965 resultados para Excess cardiac mortality.
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BACKGROUND: The arterial pulse pressure variation induced by mechanical ventilation (Delta PP) has been shown to be a predictor of fluid responsiveness. Until now, Delta PP has had to be calculated offline (from a computer recording or a paper printing of the arterial pressure curve), or to be derived from specific cardiac output monitors, limiting the widespread use of this parameter. Recently, a method has been developed for the automatic calculation and real-time monitoring of Delta PP using standard bedside monitors. Whether this method is to predict reliable predictor of fluid responsiveness remains to be determined. METHODS: We conducted a prospective clinical study in 59 mechanically ventilated patients in the postoperative period of cardiac surgery. Patients studied were considered at low risk for complications related to fluid administration (pulmonary artery occlusion pressure <20 mm Hg, left ventricular ejection fraction >= 40%). All patients were instrumented with an arterial line and a pulmonary artery catheter. Cardiac filling pressures and cardiac output were measured before and after intravascular fluid administration (20 mL/kg of lactated Ringer`s solution over 20 min), whereas Delta PP was automatically calculated and continuously monitored. RESULTS: Fluid administration increased cardiac output by at least 15% in 39 patients (66% = responders). Before fluid administration, responders and nonresponders were comparable with regard to right atrial and pulmonary artery occlusion pressures. In contrast, Delta PP was significantly greater in responders than in nonresponders, (17% +/- 3% vs 9% +/- 2%, P < 0.001). The Delta PP cut-off value of 12% allowed identification of responders with a sensitivity of 97% and a specificity of 95%. CONCLUSION: Automatic real-time monitoring of Delta PP is possible using a standard bedside rnonitor and was found to be a reliable method to predict fluid responsiveness after cardiac surgery. Additional studies are needed to determine if this technique can be used to avoid the complications of fluid administration in high-risk patients.
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Pulmonary hypertension represents an important cause of morbidity and mortality in patients with mitral stenosis who undergo cardiac surgery, especially in the postoperative period. The aim of this study was to test the hypothesis that inhaled nitric oxide (iNO) would improve the hemodynamic effects and short-term clinical outcomes of patients with mitral stenosis and severe pulmonary hypertension who undergo cardiac surgery in a randomized, controlled study. Twenty-nine patients (4 men, 25 women; mean age 46 2 years) were randomly allocated to receive iNO (n = 14) or oxygen (n = 15) for 48 hours immediately after surgery. Hemodynamic data, the use of vasoactive drugs, duration of stay, and short-term complications were assessed. No differences in baseline characteristics were observed between the groups. After 24 and 48 hours, patients receiving iNO had a significantly greater increase in cardiac index compared to patients receiving oxygen (p < 0.0001). Pulmonary vascular resistance was also more significantly reduced in patients receiving iNO versus oxygen (-117 dyne/s/cm(5), 95% confidence interval 34 to 200, vs 40 dyne/s/cm5, 95% confidence interval 34 to 100, p = 0.005) at 48 hours. Patients in the iNO group used fewer systemic vasoactive drugs.(mean 2.1 +/- 0.14 vs 2.6 +/- 0.16, p = 0.046) and had a shorter intensive care unit stay (median 2 days, interquartile range 0.25, vs median 3 days, interquartile range 7, p = 0.02). In conclusion, iNO immediately after surgery in patients with mitral stenosis and severe pulmonary hypertension improves hemodynamics and may have short-term clinical benefits. (C) 2011 Elsevier Inc. All rights reserved. (Am J Cardiol 2011;107:1040-1045)
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Bliacheriene F, Carmona MJC, Barretti CFM, Haddad CMF, Mouchalwat ES, Bortlotto MRFL, Francisco RPV, Zugaib M - Use of a Minimally Invasive Uncalibrated Cardiac Output Monitor in Patients Undergoing Cesarean Section under Spinal Anesthesia: Report of Four Cases. Background and Objectives: Hemodynamic changes are observed during cesarean section under spinal anesthesia. Non-invasive blood pressure (BP) and heart rate (HR) measurements are performed to diagnose these changes, but they are delayed and inaccurate. Other monitors such as filling pressure and cardiac output (CO) catheters with external calibration are very invasive or inaccurate. The objective of the present study was to report the cardiac output measurements obtained with a minimally invasive uncalibrated monitor (LiDCO rapid) in patients undergoing cesarean section under spinal anesthesia. Case report: After approval by the Ethics Commission, four patients agreed to participate in this study. They underwent cesarean section under spinal anesthesia while at the same time being connected to the LiDCO rapid by a radial artery line. Cardiac output, HR, and BP were recorded at baseline, after spinal anesthesia, after fetal and placental extraction, and after the infusion of oxytocin and metaraminol. We observed a fall in BP with an increase of HR and CO after spinal anesthesia and oxytocin infusion; and an increase in BP with a fall in HR and CO after bolus of the vasopressor. Conclusions: Although this monitor had not been calibrated, it showed a tendency for consistent hemodynamic data in obstetric patients and it may be used as a therapeutic guide or experimental tool.
