Diagnostic Value of High-Sensitivity Cardiac Troponin-I in Patients After Out-of-Hospital Cardiac Arrest.

Knowing the etiology of cardiac arrest (CA) is important for treatment decisions. Results of previous studies on the diagnostic role of cardiac troponin in patients resuscitated from CA are controversial, few studies were done during the era of high-sensitivity cardiac troponin-I (hs-cTnI), and kinetics of hs-cTnI was not thoroughly investigated. We aimed to explore the diagnostic value of hs-cTnI in patients resuscitated from out-of-hospital CA (OHCA). This retrospective study included 201 consecutive patients after OHCA admitted to the intensive cardiac care unit at Rambam Health Care Campus from 2016 to 2021. Patients were divided into 2 groups according to etiology of CA: group 1-patients with definite acute myocardial infarction (AMI), group 2-patients in whom AMI was excluded. Values of hs-cTnI on admission, peak hs-cTnI, and hs-cTnI upslope were compared between patients with AMI and non-AMI. Peak hs-cTnI and hs-cTnI upslope differed significantly between patients with non-AMI versus AMI CA (median 1,424 vs 32,558 ng/L, p <0.0001 and median 109 vs 2,322 ng/L/h, p <0.0001, respectively). Moreover, peak hs-cTnI and hs-cTnI upslope were found to have good discrimination performance between patients with non-AMI and AMI, with area under the curve receiver operating characteristics (ROC) curves of 0.83 and 0.80, respectively. In conclusion, in patients resuscitated from OHCA values of peak hs-cTnI and hs-cTnI upslope could be helpful in the diagnosis of etiology of CA as adjunct to other diagnostic methods.

Type of Anemia, Chronic Non-cardiovascular Illnesses, and Outcomes of Patients with ST-segment Elevation Myocardial Infarction.

OBJECTIVES: To assess the impact of different types of anemia and of concomitant non-cardiovascular chronic illnesses on outcomes of patients with ST-segment elevation myocardial infarction (STEMI) and baseline anemia admitted to the Intensive Cardiac Care Unit. METHODS: Based on the mean corpuscular volume, anemia was stratified into: microcytic (<80 fL), normocytic (≥80, <96 fL), and macrocytic (≥96 fL). Data on concomitant chronic non-cardiovascular illnesses including malignancies were carefully collected. Endpoints included in-hospital bleeding as well as all-cause mortality at long-term follow-up. RESULTS: Of 1,390 patients with STEMI, 294 patients had baseline anemia (21.2%), in whom normocytic, microcytic, and macrocytic anemia was present in 77.2%, 17.0%, and 5.8% patients, respectively. In-hospital bleeding occurred in 25 (8.5%) of the study population without significant differences between the three groups. At a mean follow-up of 5.5±3.5 years, 104 patients (35.4%) had died. Mortality was the highest in patients with macrocytic anemia, followed by patients with normocytic anemia and microcytic anemia (58.8%, 37.0%, and 20.0%, respectively; P=0.009). Chronic non-cardiovascular condition was identified as an independent predictor of both in-hospital bleeding (odds ratio=2.57, P=0.01) and long-term mortality (hazard ratio [HR] 1.54, P=0.019). Performance of coronary angiography within index hospitalization was associated with lower long-term mortality (HR 0.38, P=0.001). Mean corpuscular volume did not predict either in-hospital bleeding or mortality. CONCLUSIONS: Chronic non-cardiovascular illnesses are highly prevalent among patients with STEMI and baseline anemia, and are strongly associated with higher in-hospital bleeding and long-term mortality. Type of anemia is not related to prognosis post-STEMI.

Long-term effects of brief hypoxia due to cardiac arrest: Hippocampal reductions and memory deficits.

