Association of uric acid with mortality in patients with stable coronary artery disease

ObjectiveThe association between uric acid and cardiovascular disease is poorly studied. We undertook this study to assess whether uric acid level predicts clinical outcome in patients with stable coronary artery disease (CAD) treated with percutaneous coronary intervention (PCI).Materials/MethodsThis study included 8149 patients with stable CAD who underwent PCI. Uric acid was measured before angiography. The primary end point was 1-year mortality. Quartiles of quartiles of uric acid were: 1.49 to < 5.49 mg/dl (1st quartile; n=2032 patients), 5.49 to < 6.40 mg/dl (2nd quartile; n=1981 patients), 6.40 to < 7.50 mg/dl (3rd quartile; n=2093 patients) and 7.50 to 21.90 mg/dl (4th quartile; n=2043 patients).ResultsThere were 196 deaths during the 1-year follow-up. The numbers of deaths (Kaplan-Meier estimates) according to uric acid quartiles were: 35 deaths (1.8%) in the 1st quartile, 30 deaths (1.6%) in the 2nd quartile, 45 deaths (2.2%) in the 3rd quartile and 86 deaths (4.3%) in the 4th quartile (unadjusted hazard ratio [HR]=1.60, 95% confidence interval [CI] 1.38-1.86, P < 0.001 for each standard deviation [SD] increase in the logarithmic scale). After adjustment for traditional cardiovascular risk factors, renal function and inflammatory status, the association between uric acid and 1-year mortality remained significant (adjusted HR=1.26, 95% CI 1.07-1.48; P=0.005 for each standard deviation increase in the logarithmic scale). Uric acid improved predictivity of the multivariable model regarding mortality (P=0.040).ConclusionsElevated level of uric acid is an independent predictor of 1-year mortality in patients with stable CAD treated with PCI.     

Impact of body mass index on clinical outcome in patients with acute coronary syndromes treated with percutaneous coronary intervention

Studies that have tested the relationship between body weight as assessed by body mass index (BMI) and clinical outcome after percutaneous coronary intervention (PCI) have given contradictory results. The aim of the study was to investigate the impact of BMI on clinical outcome and assess the impact of adjustment for other cardiovascular risk factors on the relationship between obesity and clinical outcome in patients with acute coronary syndromes (ACS) following PCI. This study included 9146 patients with ACS who underwent coronary angiography and PCI: 2610 patients with ST-segment elevation acute myocardial infarction, 2792 patients with non-ST-segment elevation acute myocardial infarction, and 3744 patients with unstable angina. The primary outcome of this analysis was 1-year mortality. Quartiles of BMI were: 12.8 to <24.3 (1st quartile), 24.3 to <26.4 (2nd quartile), 26.4 to <29.1 (3rd quartile), and >29.1 to 50.7 (4th quartile). Within the first year following PCI, there were 756 deaths: 228 deaths in the 1st BMI quartile, 209 deaths in the 2nd BMI quartile, 161 deaths in the 3rd BMI quartile and 158 deaths in the 4th BMI quartile (Kaplan-Meier estimates of mortality 10.3%, 9.1%, 7.2%, and 7.0%, respectively; odds ratio [OR] = 1.51, 95% confidence interval [CI] 1.22-1.86, P < 0.001 for 1st vs 4th BMI quartile). After adjustment in the Cox proportional hazards model, the association between BMI and 1-year mortality was attenuated to the level of statistical insignificance (hazards ratio [HR] = 1.25, 95% CI 0.94–1.64; P = 0.127 for 1st vs 4th BMI quartile). In conclusion, in patients with ACS undergoing PCI, obesity as assessed with BMI was not an independent correlate of 1-year mortality.     

