Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 2005;111:2042-2049
Published online before print April 11, 2005, doi: 10.1161/01.CIR.0000162477.70955.5F
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
111/16/2042    most recent
01.CIR.0000162477.70955.5Fv1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sabatine, M. S.
Right arrow Articles by Braunwald, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sabatine, M. S.
Right arrow Articles by Braunwald, E.
Related Collections
Right arrow Acute coronary syndromes

(Circulation. 2005;111:2042-2049.)
© 2005 American Heart Association, Inc.


Coronary Heart Disease

Association of Hemoglobin Levels With Clinical Outcomes in Acute Coronary Syndromes

Marc S. Sabatine, MD, MPH; David A. Morrow, MD, MPH; Robert P. Giugliano, MD, SM; Paul B.J. Burton, MBBS, PhD; Sabina A. Murphy, MPH; Carolyn H. McCabe, BS; C. Michael Gibson, MS, MD; Eugene Braunwald, MD

From the TIMI Study Group (M.S.S., D.A.M., R.P.G., S.A.M., C.H.M., C.M.G., E.B.), Cardiovascular Division, Brigham and Women’s Hospital, Boston, Mass, and Amgen, Inc (P.B.J.B.), Thousand Oaks, Calif.

Correspondence to Marc S. Sabatine, MD, MPH, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail msabatine{at}partners.org

Received August 6, 2004; revision received December 16, 2004; accepted January 11, 2005.


*    Abstract
up arrowTop
*Abstract
down arrowIntroduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Background— In the setting of an acute coronary syndrome (ACS), anemia has the potential to worsen myocardial ischemia; however, data relating anemia to clinical outcomes in ACS remain limited.

Methods and Results— We examined the association between baseline hemoglobin values and major adverse cardiovascular events through 30 days in 39 922 patients enrolled in clinical trials of ACS. After adjustment for differences in baseline characteristics and index hospitalization treatments, a reverse J-shaped relationship between baseline hemoglobin values and major adverse cardiovascular events was observed. In patients with ST-elevation myocardial infarction, when those with hemoglobin values between 14 and 15 g/dL were used as the reference, cardiovascular mortality increased as hemoglobin levels fell below 14 g/dL, with an adjusted OR of 1.21 (95% CI 1.12 to 1.30, P<0.001) for each 1-g/dL decrement in hemoglobin. At the other end of the range of hemoglobin, patients with hemoglobin values >17 g/dL also had excess mortality (OR 1.79, 95% CI 1.18 to 2.71, P=0.007). In patients with non–ST-elevation ACS, with those with hemoglobin 15 to 16 g/dL used as the reference, the likelihood of cardiovascular death, myocardial infarction, or recurrent ischemia increased as the hemoglobin fell below 11 g/dL, with an adjusted OR of 1.45 (95% CI 1.33 to 1.58, P<0.001) for each 1 g/dL decrement in hemoglobin. Patients with hemoglobin values >16 g/dL also had an increased rate of death or ischemic events (OR 1.31, 95% CI 1.03 to 1.66, P=0.027).

Conclusions— Anemia is a powerful and independent predictor of major adverse cardiovascular events in patients across the spectrum of ACS.


Key Words: anemia • coronary disease • hemoglobin • myocardial infarction • risk factors


*    Introduction
up arrowTop
up arrowAbstract
*Introduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Anemia has been shown to be present in {approx}15% of patients presenting with acute myocardial infarction (MI) and in 43% of elderly patients with acute MI.1,2 Anemia has the potential to worsen the myocardial ischemic insult in acute MI and other acute coronary syndromes (ACS), both by decreasing the oxygen content of the blood supplied to the jeopardized myocardium3 and by increasing myocardial oxygen demand through necessitating a higher cardiac output to maintain adequate systemic oxygen delivery.4

In animal models, higher hemoglobin concentrations prevent ischemia in the setting of significant coronary artery stenoses.5,6 In human studies, anemia has been shown to be an independent risk factor for adverse cardiovascular outcomes in community cohorts,7 in patients with heart failure,8,9 and in patients undergoing percutaneous coronary intervention.10 To this point, few studies have specifically examined anemia in patients with ACS.2,11–14 We therefore examined the association between baseline hemoglobin concentration and a range of cardiovascular clinical outcomes in a broad cohort of nearly 40 000 patients across the spectrum of ACS.


