Abstract Background The term Cardiorenal Syndrome (CS) has been recently introduced to indicate the close relationship between cardiovascular and renal diseases, which are able to reciprocally influence the each other progression. In this setting the renal resistance index (RRI) has been demonstrated to be a useful parameter able to detect patients at higher risk of CS. However, there are no data about its role in predicting worsening of renal function (WRF) mediated by the intravascular administration of contrast. Aim of the Study To evaluate the role of RRI in predicting WRF after coronary angiography. METHODS We enrolled 115 patients (mean age 64 years, 73% males, 84% hypertensive, 43% diabetic, 30% with acute coronary syndrome, 21% affected by chronic heart failure, CHF, with a mean left ventricular ejection fraction, LVEF, of 51±11) with suspected coronary artery disease, stable angina, or acute coronary syndromes who have been referred for coronary angiography (with or without pre–existing renal impairment). All patients underwent medical examination, electrocardiogram, echocardiographic and chemical evaluation, and renal arterial echo–color Doppler used to calculate RRI. WRF was defined as an increase of creatinine >0.3 mg/dl and of at least 25% from baseline 24–48 hours after coronary angiography. Results After coronary angiography, 14 (12%) of the enrolled patients showed WRF. As shown in the Table, at univariate regression analysis baseline RRI was associated with WRF as well as age, peripheral artery disease, CHF, atrial fibrillation, NYHA class, LVEF, mitral regurgitation (MR), central venous pressure (CVP), tricuspid regurgitation (TR), estimated glomerular filtration rate (GFR). In a multivariate forward stepwise regression model, including all univariate predictors, history of CHF, high CVP and RRI were the only parameters significantly associated with WRF. Conclusion Our findings demonstrate that in patients undergoing coronary angiography, history of CHF, high CVP and RRI are independent predictors of WRF. RRI, but not GFR, is independently associated with WRF probably because providing additional relevant information about cardiorenal pathophysiological factors reflecting the hemodynamic status and kidney flow reserve.

Abstract Background Renal resistance index is a Doppler derived measure which is able to reflect the pathophysiological background of Cardiorenal Syndrome (CS). There are no data about the influence of the intravascular administration of contrast media on RRI and its relationship with worsening of renal function (WRF). Aim of the Study To evaluate changes in renal resistance index (RRI) after coronary angiography in patients with and without WRF. METHODS We enrolled 115 patients (mean age 64 years, 73% males, 84% hypertensive, 43% diabetic, 30% with acute coronary syndrome, 21% affected by chronic heart failure, CHF, with a mean left ventricular ejection fraction, LVEF, of 51±11) with suspected coronary artery disease, stable angina, or acute coronary syndromes who have been referred for coronary angiography (with or without pre–existing renal impairment). Renal arterial echo–color Doppler was used to calculate RRI before and 48 hours after coronary angiography. WRF was defined as an increase of creatinine >0.3 mg/dl and of at least 25% from baseline 24–48 hours after coronary angiography. Results Fourteen (12%) among the enrolled patients showed WRF. As expected, a significant increase of creatinine serum levels was observed in patients with WRF (from 1.14±0.40 to 1.71±0.49, p < 0.001) but not those without (from 0.89±0.27 to 0.92±0.28, p n.s.) WRF. On the other hand, RRI significantly increased both in patients with (from 72.8±4.3 to 76.4±5.2, p < 0.05) and without (from 63.1±7.2 to 65.4±7.1, p < 0.05). However, both at baseline and after angiography, patients with WRF showed RRI values significantly greater when compared with those without. At ROC curve analyses for WRF, the baseline and after angiography RRI sowed similar AUC (0.88 and 0.90, respectively) and for both RRI values the best cut–off was 70% (sensitivity of 79% and 93% and Specificity of 93% and 82%, respectively). As shown in the figure, the high predictive accuracy of RRI values was due to the fact that, although increased after angiography, the proportion of patients without WRF and with RRI>70% remained very low. Conclusion After coronary angiography RRI significantly increase both in patients with and without WRF. However, a larger proportion of patients with WRF present a critically increased RRI, i.e. equal or above 70%, before and after angiography probably because reflecting the pathophysiological background underlying the progression of cardiorenal syndrome.

Background: The aim was to investigate prognostic relevance of history of allergy in subjects with unstable angina treated with coronary angioplasty.Methods: Fifty-seven consecutive patients with unstable angina who underwent coronary angioplasty were enrolled in the study and were divided into two groups: those with a history of allergy (Group A, N=15); and controls (Group C, N=42). Major adverse cardiac events were recorded over a six-month follow-up period. Patients with primary or unsuccessful angioplasty and patients treated with drug eluting stent were excluded from the study.Results: Group A patients (history of allergy) showed a 46.67% incidence of major adverse cardiac events at six-month follow-up (vs. 9.52% Group C, p<0.01): results remained significant even in a multiple Cox regression analysis (hazard ratio 7.17, 95% CI 1.71-29.98, p<0.01).Conclusion: History of allergy is an independent predictor of major adverse cardiac events after coronary angioplasty in a six-month follow-up period in unstable angina. (C) 2011 SEICAP. Published by Elsevier Espana, S.L. All rights reserved.

C-reactive protein (CRP) plasmatic levels might increase in patients with acute coronary syndrome (ACS) or atherosclerosis and evaluation of CRP is relevant for prognosis in case of ischemic heart disease. This clear role played by CRP in risk stratification of cardiovascular diseases is however biased by non-cardiac determinants: genetic heritable factors, seasonal or daily variability, and gender differences probably based on hormonal differences. Also non-steroidal hormones seem to be involved in CRP determinism, in a complicated interaction not easy to extricate. Nevertheless, CRP determination in patients with ACS should be considered as crucial for its prognostic relevance, even after a careful consideration of all these bias factors.

Activated mast cells are present in human coronary atheromas, as well as in the adventitia of patients with variant angina, and may play an important role in plaque rupture and coronary vasomotion. To assess whether or not activation of mast cells is a primary event, we measured serum levels of tryptase, a specific marker of mast cell activation, in 8 patients with unstable angina during a spontaneous ischemic episode (Group 1) and in 5 patients with variant angina (Group 2) during ergonovine-induced coronary spasm. Blood samples were collected as soon as possible after the onset of pain and ECG changes (0 min), and after 5, 15 and 60 min. Tryptase levels in Group 1 were 0.13 U/l (range 0.017-0.44) at the onset of pain and significantly raised to 0.75 U/l (range 0.05-2.49) at 5 min, decreasing to 0.076 U/l (range 0.018-0.16) at 15 min and to 0.085 U/l (range 0.01-0.25) at 60 min (p = 0.035). Conversely, tryptase levels in Group 2 were 0.09 U/l (range 0.07-0.13) at 0 min, 0.11 U/l (range 0.07-0.22) at 5 min, 0.10 U/l (range 0.07-0.18) at 15 min, 0.11 U/l (range 0.07-0.17) at 60 min (NS). In conclusion, tryptase levels raise during spontaneous ischemic episodes in unstable angina, but not after ergonovine-provoked ischemia in variant angina, suggesting that a primary, yet unknown stimulus, may activate mast cells during some ischemic episodes in unstable angina.

In order to evaluate whether different clinical presentations of unstable angina are associated with a different degree or pattern of activation of the hemostatic, fibrinolytic and inflammatory systems, we measured plasma levels of thrombin-antithrombin III, plasmin-alpha2- antiplasmin complexes and C-reactive protein, as markers of activation of coagulation, fibrinolysis and inflammation respectively, in two groups of patients: 7 patients with de novo unstable angina (Group 1) and 7 patients with destabilizing unstable angina (Group 2). Blood samples were taken on admission for measuring levels of C-reactive protein and during ischemic episodes at the onset of ECG changes and pain (0 min) and after 5, 15 and 60 min in order to assess the peak values of thrombin-antithrombin III and plasmin-alpha2-antiplasmin during the episode. Thrombin-antithrombin III levels in Group 1 were 1.8 microgram/l (0.3-4.15) at 0 min and increased to 17 micrograms/l (2.8-60) after 5 to 15 min (p = 0.013); conversely thrombin-antithrombin III levels in Group 2 were 2.15 microgram/l (1.4-3.8) at 0 min and raised to 4 micrograms/l (2-43) after 5 to 15 min (NS). No significant differences in both groups were observed in plasmin-alpha2-antiplasmin levels (Group 1:650 micrograms/l, ranged 492-956, at 0 min vs 670 microgram/l, range 415-977, at peak; Group 2: 480 micrograms/l, range 274-955, at 0 min vs 502 micrograms/l, range 304-1027, at peak; NS). Inversely, C-reactive protein levels on admission were 4 mg/dl (range 2-27) in Group 1, and 1 mg/dl (range 0.6-4) in Group 2 (p = 0.006). In conclusion, patients with de novo unstable angina have significantly enhanced thrombin (but not plasmin) production during spontaneous ischemic episodes than patients with destabilizing unstable angina. Furthermore, patients with de novo unstable angina have enhanced acute phase responses than patients with destabilizing unstable angina. Our data suggest that different pathogenetic mechanisms may be responsible for acute ischemic episodes in unstable angina and may explain different response to antithrombotic therapy in unstable angina patients.