Prognostic value of uric acid in patients with ST-elevated myocardial infarction undergoing primary coronary intervention

Elevated uric acid (UA) levels have been associated with cardiovascular disease in epidemiologic studies. The relation between UA levels and long-term outcomes in patients with ST-segment elevation myocardial infarction who undergo primary percutaneous coronary intervention is not known. Data from 2,249 consecutive patients with ST-segment elevation myocardial infarction who underwent primary percutaneous coronary intervention were evaluated. Patients were divided into 2 groups with high or low UA using upper limits of normal of 6 mg/dl for women and 7 mg/dl for men. There were 1,643 patients in the low-UA group (mean age 55.9 ± 11.6 years, 85% men) and 606 patients in the high-UA group (mean age 60.5 ± 12.6 years, 76% men). Serum UA levels were 8.0 ± 1.5 mg/dl in the high-UA group and 5.2 ± 1.0 mg/dl in the low-UA group (p <0.001). The in-hospital mortality rate was significantly higher in patients with high UA levels (9% vs 2%, p <0.001), as was the rate of adverse outcomes in patients with high UA. The mean follow-up time was 24.3 months. Cardiovascular mortality, reinfarction, target vessel revascularization, heart failure, and major adverse cardiac events were all significantly higher in the high-UA group. In a multivariate analyses, high plasma UA levels were an independent predictor of major adverse cardiac events in the hospital (odds ratio 2.03, 95% confidence interval 1.25 to 3.75, p = 0.006) and during long-term follow-up (odds ratio 1.64, 95% confidence interval 1.05 to 2.56, p = 0.03). In conclusion, high UA levels on admission are independently associated with in-hospital and long-term adverse outcomes in patients with ST-segment elevation myocardial infarction who undergo primary percutaneous coronary intervention.     

Serum uric acid as an independent predictor of mortality in patients with angiographically proven coronary artery disease.

It is a matter of controversy as to whether uric acid is an independent predictor of mortality in patients with coronary artery disease (CAD) or whether it represents only an indirect marker of adverse outcome by reflecting the association between uric acid and other cardiovascular risk factors. Therefore, we studied the influence of uric acid levels on mortality in patients with CAD. In 1,017 patients with angiographically proven CAD, classic risk factors and uric acid levels were determined at enrollment. A follow-up over a median of 2.2 years (maximum 3.1) was performed. Death from all causes was defined as an end point of the study. In CAD patients with uric acid levels <303 micromol/L (5.1 mg/dl) (lowest quartile) compared with those with uric acid levels >433 micromol/L (7.1 mg/dl) (highest quartile), the mortality rate increased from 3.4% to 17.1% (fivefold increase). After adjustment for age, both sexes demonstrated an increased risk for death with increasing uric acid levels (female patients: hazard ratio [HR] 1.30, 95% confidence intervals [CI] 1.14 to 1.49, p < or = 0.001; male patients: HR 1.39 [95% CI 1.21 to 1.59], p < or = 0.001). In multivariate Cox regression analysis performed with 12 variables that influence overall mortality-including diuretic use-elevated levels of uric acid demonstrated an independent, significant positive relation to overall mortality (HR 1.23 [95% CI 1.11 to 1.36], p <0.001) in patients with CAD. Thus, uric acid is an independent predictor of mortality in patients with CAD.     

The prognostic role of serum uric acid level in patients with acute ST elevation myocardial infarction

Objectives

The role of uric acid as a prognostic factor in patients with acute ST elevation myocardial infarction is controversial. The purpose of this study was to demonstrate the relationship between serum uric acid level and mortality during admission period and 30-day period after admission.

Methods

We assessed the relation between serum uric acid level and in-hospital and short-term mortality rates in 184 patients admitted with acute ST elevation myocardial infarction. We divided the patients according to their gender and uric acid level measured on admission into four groups: group A₁: men with uric acid ⩽7 mg/dl versus group B₁: men with uric acid >7 mg/dl and group A₂: women with uric acid ⩽5.6 mg/dl versus group B₂: women with uric acid >5.6 mg/dl. The patients were followed for 30 days after admission.

Results

In-hospital mortality rate in group B₁ was higher than group A₁ [P value: 0.011, Relative risk: 13.33 (95% confidence interval: 1.55–114.7)]. Short-term all-cause mortality was significantly higher in group B₁ patients [P value: 0.037, Relative risk: 3.3 (95% confidence interval: 1.02–10.64)]. Multivariate logistic regression analysis of data showed an odds ratio of 15.23 for in-hospital mortality and odds ratio of 3.76 for short-term mortality in male hyperuricemic patients.