*    Methods
up arrowTop
up arrowAbstract
up arrowIntroduction
*Methods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Patient Populations
The study cohort eligible for these analyses consisted of 41 637 patients with ACS from the following 16 Thrombolysis In Myocardial Infarction (TIMI) trials: IIIB,15 4,16 9A,17 9B,18 10A,19 10B,20 11A,21 11B,22 12,23 14,24 16 (OPUS),25 17 (InTIME II),26 18 (TACTICS),27 20 (INTEGRITI),28 23 (ENTIRE),29 and 24 (FASTER),30 the details for which have been published. Patients with active cancer, significant liver or renal disease (typically a creatinine >2.0 mg/dL), active or recent internal bleeding, known bleeding diathesis, and other significant comorbidities were excluded from these trials.

Baseline Data and Clinical Outcomes
Baseline characteristics were recorded by the local investigators. Baseline hemoglobin values were available in 96% of patients (39 922). For patients with ST-elevation MI (STEMI), the clinical end points were cardiovascular mortality and congestive heart failure through 30 days. For patients with non–ST-elevation ACS (NSTE ACS), the clinical end points were cardiovascular mortality, MI, and recurrent myocardial ischemia through 30 days. Major bleeding was defined as intracranial bleeding or any clinically overt sign of hemorrhage that was associated with a fall in hemoglobin of >5 g/dL.31

Statistical Analyses
Patients were initially divided into categories based on 1-g/dL hemoglobin increments. Univariate associations between hemoglobin categories and other baseline demographic and clinical variables were evaluated with ANOVA and {chi}2 tests. Unadjusted event rates for the aforementioned cardiovascular end points were compared across hemoglobin categories with the {chi}2 test for trend across ordered groups. To evaluate the independent relationship between hemoglobin and cardiovascular end points at 30 days, multivariable logistic regression was used. Hemoglobin was coded as a multicategory predictor in 1-g/dL increments, and the hemoglobin category that had the lowest event rate was used as the reference group. A comprehensive search for potential confounders was conducted. Specifically, candidate variables for which we had data in >80% of subjects and that either demonstrated association with baseline hemoglobin levels (at a significance threshold of P<0.25) or were of known clinical importance were included in the final model.32 This approach yielded the following covariates: age; gender; race; hypertension; diabetes; smoking history; creatinine clearance; prior MI; prior congestive heart failure; prior percutaneous coronary intervention; prior CABG; cerebrovascular disease; peripheral arterial disease; prior aspirin, ß-blocker, ACE inhibitor, angiotensin receptor blocker, or hypolipidemic use; index hospitalization aspirin, ß-blocker, ACE inhibitor, angiotensin receptor blocker, or hypolipidemic use; index revascularization; and, for STEMI patients, anterior location of the index MI.


*    Results
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
*Results
down arrowDiscussion
down arrowReferences
 
There were a total of 25 419 patients with STEMI and 14 503 patients with NSTE ACS in whom baseline hemoglobin data were available. These patients were divided into categories based on 1-g/dL hemoglobin increments, and their baseline characteristics are shown in Tables 1 and 2Down, respectively. Across the spectrum of ACS, those with lower baseline hemoglobin levels were more likely to be older and female, were less likely to be a current smoker, had lower estimated creatinine clearances, and were less likely to undergo revascularization during their index hospitalization.


View this table:
[in this window]
[in a new window]
 
TABLE 1. Baseline Characteristics in STEMI Patients Stratified by Baseline Hemoglobin


View this table:
[in this window]
[in a new window]
 
TABLE 2. Baseline Characteristics in NSTE ACS Patients Stratified by Baseline Hemoglobin

Indicators of Severity of Acute Ischemic Insult
In patients with STEMI, the likelihood of hypotension, tachycardia, and Killip class II to IV was significantly related to baseline hemoglobin (Figures 1A through 1C, P<0.001 for each), with patients at either end of the hemoglobin spectrum being more likely to have hemodynamic disarray. Similarly, among patients with NSTE ACS, the presence of ST deviation was related to the baseline hemoglobin (P<0.001), again with a J-shaped pattern (Figure 2).



View larger version (19K):
[in this window]
[in a new window]
 
Figure 1. Prevalence of hypotension (systolic blood pressure <100 mm Hg; A), tachycardia (heart rate >100 bpm; B), and Killip class 2 to 4 (C) in patients with STEMI stratified by baseline hemoglobin values. SBP indicates systolic blood pressure; HR, heart rate.



