.73 m2. Kidney dysfunction was significantly associated with age (OR = 1.09, 95% CI 1.06 to 1.12), history of heart failure (OR = 2.13, 95% CI 1.08 to 4.17), and hypertension (OR = 2.31, 95% 1.12 to 4.74). C-reactive protein (CRP) and uric acid levels were significantly increased in patients with severe renal dysfunction (SRD) by bivariate and multivariate analyses, adjusted for gender, age and comorbidities at admission. The extent of coronary artery disease (CAD) was significantly higher in the SRD group (p < 0.001). Individuals with SRD were less likely to receive immediate evidence-based therapies (62.9% vs. 76.7% and 82.0% in those with intermediate and no/mild renal dysfunction, p < 0.001). Hospital stay was significantly longer in individuals with a greater extent of CAD, diabetes, and a history of heart failure, and was borderline significantly associated with renal dysfunction (p = 0.08). Older age, CAD severity, and renal function were associated with worsening GFR during hospitalization, whereas immediate evidence-based treatment was unrelated to a GFR change. CONCLUSIONS: Among individuals hospitalized for NSTEMI, those with SRD had a more extensive CAD and a higher prevalence of pre-existing cardiovascular disease. CRP was positively correlated with renal dysfunction and the number of involved coronary vessels, confirming its potential as a biomarker. Uric acid was associated with renal dysfunction but not with the number of diseased coronary vessels.

Portal hypertensive gastropathy.

Portal hypertensive gastropathy (PHG) is the term used to describe the endoscopic appearance of gastric mucosa seen in patients with cirrhotic or non-cirrhotic portal hypertension with a characteristic mosaic-like pattern with or without red spots. The prevalence of PHG varies from 50% to 98%, this variation of the prevalence being perhaps related to patient selection, inter- and intra-observer variation and absence of uniform criteria and classification. About 8% of the upper digestive hemorrhages in the cirrhotic patients are secondary to PHG. There is no general consensus on the endoscopic classification of PHG (the most New Italian Endoscopy Club). The exact pathogenesis of PHG is not completely understood, but the portal hypertension is the main factor involved in its development and not the severity of the hepatic disease. Gastric Antral Vascular Ectasia (GAVE) is a term used for the typical endoscopic findings of red stripes, separated by normal mucosa, most frequently seen in the gastric antrum or proximal stomach. Current therapy of PHG includes beta blockers, somatostatin and derivates, endoscopic and surgical methods including hepatic transplantation.

The role of octreotide on renal function in patients with advanced cirrhosis.

UNLABELLED: Advanced cirrhosis is characterized by arterial vasodilatation and the reduced arterial response to vasoconstrictors. Both of these are related to an increase of endothelial (prostacyclin and nitric oxide) and nonendothelial vasodilatators (glucagon) level. Experimental study had shown that the responsiveness to vasoconstrictors of the mesentery artery may be normalized by the inhibition of glucagon or nitric oxide. The aim of our study was to assess the effects on renal hemodynamics by the administration of octreotide, the synthetic somatostatin analog, an inhibitor of the release of endogenous vasodilatators. METHODS: We studied forty-six patients admitted at the University Hospital in Bucharest for advanced cirrhosis between 2000-2002. The patients aged (35-62) were divided in two groups: Group I--23 patients received intravenous octreotide by infusion of 50 microg/hour for three days; Group II--23 patients received placebo. Exclusion criteria were: A recent gastrointestinal bleeding; Hepatic encephalopathy; Serum creatinine > 1.5 mg/dl; Ultrasonographic evidence of renal disease or urinary tract obstruction. STUDY PROTOCOL: Discontinuation of pharmacological treatment with beta-blockers, nitrates and angiotensin converting enzyme inhibitors 7 days before the study; Sodium restricted diet (35 mEq/day) 2 weeks before and during the study. All the patients underwent on day 0 and 3 the following; Routine laboratory tests, Creatinine clearance for glomerular filtration rate (GRF); Urinary sodium excretion (24 hours), Water diuresis, Lithium clearance, Plasma renin activity, Plasma aldosterone concentration, Medium blood pressure, Cardiac output (by ecocardiography). CONCLUSIONS: Octreotide in a short infusion treatment induces an inhibitory effect on renin aldosterone secretion which may be responsible for the benefical effects on sodium excretion. The significant increase of MAP may be the result of an inhibition of vasodilatatory substances or an increased arterial responsiveness to vasoconstrictors. The significant effect on renal function in patients with advanced cirrhosis can be a promising therapeutic perspective in the treatment of hepatorenal syndrome.

The effects of carvedilol a nonselective beta-blocker on portal hemodynamics in cirrhosis.

UNLABELLED: Portal hypertension is the result of increased hepatic resistance and portal influx. AIM: To assess the effects of Carvedilol, a 3rd-generation nonselective beta blocker with alpha1-adrenergic activity on portal and systemic homodynamic in patients with cirrhosis and portal hypertension. METHODS: Fifty patients with cirrhosis and portal hypertension were divided into two groups and statistically compared as follows: group I - 25 patients received Carvedilol, 12.5 mg/day and group II - 25 patients received placebo for six days. All the patients had hemodynamic, endocrine and renal measurements before and after administration of Carvedilol or placebo. They underwent creatinine clearance, lithium clearance, plasma renin activity, concentration of plasma aldosteron and urinary sodium excretion. Hemodynamic effects were assessed by portal flow volume and velocity, cardiac output and medium blood pressure. RESULTS: Carvedilol significantly increased the portal blood flow and velocity (p<0.05). Carvedilol reduced the medium blood pressure (p<0.001) with statistically insignificant alterations in creatinine clearance and 24-hours urinary sodium excretion. Carvedilol also reduced the concentration of plasma aldosteron (p < 0.002). CONCLUSIONS: Carvedilol can be used as an alternative drug for the prophylactic treatment of portal hypertension with careful monitoring of blood pressure regarding its hypotensive effects.