Conclusions

Our data suggest that in the acute phase of ST elevation myocardial infarction, uric acid has a prognostic role for in-hospital and short-term (30-day) mortality in men.     

Uric acid in-hospital changes predict mortality in patients with acute myocardial infarction

Background and aimsThe prognostic impact of admission uric acid (UA) levels in patients with acute myocardial infarction (AMI) is controversial. We assessed the prognostic role of in-hospital UA changes in patients with AMI.Methods and resultsWe studied 375 consecutive patients (320 males, mean age 62.6 years) with AMI (232 with ST elevation MI) within 12 h of symptoms' onset. UA levels were daily measured throughout hospitalization and their admission and peak values were recorded. End-points were 30-day and 1-year mortality. Mortality rate at 30 days was 7.2% and at 1 year 10.9%. Patients who died within 30 days exhibited higher peak UA (10.24 mg/dl vs. 7.06 mg/dl, p < 0.001) and absolute UA elevation (1.7 mg/dl vs. 0.7 mg/dl, p < 0.001). Optimal values for predicting 30-day mortality were 9.65 mg/dl for peak UA and 2.35 mg/dl for UA elevation. Concerning 1-year mortality, deceased patients had higher peak UA levels (9.71 mg/dl vs. 7 mg/dl, p < 0.001) and absolute UA elevation (1.5 mg/dl vs. 0.6 mg/dl, p < 0.001). Optimal values for predicting 1-year mortality were 9.55 mg/dl for peak UA and 1.1 mg/dl for UA elevation. With Cox regression analysis peak UA (adjHR 1.157, p = 0.030) and UA elevation (adjHR 1.288, p = 0.009) were independent predictors of 30-day mortality. Similarly, peak UA levels (adjHR 1.204, p = 0.001) and UA elevation (adjHR 1.213, p = 0.001) predicted 1-year mortality.ConclusionsIn patients with AMI peak rather than admission UA levels, and absolute in-hospital UA elevation predict both 30-day and 1-year mortality. Serial in-hospital UA measurements add prognostic information in AMI patients.     

Uric acid within the “normal” range predict 9-year cardiovascular mortality in older individuals. The InCHIANTI study

Background and aimsIncreased uric acid levels correlate with cardiovascular disease and cardiovascular/overall mortality. To identify a uric acid threshold above which cardiovascular mortality rises, we studied the relationship between uric acid concentration and overall/cardiovascular mortality.Methods and resultsWe analyzed data from the InCHIANTI study, a cohort study of Italian community-dwelling people with 9 years of follow-up. We selected a sample of 947 individuals over 64 years of age, free from cardio-cerebrovascular disease and with available uric acid measurement at baseline. The sample was divided according to plasma uric acid tertiles. The Hazard ratio (HR) for mortality was calculated by multivariate Cox proportional hazard model. Mean age of participants was 75.3 ± 7.3 years; the mean value of uric acid was 5.1 ± 1.4 mg/dl. Over 9-years of follow-up, 342 (36.1%) participants died, 143 deaths (15.1%) were due to cardiovascular disease. Subjects with higher uric acid concentrations presented a higher cardiovascular mortality [II (4.6–5.5 mg/dl) vs I (1.8–4.5 mg/dl) tertile HR: 1.98, 95%C.I. 1.22–3.23; III (≥5.6 mg/dl) vs I tertile HR: 1.87, 95%C.I. 1.13–3.09]. We found a non-linear association between uric acid concentrations and cardiovascular mortality with the lowest mortality for values of about 4.1 mg/dl and a significant risk increment for values above 4.3 mg/dl.ConclusionIn community-dwelling older individuals free from cardio-cerebrovascular events, the lowest 9-year cardiovascular mortality was observed for uric acid values far below current target values. If confirmed, these data might represent the background for investigating the efficacy of uric acid levels reduction in similar populations.     

