Ana Paula Otaviano

Incidence and Mortality of Acute Kidney Injury after Myocardial Infarction: A Comparison between KDIGO and RIFLE Criteria

Background Acute kidney injury (AKI) increases the risk of death after acute myocardial infarction (AMI). Recently, a new AKI definition was proposed by the Kidney Disease Improving Global Outcomes (KDIGO) organization. The aim of the current study was to compare the incidence and the early and late mortality of AKI diagnosed by RIFLE and KDIGO criteria in the first 7 days of hospitalization due to an AMI. Methods and Results In total, 1,050 AMI patients were prospectively studied. AKI defined by RIFLE and KDIGO occurred in 14.8% and 36.6% of patients, respectively. By applying multivariate Cox analysis, AKI was associated with an increased adjusted hazard ratio (AHR) for 30-day death of 3.51 (95% confidence interval [CI] 2.35–5.25, p<0.001) by RIFLE and 3.99 (CI 2.59–6.15, p<0.001) by KDIGO and with an AHR for 1-year mortality of 1.84 (CI 1.12–3.01, p = 0.016) by RIFLE and 2.43 (CI 1.62–3.62, p<0.001) by KDIGO. The subgroup of patients diagnosed as non-AKI by RIFLE but as AKI by KDIGO criteria had also an increased AHR for death of 2.55 (1.52–4.28) at 30 days and 2.28 (CI 1.46–3.54) at 1 year (p<0.001). Conclusions KDIGO criteria detected substantially more AKI patients than RIFLE among AMI patients. Patients diagnosed as AKI by KDIGO but not RIFLE criteria had a significantly higher early and late mortality. In this study KDIGO criteria were more suitable for AKI diagnosis in AMI patients than RIFLE criteria.

Effect of Kidney Disease on Acute Coronary Syndrome

Chronic kidney disease (CKD) is highly prevalent worldwide and is associated with an increased risk for adverse outcomes in patients hospitalized with acute coronary syndrome (ACS). In studies including thousands of patients admitted with myocardial infarction, CKD consistently determines a poorer prognosis for ACS patients. In contrast with CKD, information about the effect of acute kidney injury (AKI) on clinical outcomes after ACS is limited. Most data come from retrospective registry databank studies of nonconsecutive patients with a significant number of patients excluded from analyses. There are no prospective studies designed to determine whether AKI strictly diagnosed by the new the Acute Kidney Injury Network (AKIN) or RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria is a risk factor for death after ACS, and there are no data comparing the RIFLE and AKIN criteria for AKI diagnosis after myocardial infarction. This article reviews the most important data on CKD and ACS and the available data on AKI and ACS. The importance of obtaining an early serum creatinine level after admission for ACS and the importance of renal function monitoring during hospitalization are stressed.

Renal function at hospital admission and mortality due to acute kidney injury after myocardial infarction.

Background The role of an impaired estimated glomerular filtration rate (eGFR) at hospital admission in the outcome of acute kidney injury (AKI) after acute myocardial infarction (AMI) has been underreported. The aim of this study was to assess the influence of an admission eGFR<60 mL/min/1.73 m2 on the incidence and early and late mortality of AMI-associated AKI. Methods A prospective study of 828 AMI patients was performed. AKI was defined as a serum creatinine increase of ≥50% from the time of admission (RIFLE criteria) in the first 7 days of hospitalization. Patients were divided into subgroups according to their eGFR upon hospital admission (MDRD formula, mL/min/1.73 m2) and the development of AKI: eGFR≥60 without AKI, eGFR<60 without AKI, eGFR≥60 with AKI and eGFR<60 with AKI. Results Overall, 14.6% of the patients in this study developed AKI. The admission eGFR had no impact on the incidence of AKI. However, the admission eGFR was associated with the outcome of AMI-associated AKI. The adjusted hazard ratios (AHR, Cox multivariate analysis) for 30-day mortality were 2.00 (95% CI 1.11–3.61) for eGFR<60 without AKI, 4.76 (95% CI 2.45–9.26) for eGFR≥60 with AKI and 6.27 (95% CI 3.20–12.29) for eGFR<60 with AKI. Only an admission eGFR of <60 with AKI was significantly associated with a 30-day to 1-year mortality hazard (AHR 3.05, 95% CI 1.50–6.19). Conclusions AKI development was associated with an increased early mortality hazard in AMI patients with either preserved or impaired admission eGFR. Only the association of impaired admission eGFR and AKI was associated with an increased hazard for late mortality among these patients.

Outcome of Chagas cardiomyopathy in comparison to ischemic cardiomyopathy

BACKGROUND Chagas cardiomyopathy and ischemic heart disease (IHD) are frequent causes of chronic systolic heart failure (CHF) in areas where the former is endemic. Nonetheless, a specific comparison of outcome and role of etiology of CHF failure has not been performed in patients with both conditions. METHODS Two-hundred twenty two patients with Chagas cardiomyopathy and 79 with IHD with CHF were included in the study. A Cox proportional hazards model was used to establish independent predictors of mortality for the studied population. Survival analysis was performed with the Kaplan-Meir product limit method. RESULTS In the multivariable model, Beta-Blocker therapy [(hazard ratio (HR)=0.36; 95% confidence interval (CI) 0.24 to 0.52; p<0.005)], Chagas etiology of CHF (HR=3.6; 95% CI 2.0 to 6.5; p<0.005), serum sodium levels (HR=0.95; 95% CI 0.91 to 0.98; p<0.005), digoxin use (HR=2.1; 95% CI 1.19 to 3.80, p=0.01), and spironolactone use (HR=1.7; 95% CI 1.10 to 2.80; p=0.02) were determined independent predictors of all-cause mortality for this cohort. Probability of survival at 12, 24, 36, 48, and 60 months was 92%, 92%, 88%, 81%, and 78%, respectively, in IHD patients, and 79%, 61%, 49%, 41%, and 35%, respectively, in Chagas cardiomyopathy patients (p<0.005). CONCLUSION Outcome in patients with chronic systolic heart failure secondary to Chagas cardiomyopathy is poorer than that seen in those with IHD.

Comparação do desfecho entre a cardiopatia chagásica e a miocardiopatia dilatada idiopática

FUNDAMENTO: Pouco se sabe sobre o desfecho dos pacientes com cardiopatia chagasica, em comparacao aos pacientes com miocardiopatia dilatada idiopatica na era contemporânea. OBJETIVO: Comparar o desfecho dos pacientes chagasicos com insuficiencia cardiaca sistolica cronica decorrente da cardiopatia chagasica ao observado em pacientes com MDI na era contemporânea. METODOS: Foi incluido um total de 352 pacientes (246 com cardiomiopatia chagasica e 106 com miocardiopatia dilatada idiopatica), seguidos prospectivamente em nossa Instituicao, de janeiro de 2000 a janeiro de 2008. Todos os pacientes receberam tratamento clinico contemporâneo padrao. RESULTADOS: Na analise multivariada com o modelo de risco proporcional de Cox, o uso da digoxina (relacao de risco = 3,17; intervalo de confianca de 95%, de 1,62 a 6,18; p = 0,001) necessitou de suporte inotropico (relacao de risco = 2,08; intervalo de confianca de 95%, de 1,43 a 3,02; p < 0,005). A fracao de ejecao do ventriculo esquerdo (relacao de risco = 0,97; intervalo de confianca de 95%, de 0,95 a 0,99; p < 0,005) e a etiologia da cardiopatia chagasica (relacao de risco = 3,29; intervalo de confianca de 95%, de 1,89 a 5,73; p < 0,005) foram associadas positivamente a mortalidade, enquanto a terapia com betabloqueadores (relacao de risco = 0,39; intervalo de confianca de 95%, de 0,26 a 0,56; p < 0,005) foi associada negativamente a mortalidade. A probabilidade de sobrevida para pacientes com cardiomiopatia chagasica em oito, 24 e 49 meses foi de 83%, 61% e 41%, respectivamente. Ja para pacientes com cardiomiopatia dilatada idiopatica, foi de 97%, 92% e 82%, respectivamente (p < 0,005). CONCLUSAO: Na era atual do tratamento da insuficiencia cardiaca, os pacientes com cardiomiopatia chagasica tem um desfecho pior em comparacao aos pacientes com cardiomiopatia dilatada idiopatica.

Prognosis of patients with chronic systolic heart failure: Chagas disease versus systemic arterial hypertension

Chagas disease is a major health problem in South American because it affects 11 million people; 90 million are at risk of acquiring the disease, and about 12,500 persons die of the disease yearly [1]. Furthermore, Chagas disease has become global because of international immigration. It is caused by the protozoan Trypanosoma cruzi, which is transmitted to humans through the contact of feces of blood-sucking bugs with human mucosa. Many years after infection, about 30% of patients develop chronic cardiomyopathy, whichmanifests by life-threatening ventricular arrhythmias [2], chronic systolic heart failure (CHF) [3], sudden cardiac death [4], and thromboembolism [5]. Chagas disease is the principal cause of CHF in referral centers where the disease is endemic. Prognosis for patients with CHF secondary to Chagas cardiomyopathy is very poor, with an annual mortality around 20% [6]. Overall, outcome for CHF secondary to Chagas cardiomyopathy is poor to that found in non-Chagas disease heart failure [7]. Systemic arterial hypertension (SAH)may affect about 33% of patients with chronic Chagas disease, and 8% of them develop CHF [8]. The purpose of this investigationwas to compare outcome of patients with CHF secondary to Chagas cardiomyopathywith thosewith CHF secondary to SAH in view of lack of such data in the medical literature. All patients with the diagnosis of CHF secondary to either Chagas cardiomyopathy or SAH routinely followed at our Cardiomyopathy Outpatient Service from January, 2000 to January, 2008 were initially considered for the study. Patients were entered in the study if they had 1) positive serology for Chagas disease and left ventricular systolic dysfunction or 2) SAH (systolic blood pressure N 140 × 90 mmHg) at physical examination on admission or normal systemic arterial pressure but with a history of SAH treated with antihypertensive medication at study entry associated with left ventricular systolic dysfunction, as previously reported. Details of this patients cohort have been described elsewhere [9]. All Chagas disease heart failure patients were treated as previously described [10], whereas hypertensive patients received standard treatment for CHF. The daily dose of each medication at the last follow-up visit before study close was noted. The T test for unpaired sample was used to compare continuous variables between patients with CHF secondary to Chagas cardiomyopathy and those with CHF secondary to SAH at baseline. A Cox proportional hazard models, adjusted for confounders, were used to determine independent predictors of mortality for this specific patient population. Kaplan–Meier survival curves were constructed to estimate survival probability for both groups, and the log-rank sum test was used to compare survival probability between both patient groups. Differences at the level of p b 0.05 were considered of statistical significance. Table 1 lists the comparison of relevant clinical characteristics at baseline of patients with CHF secondary to Chagas cardiomyopathy and those with CHF secondary to SAH. Of interest, mean daily dose of carvedilol (21.7 ± 17.4 mg × 34.4 ± 19.7 mg; p b 0.005) and metoprolol succinate (106.2 ± 67.6 mg × 144.3 ± 65.4 mg; p b 0.06) was lower in Chagas disease patients than in those with SAH with CHF. Onmultivariable analysis, Beta-Blocker therapy [Hazard Ratio (HR)= 0.31; 95% Confidence Interval (95%) 0.2 to 0.44; p b 0.005], Chagas etiology of heart failure (HR= 2.2; 95% CI 1.47 to 3.40; p b 0.005), need of inotropic support (HR= 1.72; 95% CI 1.19 to 2.47; p= 0.004), left ventricular diastolic diameter (HR= 1.02; 95% CI 1.19 to 2.47; p= 0.002) and serum sodium levels (HR= 0.95; 95% CI 0.91 to 0.98; p= 0.006) were independent predictors of all-cause mortality. Overall, patients were followed for 33 ± 21 months. Probability of survival for patients with CHF secondary to Chagas cardiomyopathy at 12, 24, 36, 48, and 60 months was 76%, 56%, 45%, 37%, and 29%, respectively; nonetheless, probability of survival for those with CHF secondary to SAH at 12, 24, 36, 48, and 60 months was 96%, 92%, 82%, 77%, and 73%, respectively (p b 0.05). Fig. 1 illustrates these data.

Clinical course of patients with chronic systolic heart failure due to the association of Chagas disease and systemic arterial hypertension

rosuvastatin on coronary atheroma in stable coronary artery disease: multicenter coronary atherosclerosis study measuring effects of rosuvastatin using intravascular ultrasound in Japanese subjects (COSMOS). Circ J 2009;73:2110–7. [5] Smith Jr SC, Allen J, Blair SN, Bonow RO, Brass LM, Fonarow GC, et al. AHA/ACC guidelines for secondary prevention for patients with coronary and other atherosclerotic vascular disease: 2006 update: endorsed by the National Heart, Lung, and Blood Institute. Circulation 2006;113:2363–72. [6] Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation 2002;106:3143–421. [7] Grundy SM, Cleeman JI, Merz CN, Brewer Jr HB, Clark LT, Hunninghake DB, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation 2004;110:227–39. [8] Deedwania P, Singh V, Davidson MH. Low high-density lipoprotein cholesterol and increased cardiovascular disease risk: an analysis of statin clinical trials. Am J Cardiol 2009;104:3E–9E. [9] Barter P, Gotto AM, LaRosa JC, Maroni J, Szarek M, Grundy SM, et al. HDL cholesterol, very low levels of LDL cholesterol, and cardiovascular events. N Engl J Med 2007;357:1301–10. [10] Gordon DJ, Probstfield JL, Garrison RJ, Neaton JD, Castelli WP, Knoke JD, et al. Highdensity lipoprotein cholesterol and cardiovascular disease: Four prospectiveAmerican studies. Circulation 1989;79:8–15. [11] Shewan LG, Coats AJ. Ethics authorship publishing scientific articles Int J Cardiol 2010;144:1–2.