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BACKGROUND Reliable preprocedural risk scores for the prediction of Contrast-Induced Acute Kidney Injury (CI-AKI) following Percutaneous Coronary Intervention (pPCI) in patients with ST-elevation myocardial infarction (STEMI) are lacking. Aim of this study was to derive and validate a preprocedural Risk Score in this setting. METHODS Two prospectively enrolled patient cohorts were used for derivation and validation (n = 3,736). CI-AKI was defined as creatinine increase ≥0.5 mg/dl 75 years, anterior MI (3 points), Killip class IV (4 points), estimated GFR

Background: Mitochondrial biomarkers have been investigated in different critical settings, including ST-elevation myocardial infarction (STEMI). Whether they provide prognostic information in STEMI, complementary to troponins, has not been fully elucidated. We prospectively explored the in-hospital and long-term prognostic implications of cytochrome c and cell-free mitochondrial DNA (mtDNA) in STEMI patients undergoing primary percutaneous coronary intervention. Methods: We measured cytochrome c and mtDNA at admission in 466 patients. Patients were grouped according to mitochondrial biomarkers detection: group 1 (&minus, /&minus, no biomarker detected, n = 28), group 2 (&minus, /+, only one biomarker detected, n = 283), group 3 (+/+, both biomarkers detected, n = 155). A composite of in-hospital mortality, cardiogenic shock, and acute pulmonary edema was the primary endpoint. Four-year all-cause mortality was the secondary endpoint. Results: Progressively lower left ventricular ejection fractions (52 &plusmn, 8%, 49 &plusmn, 8%, 47 &plusmn, 9%, p = 0.006) and higher troponin I peaks (54 &plusmn, 44, 73 &plusmn, 66, 106 &plusmn, 81 ng/mL, p = 0.001) were found across the groups. An increase in primary (4%, 14%, 19%, p = 0.03) and secondary (10%, 15%, 23%, p = 0.02) endpoint rate was observed going from group 1 to group 3. The adjusted odds ratio increment of the primary endpoint from one group to the next was 1.65 (95% CI 1.04&ndash, 2.61, p = 0.03), while the adjusted hazard ratio increment of the secondary endpoint was 1.55 (95% CI 1.12&ndash, 2.52, p = 0.03). The addition of study group allocation to admission troponin I reclassified 12% and 22% of patients for the primary and secondary endpoint, respectively. Conclusions: Detection of mitochondrial biomarkers is common in STEMI and seems to be associated with in-hospital and long-term outcome independently of troponin.

Background: Patients hospitalized with acute myocardial infarction (AMI) are often on prior single antiplatelet therapy (SAPT) or a dual antiplatelet therapy (DAPT). Whether chronic SAPT or DAPT is beneficial or associated with an increased risk in AMI is still controversial. Methods and Results: We prospectively enrolled 1718 consecutive patients with AMI (798 ST-segment elevation myocardial infarction and 920 non-ST-segment elevation myocardial infarction) who were divided according to their chronic APT (no APT, SAPT, or DAPT). The study primary end point was the infarct size, as estimated by troponin I peak. Incidence of major bleeding was also evaluated. Five hundred thirty-six (31%) patients were on chronic SAPT and 215 (13%) on DAPT. A graded increase in Global Registry of Acute Coronary Events (GRACE) and Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines (CRUSADE) risk scores was found going from patients without APT to those with DAPT, while a progressive smaller troponin I peak was observed with the increasing number of chronic antiplatelet agents (11.2 [interquartile range: 2-45] ng/mL, 6.6 [1-33] ng/mL, and 4.1 [1-24] ng/mL; P < .001 for trend). This result was maintained after adjustment for baseline ischemic risk profile (GRACE score) and other major confounders ( P < .001). The incidence of bleeding was higher in patients on chronic APT than in those without APT (5.2% vs 2.4%; P = .002). However, when the bleeding risk was adjusted for the CRUSADE risk score, chronic SAPT (odds ratio [OR]: 1.40, 95% confidence interval [CI]: 0.77-2.53) and DAPT (OR: 0.70, 95% CI: 0.29-1.70) were not associated with an increased bleeding risk. Conclusion: In patients with AMI, chronic APT is associated with higher baseline ischemic and bleeding risks. Despite this and unexpectedly, they have a smaller infarct size and similar adjusted bleeding risk.

