-
Giancarlo Marenzi,
Angelo Cabiati,
Silvio V Bertoli,
Emilio Assanelli,
Ivana Marana,
Monica De Metrio,
Mara Rubino,
Marco Moltrasio, Marco Grazi,
Jeness Campodonico,
Valentina Milazzo,
Fabrizio Veglia,
Gianfranco Lauri,
Antonio L Bartorelli
[show abstract]
[hide abstract]
ABSTRACT: Acute kidney injury (AKI) occurs frequently in patients with acute coronary syndromes (ACS) and is associated with adverse short- and long-term outcomes. To date, however, no standardized definition of AKI has been used for patients with ACS. As a result, information on its true incidence and the clinical and prognostic relevance according to the severity of renal function deterioration are still lacking. We retrospectively studied 3,210 patients with ACS. AKI was identified on the basis of the changes in serum creatinine during hospitalization according to the AKI Network criteria. Overall, 409 patients (13%) developed AKI: 262 (64%) had stage 1, 25 (6%) stage 2, and 122 (30%) stage 3 AKI. In-hospital mortality was greater in patients with AKI than in those without AKI (21% vs 1%; p <0.001). The adjusted risk of death increased with increasing AKI severity. Compared to no AKI, the adjusted odds ratio for death was 3.5 (95% confidence interval 1.79 to 6.83) with stage 1 AKI and 31.2 (95% confidence interval 16.96 to 57.45) with stage 2 to 3 AKI. A significant parallel increase in major adverse cardiac events was also observed comparing patients without AKI and those with stage 2 to 3 AKI. In conclusion, in patients with ACS, AKI is a frequent complication, and the graded increase of its severity, as assessed using the AKI Network classification, is associated with a progressive increased risk of in-hospital morbidity and mortality.
The American journal of cardiology 12/2012; · 3.58 Impact Factor
-
Giancarlo Marenzi,
Monica De Metrio,
Mara Rubino,
Gianfranco Lauri,
Annalisa Cavallero,
Emilio Assanelli, Marco Grazi,
Marco Moltrasio,
Ivana Marana,
Jeness Campodonico,
Andrea Discacciati,
Fabrizio Veglia,
Antonio L Bartorelli
[show abstract]
[hide abstract]
ABSTRACT: Acute hyperglycemia and contrast-induced nephropathy (CIN) are frequently observed in ST-elevation acute myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI), and both are associated with an increased mortality rate. We investigated the possible association between acute hyperglycemia and CIN in patients undergoing primary PCI.
We prospectively enrolled 780 STEMI patients undergoing primary PCI. For each patient, plasma glucose levels were assessed at hospital admission. Acute hyperglycemia was defined as glucose levels>198 mg/dL (11 mmol/L). Contrast-induced nephropathy was defined as an increase in serum creatinine>25% from baseline in the first 72 hours.
Overall, 148 (19%) patients had acute hyperglycemia; and 113 (14.5%) patients developed CIN. Patients with acute hyperglycemia had a 2-fold higher incidence of CIN than those without acute hyperglycemia (27% vs 12%, P<.001). In-hospital mortality was higher in patients with acute hyperglycemia than in those without acute hyperglycemia (12% vs 3%, P<.001). Mortality rate was also higher in patients developing CIN than in those without this renal complication (27% vs 0.9%, P<.001). Patients with acute hyperglycemia that developed CIN had the highest mortality rate (38%). Acute hyperglycemia was an independent predictor of CIN and in-hospital mortality.
In STEMI patients undergoing primary PCI, acute hyperglycemia is associated with an increased risk for CIN and with increased in-hospital mortality.
American heart journal 12/2010; 160(6):1170-7. · 4.65 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Despite emergency coronary revascularization coupled with medical stabilization, intra-aortic balloon pump and ventricular assist devices have significantly improved survival in patients with cardiogenic shock complicating acute myocardial infarction, mortality still remains excessively high, being actually about 30-40%. Future research should focus on new therapeutic strategies, aimed to further decrease mortality rate of these patients.