OBJECTIVE: To examine the effects of brief hypoxia (<7 min) due to cardiac arrest on the integrity of the brain and performance on memory and executive functions tasks. METHODS: Patients after out-of-hospital cardiac arrest (CA) (n = 9), who were deemed neurologically intact on discharge, were compared to matched patients with myocardial infarction (MI) (n = 9). A battery of clinical and experimental memory and executive functions neuropsychological tests were administered and MRI scans for all patients were collected. Measures of subcortical and cortical volumes and cortical thickness were obtained using FreeSurfer. Manual segmentations of the hippocampus were also performed. APACHE-II scores were calculated based on metrics collected at admission to ICCU for all patients. RESULTS: Significant differences between the two groups were observed on several verbal memory tests. Both hippocampi were significantly reduced (p < 0.05) in the CA patients, relative to MI patients. Hippocampal subfields segmentation showed significantly reduced presubiculum volumes bilaterally. CA patients had on average 10% reduction in volumes bilaterally across hippocampal subfields. No cortical thickness differences survived correction. Significant correlations were observed in the CA group only between the hippocampal volumes and performance on verbal memory tasks, including recollection. Hippocampal volumes and several memory measures (but not other cognitive domains) were strongly correlated with APACHE-II scores on admission in the CA group, but not in the MI group CONCLUSIONS: Chronic patients with cardiac arrest who were discharged from hospital in "good neurological condition" showed an average of 10% reduction in hippocampal volume bilaterally and significant verbal memory deficits relative to matched controls with myocardial infarction, suggesting even brief hypoxic periods suffice to lead to specific hippocampal damage.

Acute Kidney Injury After Primary Angioplasty: Is Contrast-Induced Nephropathy the Culprit?

BACKGROUND: Acute kidney injury (AKI) following primary percutaneous coronary intervention (pPCI) is frequently interpreted as contrast-induced AKI but may result from other insults. We aimed to determine the causal association of contrast material exposure and the incidence of AKI following pPCI using a control group of propensity score-matched patients with ST-segment-elevation myocardial infarction who were not exposed to contrast material. METHODS AND RESULTS: We studied 2025 patients with ST-segment-elevation myocardial infarction who underwent pPCI and 1025 patients receiving fibrinolysis or no reperfusion who were not exposed to contrast material during the first 72 hours of hospital stay (control group). AKI was defined as creatinine of ≥0.5 mg/dL or >25% rise within 72 hours. AKI rates were similar in the pPCI and control groups (10.3% versus 12.1%, respectively; P=0.38). Propensity score matching resulted in 931 matched pairs with PCI and no PCI, with balanced baseline covariates (standardized difference <0.1). Among propensity score-matched patients, AKI rates were not significantly different with and without PCI (8.6% versus 10.9%, P=0.12). In the pPCI cohort, independent predictors of AKI included age ≥70 years, insulin-treated diabetes mellitus, diuretic therapy, anterior infarction, baseline estimated glomerular filtration rate, and variables related to the presence of pump failure (higher Killip class, intra-aortic balloon pump use) and reduced left ventricular ejection fraction but not contrast material dose. A risk score based on the PCI cohort had similar discriminatory capacity for AKI in the control group (C statistic 0.81±0.02 and 0.78±0.02, respectively; P=0.26). CONCLUSIONS: The development of AKI in patients with ST-segment-elevation myocardial infarction undergoing pPCI is mainly related to older age, baseline estimated glomerular filtration rate, heart failure, and hemodynamic instability. Risk for AKI is similar among ST-segment-elevation myocardial infarction patients with and without contrast material exposure.

Conduction abnormalities during dipyridamole stress testing.

Pharmacological stress tests using dipyridamole are considered to be safe. However, cases of atrioventricular (AV) block have been reported. We retrospectively analyzed ECG at baseline and during dipyridamole stress tests of 2010 consecutive patients (patients with second or third degree AV block were excluded). At baseline, 350 (17.4%) patients had conduction abnormalities. Following dipyridamole infusion 16 patients (0.8%) developed a transient change in AV conduction (15 patients) and or sinus arrest (1 patient). Compared to patients without baseline conduction abnormalities, patients with any conduction abnormalities at baseline were at a higher risk for the development of AV block after dipyridamole infusion [0.3% vs 3.14%, respectively; P < .0001].

Real-World Use of Novel P2Y12 Inhibitors in Patients with Acute Myocardial Infarction: A Treatment Paradox.

OBJECTIVE: To assess the real-world use, clinical outcomes, and adherence to novel P2Y12 inhibitors. METHODS: We evaluated 1,093 consecutive acute myocardial infarction patients undergoing a percutaneous intervention. Patients were derived from a prospective, multicenter, nationwide registry and were followed for 30 days; 381 patients (35%) received clopidogrel, 468 (43%) received prasugrel, and 244 (22%) received ticagrelor. Patients treated with clopidogrel were older and more likely to suffer from chronic renal failure and stroke and/or present with non-ST-elevation myocardial infarction (NSTEMI) (p < 0.01 for all). Independent predictors of undertreatment with novel P2Y12 inhibitors included: older age (OR 0.17; 95% CI 0.1-0.27, p < 0.0001), a prior stroke (OR 0.41; 95% CI 0.2-0.68, p = 0.008), and NSTEMI (OR 0.37; 95% CI 0.26-0.54, p < 0.0001). RESULTS: Novel P2Y12 inhibitors were associated with a lower incidence of cardiovascular events, major bleeding, and/or death (7.6 vs.11%, HR 0.67; 95% CI 0.43-1, p = 0.05). However, after a multivariate analysis this trend was not statistically significant. Patients discharged with ticagrelor versus thienopyridines demonstrated a higher rate of crossover to other P2Y12 inhibitors (11 vs. 5%, p = 0.03). CONCLUSIONS: In a real-world cohort, there was an underutilization of novel P2Y12 inhibitors which was more pronounced in higher-risk subsets that might benefit from novel P2Y12 inhibitors at least as much as other patients.

Time Dependence of the Effect of Right Ventricular Dysfunction on Clinical Outcomes After Myocardial Infarction: Role of Pulmonary Hypertension.

BACKGROUND: The clinical importance of right ventricular (RV) function in acute myocardial infarction is well recognized, but the impact of concomitant pulmonary hypertension (PH) has not been studied. METHODS AND RESULTS: We studied 1044 patients with acute myocardial infarction. Patients were classified into 4 groups according to the presence or absence of RV dysfunction and PH, defined as pulmonary artery systolic pressure >35 mm Hg: normal right ventricle without PH (n=509), normal right ventricle and PH (n=373), RV dysfunction without PH (n=64), and RV dysfunction and PH (n=98). A landmark analysis of early (admission to 30 days) and late (31 days to 8 years) mortality and readmission for heart failure was performed. In the first 30 days, RV dysfunction without PH was associated with a high mortality risk (adjusted hazard ratio 5.56, 95% CI 2.05-15.09, P<0.0001 compared with normal RV and no PH). In contrast, after 30 days, mortality rates among patients with RV dysfunction were increased only when PH was also present. Compared with patients having neither RV dysfunction nor PH, the adjusted hazard ratio for mortality was 1.44 (95% CI 0.68-3.04, P=0.34) in RV dysfunction without PH and 2.52 (95% CI 1.64-3.87, P<0.0001) in RV dysfunction with PH. PH with or without RV dysfunction was associated with increased risk for heart failure. CONCLUSION: In the absence of elevated pulmonary pressures, the risk associated with RV dysfunction after acute myocardial infarction is entirely confined to the first 30 days. Beyond 30 days, PH is the stronger risk factor for long-term mortality and readmission for heart failure.

Heart failure in patients with diabetes undergoing primary percutaneous coronary intervention.

INTRODUCTION: Diabetes mellitus is associated with increased risk after acute coronary syndromes. Primary percutaneous coronary intervention is the most effective method of reperfusion for acute ST-elevation myocardial infarction and can limit the ischaemic damage to the left ventricle. However, there are few data on the impact of diabetes mellitus on the risk of heart failure following primary percutaneous coronary intervention. METHODS: We studied 958 ST-elevation myocardial infarction patients treated with primary percutaneous coronary intervention, of whom 263 (27.5%) had diabetes mellitus, with 67 (7.0%) treated with insulin. The primary end points of the study were re-admission for heart failure. Secondary end points were all-cause mortality and recurrent infarctions. The follow-up period was 5 years after hospital discharge. RESULTS: The cumulative incidence of re-admission for heart failure was 8.4%, 15.2% and 26.7% in patients without diabetes mellitus, non-insulin-treated and insulin-treated diabetes mellitus, respectively. Compared with patients without diabetes mellitus, the adjusted hazard ratio for heart failure was 1.95 (95% confidence intervals 1.30-2.93) and 3.09 (95% confidence intervals 1.71-5.60) in non-insulin-treated and insulin-treated diabetes mellitus, respectively. The corresponding hazard ratios for mortality were 1.03 (95% confidence intervals 0.68-1.55) and 2.04 (95% confidence intervals 1.22-3.42), respectively. There was a J-shaped association between fasting glucose levels in the acute phase and risk of mortality (P=0.0001) and a direct association with heart failure (P=0.03). CONCLUSION: Despite modern treatment of ST-elevation myocardial infarction and high levels of guideline-based medical care, diabetes mellitus had an independent adverse effect on the risk of re-admissions for heart failure, which was particularly high among insulin-treated patients.

Severe burns in a patient after out-of-hospital CPR.

We present a case of a patient after prolonged cardio-pulmonary resuscitation on hot asphalt, who suffered from first and second degree burns which worsened during hospitalization. The patient was treated with therapeutic hypothermia. Possible effect of therapeutic hypothermia on the course of burns is discussed.

Impact of functional mitral regurgitation on right ventricular function and outcome in patients with right ventricular infarction.

Right ventricular (RV) infarction is associated with increased mortality. Functional mitral regurgitation (FMR) may complicate inferoposterior infarction with RV involvement leading to pulmonary hypertension and increased RV afterload, potentially exacerbating RV remodeling and dysfunction. We studied 179 patients with inferior wall left ventricular (LV) ST-elevation myocardial infarction and RV infarction. The presence and severity of FMR and RV function were assessed by echocardiography. FMR was diagnosed based on echocardiographic criteria and when the severity of regurgitation was ≥moderate. Eighteen patients (10.0%) had ≥moderate FMR. Estimated pulmonary artery systolic pressure was higher in patients with FMR than in patients without FMR (43 ± 10 vs 34 ± 10 mmHg, respectively, p = 0.002). RV systolic dysfunction was present in 76 patients (42.5%). FMR was a strong predictor of RV dysfunction (odds ratio 5.35, 95% confidence interval [CI] 1.65 to 17.48, p = 0.005) independent of reperfusion therapy. During a median follow-up of 4.1 years, 20 (12.4%) and 10 (55.6%) deaths occurred in patients with and without FMR, respectively (p <0.001). In a multivariable Cox regression model, compared with patients without FMR and with normal RV function, the adjusted hazard ratio for mortality was 1.02 in patients without FMR and with RV dysfunction (95% CI 0.39 to 2.69, p = 0.97) and 3.62 in patients with FMR with RV dysfunction (95% CI 1.33 to 9.85, p = 0.01). In conclusion, in patients with RV infarction, the development of concomitant hemodynamically significant FMR is associated with RV dysfunction. The risk for mortality is increased predominantly in patients with both RV dysfunction and FMR.

The relation between serum phosphorus levels and clinical outcomes after acute myocardial infarction.

BACKGROUND: Elevated serum phosphorus levels have been linked with cardiovascular disease and mortality with conflicting results, especially in the presence of normal renal function. METHODS: We studied the association between serum phosphorus levels and clinical outcomes in 1663 patients with acute myocardial infarction (AMI). Patients were categorized into 4 groups based on serum phosphorus levels (<2.50, 2.51-3.5, 3.51-4.50 and >4.50 mg/dL). Cox proportional-hazards models were used to examine the association between serum phosphorus and clinical outcomes after adjustment for potential confounders. RESULTS: The mean follow up was 45 months. The lowest mortality occurred in patients with serum phosphorus between 2.5-3.5 mg/dL, with a multivariable-adjusted hazard ratio of 1.24 (95% CI 0.85-1.80), 1.35 (95% CI 1.05-1.74), and 1.75 (95% CI 1.27-2.40) in patients with serum phosphorus of <2.50, 3.51-4.50 and >4.50 mg/dL, respectively. Higher phosphorus levels were also associated with increased risk of heart failure, but not the risk of myocardial infarction or stroke. The effect of elevated phosphorus was more pronounced in patients with chronic kidney disease (CKD). The hazard ratio for mortality in patients with serum phosphorus >4.5 mg/dL compared to patients with serum phosphorus 2.50-3.50 mg/dL was 2.34 (95% CI 1.55-3.54) with CKD and 1.53 (95% CI 0.87-2.69) without CKD. CONCLUSION: We found a graded, independent association between serum phosphorus and all-cause mortality and heart failure in patients after AMI. The risk for mortality appears to increase with serum phosphorus levels within the normal range and is more prominent in the presence of CKD.

Utility of pulmonary hypertension for the prediction of heart failure following acute myocardial infarction.

Pulmonary hypertension (PH) is usually perceived as a complication of established heart failure (HF) rather than as a predictor of HF or a marker of subclinical HF. PH may develop because of cardiac alterations that result in increased filling pressures after acute myocardial infarction (AMI). We hypothesized that PH might be a useful marker to predict the risk of HF after AMI. We studied 1,054 patients with AMI. Pulmonary artery systolic pressure (PASP) was estimated using echocardiography at the index admission and PH was defined as a PASP >35 mm Hg. The primary end point was readmission for HF at 1 year. PH was present in 471 patients (44.6%) and was strongly associated with age, decreased ejection fraction, advanced diastolic dysfunction, and moderate/severe mitral regurgitation (p <0.0001 for all comparisons). Area under the receiver operating characteristic curve was significantly higher for estimated PASP (0.74 ± 0.02) compared to other echocardiographic parameters (p = 0.02 to 0.0003). After adjustments for clinical and echocardiographic variables in a Cox model, PH was associated with a hazard ratio of 3.10 for HF (95% confidence interval 1.31 to 2.57, p <0.0001). After adding estimated PASP to a model containing clinical and echocardiographic risk factors, net reclassification improvement was 0.21 (95% confidence interval 0.11 to 0.31, p <0.0001). In conclusion, PASP integrates the severity of multiple hemodynamic determinants of increased left atrial pressures that lead to an increase in pulmonary venous pressure. In AMI, PH at the index admission is a useful marker in unmasking latent subclinical HF and predicting the development of overt HF.

The impact of body mass index on clinical outcomes after acute myocardial infarction.

BACKGROUND: Several studies indicated that an elevated body mass index (BMI) is associated with a lower rate of mortality in patients with acute myocardial infarction (AMI). However, the existence of the obesity paradox in AMI patients remains controversial. METHODS: We examined the association of BMI and clinical outcomes in 2157 patient with AMI (mean follow-up of 26 months). BMI was categorized into 9 groups (<18.5, 18.5 to 20.9, 21.0 to 23.4, 23.5 to 24.9, 25.0 to 26.4, 26.5 to 27.9, 28.0 to 29.9, 30.0 to 34.9, and ≥35.0 kg/m2). Cox regression was used to calculate hazard ratios (HR) for the various BMI categories, adjusting for the clinical variables, left ventricular ejection fraction, and hemoglobin level. RESULTS: BMI had a U-shaped association with mortality. Relative to the lowest mortality group (BMI of 26.5 to 27.9 kg/m2), the adjusted HRs for mortality were increased only in the lower (HR 2.3; 95% CI 1.3-4.2) and upper (HR 1.8; 95% 1.2-2.9) BMI categories. There was a significant interaction between BMI and anemia (P=0.0003) such that the U-shaped relationship between BMI and mortality was present mainly in patients with anemia. Patients in the lower and upper BMI categories and concomitant anemia had a striking increase in mortality (adjusted HR 5.1, 95% CI 1.9-11.7 and 3.2, 95% CI 1.5-7.0, respectively). CONCLUSION: Both obesity and underweight are associated with increased mortality in patients with AMI. The risk of mortality is particularly high among underweight and obese patients with anemia.

Incidence of early left ventricular thrombus after acute anterior wall myocardial infarction in the primary coronary intervention era.

BACKGROUND: Rapid reperfusion has been shown to decrease mortality and improve left ventricular (LV) function. Previous studies have reported that LV thrombus (LVT) is a major complication of ST-segment elevation acute anterior wall myocardial infarction (AMI). There are little data on LVT in the current primary percutaneous coronary intervention (PPCI) era. We sought to demonstrate the incidence of LVT after AMI in patients treated with PPCI compared with those treated with thrombolysis or with conservative management. METHODS: In a 6-year period, 642 patients with anterior wall AMI and echocardiography were treated with PPCI (n = 297), thrombolysis (n = 128), or conservative treatment (n = 217). Left ventricular thrombus was defined as an echodense mass adjacent to an abnormally contracting myocardial segment. RESULTS: The rate of LVT among anterior wall AMI was 6.2%. Predictors for LVT were reduced ejection fraction (adjusted relative risk 0.71, 95% CI 0.52-0.96) and severe mitral regurgitation (adjusted relative risk 2.48, 95% CI 1.0-6.44). There was no statistical difference in LVT rate according to treatment: 21 (7.1%) of 297 patients in the PPCI group, 10 (7.8%) of 128 patients in the thrombolytic group, and 9 (4.1%) of 217 patients in the conservative group (P = .28). Those in the thrombolytic group were characterized by shorter duration from symptom onset and were generally also treated with heparin/low-molecular weight heparin. CONCLUSIONS: This is the largest report to evaluate the incidence of LVT formation after AMI. In the current era of rapid reperfusion by PPCI, the rate of thrombus formation is similar to that reported in the past and not different than for patients currently treated conservatively or with thrombolysis.

Impact of platelet glycoprotein IIb/IIIa receptor inhibitors on renal function in patients with ST-segment elevation myocardial infarction treated with primary or rescue percutaneous coronary intervention.

AIMS: Worsening renal function in patients undergoing percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) is associated with adverse clinical outcomes. We hypothesised that platelet glycoprotein IIb/IIIa receptor inhibitors (GPI) may decrease the rate of renal function deterioration in these patients through attenuation of platelet aggregation and the possible improvement of renal rheology and haemodynamics. METHODS AND RESULTS: Based on prospectively collected data, we analysed rates of renal function deterioration in 603 consecutive patients (mean age 58+/-13 years, males 82%) with STEMI treated with primary or rescue PCI. Renal function deterioration was defined as an increase in serum creatinine level of >or=25% and/or >or=0.5 mg/dl at any time point post-PCI during index hospitalisation compared with baseline value. Outcomes were stratified by treatment with GPI. Patients treated with GPI (n=442) vs. patients who were not treated with GPI (n=161) had significantly lower rates of serum creatinine increase of >or=25% compared with baseline (22.9% vs. 31.9%, P=0.02, respectively), of serum creatinine increase >or=0.5 g/dL (4.1% vs. 8.8%, P=0.02). Treatment with GPI was associated with significantly lower mean maximal increase in serum creatinine level compared with baseline value (0.14+/-0.38 vs. 0.25+/-0.45 mg/dL, P=0.005). Rates of major bleeding did not differ significantly between the two groups (7.3% vs. 5.9%; P=0.42), while 30-day mortality was significantly lower in patients treated with GPI (2.3% vs. 7.5%; P=0.005). By multivariable analysis, treatment with GPI was an independent predictor of freedom from renal function deterioration (odds ratio 0.53; 95% confidence interval 0.33-0.86; P=0.01). CONCLUSIONS: In this analysis, administration of GPI to patients with STEMI treated with primary PCI was associated with lower rates of worsening renal function and lower 30-day mortality.

Identification of the gene causing long QT syndrome in an Israeli family.

BACKGROUND: Long QT syndrome is an inherited cardiac disease, associated with malignant arrhythmias and sudden cardiac death. OBJECTIVES: To map and identify the gene responsible for LQTS in an Israeli family. METHODS: A large family was screened for LQTS after one of them was successfully resuscitated from ventricular fibrillation. The DNA was examined for suspicious loci by whole genome screening and the coding region of the LQT2 gene was sequenced. RESULTS: Nine family members, 6 males and 3 females, age (median and interquartile range) 26 years (13, 46), who were characterized by a unique T wave pattern were diagnosed as carrying the mutant gene. The LQTS-causing gene was mapped to chromosome 7 with the A614V mutation. All of the affected members in the family were correctly identified by electrocardiogram. Corrected QT duration was inversely associated with age in the affected family members and decreased with age. CONCLUSIONS: Careful inspection of the ECG can correctly identify LQTS in some families. Genetic analysis is needed to confirm the diagnosis and enable the correct therapy in this disease.

Relation of statin therapy to risk of heart failure after acute myocardial infarction.

Recent studies suggest that statin therapy reduces hospitalizations for heart failure (HF). However, few data exist regarding the role of statins in preventing HF after acute myocardial infarction (AMI). In addition, the potential impact of left ventricular (LV) ejection fraction (EF) and coexisting functional mitral regurgitation (MR) on the efficacy of statin therapy was not considered. We prospectively studied 1,563 patients with AMI. The primary endpoint was readmission for the treatment of HF. The effect of statin therapy initiated before hospital discharge was evaluated using a Cox model, adjusting for clinical variables, a propensity score for statin therapy, LVEF, and MR grade. Patients with recurrent infarctions were censored. Statins were prescribed in 1,048 patients (67.1%) before hospital discharge. During a median follow-up of 17 months, admissions for HF were lower in patients receiving statins (6.5% vs 14.8%; unadjusted hazard ratio 0.45, 95% confidence interval 0.32 to 0.63, p <0.0001). In a multivariable Cox model, statin therapy was associated with a significant reduction of hospitalization for HF (HR 0.62, 95% confidence interval 0.43 to 0.89, p = 0.009). There was a significant interaction between MR and statin therapy (p = 0.039), such that the beneficial effect of statins on HF hospitalizations was most pronounced in patients without concomitant MR and absent in patients with hemodynamically significant MR. In conclusion, in patients with AMI statin therapy initiated before hospital discharge significantly reduces subsequent hospitalizations for HF. The effect of statins is driven largely by the reduction in events in patients without concomitant hemodynamically significant MR.

Impact of red blood cell transfusion on clinical outcomes in patients with acute myocardial infarction.

Divergent views remain regarding the safety of treating anemia with red blood cell (RBC) transfusion in patients with acute coronary syndrome (ACS). We used a prospective database to study effect of RBC transfusion in patients with acute myocardial infarction (MI; n = 2,358). Cox regression models were used to determine the association between RBC transfusion and 6-month outcomes, incorporating transfusion as a time-dependent variable. The models adjusted for baseline variables, propensity for transfusion, and nadir hemoglobin previous to the transfusion. One hundred ninety-two patients (8.1%) received RBC transfusion. Six-month mortality rates were higher in patients receiving transfusion (28.1% vs 11.7%, p <0.0001). The adjusted hazard ratio (HR) for mortality was 1.9 in transfused patients (95% confidence interval [CI] 1.3 to 2.9). Interaction between RBC transfusion and nadir hemoglobin with respect to mortality (p = 0.004) was significant. Stratified analyses showed a protective effect of transfusion in patients with nadir hemoglobin < or=8 g/dL (adjusted HR 0.13, 95% CI 0.03 to 0.65, p = 0.013). By contrast, transfusion was associated with increased mortality in patients with nadir hemoglobin >8 g/dL (adjusted HR 2.2, 95% CI 1.5 to 3.3; p <0.0001). Similar results were obtained for the composite end point of death/MI/heart failure (p for interaction = 0.04). In conclusion, RBC transfusion in patients with acute MI and hemoglobin < or =8 g/dL may be appropriate. The increased mortality observed in transfused patients with nadir hemoglobin above 8 g/dL underscores the clinical difficulty of balancing risks and benefits of RBC transfusion in the setting of ACS.

Troponin-positive, CK-MB-negative acute myocardial infarction: clinical, electrocardiographic and angiographic characteristics.

OBJECTIVES: We assessed the clinical, electrocardiographic (ECG) and angiographic characteristics of patients with acute coronary syndrome, increased troponin I (cTn-I) levels and normal creatine kinase levels. BACKGROUND: Cardiac troponins are part of the new definition of acute myocardial infarction by the European Society of Cardiology and the American College of Cardiology. However, there are limited data regarding the angiographic characteristics of these patients. METHODS: Between 1/2002 and 7/2004, a total of 50 consecutive cTn-I-positive, creatine kinase-negative patients were admitted to the intensive coronary care unit of our institution and underwent coronary angiography. RESULTS: The mean cTn-I level was 10.7 +/- 13.5 mcg/L and the mean creatine kinase was 106 +/- 40 U/L (normal < 180 U/L). Admission ECG showed inverted T-waves in 42% of patients, ST-segment elevation in 36%, ST-segment depression in 20% and a normal ECG in 20%. A total of 168 lesions were analyzed, and 47 (28%) of these were considered to be nonsignificant lesions (< 50% diameter stenosis). Seven patients had normal or nonsignificant coronary artery disease (CAD) and the remainder had at least single-vessel disease. There were 12 patients with stenosis in the left main coronary artery, 6 patients had a visible clot in the artery, 5 of them located in the right coronary artery and 1 in the left circumflex. A total of 37 patients underwent coronary revascularization, the majority (62%) percutaneously, the rest were treated conservatively. CONCLUSIONS: Increased cTn-I levels in the presence of rest pain and normal creatine kinase is not a spurious finding, but may actually be a marker of advanced CAD. However, some of these patients may also have nonsignificant CAD.

Predictors of outcome and the lack of effect of percutaneous coronary intervention across the risk strata in patients with persistent total occlusion after myocardial infarction: Results from the OAT (Occluded Artery Trial) study.

OBJECTIVES: This study sought to determine predictors of outcome and examine the influence of baseline risk on therapeutic impact of late mechanical opening of a persistently occluded infarct related artery after myocardial infarction in stable patients. BACKGROUND: Previous studies in patients with acute coronary syndromes suggest that the impact of infarct-related artery recanalization on clinical outcome is greatest in patients at highest risk. METHODS: Of 2,201 patients (age 58.6 +/- 11.0 years) with infarct-related artery occlusion on days 3 to 28 after myocardial infarction in the OAT (Occluded Artery Trial) study, 1,101 were assigned to percutaneous coronary intervention (PCI) and 1,100 to medical therapy alone and followed for a mean of 3.2 years. The primary end point was a composite of death, reinfarction, or New York Heart Association functional class IV heart failure. Interaction of treatment effect with tertiles of predicted survival were examined using the Cox survival model. RESULTS: The 5-year rate for the primary end point was 18.9% versus 16.1% for patients assigned to PCI and medical treatment alone, respectively (hazard ratio [HR]: 1.14, 95% confidence interval [CI]: 0.92 to 1.43, p 0.23). Lack of benefit of PCI was consistent across the risk spectrum for both the primary end point and total mortality, including for the highest tertile (33.9% PCI vs. 27.3% medical treatment alone, HR: 1.27, 99% CI: 0.87 to 1.85 primary end point and 23.5% PCI vs. 21.7% medical treatment alone, HR: 1.16, 99% CI: 0.73 to 1.85 mortality). The independent predictors of the composite outcome were history of heart failure (HR: 2.06, p < 0.001), peripheral vascular disease (HR: 1.93, p 0.001), diabetes (HR: 1.49, p 0.002), rales (HR: 1.88, p < 0.001), decreasing ejection fraction (HR: 1.48 per 10%, p < 0.001), decreasing days from myocardial infarction to randomization (HR: 1.04 per day, p < 0.001), and decreasing glomerular filtration rate (HR: 1.11 per 10 ml/min/1.73 m(2), p < 0.001). CONCLUSIONS: In the OAT study, there was no variation in the effect of PCI on clinical outcomes at different levels of patient risk, including the subset with very high event rates. (Occluded Artery Trial [OAT]; NCT00004562)