Early invasive strategies for acute coronary syndromes

Early coronary angiography and percutaneous or operative revascularization is now the treatment of choice for both ST- and non-ST-segment elevation acute coronary syndromes (ACS). In non-ST-segment elevation ACS this strategy produces a 18% to 22% reduction in ischemic outcomes at 6 months and prevents 1.7 deaths, 2.0 nonfatal infarcts and 20 readmissions per 100 treated patients at 1-year follow-up. Early angiography allows definition of coronary anatomy and assessment of left ventricular function, both important predictors of long-term risk. Intracoronary stenting and intravenous glycoprotein IIb/IIIa antagonists have improved outcome in percutaneous revascularization and should be used in the majority of ACS patients undergoing PCI. Initial costs are higher with an early invasive strategy; however, these are offset by reductions in rehospitalizations and later ischemic complications.     

Comparison of five-year outcomes of patients with and without chronic total occlusion of noninfarct coronary artery after primary coronary intervention for ST-segment elevation acute myocardial infarction

The aim of the present study was to evaluate the effect of concurrent chronic total occlusion (CTO) in a noninfarct-related artery (IRA) on the long-term prognosis in patients with ST-segment elevation myocardial infarction and multivessel coronary disease. Of 1,658 consecutive patients with ST-segment elevation myocardial infarction, 666 with multivessel coronary disease who underwent percutaneous coronary intervention from 1999 to 2004 were included in the present analysis. The patients were divided into 2 groups: no CTO and CTO. The first group included 462 patients without CTO (69%) and the second group included 204 patients with CTO in a non-IRA (31%). The in-hospital mortality rate was 6.3% and 21.1% (p < 0.0001) and the 5-year mortality rate was 22.5% and 40.2% (p < 0.0001) for the no-CTO and CTO patients, respectively. Multivariate analysis revealed that after correction for baseline differences CTO in a non-IRA was a strong, independent predictor of 5-year mortality in patients undergoing percutaneous coronary intervention (hazard ratio 1.85; 95% confidence interval 1.35 to 2.53; p = 0.0001). In conclusion, the presence of CTO in a non-IRA in patients with ST-segment elevation myocardial infarction and multivessel coronary disease is a strong and independent risk factor for greater 5-year mortality.     

Relationship of C-reactive protein levels with angiographic findings and markers of necrosis in non-ST-segment elevation acute coronary syndrome

INTRODUCTION AND OBJECTIVES: The mechanism responsible for elevated C-reactive protein levels (inflammation of the ruptured atherosclerotic plaque or myocardial necrosis) in acute coronary syndromes is controversial. The aim of this study was to investigate the relationship between C-reactive protein levels and angiographic complexity of the culprit lesion and troponin elevation in patients with non-ST elevation acute coronary syndromes. PATIENTS AND METHOD: The study group consisted of 125 patients with single-vessel disease. Troponin-I and C-reactive protein were measured, and the complexity of the culprit lesion was analyzed (TIMI flow and thrombus). Information on age, sex, smoking habit, hypertension, hypercholesterolemia and diabetes was obtained from the medical record. RESULTS: The quartile distribution of C-reactive protein showed more patients with TIMI flow < 3 (31%, 28%, 18%, and 55%; P=.02), thrombus (3%, 6%, 7%, and 28%; P=.007) and troponin-I elevation (19%, 44%, 50%, and 66%; P=.003) in the fourth quartile. Multivariate analysis showed both thrombus (OR = 4.1; 95% CI, 1.2-14.3; P=.03) and troponin elevation (OR = 2.6; 95% CI, 1.1-6.3; P=.03) to be associated with C-reactive protein > 18 mg/L (fourth quartile cut-off). When treated as a continuous variable, higher levels of C-reactive protein were also associated with thrombus (P=.02) and troponin elevation (P=.003). No other clinical variables were related with C-reactive protein levels. CONCLUSIONS: Both angiographic complexity of the culprit lesion and elevated troponin level are related with increased C-reactive protein levels in non-ST elevation acute coronary syndromes.     

Renal failure after percutaneous coronary intervention is associated with high mortality.