Recenti progressi in medicina 03/2010; 101(3):99-105.
-
Annals of internal medicine 06/2009; 150(10):738-40. · 16.73 Impact Factor
-
Giancarlo Marenzi,
Emilio Assanelli,
Jeness Campodonico,
Gianfranco Lauri,
Ivana Marana,
Monica De Metrio,
Marco Moltrasio, Marco Grazi,
Mara Rubino,
Fabrizio Veglia,
Franco Fabbiocchi,
Antonio L Bartorelli
[show abstract]
[hide abstract]
ABSTRACT: Contrast-induced nephropathy (CIN) frequently occurs in patients with acute ST-segment elevation myocardial infarction (STEMI) who are undergoing primary percutaneous coronary intervention, and CIN is associated with a more complicated clinical course and increased mortality.
To investigate the association between absolute and weight- and creatinine-adjusted contrast volume, CIN incidence, and clinical outcome in the era of mechanical reperfusion of STEMI.
Prospective, observational study.
A university cardiology center in Milan, Italy.
561 consecutive patients with STEMI who were undergoing primary percutaneous coronary intervention.
For each patient, the maximum contrast dose was calculated, according to the formula (5 x body weight [kg])/serum creatinine, and the contrast ratio, defined as the ratio between the contrast volume administered and the maximum dose calculated, was assessed. An increase in serum creatinine of more than 25% from baseline was defined as CIN.
115 (20.5%) patients developed CIN. In-hospital mortality was higher among patients with CIN than those without CIN (21.4% vs. 0.9%; P < 0.001). The maximum contrast dose was exceeded in 130 (23%) patients. Patients who received more than the maximum contrast dose (contrast ratio >1) had a more complicated in-hospital clinical course and higher mortality rate (13% vs. 2.8%; P < 0.001) than did patients with a contrast ratio less than 1. Development of CIN was associated with both contrast volume and contrast ratio.
The association between contrast volume and outcomes was observed in a single center and could be due to comorbid conditions, disease severity, or an unknown factor.
During primary percutaneous coronary intervention for STEMI, higher contrast volume is associated with higher rates of CIN and mortality; however, further study is needed to determine whether limiting contrast volume would improve patient outcome.
Centro Cardiologico Monzino, Institute of Cardiology, University of Milan.
Annals of internal medicine 02/2009; 150(3):170-7. · 16.73 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Risk stratification of patients with ST-elevation myocardial infarction (STEMI) undergoing primary angioplasty is important in order to predict outcomes and to delineate targeted therapeutic strategies. Although the prognostic implications of reduced left ventricular ejection fraction (LVEF) and creatinine clearance (CrCl) have been recognized, the clinical and prognostic impact of their combination has never been prospectively evaluated.
We stratified 467 patients with STEMI undergoing primary angioplasty according to LVEF and CrCl values at admission: CrCl > 60 mL/min and LVEF > 40% (group 1, n = 261); CrCl < or = 60 mL/min and LVEF > 40% (group 2, n = 113); CrCl > 60 mL/min and LVEF < or = 40% (group 3, n = 60); CrCl < or = 60 mL/min and LVEF < or = 40% (group 4, n = 33).
Inhospital mortality was different in the 4 groups (1% in group 1, 3% in group 2, 15% in group 3, 30% in group 4) (P < .001). The incidence of combined end point of death, acute pulmonary edema, cardiogenic shock, and acute renal failure requiring mechanical support increased progressively from group 1 to group 4 (5%, 17%, 33%, and 48%, respectively) (P < .001). We found a significant gradient of risk in terms of inhospital mortality and combined end point when patients outcome was evaluated according to the presence of both normal LVEF and CrCl (group 1), impairment in only 1 of these 2 parameters (group 2 and 3 pooled together), and combined LVEF and CrCl reductions (group 4).