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Background: This study was designed to evaluate serum potassium level variation in a porcine model of hemorrhagic shock ( HS). Methods: Eight pigs were studied in a controlled hemorrhage model of HS. Blood withdrawal began at a 50 mL/min to 70 mL/min rate, adjusted to reach a mean arterial pressure ( MAP) level of 60 mm Hg in 10 minutes. When MAP reached 60 mm Hg, the blood withdrawal rate was adjusted to maintain a MAP decrease rate of 10 mm Hg every 2 minutes to 4 minutes. Arterial and mixed venous blood samples were collected at MAP levels of 60 mm Hg, 50 mm Hg, 40 mm Hg, 30 mm Hg, 20 mm Hg, and 10 mm Hg and analyzed for oxygen saturation, PO(2), PCO(2), potassium, lactate, bicarbonate, hemoglobin, pH, and standard base excess. Results: Significant increase in serum potassium occurred early in all animals. The rate of rise in serum potassium and its levels accompanied the hemodynamic deterioration. Hyperkalemia ( K >5 mmol/L) incidence was 12.5% at 60 mm Hg and 50 mm Hg, 62.5% at 40 mm Hg, 87.5% at 30 mm Hg, and 100% at 20 mm Hg. Strong correlations were found between potassium levels and lactate ( R = 0.82), SvO(2) ( R = 0.87), Delta pH ( R = 0.83), and Delta PCO(2) ( R = 0.82). Conclusions: Serum potassium increase accompanies the onset of HS. The rise in serum potassium was directly related to the hemodynamic deterioration of HS and strongly correlated with markers of tissue hypoxia.
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Background: Sudden unexpected cardiac death (SUCD) accounts for approximately 25% of deaths from ischaemic heart disease (IHD) but is relatively poorly understood because of the difficulties involved in researching aetiology. Clinical differences between instances of SUCD and those cases of acute chest pain that survive long enough to be proven as myocardial infarction but are eventually fatal might reflect differences in aetiology. Aims: To determine the risk factors for sudden unexpected cardiac death in Tasmanian men. Methods: A population-based case-control method was used with the study population, an estimated 125,225 men aged 25-74 years living in the island State of Tasmania, Australia. The case group of 102 men who had a SUCD was validated using necropsy reports, hospital records and information provided by the usual general practitioner. Cases were matched with 204 community controls. Spouses or partners of eligible subjects answered a detailed questionnaire. Multi-variate odds ratios (ORs) for risk factors were calculated using stepwise analysis. Results: Risk factors measured included: smoking habit, treated hypertension, hypercholesterolaemia, diabetes mellitus, family history of LHD, alcohol intake and exercise habits. Independent risk factors for SUCD were: history of diabetes mellitus (OR=4.2, 95% CI: 1.39, 12.81), current smoking status (OR=3.5, 95% CI: 1.80, 6.82), and family history of IHD (OR=2.6, 95% CI: 1.34, 4.92). Conclusions: Some accepted risk factors for acute myocardial infarction (AMI) also predict sudden death in men with no history of coronary disease. Efforts to reduce smoking, the incidence of diabetes mellitus and mean blood pressure must be continued as SUCD is, by definition, untreatable but is potentially avoidable in many instances.
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SETTING: Chronic obstructive pulmonary disease (COPD) is the third leading cause of death among adults in Brazil. OBJECTIVE: To evaluate the mortality and hospitalisation trends in Brazil caused by COPD during the period 1996-2008. DESIGN: We used the health official statistics system to obtain data about mortality (1996-2008) and morbidity (1998-2008) due to COPD and all respiratory diseases (tuberculosis: codes A15-16; lung cancer: code C34, and all diseases coded from J40 to 47 in the 10th Revision of the International Classification of Diseases) as the underlying cause, in persons aged 45-74 years. We used the Joinpoint Regression Program log-linear model using Poisson regression that creates a Monte Carlo permutation test to identify points where trend lines change significantly in magnitude/direction to verify peaks and trends. RESULTS: The annual per cent change in age-adjusted death rates due to COPD declined by 2.7% in men (95%CI -3.6 to -1.8) and -2.0% (95%CI -2.9 to -1.0) in women; and due to all respiratory causes it declined by -1.7% (95%CI 2.4 to -1.0) in men and -1.1% (95%CI -1.8 to -0.3) in women. Although hospitalisation rates for COPD are declining, the hospital admission fatality rate increased in both sexes. CONCLUSION: COPD is still a leading cause of mortality in Brazil despite the observed decline in the mortality/hospitalisation rates for both sexes.