Renal failure is a marker of poor outcome in the general population. Renal failure after percutaneous coronary artery intervention (PCI) is associated with an increased hazard of in-hospital mortality. We hypothesized that post-PCI renal insufficiency would be a predictor of long-term mortality in patients undergoing PCI who survive for over 30 days after the procedure. A retrospective analysis was conducted from a registry of 9,067 patients undergoing PCI at our center from 1997 to 2001. A rise in creatinine by 1 mg/dl from baseline was defined as post-PCI renal insufficiency. Vital status was assessed using Social Security Death Index. There were a total of 996 deaths over a mean follow-up period of 3.2 years. In a multivariate analysis, history of recent acute myocardial infarction, older age, insulin-dependent diabetes, baseline creatinine greater than 1.5 mg/dl, and presence of mitral regurgitation were associated with post-PCI renal insufficiency. Developing post-PCI renal insufficiency was associated with a 4.31-fold hazard of mortality in univariate analysis and a 1.77-fold hazard after adjustment for known predictors of mortality after PCI. The 1-year survival in patients with renal failure was 70.3% +/- 3.91%, compared to a survival of 93.6% +/- 0.27% in those without any post-PCI renal insufficiency (P < 0.0001). Acute renal insufficiency after PCI is a strong and independent predictor of long-term mortality in patients who survived for 30 days after the procedure.     

Effect of abciximab on clinical and angiographic restenosis in patients with non-ST-segment elevation acute coronary syndromes

The ISAR-REACT 2 trial was designed to assess the effect of abciximab in patients with acute coronary syndromes undergoing percutaneous coronary intervention after a 600-mg loading dose of clopidogrel. The aim of the present study was to investigate the impact of abciximab on clinical and angiographic restenosis after coronary stenting in patients with acute coronary syndromes. The angiographic substudy included 1,544 patients from the ISAR-REACT 2 trial randomly assigned to abciximab (771 patients) or placebo (773 patients). All patients were scheduled for routine angiographic follow-up at 6 to 8 months after intervention. The primary end point was incidence of angiographic in-segment binary restenosis. The secondary end point was 1-year incidence of target-lesion revascularization. Binary restenosis was observed in 21.9% of patients in the abciximab group and 24.5% of patients in the placebo group (p=0.29). Percentages of in-stent (29+/-22% vs 33+/-24%; p=0.02) and in-segment (35+/-20% vs 38+/-21%; p=0.04) diameter stenoses were significantly lower in the abciximab group than the placebo group. There was a strong trend toward lower 1-year incidence of target-lesion revascularization in patients treated with abciximab than in patients treated with placebo (13.6% vs 16.8%; p=0.08). In conclusion, in patients with non-ST-segment elevation acute coronary syndromes undergoing early percutaneous coronary intervention with stenting after a 600-mg loading dose of clopidogrel, abciximab therapy may have a slight positive impact on the prevention of restenosis.     

Prognostic value of admission hemoglobin levels in ST-segment elevation myocardial infarction patients presenting with cardiogenic shock

Even in the era of primary percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI) complicated by cardiogenic shock (CS), mortality remains high. Whether admission hemoglobin (Hb) concentration is a predictor of mortality in patients with CS treated with primary PCI is unexplored. We assessed the relation between admission Hb concentration and 1-year mortality in patients with STEMI and CS who were treated with PCI at admission. We investigated a cohort of 265 patients with STEMI with CS on admission. Patients were categorized in 3 groups according to plasma Hb levels at admission: 9.6 g/dl (group I, n = 22), 9.6 to 12 g/dl (group II, n = 59), and >12 g/dl (group III, n = 184). All-cause mortality at 1 year was 64%, 46%, and 35% for groups I, II, and III, respectively (p = 0.007). Multivariate logistic regression analysis showed that the odds for mortality increased 17% for every 1.0 g/dl decrease in plasma Hb (odds ratio 1.17, 95% confidence interval 1.01 to 1.35, p = 0.042). In conclusion, admission Hb concentration is an independent predictor for 1-year mortality in patients with STEMI undergoing primary PCI.     