Reduced LVEF and CrCl are strong independent predictors of increased inhospital morbidity and mortality, and their combined evaluation provides a simple tool for early risk stratification in patients with STEMI treated with primary angioplasty.
American heart journal 05/2007; 153(5):755-62. · 4.65 Impact Factor
-
Giancarlo Marenzi,
Emilio Assanelli,
Ivana Marana,
Gianfranco Lauri,
Jeness Campodonico, Marco Grazi,
Monica De Metrio,
Stefano Galli,
Franco Fabbiocchi,
Piero Montorsi,
Fabrizio Veglia,
Antonio L Bartorelli
[show abstract]
[hide abstract]
ABSTRACT: Patients with acute myocardial infarction undergoing primary angioplasty are at high risk for contrast-medium-induced nephropathy because of hemodynamic instability, the need for a high volume of contrast medium, and the lack of effective prophylaxis. We investigated the antioxidant N-acetylcysteine for the prevention of contrast-medium-induced nephropathy in patients undergoing primary angioplasty.
We randomly assigned 354 consecutive patients undergoing primary angioplasty to one of three groups: 116 patients were assigned to a standard dose of N-acetylcysteine (a 600-mg intravenous bolus before primary angioplasty and 600 mg orally twice daily for the 48 hours after angioplasty), 119 patients to a double dose of N-acetylcysteine (a 1200-mg intravenous bolus and 1200 mg orally twice daily for the 48 hours after intervention), and 119 patients to placebo.
The serum creatinine concentration increased 25 percent or more from baseline after primary angioplasty in 39 of the control patients (33 percent), 17 of the patients receiving standard-dose N-acetylcysteine (15 percent), and 10 patients receiving high-dose N-acetylcysteine (8 percent, P<0.001). Overall in-hospital mortality was higher in patients with contrast-medium-induced nephropathy than in those without such nephropathy (26 percent vs. 1 percent, P<0.001). Thirteen patients (11 percent) in the control group died, as did five (4 percent) in the standard-dose N-acetylcysteine group and three (3 percent) in the high-dose N-acetylcysteine group (P=0.02). The rate for the composite end point of death, acute renal failure requiring temporary renal-replacement therapy, or the need for mechanical ventilation was 21 (18 percent), 8 (7 percent), and 6 (5 percent) in the three groups, respectively (P=0.002).
Intravenous and oral N-acetylcysteine may prevent contrast-medium-induced nephropathy with a dose-dependent effect in patients treated with primary angioplasty and may improve hospital outcome. (ClinicalTrials.gov number, NCT00237614[ClinicalTrials.gov]).
New England Journal of Medicine 07/2006; 354(26):2773-82. · 53.30 Impact Factor
-
Giancarlo Marenzi,
Gianfranco Lauri,
Jeness Campodonico,
Ivana Marana,
Emilio Assanelli,
Monica De Metrio, Marco Grazi,
Fabrizio Veglia,
Franco Fabbiocchi,
Piero Montorsi,
Antonio L Bartorelli
[show abstract]
[hide abstract]
ABSTRACT: Contrast-induced nephropathy is a complication of contrast medium administration during diagnostic and interventional procedures, with important prognostic relevance. Patients with chronic kidney disease have a higher risk for contrast-induced nephropathy and poorer outcome. In patients with chronic kidney disease, hemofiltration reduces contrast-induced nephropathy incidence and improves long-term survival. We assessed the mechanisms involved in the prophylactic effect of hemofiltration and of the most effective hemofiltration protocol to prevent contrast-induced nephropathy in patients with chronic kidney disease.
We randomized 92 patients with chronic kidney disease (creatinine clearance < or =30 mL/min) to three different prophylactic treatments: intravenous hydration with isotonic saline (1 mL x kg x h for 12 hours before and after contrast exposure, control group; n = 30); intravenous hydration for 12 hours before contrast exposure, followed by hemofiltration for 18 to 24 hours after contrast exposure (post-hemofiltration group; n = 31), and hemofiltration performed for 6 hours before and for 18 to 24 hours after contrast exposure (pre/post-hemofiltration group; n = 31). The incidence of contrast-induced nephropathy (>25% increase in creatinine) and the in-hospital clinical course were compared in the three groups.
Twelve patients (40%) in the control group, 8 patients (26%) in the post-hemofiltration group, and 1 patient (3%) in the pre/post-hemofiltration group experienced contrast-induced nephropathy (P = .0013); hemodialysis was required in 9 (30%), three (10%), and zero (0%) patients, respectively (P = .002). In-hospital mortality was 20%, 10%, and 0%, respectively (P = .03).
Hemofiltration is an effective strategy for contrast-induced nephropathy prevention in patients with chronic kidney disease who are undergoing cardiovascular procedures. Pre-hemofiltration is required to obtain the full clinical benefit, suggesting that, among different mechanisms possibly involved, high-volume controlled hydration before contrast media exposure plays a major role.
The American journal of medicine 02/2006; 119(2):155-62. · 4.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The aim of this research was to assess the incidence, clinical predictors, and outcome of contrast-induced nephropathy (CIN) after primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI).
Contrast-induced nephropathy is associated with significant morbidity and mortality after PCI. Patients undergoing primary PCI may be at higher risk of CIN because of hemodynamic instability and unfeasibility of adequate prophylaxis.
In 208 consecutive AMI patients undergoing primary PCI, we measured serum creatinine concentration (Cr) at baseline and each day for the following three days. Contrast-induced nephropathy was defined as a rise in Cr >0.5 mg/dl.
Overall, CIN occurred in 40 (19%) patients. Of the 160 patients with baseline Cr clearance >/=60 ml/min, only 21 (13%) developed CIN, whereas it occurred in 19 (40%) of those with Cr clearance <60 ml/min (p < 0.0001). In multivariate analysis, age >75 years (odds ratio [OR] 5.28, 95% confidence interval [CI] 1.98 to 14.05; p = 0.0009), anterior infarction (OR 2.17, 95% CI 0.88 to 5.34; p = 0.09), time-to-reperfusion >6 h (OR 2.51, 95% CI 1.01 to 6.16; p = 0.04), contrast agent volume >300 ml (OR 2.80, 95% CI 1.17 to 6.68; p = 0.02) and use of intraaortic balloon (OR 15.51, 95% CI 4.65 to 51.64; p < 0.0001) were independent correlates of CIN. Patients developing CIN had longer hospital stay (13 +/- 7 days vs. 8 +/- 3 days; p < 0.001), more complicated clinical course, and significantly higher mortality rate (31% vs. 0.6%; p < 0.001).
Contrast-induced nephropathy frequently complicates primary PCI, even in patients with normal renal function. It is associated with higher in-hospital complication rate and mortality. Thus, preventive strategies are needed, particularly in high-risk patients.
Journal of the American College of Cardiology 12/2004; 44(9):1780-5. · 14.16 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Nephropathy induced by exposure to radiocontrast agents, a possible complication of percutaneous coronary interventions, is associated with significant in-hospital and long-term morbidity and mortality. Patients with preexisting renal failure are at particularly high risk. We investigated the role of hemofiltration, as compared with isotonic-saline hydration, in preventing contrast-agent-induced nephropathy in patients with renal failure.
We studied 114 consecutive patients with chronic renal failure (serum creatinine concentration, >2 mg per deciliter [176.8 micromol per liter]) who were undergoing coronary interventions. We randomly assigned them to either hemofiltration in an intensive care unit (ICU) (58 patients, with a mean [+/-SD] serum creatinine concentration of 3.0+/-1.0 mg per deciliter [265.2+/-88.4 micromol per liter]) or isotonic-saline hydration at a rate of 1 ml per kilogram of body weight per hour given in a step-down unit (56 patients, with a mean serum creatinine concentration of 3.1+/-1.0 mg per deciliter [274.0+/-88.4 micromol per liter]). Hemofiltration (fluid replacement rate, 1000 ml per hour without weight loss) and saline hydration were initiated 4 to 8 hours before the coronary intervention and were continued for 18 to 24 hours after the procedure was completed.
An increase in the serum creatinine concentration of more than 25 percent from the base-line value after the coronary intervention occurred less frequently among the patients in the hemofiltration group than among the control patients (5 percent vs. 50 percent, P<0.001). Temporary renal-replacement therapy (hemodialysis or hemofiltration) was required in 25 percent of the control patients and in 3 percent of the patients in the hemofiltration group. The rate of in-hospital events was 9 percent in the hemofiltration group and 52 percent in the control group (P<0.001). In-hospital mortality was 2 percent in the hemofiltration group and 14 percent in the control group (P=0.02), and the cumulative one-year mortality was 10 percent and 30 percent, respectively (P=0.01).
In patients with chronic renal failure who are undergoing percutaneous coronary interventions, periprocedural hemofiltration given in an ICU setting appears to be effective in preventing the deterioration of renal function due to contrast-agent-induced nephropathy and is associated with improved in-hospital and long-term outcomes.
New England Journal of Medicine 10/2003; 349(14):1333-40. · 53.30 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Acute renal failure (ARF) requiring hemodialysis after percutaneous coronary interventions (PCI) is a serious complication with poor prognosis. Hemodialysis-induced hypotension may have deleterious cardiovascular effects, especially in high-risk patients. Ultrafiltrate removal and simultaneous fluid replacement with a solution similar to plasma for high-volume controlled hydration can be obtained with hemodynamic stability by continuous veno-venous hemofiltration (CVVH). We prospectively assessed the safety and effectiveness of percutaneous CVVH (Y-shaped double-lumen catheter, circuit originating from and terminating in the femoral vein) in 33 consecutive patients (23 men and 10 women; mean age, 69 +/- 9 years) who, after PCI, developed oligo-anuric ARF, associated in 20 of them with congestive heart failure. All patients received a concomitant infusion of furosemide (500-1000 mg/day) and dopamine (2 microg/kg/min). During CVVH, the average fluid volume replacement and body fluid net reduction were 1000 +/- 247 and 75 +/- 48 ml/hr, respectively. Treatment with CVVH continued for 4.7 +/- 2.7 days and corrected fluid overload in all cases. No patient experienced systemic hypotension or hypovolemia. Diuresis recovered in 32 (97%) patients, who showed a parallel improvement of renal function parameters. One patient required chronic dialysis. In-hospital and 1-year mortality was 9.1% and 27.3%, respectively. In conclusion, our data indicate that CVVH is a safe and effective therapy of radiocontrast-induced ARF following PCI. It temporarily replaces renal function without deleterious cardiovascular effects, allowing the kidney to recover from the nephrotoxic injury. However, despite promising early results, large randomized trials are required to define the role of CVVH in ARF after PCI.
Catheterization and Cardiovascular Interventions 02/2003; 58(1):59-64. · 2.29 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: We investigated the relationship between plasma renin activity (PRA) and serum ([sNa(+)]) and urinary ([uNa(+)]) sodium concentrations in 124 congestive heart failure (CHF) patients (II-IV NYHA class) and 20 healthy subjects. According to PRA (> or <3 ng ml(-1) h(-1)) and [sNa(+)] (> or <135 mEq l(-1)), patients were classified as Group A (normal PRA and normal [sNa(+)], n=39), Group B (increased PRA and normal [sNa(+)], n=62) and Group C (low [sNa(+)], n=23). Measurements were performed at rest and, in 26 cases, after extracorporeal ultrafiltration (UF). At rest, [sNa(+)] and [uNa(+)], and their difference ([sNa(+)]-[uNa(+)]), were linearly correlated with PRA, but the values did not allow differentiation of control subjects from patients or differentiation of patients with from those without renin-angiotensin system (RAS) activation. Conversely, the [sNa(+)]/[uNa(+)] ratio showed the best correlation with PRA (r=0.79, P<0.0001). UF-induced PRA changes were linearly correlated with [sNa(+)]/[uNa(+)] ratio changes (r=0.67, P=0.002), but not with those of [sNa(+)], [uNa(+)] and [sNa(+)]-[uNa(+)]. In CHF, the [sNa(+)]/[uNa(+)] ratio best correlates with PRA and reflects the basal activity as well as the rapid changes (as those induced by UF) of the RAS. Therefore, it can be considered a strong and easily available marker of PRA.
European Journal of Heart Failure 10/2002; 4(5):597-603. · 4.90 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: OBJECTIVESThe goal of this study was to investigate the hemodynamic and circulatory adjustments to extracorporeal ultrafiltration (UF) in refractory congestive heart failure (rCHF).BACKGROUNDIn rCHF, UF allows clinical improvement and restores diuretic efficacy. However, in the course of a UF session, patients are exposed to rapid variations of body fluid composition so that, as fluid is withdrawn from the intravascular compartment, hypotension or even shock could occur.METHODSIn 24 patients with rCHF undergoing UF, we measured, after every liter of plasma water removed, hemodynamics, blood gas analysis (in both systemic and pulmonary arteries), plasma volume changes (PV) and plasma refilling rate (PRR). The PV and PRR were calculated by considering hematocrit and ultrafiltrate volume.RESULTSIn all patients, UF was performed safely, without side effects or hemodynamic instability (ultrafiltrate = 4,880 ± 896 ml). Mean right atrial, pulmonary artery and wedge pressures progressively reduced during the procedure. Cardiac output increased at the end of the procedure and, to a greater extent, 24 h later, in relation to the increase of stroke volume. Heart rate and systemic vascular resistance did not increase, and other peripheral biochemical parameters did not worsen during UF. Intravascular volume remained stable throughout the entire duration of the procedure, indicating that a proportional volume of fluid was refilled from the congested parenchyma.CONCLUSIONSIn patients with rCHF, subtraction of plasma water by UF is associated with hemodynamic improvement. Fluid refilling from the overhydrated interstitium is the major compensatory mechanism for intravascular fluid removal, and hypotension does not occur when plasma refilling rate is adequate to prevent hypovolemia.
Journal of the American College of Cardiology 11/2001; · 14.16 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Background: In chronic heart failure (CHF), cardiac dysfunction is considered the major determinant of neurohumoral activation but the role of renal impairment has not been defined. We investigated the relationship between both cardiac and renal dysfunction and neurohumoral activation, and their possible influence on prognosis.
Methods: Hemodynamics, renal function, plasma neurohormones, and long-term follow-up were evaluated in 148 CHF patients, grouped according to systolic volume index (SVI) and serum creatinine (CRE) values: SVI > 28 mL/m2 and CRE < 1.5 mg/dL (group I, n = 55), SVI < 28 mL/m2 and CRE < 1.5 mg/dL (group II, n = 37), SVI > 28 mL/m2 and CRE > 1.5 mg/dL (group III, n = 25), SVI < 28 mL/m2 and CRE > 1.5 mg/dL (group IV, n = 31).
Results: Neurohormones progressively increased from Group I through IV and correlated with both cardiac and renal function. The hemodynamic pattern was similar in patients with normal or abnormal renal function, whereas neurohormones were only moderately increased in the former group and markedly increased in the latter group. Long-term survival progressively decreased from Group I through IV and was significantly poorer in patients with renal dysfunction.
Conclusions: Our study confirms that, in CHF, neurohumoral activation is strictly related to long-term survival and that many factors contribute to its development and progression; among these, cardiac and renal dysfunction seem to play a major role.
The American Journal of the Medical Sciences 05/2001; 321(6):359-366. · 1.39 Impact Factor