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This study of breast cancer survival is based on analysis of five-year relative survival of 38 362 cases of invasive breast cancer in New South Wales (NSW) women, incident between 1972 and 1991, with follow-up to 1992, using data from the population-based NSW Central Cancer Registry. Survival was ascertained by matching the registry file of breast cancers against NSW death certificates from 1972 to 1992, mainly by automated probabilistic linkage. Absolute survival of cases was compared with expected survival of age- and period-matched NSW women. Proportional hazard regression analysis was used for examination of the effects on excess mortality of age, period of diagnosis and degree of spread at diagnosis. Relative survival at five years increased from 70 per cent in 1972-1976 to 77 per cent in 1987-1991. Survival improved during the 1970s and in the late 1980s. Regression analysis suggested that part of the improved survival in the late 1980s was due to lesser degree of spread at diagnosis, whereas the improved survival during the 1970s may have been due to treatment. Survival was better for those aged 40-49 years (RR = 0.86) and worse for those aged greater than or equal to 70 years (RR = 1.22) compared with the referent group (60-69 years). Excess mortality was much less for those with invasive localised disease than those with regional spread (RR = 3.1) or metastatic cancer (RR = 15.5) at diagnosis. For the most recent period (1987-1991), relative five-year survival was 90, 70 and 18 per cent, respectively, for the three degree-of-spread categories.
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Breast cancer five-year relative survival was calculated for 16 urban and rural regions in New South Wales (NSW) for cases incident in 1980-1991. Survival analysis employed cancer registry data linked with the death register, and age- and period-matched regional mortality of NSW women, Proportional hazard regression analysis was used to compare excess mortality in breast cancer cases in each region. The effect of region was significant (P < 0.05) in the analysis, after age and the follow-up variable (and their intel action) were adjusted for, although no region was significantly different from the referent group (chosen because of average relative five-year survival). When degree of spread and its interactions were entered into che model, the effect of region became nonsignificant. A significant linear trend (P < 0.05) in the adjusted relative risk for excess mortality in breast cancer cases was noted when regions were divided into quartiles based on socioeconomic status, with higher relative risk in low-socioeconomic-status groups; this effect also disappeared with adjustment for degree of spread at diagnosis. There was no general effect of rurality versus capital city or other metropolitan centres. This study demonstrates a small effect of region of residence and implied socioeconomic status on breast cancer survival in NSW women, but this becomes nonsignificant when the data are adjusted for degree of spread at diagnosis, This suggests that earlier diagnosis would he of benefit in reducing minor inequalities in breast cancer survival in NSW women.
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Social surveys have established dose-response relationships between aircraft noise and annoyance, with a number of psychological symptoms being positively related to annoyance. Evidence that exposure to aircraft noise is associated with higher psychiatric hospital admission rates is mixed. Some evidence exists of an association between aircraft noise exposure and use of psychotropic medications. People with a pre-existing psychological or psychiatric condition may be more susceptible to the effects of exposure to aircraft noise. Aircraft noise can produce effects on electroencephalogram sleep patterns and cause wakefulness and difficulty in sleeping. Attendances at general practitioners, self-reported health problems and use of medications, have been associated with exposure to aircraft noise, but some findings are inconsistent. Some association between aircraft noise exposure and elevated mean blood pressure has been observed in cross-sectional studies of schoolchildren, but with little confirmation from cohort studies. There is no convincing evidence to suggest that all-cause or cause-specific mortality is increased by exposure to aircraft noise. There is no strong evidence that aircraft noise has significant perinatal effects. Using the World Health Organization definition of health, which includes positive mental and social wellbeing, aircraft noise is responsible for considerable ill-health. However, population-based studies have not found strong evidence that people living near or under aircraft flight paths suffer higher rates of clinical morbidity or mortality as a consequence of exposure to aircraft noise. A dearth of high quality studies in this area precludes drawing substantive conclusions.