The Prognostic Value of Serum Creatinine on Admission in Fibrinolytic-Eligible Patients with Acute Myocardial Infarction

Background: Previous studies have demonstrated that impaired renal function is associated with unfavourable outcomes in patients with acute coronary syndromes and following percutaneous coronary intervention. Methods: We hypothesized that serum creatinine (Cr) on admission is a useful predictor of mortality in fibrinolytic-eligible patients with ST-elevation myocardial infarction (MI). Data were collected from 352 patients with ST-elevation MI, 89% of patients underwent early invasive management. Results: 30-day and 6-month mortality were increased among patients with mild to moderate (Cr > 1.2–2.8 mg/dl) renal dysfunction compared to patients with normal (Cr 1.2 mg/dl) renal function (3.4% vs. 16.1%, p < 0.001 and 4.5% vs. 19.5%, p < 0.001). After adjustment for previously identified correlates of mortality in a multiple logistic regression model, higher Cr on admission remained independently associated with increased mortality (30-day, OR 4.78, 95%CI 1.55–14.73, p = 0.006; 6-month, 3.82 (1.45–10.11), p = 0.007). The incidence of mortality was reduced among those patients with renal dysfunction that also underwent acute percutaneous coronary intervention [30-day, OR 0.13, 95%CI 0.02–1.06, p < 0.03; 6-month, 0.23 (0.05–1.07), p < 0.05]. Conclusion: Cr on admission is a strong and independent predictor of mortality in patients with ST-elevation MI. This association does not appear to be mediated by reduced fibrinolytic efficacy, or by higher reinfarction rates among patients with renal dysfunction. Cr on admission is a rapid and widely available marker to identify high-risk patients with ST-elevation MI that have additional improvements in survival when treated with percutaneous coronary intervention.     

Relation of serum uric acid with metabolic risk factors in asymptomatic middle-aged Brazilian men

This study in 352 asymptomatic middle-aged Brazilian men demonstrated that serum uric acid increases linearly with an increasing number (0 to >/=3) of metabolic risk factors (5.78 +/- 1.1, 6.14 +/- 1.0, 6.27 +/- 1.1, and 6.79 +/- 1.3, p <0.001). In patients who had >/=3 metabolic risk factors, there was a higher prevalence of serum uric acid in the highest quartile (7.2 to 10.3 mg/dl) than in the lowest quartile (2.6 to 5.4 mg/dl, 35% vs 12%, p <0.001). Mean serum levels of uric acid were higher in those who had an abnormal ratio of >/=3 for triglyceride to high-density lipoprotein (suggesting insulin resistance) than in those who had a normal ratio (6.6 +/- 1.2 vs 5.87 +/- 1 mg/dl, p <0.001).     

Elevated serum uric acid is associated with a greater inflammatory response and with short- and long-term mortality in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention

Background and aimsDespite elevated serum uric acid (eSUA) has been identified as independent risk factor for cardiovascular diseases, its prognostic value in the setting of ST-segment elevation myocardial infarction (STEMI) is still controversial. Although the mechanisms of this possible relationship are unsettled it has been suggested that eSUA could trigger the inflammatory response. This study sought to investigate the association between eSUA with short- and long-term mortality and with inflammatory response in patients with STEMI treated with primary percutaneous coronary intervention (pPCI).Methods and resultsBlood samples were collected on admission and at 24 and 48 h after pPCI: the inflammatory biomarkers C-reactive protein (CRP), neutrophil count and neutrophil to lymphocytes ratio (NLR) were considered. Baseline eSUA was defined as ≥6.8 mg/dl. Cumulative 30-days and 1-year mortalities were estimated using the Kaplan-Meyer analysis. Multivariable analyses were performed by Cox proportional hazard models.In the 2369 patients with STEMI considered, 30-day mortality was 5.8% among patients with eSUA and 2% among patient with normal SUA level (p < 0.001); 1-year mortality was 8.5% vs 4%, respectively (p < 0.001). At multivariable analyses eSUA was an independent predictor of 30-day mortality (HR 1.196, 95%CI 1.006–1.321, p = 0.042) and 1-year mortality (HR 1.178, 95%CI 1.052–1.320, p = 0.005). eSUA patients presented higher values in on admission CRP (p < 0.001) and in neutrophil count and NLR at 24 h (respectively, p = 0.020 and p < 0.001) and at 48 h (p = 0.018 and p < 0.001) compared to patients with normal SUA levels.ConclusionsElevated serum uric acid is associated with higher short- and long-term mortality and with a greater inflammatory response after reperfusion in patients with STEMI treated with primary PCI.     