OBJECTIVE Acute hyperglycemia is a powerful predictor of poor prognosis in acute myocardial infarction (AMI), particularly in patients without diabetes. This emphasizes the importance of an acute glycemic rise rather than glycemia level at admission alone. We investigated in AMI whether the combined evaluation of acute and chronic glycemic levels, as compared with admission glycemia alone, may have a better prognostic value. RESEARCH DESIGN AND METHODS We prospectively measured admission glycemia and estimated average chronic glucose levels (mg/dL) by the following formula: [(28.7 × glycosylated hemoglobin %) − 46.7], and calculated the acute-to-chronic (A/C) glycemic ratio in 1,553 consecutive AMI patients (mean ± SD age 67 ± 13 years). The primary end point was the combination of in-hospital mortality, acute pulmonary edema, and cardiogenic shock. RESULTS The primary end point rate increased in parallel with A/C glycemic ratio tertiles (5%, 8%, and 20%, respectively; P for trend CONCLUSIONS In AMI patients with diabetes, A/C glycemic ratio is a better predictor of in-hospital morbidity and mortality than glycemia at admission.

OBJECTIVE ST-segment elevation myocardial infarction (STEMI) patients with type 2 diabetes mellitus (DM) have higher in-hospital mortality than those without. Since cardiac and renal functions are the main variables associated with outcome in STEMI, we hypothesized that this prognostic disparity may depend on a higher rate of cardiac and renal dysfunction in DM patients. RESEARCH DESIGN AND METHODS We retrospectively analyzed 5,152 STEMI patients treated with primary angioplasty. Left ventricular ejection fraction (LVEF) and estimated glomerular filtration rate (eGFR) were evaluated at hospital admission. The primary end point was in-hospital mortality. A composite of in-hospital mortality, cardiogenic shock, and acute kidney injury was the secondary end point. RESULTS There were 879 patients (17%) with DM. The incidence of LVEF ≤40% (30% vs. 22%), eGFR ≤60 mL/min/1.73 m2 (27% vs. 18%), or both (12% vs. 6%) was higher (P < 0.001 for all comparisons) in DM patients. In-hospital mortality was higher in DM patients than in non-DM patients (6.1% vs. 3.5%; P = 0.002), with an unadjusted odds ratio (OR) of 1.81 (95% CI 1.31–2.49; P < 0.001). However, DM was no longer associated with an increased mortality risk after adjustment for cardiac and renal function (OR 1.03, 95% CI 0.68–1.56; P = 0.89). A similar behavior was observed for the secondary end point, with an unadjusted OR for DM of 1.52 (95% CI 1.25–1.85; P < 0.001) and an OR after adjustment for cardiac and renal function of 1.07 (95% CI 0.85–1.36; P = 0.53). CONCLUSIONS The study indicates that the increased in-hospital mortality and morbidity of DM patients with STEMI is mainly driven by their underlying cardio-renal dysfunction.

Background: Atrial fibrillation (AF) is a frequent complication of acute myocardial infarction (AMI) and is associated with a worse prognosis. Patients with chronic kidney disease are more likely to develop AF. Whether the association between AF and glomerular filtration rate (GFR) is also true in AMI has never been investigated. Methods: We prospectively enrolled 2445 AMI patients. New-onset AF was recorded during hospitalization. Estimated GFR was estimated at admission, and patients were grouped according to their GFR (group 1 (n = 1887): GFR &gt, 60, group 2 (n = 492): GFR 60&ndash, 30, group 3 (n = 66): GFR &lt, 30 mL/min/1.73 m2). The primary endpoint was AF incidence. In-hospital and long-term (median 5 years) mortality were secondary endpoints. Results: The AF incidence in the population was 10%, and it was 8%, 16%, 24% in groups 1, 2, 3, respectively (p &lt, 0.0001). In the overall population, AF was associated with a higher in-hospital (5% vs. 1%, p &lt, 0.0001) and long-term (34% vs. 13%, 0.0001) mortality. In each study group, in-hospital mortality was higher in AF patients (3.5% vs. 0.5%, 6.5% vs. 3.0%, 19% vs. 8%, respectively, 0.0001). A similar trend was observed for long-term mortality in three groups (20% vs. 9%, 51% vs. 24%, 81% vs. 50%, 0.0001). The higher risk of in-hospital and long-term mortality associated with AF in each group was confirmed after adjustment for major confounders. Conclusions: This study demonstrates that new-onset AF incidence during AMI, as well as the associated in-hospital and long-term mortality, increases in parallel with GFR reduction assessed at admission.

High-sensitivity C-reactive protein (hs-CRP) is the most used inflammatory marker in acute myocardial infarction (AMI) and its levels are associated with outcome. Diabetes mellitus (DM) is a frequent comorbidity in AMI and it is characterized by some degree of chronic inflammation. Thus, detection

Background In acute myocardial infarction, acute hyperglycemia is a predictor of acute kidney injury ( AKI ), particularly in patients without diabetes mellitus. This emphasizes the importance of an acute glycemic rise rather than glycemia level at admission. We investigated whether, in diabetic patients with acute myocardial infarction, the combined evaluation of acute and chronic glycemic levels may have better prognostic value for AKI than admission glycemia. Methods and Results At admission, we prospectively measured glycemia and estimated average chronic glucose levels (mg/dL) using glycosylated hemoglobin (HbA 1c ), according to the following formula: 28.7×HbA 1c (%)−46.7. We evaluated the association with AKI of the acute/chronic glycemic ratio and of the difference between acute and chronic glycemia (Δ A−C ). We enrolled 474 diabetic patients with acute myocardial infarction. Of them, 77 (16%) experienced AKI . The incidence of AKI increased in parallel with the acute/chronic glycemic ratio (12%, 14%, 22%; P =0.02 for trend) and Δ A−C (13%, 13%, 23%; P =0.01) but not with admission glycemic tertiles ( P =0.22). At receiver operating characteristic analysis, the acute/chronic glycemic ratio (area under the curve: 0.62 [95% confidence interval, 0.55–0.69]; P =0.001) and Δ A−C (area under the curve: 0.62 [95% confidence interval, 0.54–0.69]; P =0.002) accurately predicted AKI , without difference in the area under the curve between them ( P =0.53). At reclassification analysis, the addition of the acute/chronic glycemic ratio and Δ A−C to acute glycemia allowed proper AKI risk prediction in 16% of patients. Conclusions In diabetic patients with acute myocardial infarction, AKI is better predicted by the combined evaluation of acute and chronic glycemic values than by assessment of admission glycemia alone.

To investigate whether admission B-type natriuretic peptide levels predict the development of acute kidney injury in acute coronary syndromes.Prospective study.Single-center study, 13-bed intensive cardiac care unit at a University Cardiological Center.Six-hundred thirty-nine acute coronary syndromes patients undergoing emergency and urgent percutaneous coronary intervention.None.We measured B-type natriuretic peptide at hospital admission in acute coronary syndromes patients (55% ST-elevation myocardial infarction and 45% non-ST-elevation myocardial infarction). Acute kidney injury was classified according to the Acute Kidney Injury Network criteria: stage 1 was defined as a serum creatinine increase greater than or equal to 0.3 mg/dL from baseline; stage 2 as a serum creatinine increase greater than two- to three-fold from baseline; stage 3 as a serum creatinine increase greater than three-fold from baseline, or greater than or equal to 4.0 mg/dL with an acute increase greater than 0.5 mg/dL, or need for renal replacement therapy. Acute kidney injury was developed in 85 patients (13%) and had a higher in-hospital mortality than patients without acute kidney injury (14% vs 1%; p0.001). B-type natriuretic peptide levels were higher in acute kidney injury patients than in those without acute kidney injury (264 [112-957] vs 98 [44-271] pg/mL; p0.001) and showed a significant gradient according to acute kidney injury severity (224 [96-660] pg/mL in stage 1 and 939 [124-1,650] pg/mL in stage 2-3 acute kidney injury; p0.001). The risk of developing acute kidney injury increased in parallel with B-type natriuretic peptide quartiles (5%, 9%, 15%, and 24%, respectively; p0.001). When B-type natriuretic peptide was evaluated, in terms of capacity to predict acute kidney injury, the area under the curve was 0.702 (95% CI, 0.642-0.762).In patients hospitalized with acute coronary syndromes, B-type natriuretic peptide levels measured at admission are associated with acute kidney injury as well as its severity.

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%; p0.001). 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.

We evaluated the rate of use, clinical predictors, and in-hospital outcome of renal replacement therapy (RRT) in acute myocardial infarction (AMI) patients.All consecutive AMI patients admitted to the Coronary Care Unit between January 1st, 2005 and December 31st, 2015 were identified through a search of our prospectively collected clinical database. Patients were grouped according to whether they required RRT or not.Two-thousand-eight-hundred-thirty-nine AMI patients were included. Eighty-three (3%) AMI patients underwent RRT. Variables confirmed at cross validation analysis to be associated with RRT were: admission creatinine1.5mg/dl (OR 16.9, 95% CI 10.4-27.3), cardiogenic shock (OR 23.0, 95% CI 14.4-36.8), atrial fibrillation (OR 8.6, 95% CI 5.5-13.4), mechanical ventilation (OR 22.6, 95% CI 14.2-36.0), diabetes mellitus (OR 4.8, 95% CI 3.1-7.4), and left ventricular ejection fraction40% (OR 9.1, 95% CI 5.6-14.7). The AUC for RRT with the combination of these predictors was 0.96 (95% CI 0.94-0.97; P0.001). In-hospital mortality was significantly higher in RRT patients (41% vs. 2.1%, P0.001). Oligoanuria as indication for RRT (OR 5.1, 95% CI 1.7-15.4), atrial fibrillation (OR 4.3, 95% CI 1.6-11.5), mechanical ventilation (OR 20.8, 95% CI 6.1-70.4), and cardiogenic shock (OR 12.9, 95% CI 4.4-38.3) independently predicted mortality in RRT-treated patients. The AUC for in-hospital mortality prediction with the combination of these variables was 0.92 (95% CI 0.87-0.98; P0.001).Patients with AMI undergoing RRT had strikingly high in-hospital mortality. Use of RRT and its associated mortality were accurately predicted by easily obtainable clinical variables.

Pericardial effusion is characterized by progressive accumulation of fluid within the pericardial space, resulting in increased intra-pericardial pressure and compression of the heart. As B-type natriuretic peptide (BNP) is secreted by the ventricles in response to increased myocardial stretch, we hypothesized that pericardial effusion, as well as its resolution, might influence BNP plasma levels.We prospectively measured, in 146 consecutive patients with pericardial effusion, BNP plasma levels at baseline, soon after, and 24h after pericardiocentesis. A scoring system based on 7 clinical and echocardiographic parameters was developed, and patients were classified according to the number of variables as having low (0-2), intermediate (3-4), or high (5-7) severity score.Out of the 146 patients, 42 (29%) had normal values (100pg/ml), whereas 104 (71%) had high BNP values at baseline. In the whole population, baseline BNP levels significantly decreased as the severity score increased (r=-0.21; P=0.01). 24h after pericardiocentesis, a significant increase in BNP was observed in patients with intermediate (P=0.004) score and with high (P0.001) severity score; no increase occurred in low score patients (P=0.56). The higher was the severity score, the steeper was the increase in BNP through the three time-points considered (P=0.04).The results of the present study show that BNP plasma levels are suppressed in the presence of severe pericardial effusion, and that they rise after pericardiocentesis. Future studies should investigate the role of BNP in assisting clinicians in the decision-making process of pericardial fluid drainage.

The effects of percutaneous transluminal renal angioplasty (PTRA) on the renal function of stenotic kidneys are usually assessed by evaluating the changes in serum creatinine, which is quite a rough indicator of glomerular filtration rate (GFR). In 27 hypertensive patients with 19 atherosclerotic and 11 fibromuscular significant renal artery stenoses, we investigated with renal scintigraphy the short-term (5 days) and long-term (10 months) effects of a technically successful PTRA (in seven cases combined with a stent implantation) on GFR of the stenotic and contralateral kidneys; these measurements were combined with those of plasma renin activity (PRA) and of angiotensin II (AII). We found that in short-term studies after PTRA GFR rose from 29.7 ± 3.5 to 34.6 ± 3.1 mL/min and from 36.9 ± 4.0 to 45.1 ± 4.3 mL/min, respectively, in atherosclerotic and fibromuscular poststenotic kidneys. In long-term studies GFR further and significantly increased, to 37.8 ± 3.2 mL/min in the former group, whereas it stabilized in the latter group (46.0 ± 3.6 mL/min). In patients with fibromuscular stenosis these changes in GFR were associated with clear-cut reductions in blood pressure (BP), PRA, and AII; these decrements also occurred in patients with atherosclerotic stenosis but to a much lesser extent. We also found that in short- and long-term studies the percent of PTRA-induced increments of GFR in the poststenotic kidneys were inversely correlated with the baseline values of GFR. In addition, the absolute and percent increments of GFR were positively correlated with the basal levels of AII. Thus the time course of the improvement in GFR after angioplasty may differ in kidneys, depending on the etiology of the stenosis, in that in those with fibromuscular stenosis it was entirely apparent within a few days whereas in those with atherosclerotic stenosis it required several months to be fully expressed. Also, it appears that the more compromised kidneys are those that benefit most from the dilatation and that AII levels are useful indicators of the possibility that the stenotic kidney will have a favorable functional outcome in terms of restoration of renal blood flow.

In acute coronary syndromes (ACS), serum creatinine (sCr) levels have short- and long-term prognostic value. However, it is possible that repeated evaluations of sCr during hospitalization, rather than measuring sCr value at admission only, might improve risk assessment. We investigated the relationship between sCr baseline value, its changes, and in-hospital mortality in patients hospitalized with ACS.In 2,756 ACS patients, sCr was measured at hospital admission and then daily, until discharge from coronary care unit. Patients were grouped according to the maximum sCr change observed:0.3 mg/dL change from baseline (stable renal function [SRF] group), ≥0.3 mg/dL decrease (improved renal function [IRF] group), and ≥0.3 mg/dL increase (worsening renal function [WRF] group).Of the 2,756 patients, 2,163 (78%) had SRF, 292 (11%) had IRF, and 301 (11%) had WRF. In-hospital mortality in the 3 groups was 0.5%, 2%, and 14% (P.001), respectively. Peak sCr value was a more powerful predictor of mortality (area under the curve 0.86, 95% CI 0.81-0.92) than the initial sCr value (area under the curve 0.69, 95% CI 0.63-0.77; P.001). When sCr and its change patterns during coronary care unit stay were evaluated together, improved mortality risk stratification was found.In ACS patients, daily sCr value and its change pattern are stronger predictors of in-hospital mortality than the initial sCr value only; thus, their combined evaluation provides a more accurate and dynamic stratification of patients' risk. Finally, the intermediate mortality risk of IRF patients possibly reflects acute kidney injury started before hospitalization.

Pericardial effusion (PE) is characterized by accumulation of fluid within the pericardium, resulting in heart compression. As B-type natriuretic peptide (BNP) is secreted by the ventricles in response to increased myocardial stretch, we hypothesized that PE and its resolution might influence BNP

Metastases to the cardiac ventricles are rare and, unfortunately, often follow a rapidly fatal course.1,2 Occasionally, they cause symptomatic ventricular arrhythmias (VAs) for which limited therapeutic options exist, such as antiarrhythmic drugs, whereas the use of catheter ablation, to our knowledge, has never been reported to date. We present the case of a 27-year-old man with a metastatic tumor in the left ventricle and intractable malignant VAs. In February 2009, the patient had been diagnosed with a gluteal sarcoma and initially treated with combined chemotherapy (including anthracyclines) and radiation. Since December 2009, a mild reduction in left ventricular ejection fraction (45%) was detected, and since January 2010, frequent monomorphic premature ventricular contractions (PVCs) and nonsustained ventricular tachycardias (VTs) were documented. Treatment with amiodarone proved helpful, and no life-threatening VAs could be induced on standard electrophysiological study.3 Since April 2010, however, the patient suffered from multiple drug-refractory episodes of sustained VT and ventricular fibrillation, requiring several direct current shocks (Figure 1). His left ventricular ejection fraction had remained stable. Electrical storm resulted in immediate hemodynamic instability and dramatically affected his quality of life. The patient was referred to our institution, where multiple antiarrhythmic drug combinations were tested, both orally and intravenously, allowing a relative stabilization of cardiac rhythm. Cardiac MRI showed a T2-hyperintense, weakly gadolinium-enhanced area at the basis of the anterior papillary muscle, compatible with metastatic infiltration (Figure 2, online-only Data Supplement Movie 1). An oncology consultation hypothesized a life expectancy of

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 levels198 mg/dL (11 mmol/L). Contrast-induced nephropathy was defined as an increase in serum creatinine25% 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.

To evaluate the clinical and prognostic relevance of acute kidney injury (AKI) in the setting of ST-elevation acute myocardial infarction (STEMI) complicated by cardiogenic shock (CS).Prospective study.Single-center study, 13-bed intensive cardiac care unit at a University Cardiological Center.Ninety-seven consecutive STEMI patients with CS at admission, undergoing intra-aortic balloon pump (IABP) support and primary percutaneous coronary intervention (PCI).None.We measured serum creatinine at baseline and each day for the following 3 days. Acute kidney injury was defined as a rise in creatinine25% from baseline. Overall, AKI occurred in 52 (55%) patients, and in 12 of these patients, a renal replacement therapy was required. In multivariate analysis, age75 yrs (p = .005), left ventricular ejection fractionor = 40% (p = .009), and use of mechanical ventilation (p = .01) were independent predictors of AKI. Patients developing AKI had a longer hospital stay, a more complicated clinical course, and significantly higher mortality rate (50% vs. 2.2%; p.001) than patients without AKI. In our population, AKI was the strongest independent predictor of in-hospital mortality (relative risk 12.3, 95% confidence intervals 1.78 to 84.9; p.001).In patients with STEMI complicated by CS, AKI represents a frequent clinical complication associated with a poor prognosis.

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: CrCl60 mL/min and LVEF40% (group 1, n = 261); CrClor = 60 mL/min and LVEF40% (group 2, n = 113); CrCl60 mL/min and LVEFor = 40% (group 3, n = 60); CrClor = 60 mL/min and LVEFor = 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.

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.

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%; P0.001). The maximum contrast dose was exceeded in 130 (23%) patients. Patients who received more than the maximum contrast dose (contrast ratio1) had a more complicated in-hospital clinical course and higher mortality rate (13% vs. 2.8%; P0.001) 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.

ObjectivesThe 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).BackgroundContrast-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.MethodsIn 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.ResultsOverall, 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 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).ConclusionsContrast-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.

Objective To assess whether the hypoxia associated with exposure to high altitude affects plasma endothelin-1 levels, and whether changes in endothelin-1 are related to those in systemic and pulmonary blood pressure. Design Eight normal subjects ascended Mount Everest to an altitude of 5050 m within a period of 8 days (study 1) and 10 ascended Mount Rosa in the Italian Alps to an altitude of 4559 m within 2 days (study 2). In study 1 systemic blood pressure, heart rate, haematocrit, haemoglobin oxygen saturation (evaluated by percutaneous oximetry) and venous plasma endothelin-1 were measured several times during the ascent, and twice more during the time spent at high altitude. In study 2 the same parameters as well as systolic pulmonary pressure by echocardiography were evaluated on the second day of resting at 4559 m. In both studies, data obtained during the expeditions were compared with those collected from the same subjects at sea level. Results In study 1 plasma endothelin-1 increased progressively up to 4240 m (from 1.8 +/- 0.1 pg/ml at sea level to 2.7 +/- 0.2 pg/ml) and decreased slightly thereafter; these increments were directly related to the decrements in percutaneous oxygen saturation, which, at that altitude, fell from 98.6 +/- 0.2% at sea level to 80.8 +/- 0.4%. Blood pressure and haematocrit also rose in response to exposure to high altitude but these changes were not related to changes in endothelin-1. In study 2 the increments in plasma endothelin-1 were similar to those observed in study 1 and the changes again correlated with changes in oxygen saturation as well as with those in systolic pulmonary pressure. On average, systolic pulmonary pressure increased from 19 +/- 1 to 26 +/- 1.9 mmHg, whereas systemic blood pressure and haematocrit were unchanged. Conclusion Exposure to high altitude is associated with consistent increases in plasma endothelin-1. This is probably the result of augmented secretion of the peptide in response to hypoxia and may contribute to the physiological adaptation of the pulmonary circulation to this condition.