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Objectives: We sought to compare long-term outcomes after coronary bypass surgery with and without an internal thoracic artery graft. Methods: We analyzed clinical outcomes over a median follow-up of 6.7 years among 3,087 patients who received coronary bypass surgery as participants in one of 8 clinical trials comparing surgical intervention with angioplasty. We used 2 statistical methods (covariate adjustment and propensity score matching) to adjust for the nonrandomized selection of internal thoracic artery grafts. Results: Internal thoracic artery grafting was associated with lower mortality, with hazard ratios of 0.77 (confidence interval, 0.62-0.97; P = .02) for covariate adjustment and 0.77 (confidence interval, 0.57-1.05; P = .10) for propensity score matching. The composite end point of death or myocardial infarction was reduced to a similar extent, with hazard ratios of 0.83 (confidence interval, 0.69-1.00; P = .05) for covariate adjustment to 0.78 (confidence interval, 0.61-1.00; P = .05) for propensity score matching. There was a trend toward less angina at 1 year, with odds ratios of 0.81 (confidence interval, 0.61-1.09; P = .16) in the covariate-adjusted model and 0.81 (confidence interval, 0.55-1.19; P = .28) in the propensity score-adjusted model. Conclusions: Use of an internal thoracic artery graft during coronary bypass surgery seems to improve long-term clinical outcomes. (J Thorac Cardiovasc Surg 2011; 142: 829-35)
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In human heart there is now evidence for the involvement of four beta-adrenoceptor populations, three identical to the recombinant beta(1)-, beta(2)- and beta(3)-adrenoceptors, and a fourth as yet uncloned putative beta-adrenoceptor population, which we designate provisionally as the cardiac putative beta(4)-adrenoceptor. This review described novel features of beta-adrenoceptors as modulators of cardiac systolic and diastolic function. We also discuss evidence for modulation by unoccupied beta(1)- and beta(2)-adrenoceptors. Human cardiac and recombinant beta(1)- and beta(2)-adrenoceptors are both mainly coupled to adenylyl cyclase through Gs protein, the latter more tightly than the former. Activation of both human beta(1)- and beta(2)-adrenoceptors not only increases cardiac force during systole but also hastens relaxation through cyclic AMP-dependent phosphorylation of phospholamban and troponin I, thereby facilitating diastolic function. Furthermore, both beta(1) and beta(2)-adrenoceptors can mediate experimental arrhythmias in human cardiac preparations elicited by noradrenaline and adrenaline. Human ventricular beta(3)-adrenoceptors appear to be coupled to a pertussis toxin-sensitive protein (Gi?). beta(3)-Adrenoceptor-selective agonists shorten the action potential and cause cardiodepression, suggesting direct coupling of a Gi protein to a K+ channel. In a variety of species, including man, cardiac putative beta(4)-adrenoceptors mediate cardiostimulant effects of non-conventional partial agonists, i.e. high affinity beta(1)- and beta(2)-adrenoceptor blockers that cause agonist effects at concentrations considerably higher than those that block these receptors. Putative beta(4)-adrenoceptors appear to be coupled positively to a cyclic AMP-dependent cascade and can undergo some desensitisation.
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Background. The incidence of unexplained sudden death (SD) and the factors involved in its occurrence in patients with chronic kidney disease are not well known. Methods. We investigated the incidence and the role of co-morbidities in unexplained SD in 1139 haemodialysis patients on the renal transplant waiting list. Results. Forty-four patients died from SD of undetermined causes (20% of all deaths; 3.9 deaths/1000 patients per year), while 178 died from other causes and 917 survived. SD patients were older and likely to have diabetes, hypertension, past/present cardiovascular disease, higher left ventricular mass index, and lower ejection fraction. Multivariate analysis showed that cardiovascular disease of any type was the only independent predictor of SD (P = 0.0001, HR = 2.13, 95% CI 1.46-3.22). Alterations closely associated with ischaemic heart disease like angina, previous myocardial infarction and altered myocardial scan were not independent predictors of SD. The incidence of unexplained SD in these haemodialysis patients is high and probably a consequence of pre-existing cardiovascular disease. Conclusions. Factors influencing SD in dialysis patients are not substantially different from factors in the general population. The role played by ischaemic heart disease in this context needs further evaluation.
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Objective: To evaluate whether the number of vessels disease has an impact on clinical outcomes as well as on therapeutic results accordingly to medical, percutaneous, or surgery treatment in chronic coronary artery disease. Methods: We evaluated 825 individuals enrolled in MASS study, a randomized study to compare treatment options for single or multivessel coronary artery disease with preserved left ventricular function, prospectively followed during 5 years. The incidence of overall mortality and the composite end-point of death, myocardial infarction, and refractory angina were compared in three groups: single vessel disease (SVD n = 214), two-vessel disease (2VD n = 253) and three-vessel disease (3VD n = 358). The relationship between baseline variables and the composite end-point was assessed using a Cox proportional hazards survival model. Results: Most baseline characteristics were similar among groups, except age (younger in SVD and older in 3VD, p < 0.001), lower incidence of hypertension in SVD (p < 0.0001), and lower levels of total and LDL-cholesterol in 3VD (p = 0.004 and p = 0.005, respectively). There were no statistical differences in composite end-point in 5 years among groups independent of the kind of treatment; however, there was a higher mortality rate in 3VD (p < 0.001). When we stratified our analysis for each treatment option, bypass surgery was associated with a tower number of composite end-point in all groups (SVD p < 0.001, 2VD p = 0.002, 3VD p < 0.001). In multivariate analysis, we found higher mortality risk in 3VD comparing to SVD (p = 0.005, HR 3.14, 95%Cl 1.4-7.0). Conclusion: Three-vessel disease was associated with worse prognosis compared to single-or two-vessel disease in patients with stable coronary disease and preserved ventricular function at 5-year follow-up. In addition, event-free survival rates were higher after bypass surgery, independent of the number of vessels diseased in these subsets of patients. (c) 2008 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.
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Objectives: To evaluate clinical and echocardiographic variables that could be used to predict outcomes in patients with asymptomatic severe aortic valve stenosis. Management of asymptomatic severe aortic stenosis is controversial. Because prophylactic surgery may be protective, independent predictors of events that could justify early surgery have been sought. Methods: Outpatients (n= 133; mean [+/- SD] age, 66.2 +/- 13.6 years) with isolated severe asymptomatic aortic stenosis but normal left ventricular function and no previous myocardial infarction were followed up prospectively at a tertiary care hospital. Interventions: We use a ""wait-for-events"" strategy. Clinical and echocardiographic variables were analyzed. Results: Nineteen patients developed angina; 40, dyspnea; 5, syncope; and 7, sudden death during a mean follow-up period of 3.30 +/- 1.87 years. Event-free survival was 90.2 +/- 2.6% at 1 year, 73.4 +/-.9% at 2 years, 70.7 +/- 4.3% at 3 years, 57.8 +/- 4.7% at 4 years, 40.3 +/- 5.0% at 5 years, and 33.3 +/- 5.2% at 6 years. The mean follow-up period until sudden death (1.32 +/- 1.11 years) was shorter than that for dyspnea (2.44 +/- 1.84 years), syncope (2.87 +/- 1.26 years) and angina (3.03 +/- 1.68 years). Cox regression analysis disclosed only reduced but within normal limits ejection fraction as independent predictor of total events. Conclusions: Management on ""wait-for-events"" strategy is generally safe. Progressive left ventricular ejection fraction reduction even within normal limits identified patients at high risk for events in whom valve replacement surgery should be considered. (c) 2007 Elsevier Ireland Ltd. All rights reserved.
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Introduction. Chagas` disease is endemic in South America. Objective. This research reviewed the experience with cardiac transplantation in Chagas` disease, emphasizing reactivation, immunosuppression, and mortality. Methods. Over 25 years from March 1985 to March 2010, 107/409 (26.2%) patients with Chagas` disease underwent heart transplantation, patients including 74 (71.1%) men and 72 (67.2%), in functional class IV with 33 (30.8%) on vasopressors and 17 (10.7%) on mechanical circulatory support. Results. The diagnosis of disease reactivation was performed by identifying the parasite in the myocardium (n = 23; 71.8%) in the subcutaneous tissue (n = 8; 25.0%), in blood (n = 11; 34.3%), or in central nervous tissue (n = 1; 3.1%). Hospital mortality was 17.7% (n = 19) due to infection (n = 6; 31.5%), graft dysfunction (n = 6; 31.5%), rejection (n 4; 21.1%), or sudden death (n = 2; 10.5%). Late mortality was 27 (25.2%) cases, which were distributed as: rejection (n = 6; 22.2%), infection (n = 6; 22.2%), (n = lymphoma 4; 14.8%), sarcoma (n = 2; 7.4%), for constrictive pericarditis (n = 2; 7.4%) reactivation of Chagas` disease in the central nervous system (n = 1; 7.1%). Conclusions. Transplantation in Chagas` disease has peculiar problems that differ from other etiologies due to the possibility of disease reactivation and the increased possibility of emergence of cancers. However, transplantation is the only treatment able to modify the natural progression of the disease in its terminal phase. Early diagnosis and rapid introduction of benzonidazole reverses the histological patterns. Immunosuppression, especially steroids, predisposes to the development of cancer and disease reactivation.