Integrating antithrombin and antiplatelet therapies with early invasive management for non-ST-segment elevation acute coronary syndromes

Non-ST-segment elevation acute coronary syndromes are a dramatic manifestation of coronary artery disease. Multiple clinical trials have shown that early cardiac catheterization improves clinical outcomes in patients with non-ST-segment elevation acute coronary syndromes. Many antithrombotic agents effectively manage unstable coronary syndromes and serve as adjuncts to percutaneous coronary intervention. Yet, the growing number of pharmacologic agents makes early management of non-ST-segment elevation acute coronary syndromes increasingly complex. We review the current evidence regarding the optimal integration of early antithrombotic and antiplatelet therapies with early coronary angiography and subsequent revascularization.     

Predictive factors of major adverse cardiac events in acute myocardial infarction patients complicated by cardiogenic shock undergoing primary percutaneous coronary intervention.

BACKGROUND: The aim of this study was to assess in-hospital mortality and major adverse cardiac events (MACE) during long-term clinical follow-up of patients who developed cardiogenic shock (CS) after acute myocardial infarction (AMI) and who underwent primary percutaneous coronary intervention (PCI). METHODS AND RESULTS: The data from 147 patients with CS after AMI (61.7 +/-10.4 years, M:F =156:99) who underwent primary PCI at Chonnam National University Hospital between January 1999 and December 2002 were analyzed: clinical characteristics, coronary angiographic findings and mortality during admission, and MACE during a 1-year clinical follow-up. Of the enrolled patients, 121 patients survived (group I, M:F =94:27) and 26 died (group II, M:F =14:12) during admission. By binary logistic regression analysis, in-hospital death was associated with low Thrombolysis In Myocardial Infarction (TIMI) flow after coronary revascularization (p=0.02, odds ratio (OR) =1.3). Eighty-nine patients (60.5%) survived without MACE during the 1-year clinical follow-up and MACE was associated with a C-reactive protein (CRP) of more than 1 mg/dl (p=0.002, OR =6.3) and low TIMI flow after coronary revascularization (p<0.001, OR =7.8). CONCLUSIONS: Primary PCI achieving TIMI 3 flow reduces in-hospital death in AMI with CS. High concentration of CRP and low TIMI flow are associated with MACE during long-term clinical follow-up.     

Usefulness of adiponectin as a predictor of all cause mortality in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention

Substantial evidence points to a protective role of adiponectin against atherosclerosis and cardiovascular (CV) disease. However, in the setting of an acute myocardial infarction (AMI), the role of adiponectin has not previously been studied. Consequently, the aim of this study was to investigate the prognostic role of adiponectin after AMI in a large population of patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention. A total of 735 consecutive patients with ST-segment elevation myocardial infarction admitted to a single high-volume invasive heart center and treated with primary percutaneous coronary intervention from September 2006 to December 2008 were included. Blood samples were drawn immediately before the invasive procedure. Plasma adiponectin was measured using a validated immunoassay. End points were all-cause mortality, CV mortality, and admission for new AMI or heart failure. The median follow-up time was 27 months (interquartile range 22 to 33). Patients with high adiponectin (quartile 4) had increased mortality compared to patients with low adiponectin (quartiles 1 to 3) (log-rank p <0.001). After adjustment for conventional risk factors (age, gender, smoking, hypertension, hypercholesterolemia, diabetes, body mass index, C-reactive protein, peak troponin I, creatinine, estimated glomerular filtration rate, previous AMI, multivessel disease, complex lesions, left anterior descending coronary artery lesion, and symptom-to-balloon time) by Cox regression analysis, high adiponectin remained an independent predictor of all-cause mortality (hazard ratio 2.1, 95% confidence interval 1.3 to 3.2, p = 0.001) and CV mortality (hazard ratio 2.6, 95% confidence interval 1.5 to 4.5, p = 0.001). In conclusion, increased plasma adiponectin independently predicts all-cause and CV mortality in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention.