Marcelo A. Nakazone

Prognostic value of acute kidney injury after cardiac surgery according to kidney disease: improving global outcomes definition and staging (KDIGO) criteria.

Objectives The definition of acute renal failure has been recently reviewed, and the term acute kidney injury (AKI) was proposed to cover the entire spectrum of the syndrome, ranging from small changes in renal function markers to dialysis needs. This study was aimed to evaluate the incidence, morbidity and mortality associated with AKI (based on KDIGO criteria) in patients after cardiac surgery (coronary artery bypass grafting or cardiac valve surgery) and to determine the value of this feature as a predictor of hospital mortality (30 days). Methods From January 2003 to June 2013, a total of 2,804 patients underwent cardiac surgery in our service. Cox proportional hazard models were used to determine the association between the development of AKI and 30-day mortality. Results A total of 1,175 (42%) patients met the diagnostic criteria for AKI based on KDIGO classification during the first 7 postoperative days: 978 (35%) patients met the diagnostic criteria for stage 1 while 100 (4%) patients met the diagnostic criteria for stage 2 and 97 (3%) patients met the diagnostic criteria for stage 3. A total of 63 (2%) patients required dialysis treatment. Overall, the 30-day mortality was 7.1% (2.2%) for patients without AKI and 8.2%, 31% and 55% for patients with AKI at stages 1, 2 and 3, respectively. The KDIGO stage 3 patients who did not require dialysis had a mortality rate of 41%, while the mortality of dialysis patients was 62%. The adjusted Cox regression analysis revealed that AKI based on KDIGO criteria (stages 1–3) was an independent predictor of 30-day mortality (P<0.001 for all. Hazard ratio = 3.35, 11.94 and 24.85). Conclusion In the population evaluated in the present study, even slight changes in the renal function based on KDIGO criteria were considered as independent predictors of 30-day mortality after cardiac surgery.

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.

Implantable Cardioverter-Defibrillator therapy for primary prevention of sudden cardiac death in patients with severe Chagas cardiomyopathy

Sudden cardiac death (SCD) affects about half of patients who died of Chagas disease followed at a referral center, and may victim up to 20% of patients without any evidence of heart disease [1]. In the vast majority of cases, SCD is caused by either sustained ventricular tachycardia (VT) degenerating into ventricular fibrillation (VF) or direct VF [1]. In patients with non-Chagas disease dilated cardiomyopathy and left ventricular ejection fraction b35%, Implantable CardioverterDefibrillator (ICD) delivered-therapy has been recommended by international guidelines to avert SCD [2]. Conversely, the impact of ICD therapy in patients with Chagas cardiomyopathy and a left ventricular ejection fraction b35% is unknown. Accordingly, we report herein our initial experience with ICD-delivered therapy in patients with severe Chagas cardiomyopathy. From January, 2006 to December, 2009, a total of 32 patients routinely followed at the Cardiomyopathy Outpatient Service of our Institution received ICD therapy for primary prevention of SCD. The study was approved by the Local Ethical Committee (protocol 3626/ 2010). Inclusion criteria were a left ventricular ejection fraction b35% at radionuclide ventriculography, receiving standard therapy for chronic systolic heart failure, and to have a reasonable expectation of 1-year survival after device implantation [2]. All patients were on New York Heart Association class II at the time of ICD implantation and none had syncope before device implantation. Nineteen (59%) patients had a positive serology for Chagas disease and were considered to have Chagas cardiomyopathy, whereas the remaining 13 (41%) patients had non-Chagas disease dilated cardiomyopathy. Device therapy consisted of antitachycardia pacing (ATP) or shock. ATP was the initial therapy for VT. Shock was the initial therapy when heart rate was higher than 200 beats per minute (VF zone), when ATP accelerated VT heart rate, or when ATP failed to abolish VT. Baseline characteristics of the study population are given in Table 1. It is noteworthy that 87% patients were on Beta-Blocker therapy. Sustained VT was detected in 4 (21%) of 19 patients with Chagas cardiomyopathy and in 2 (15%) patients with non-Chagas cardiomyopathy (pN0.05). VF was observed in 4 Chagas cardiomyopathy (21%) patients and in 2 (15%) non-Chagas cardiomyopathy patients (pN0.05). Overall, 10 (31%) patients were shocked. In total, shock occurrence was necessary to terminate 136 out of 172 (79%) episodes of VT/VF. Inappropriate shock occurred in 4 (12%) patients; 2 (10%) in Chagas and 2 (14%) in non-Chagas cardiomyopathy patients (pN0.05). A total of 101 episodes of VFwere observed in 6 patients. Median of episodes per patient was 6.5 (3, 38). Ninety-four episodes of VF were observed in four Chagas and 7 episodes of VF in two non-Chagas cardiomyopathy patients (p=0.03). Median time to first event was 78 (34, 151) days in Chagas and 173 (71, 593) days in non-Chagas cardiomyopathy patients (pb0.005). Median time to VF was 80 (22, 147) days in Chagas cardiomyopathy patients and 151 (43, 804) days in non-Chagas cardiomyopathy patients (pb0.005). Probability of freedom from shock occurrence was similar in Chagas and non-Chagas cardiomyopathy patients (Fig. 1). Median follow upwas 292 (78, 845) days in Chagas and 654 (158, 987) days in non-Chagas cardiomyopathy patients (pb0.005). Three (9%) patients died during the study period; 2 in Chagas and 1 in non-Chagas patients (pN0.05). The frequency of shock occurrence observed in our Chagas cardiomyopathy cohort in this study was similar to that reported in patients with non-Chagas cardiomyopathy [3]. The lower mortality rate observed in our study in comparison to studies of secondary prevention of SCD [4] in Chagas disease patients may partially be explained by the lower frequency of shock occurrence. Also, the frequency of shock episodes observed in this investigation was lower than that seen in Chagas disease patients receiving ICD therapy for secondary prevention of SCD [4–6]. This can account, at least in part, for the similarity of mortality rate observed in our study in comparison to that seen in non-Chagas cardiomyopathy patients [7]. The higher frequency of VF episodes/per patient observed in Chagas cardiomyopathy patients in this study can also reflect the characteristics of the pathogenesis of Chagas disease [8]. In patients with Chagas cardiomyopathy, foci of confluent fibrosis intermingled with mononuclear cell infiltrate disseminated throughout the myocardium are frequently seen. Moreover, myocardial ischemia

Exposure to pesticides and heterozygote genotype of GSTP1-Alw26I are associated to Parkinson's disease

OBJECTIVE This study aimed to analyze the frequency of GSTP1-Alw26I polymorphism and to estimate its association with toxic substances in Parkinsons disease (PD). METHODS A study group with 154 patients - subdivided into familial and sporadic PD groups - and 158 elderly individuals without the disease (control group) were evaluated. GSTP1-Alw26I polymorphism was analyzed by polymerase chain reaction/restriction fragment length polymorphism (PCR-RFLP). RESULTS Patients were significantly more exposed to pesticides compared with the control group (p=0.0004), and the heterozygote genotype associated to exposure to pesticides also prevailed in patients (p=0.0001). Wild homozygote genotype was related to tobacco use (p=0.043) and alcoholism (p=0.033) in familial PD patients. CONCLUSION Exposure to pesticides is associated to PD, whose effect can be enhanced when combined with the heterozygote genotype of GSTP1-Alw26I. Also, large genetic and environmental studies considering tobacco use, alcoholism, GSTP1 and PD are necessary to confirm our findings.

Do We Need to Personalize Renal Function Assessment in the Stratification of Patients Undergoing Cardiac Surgery

Background Renal dysfunction is an independent predictor of morbidity and mortality in cardiac surgery. For a better assessment of renal function, calculation of creatinine clearance (CC) may be necessary. Objective To objectively evaluate whether CC is a better risk predictor than serum creatinine (SC) in patients undergoing cardiac surgery. Methods Analysis of 3,285 patients registered in a prospective, consecutive and mandatory manner in the Sao Paulo Registry of Cardiovascular Surgery (REPLICCAR) between November 2013 and January 2015. Values of SC, CC (Cockcroft-Gault) and EuroSCORE II were obtained. Association analysis of SC and CC with morbidity and mortality was performed by calibration and discrimination tests. Independent multivariate models with SC and CC were generated by multiple logistic regression to predict morbidity and mortality following cardiac surgery. Results Despite the association between SC and mortality, it did not calibrate properly the risk groups. There was an association between CC and mortality with good calibration of risk groups. In mortality risk prediction, SC was uncalibrated with values > 1.35 mg /dL (p < 0.001). The ROC curve showed that CC is better than SC in predicting both morbidity and mortality risk. In the multivariate model without CC, SC was the only predictor of morbidity, whereas in the model without SC, CC was not only a mortality predictor, but also the only morbidity predictor. Conclusion Compared with SC, CC is a better parameter of renal function in risk stratification of patients undergoing cardiac surgery.

Gait Speed improves EuroSCORE II prediction

Traditionally cardiac surgery risk scores have worse performance in elderly patients. Frailty evaluation may improve EuroSCORE II accuracy in predicting morbimortality