View larger version (10K):
[in this window]
[in a new window]
 
Figure 2. Prevalence of ST deviation in patients with NSTE ACS stratified by baseline hemoglobin values.

Unadjusted Event Rates
The unadjusted rates of cardiovascular clinical events through 30 days in patients with STEMI and NSTE ACS categorized by baseline hemoglobin are shown in Tables 3 and 4Down, respectively. In general, adverse clinical event rates were higher in those with lower hemoglobin values and tended to decrease with increasing hemoglobin levels. For patients with STEMI, there were highly statistically significant trends for cardiovascular death (P<0.001), congestive heart failure (P<0.001), and the composite (P<0.001). For patients with NSTE ACS, there were highly significant trends for cardiovascular death (P<0.001) and recurrent ischemia (P<0.001), a trend for MI (P=0.19), and a highly significant trend for their composite (P<0.001). In both STEMI and NSTE ACS patients, the rate of adverse events started to increase in those with very high hemoglobin values (>16 to 17 g/dL). The rates of TIMI major bleeding were low ({approx}5%) and were not associated with hemoglobin levels in either STEMI (P=0.49) or NSTE ACS (P=0.19) patients.


View this table:
[in this window]
[in a new window]
 
TABLE 3. Clinical Outcomes Through 30 Days in STEMI Patients Stratified by Baseline Hemoglobin


View this table:
[in this window]
[in a new window]
 
TABLE 4. Clinical Outcomes Through 30 Days in NSTE ACS Patients Stratified by Baseline Hemoglobin

Adjusted ORs
Given imbalances in important baseline characteristics, multivariable logistic regression was used to evaluate the independent relationship between hemoglobin and clinical outcomes after adjustment for a wide range of covariates, including demographics, cardiac risk factors, prior cardiac disease, medications and revascularization procedures, location of STEMI, and index medications and revascularization (c-statistics for models were 0.84 for STEMI and 0.71 for NSTE ACS). Figure 3 shows a plot of the adjusted OR and 95% CI for 30-day cardiovascular mortality in patients with STEMI categorized by 1-g/dL hemoglobin increments. A nonmonotonic, reverse J-shaped relationship is evident. With patients with hemoglobin values of 14 to 15 g/dL as the reference, cardiovascular mortality increased as hemoglobin levels fell below 14 g/dL, with an adjusted OR of 1.21 (95% CI 1.12 to 1.30, P<0.001) for each 1-g/dL decrement in hemoglobin. When systolic blood pressure, heart rate, and Killip class were added to the model, the adjusted OR was essentially unchanged (OR 1.20, 95% CI 1.11 to 1.29). Similarly, when in-hospital medications were excluded from the model, the adjusted OR was again essentially unchanged (OR 1.23, 95% CI 1.11 to 1.29). For all patients with a baseline hemoglobin <14 g/dL, the adjusted OR of cardiovascular death was 1.35 (95% CI 1.11 to 1.64, P=0.003). Reflecting the J-shaped relationship, patients with very high hemoglobin values (>17 g/dL) also had an increased risk of dying (adjusted OR 1.79, 95% CI 1.18 to 2.71, P=0.007). A similar relationship was seen between baseline hemoglobin and the risk of heart failure. Those with a hemoglobin <14 g/dL were at increased risk of developing heart failure (adjusted OR 1.20, 95% CI 1.05 to 1.38, P=0.009), as were those with a hemoglobin >17 g/dL (adjusted OR 1.67, 95% CI 1.27 to 2.20, P<0.001).



View larger version (20K):
[in this window]
[in a new window]
 
Figure 3. Unadjusted and adjusted ORs and 95% CIs for association between baseline hemoglobin concentration and cardiovascular mortality through 30 days in patients with STEMI. Adjusted for age; gender; race; hypertension; diabetes; smoking history; renal disease; prior MI; prior heart failure; prior percutaneous coronary intervention; prior CABG; cerebrovascular disease; peripheral arterial disease; prior aspirin, ß-blocker, ACE inhibitor or angiotensin receptor blocker, and hypolipidemic use; anterior MI; index hospitalization aspirin, ß-blocker, ACE inhibitor or angiotensin receptor blocker, and hypolipidemic use; and index revascularization. CV indicates cardiovascular; Hgb, hemoglobin; and n, number of patients.

Figure 4 shows a plot of the adjusted OR and 95% CI for the composite of cardiovascular death, MI, or recurrent ischemia through 30 days in patients with NSTE ACS categorized by 1-g/dL hemoglobin increments. Increased risk of the composite end point becomes apparent as hemoglobin values fall below 11 g/dL. With patients with hemoglobin values of 15 to 16 g/dL as the reference, the risk of cardiovascular death, MI, or recurrent ischemia increased as hemoglobin levels fell below 11 g/dL, with an adjusted OR of 1.45 (95% CI 1.33 to 1.58, P<0.001) for each 1-g/dL decrement in hemoglobin. When in-hospital medications were excluded from the model, the adjusted OR was identical (OR 1.45, 95% CI 1.33 to 1.58). For all patients with a baseline hemoglobin <11 g/dL, the adjusted OR of the composite end point was 2.26 (95% CI 1.83 to 2.79, P<0.001). Directionally consistent associations were seen between hemoglobin and the individual components of the composite end point, including cardiovascular death (adjusted OR 1.35, 95% CI 0.74 to 2.45), MI (adjusted OR 1.63, 95% CI 1.07 to 2.48), and recurrent ischemia (adjusted OR 2.60, 95% CI 2.08 to 3.26). Again, reflecting the J-shaped relationship, patients with baseline hemoglobin values >16 g/dL were also at an increased risk for the composite end point (adjusted OR 1.31, 95% CI 1.03 to 1.66, P=0.027).



View larger version (23K):
[in this window]
[in a new window]
 
Figure 4. Unadjusted and adjusted ORs and 95% CIs for association between baseline hemoglobin concentration and cardiovascular death, MI, or recurrent ischemia through 30 days in patients with NSTE ACS. Adjusted for age; gender; race; hypertension; diabetes; smoking history; renal disease; prior MI; prior heart failure; prior percutaneous coronary intervention; prior CABG; cerebrovascular disease; peripheral arterial disease; prior aspirin, ß-blocker, ACE inhibitor or angiotensin receptor blocker, and hypolipidemic use; index hospitalization aspirin, ß-blocker, ACE inhibitor or angiotensin receptor blocker, and hypolipidemic use; and index revascularization. CVD indicates cardiovascular death; RI, recurrent ischemia; Hgb, hemoglobin; and n, number of patients.

Transfusion
A total of 4.6% of patients with STEMI and 2.7% percent of patients with NSTE ACS received transfusions with whole blood or packed red blood cells. Approximately 80% of these transfusions were in the setting of bleeding. In STEMI patients, when transfusion, interaction terms between transfusion and hemoglobin, and bleeding were added to the aforementioned multivariable model, transfusion was associated with a decreased risk of cardiovascular death when the baseline hemoglobin was <12 g/dL (adjusted OR 0.42, 95% CI 0.20 to 0.89) but not when hemoglobin was ≥12 g/dL (adjusted OR 1.42, 95% CI 0.94 to 2.17). In NSTE ACS, transfusion appeared to be associated with an increased risk of the composite end point (adjusted OR 1.54, 95% CI 1.14 to 2.09), regardless of the hemoglobin concentration.


*    Discussion
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
In a broad cohort of patients with ACS, we found large, highly statistically significant, and independent associations between low hemoglobin concentrations and adverse cardiovascular outcomes. Among patients with STEMI, there was a progressive increase in cardiovascular mortality and heart failure as the baseline hemoglobin dropped below 14 g/dL. In patients with NSTE ACS, an increased odds of cardiovascular death, MI, or recurrent ischemia became apparent when the baseline hemoglobin fell below 11 g/dL.

To this point, data linking anemia and adverse outcomes in ACS have been limited. In one study that examined a database of discharge abstract information in patients admitted with MI, those identified as anemic on the basis of International Classification of Diseases, 9th Revision (ICD-9) coding were not found to have a higher mortality.11 In contrast, in a large database study of elderly Medicare beneficiaries with acute MI in which actual hematocrit data were used, a powerful, albeit unadjusted, relationship between hematocrit on admission and all-cause 30-day mortality was found. Similar to the present study, there was a dose-response effect, with progressively lower survival rates with more profound degrees of anemia.2 In a small study of 444 consecutive patients with NSTE ACS admitted to the coronary unit of a single medical center, those with hemoglobin concentrations below 12.8 g/dL were at significantly increased risk of death or MI.12 In a study of 936 women undergoing evaluation for chest pain, hemoglobin was an independent predictor of adverse cardiovascular outcomes, with a 20% increased risk for each 1-g/dL decrement in hemoglobin.33 Among patients undergoing percutaneous coronary intervention for ACS, anemia was associated with an increased risk of periprocedural MI and major adverse cardiovascular events through 30 days.13,14

After careful adjustment for a broad array of baseline characteristics, we found a striking dose-response relationship across the spectrum of ACS. Anemia has been shown to significantly decrease oxygen delivery to myocardium downstream of coronary stenoses.3 Anemia also increases myocardial oxygen demand through necessitating a higher stroke volume and heart rate to maintain adequate systemic oxygen delivery.4 The combination of these processes may explain the pathophysiology underlying the progressively worse outcomes we observed in patients with ACS with lower baseline hemoglobin concentrations. Interestingly, the thresholds below which patients were at increased risk for major adverse cardiovascular events differed between STEMI and NSTE ACS. This may reflect differences in the mechanisms by which anemia predisposes to adverse cardiovascular events in the 2 types of ACS. In STEMI, even mildly reduced hemoglobin concentrations at the abrupt onset of the coronary occlusion may significantly attenuate the ability of collateral flow from nearby patent vessels to limit the extent of myocardial necrosis and peri-infarct ischemia. We did not have scintigraphic or core laboratory biochemical measurements of infarct size in the present cohort to test this theory directly; however, consistent with this hypothesis is our finding that worsening degrees of anemia were associated with progressively higher rates of hypotension, tachycardia, and heart failure. For NSTE ACS, coronary occlusion is usually subtotal, and the likelihood of death and recurrent ischemic events over the ensuing days may reflect a delicate balance between myocardial oxygen supply and demand. In the setting of aggressive antiischemic pharmacological therapy, a more profound degree of anemia may be necessary to predispose a patient to recurrent ischemic events.

In both types of ACS, patients with very high baseline hemoglobin (>16 to 17 g/dL) also were at greater risk for adverse cardiovascular events, a finding supported by observations from other studies.34 The pathophysiological basis for these observations may be that high hemoglobin concentrations can increase blood viscosity. This, in turn, can increase coronary vascular resistance and decrease coronary blood flow,35 predispose to thrombosis,36 and increase myocardial work.37

Potential limitations of this study should be considered. The present study population was derived from clinical trials rather than unselected community cohorts; however, the inclusion and exclusion criteria differed between these 16 trials, thus potentially strengthening the generalizability of our findings. Moreover, the use of clinical trials allowed us to gather data prospectively on important baseline characteristics and clinical outcomes from dedicated case report forms rather than, for example, unconfirmed ICD-9 coding on discharge summaries. Furthermore, we used actual hemoglobin values, thereby minimizing misclassification and permitting a quantitative approach to the definition of anemia. The cause of anemia in patients in the present study was unknown, although patients with recent bleeding, known bleeding diathesis, or significant renal or hematologic-oncological diseases (all important potential confounders) were excluded from these trials. We did not measure erythropoietin levels in these patients. In addition to stimulating erythrocyte precursors, erythropoietin has multiple cardiovascular effects that range from myocardial protection and angiogenesis to activation of platelets and upregulation of plasminogen activator inhibitor-1.38 Thus, some of our observations may be due to low or high erythropoietin levels rather than anemia per se. Lastly, comorbidities associated with hemoglobin and prognosis or differences in treatment influenced by the baseline hemoglobin had the potential to confound our analyses; however, we conducted a comprehensive search for potential confounders and included a broad group of prognostic and treatment-related variables in our multivariable analyses. Although incompletely or unmeasured comorbidities could cause residual confounding, given the breadth of covariates adjusted for in the present analyses, the impact is likely to be small.

If the association between hemoglobin levels and adverse cardiovascular events is, in fact, causal, the present findings would support the current practice guidelines from the American College of Cardiology/American Heart Association that suggest screening for and correcting anemia in ACS.39,40 The guidelines, however, do not specify what hemoglobin level to target. Studies of transfusion thresholds have provided some data relevant to patients with coronary disease. In a randomized clinical trial in critical illness, there was no apparent benefit to a more liberal transfusion strategy (hemoglobin target 10 to 12 g/dL) versus a more restrictive strategy (target 7 to 9 g/dL)41; however, in an analysis specifically restricted to those with ischemic heart disease, there was a trend toward higher mortality in those who were randomized to a restrictive strategy.42 Two recent nonrandomized studies have yielded conflicting results. In a study of patients with ACS, transfusion was associated with an increased risk of 30-day mortality, although this effect was no longer apparent if the nadir hematocrit was below 25%.43 In contrast, in elderly patients with acute MI, transfusion appeared to be beneficial if the hematocrit was <33%.2 The present data show a reduction in cardiovascular mortality with transfusion in STEMI patients with a hemoglobin <12 g/dL (approximately equivalent to a hematocrit <36%) but an increased risk of cardiovascular death, MI, or recurrent ischemia in patients with NSTE ACS who were transfused; however, we would underscore that all nonrandomized comparisons must be viewed with caution because, despite multivariable analyses, there can be residual confounding by indication, with physicians more likely to transfuse sicker patients. Only randomized trials can definitely resolve the benefit of transfusions in ACS.

In conclusion, we have found that in 39 922 patients with ACS enrolled in clinical trials, anemia was a powerful predictor of cardiovascular mortality and ischemic events. The graded relationship between hemoglobin levels and clinical outcomes persisted after adjustment for a wide array of baseline prognostic factors and in-hospital treatments. Given these data, a prospective, randomized clinical trial may be warranted to determine whether precise targeting of hemoglobin levels improves outcomes in patients with ACS.


*    Acknowledgments
 
Dr Sabatine is supported in part by National Heart, Lung, and Blood Institute grants R01 HL072879 and R01 HL072872. Statistical analyses supported by Amgen, Inc.


*    References
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
up arrowDiscussion
*References
 
1. Chesebro JH, Knatterud G, Roberts R, Borer J, Cohen LS, Dalen J, Dodge HT, Francis CK, Hillis D, Ludbrook P. Thrombolysis in Myocardial Infarction (TIMI) Trial, phase I: a comparison between intravenous tissue plasminogen activator and intravenous streptokinase: clinical findings through hospital discharge. Circulation. 1987; 76: 142–154.[Abstract/Free Full Text]

2. Wu WC, Rathore SS, Wang Y, Radford MJ, Krumholz HM. Blood transfusion in elderly patients with acute myocardial infarction. N Engl J Med. 2001; 345: 1230–1236.[Abstract/Free Full Text]

3. Most AS, Ruocco NA Jr, Gewirtz H. Effect of a reduction in blood viscosity on maximal myocardial oxygen delivery distal to a moderate coronary stenosis. Circulation. 1986; 74: 1085–1092.[Abstract/Free Full Text]

4. Levy PS, Quigley RL, Gould SA. Acute dilutional anemia and critical left anterior descending coronary artery stenosis impairs end organ oxygen delivery. J Trauma. 1996; 41: 416–423.[Medline] [Order article via Infotrieve]

5. Yoshikawa H, Powell WJ Jr, Bland JH, Lowenstein E. Effect of acute anemia on experimental myocardial ischemia. Am J Cardiol. 1973; 32: 670–678.[CrossRef][Medline] [Order article via Infotrieve]

6. Levy PS, Kim SJ, Eckel PK, Chavez R, Ismail EF, Gould SA, Ramez Salem M, Crystal GJ. Limit to cardiac compensation during acute isovolemic hemodilution: influence of coronary stenosis. Am J Physiol. 1993; 265: H340–H349.[Medline] [Order article via Infotrieve]

7. Sarnak MJ, Tighiouart H, Manjunath G, MacLeod B, Griffith J, Salem D, Levey AS. Anemia as a risk factor for cardiovascular disease in the Atherosclerosis Risk in Communities (ARIC) study. J Am Coll Cardiol. 2002; 40: 27–33.[Abstract/Free Full Text]

8. Al-Ahmad A, Rand WM, Manjunath G, Konstam MA, Salem DN, Levey AS, Sarnak MJ. Reduced kidney function and anemia as risk factors for mortality in patients with left ventricular dysfunction. J Am Coll Cardiol. 2001; 38: 955–962.[Abstract/Free Full Text]

9. Ezekowitz JA, McAlister FA, Armstrong PW. Anemia is common in heart failure and is associated with poor outcomes: insights from a cohort of 12 065 patients with new-onset heart failure. Circulation. 2003; 107: 223–225.[Abstract/Free Full Text]

10. McKechnie RS, Smith D, Montoye C, Kline-Rogers E, O’Donnell MJ, DeFranco AC, Meengs WL, McNamara R, McGinnity JG, Patel K, Share D, Riba A, Khanal S, Moscucci M. Prognostic implication of anemia on in-hospital outcomes after percutaneous coronary intervention. Circulation. 2004; 110: 271–277.[Abstract/Free Full Text]

11. Al Falluji N, Lawrence-Nelson J, Kostis JB, Lacy CR, Ranjan R, Wilson AC. Effect of anemia on 1-year mortality in patients with acute myocardial infarction. Am Heart J. 2002; 144: 636–641.[Medline] [Order article via Infotrieve]

12. Goncalves AG, Ferreira J, Aguiar C, Trabulo M, Silva JA, Seabra-Gomes R. Prognostic value of baseline hemoglobin in acute coronary syndromes. Circulation. 2002; 106 (suppl II): II-402.

13. Lee PC, Kini AS, Ahsan C, Fisher E, Sharma SK. Anemia is an independent predictor of mortality after percutaneous coronary intervention. J Am Coll Cardiol. 2004; 44: 541–546.[Abstract/Free Full Text]

14. Nikolsky E, Aymong ED, Halkin A, Grines CL, Cox DA, Garcia E, Mehran R, Tcheng JE, Griffin JJ, Guagliumi G, Stuckey T, Turco M, Cohen DA, Negoita M, Lansky AJ, Stone GW. Impact of anemia in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention: analysis from the Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications (CADILLAC) Trial. J Am Coll Cardiol. 2004; 44: 547–553.[Abstract/Free Full Text]

15. The TIMI IIIB Investigators. Effects of tissue plasminogen activator and a comparison of early invasive and conservative strategies in unstable angina and non-Q-wave myocardial infarction: results of the TIMI IIIB Trial. Circulation. 1994; 89: 1545–1556.[Abstract/Free Full Text]

16. Cannon CP, McCabe CH, Diver DJ, Herson S, Greene RM, Shah PK, Sequeira RF, Leya F, Kirshenbaum JM, Magorien RD, Palmeri ST, Davis V, Gibson CM, Poole WK, Braunwald E, the TIMI 4 Investigators. Comparison of front-loaded recombinant tissue-type plasminogen activator, anistreplase and combination thrombolytic therapy for acute myocardial infarction: results of the Thrombolysis in Myocardial Infarction (TIMI) 4 Trial. J Am Coll Cardiol. 1994; 24: 1602–1610.[Abstract]

17. Antman EM, for the TIMI 9A Investigators. Hirudin in acute myocardial infarction: safety report from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction (TIMI) 9A trial. Circulation. 1994; 90: 1624–1630.[Abstract/Free Full Text]

18. Antman EM, for the TIMI 9B Investigators. Hirudin in acute myocardial infarction: thrombolysis and thrombin inhibitors in myocardial infarction (TIMI) 9B trial. Circulation. 1996; 94: 911–922.[Abstract/Free Full Text]

19. Cannon CP, McCabe CH, Gibson CM, Ghali M, Sequeira RF, McKendall GR, Breed J, Modi NB, Fox NL, Tracy RP, Love TW, Braunwald E. TNK-tissue plasminogen activator in acute myocardial infarction: results of the Thrombolysis in Myocardial Infarction (TIMI) 10A dose-ranging trial. Circulation. 1997; 95: 351–356.[Abstract/Free Full Text]

20. Cannon CP, Gibson CM, McCabe CH, Adgey AA, Schweiger MJ, Sequeira RF, Grollier G, Giugliano RP, Frey M, Mueller HS, Steingart RM, Weaver WD, Van de Werf F, Braunwald E, for the Thrombolysis in Myocardial Infarction (TIMI) 10B Investigators. TNK-tissue plasminogen activator compared with front-loaded alteplase in acute myocardial infarction: results of the TIMI 10B trial. Circulation. 1998; 98: 2805–2814.[Abstract/Free Full Text]

21. The Thrombolysis in Myocardial Infarction (TIMI) 11A Trial Investigators. Dose-ranging trial of enoxaparin for unstable angina: results of TIMI 11A. J Am Coll Cardiol. 1997; 29: 1474–1482.[Abstract]

22. Antman EM, McCabe CH, Gurfinkel EP, Turpie AGG, Bernink PJLM, Salein D, Bayes de Luna A, Fox K, Lablanche J-M, Radley D, Premmereur J, Braunwald E, for the TIMI 11B Investigators. Enoxaparin prevents death and cardiac ischemic events in unstable angina/non-Q-wave myocardial infarction: results of the Thrombolysis In Myocardial Infarction (TIMI) 11B trial. Circulation. 1999; 100: 1593–1601.[Abstract/Free Full Text]

23. Cannon CP, McCabe CH, Borzak S, Henry TD, Tischler MD, Mueller HS, Feldman R, Palmeri ST, Ault K, Hamilton SA, Rothman JM, Novotny WF, Braunwald E, for the TIMI 12 Investigators. Randomized trial of an oral platelet glycoprotein IIb/IIIa antagonist, sibrafiban, in patients after an acute coronary syndrome: results of the TIMI 12 trial. Circulation. 1998; 97: 340–349.[Abstract/Free Full Text]

24. Antman EM, Giugliano RP, Gibson CM, McCabe CH, Coussement P, Kleiman NS, Vahanian A, Adgey AAJ, Menown I, Rupprecht H-J, Van der Wieken R, Ducas J, Scherer J, Anderson K, Van der Werf F, Braunwald E, for the TIMI 14 Investigators. Abciximab facilitates the rate and extent of thrombolysis: results of the Thrombolysis in Myocardial Infarction (TIMI) 14 trial. Circulation. 1999; 99: 2720–2732.[Abstract/Free Full Text]

25. Cannon CP, McCabe CH, Wilcox RG, Langer A, Caspi A, Berink P, Lopez-Sendon J, Toman J, Charlesworth A, Anders RJ, Alexander JC, Skene A, Braunwald E. Oral glycoprotein IIb/IIIa inhibition with orbofiban in patients with unstable coronary syndromes (OPUS-TIMI 16) trial. Circulation. 2000; 102: 149–156.[Abstract/Free Full Text]

26. The InTIME-II Investigators. Intravenous NPA for the Treatment of Infarcting Myocardium Early: InTIME-II, a double-blind comparison of single-bolus lanoteplase vs accelerated alteplase for the treatment of patients with acute myocardial infarction. Eur Heart J. 2000; 21: 2005–2013.[Abstract/Free Full Text]

27. Cannon CP, Weintraub WS, Demopoulos LA, Vicari R, Frey MJ, Lakkis N, Neumann FJ, Robertson DH, DeLucca PT, DiBattiste PM, Gibson CM, Braunwald E, for the Tactics-Thrombolysis in Myocardial Infarction 18 Investigators. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med. 2001; 344: 1879–1887.[Abstract/Free Full Text]

28. Giugliano RP, Roe MT, Harrington RA, Gibson CM, Zeymer U, Van de Werf F, Baran KW, Hobbach HP, Woodlief LH, Hannan KL, Greenberg S, Miller J, Kitt MM, Strony J, McCabe CH, Braunwald E, Califf RM. Combination reperfusion therapy with eptifibatide and reduced-dose tenecteplase for ST-elevation myocardial infarction: results of the Integrilin and Tenecteplase in Acute Myocardial Infarction (INTEGRITI) phase II angiographic trial. J Am Coll Cardiol. 2003; 41: 1251–1260.[Abstract/Free Full Text]

29. Antman EM, Louwerenburg HW, Baars HF, Wesdorp JC, Hamer B, Bassand JP, Bigonzi F, Pisapia G, Gibson CM, Heidbuchel H, Braunwald E, Van de Werf F. Enoxaparin as adjunctive antithrombin therapy for ST-elevation myocardial infarction: results of the ENTIRE-Thrombolysis in Myocardial Infarction (TIMI) 23 Trial. Circulation. 2002; 105: 1642–1649.[Abstract/Free Full Text]

30. Ohman EM. FASTER-TIMI 24. Presented at the 18th International Symposium on Thrombolysis and Interventional Therapy in Acute Myocardial Infarction, November 16, 2002, Chicago, Ill.

31. Bovill EG, Terrin ML, Stump DC, Berke AD, Frederick M, Collen D, Feit F, Gore JM, Hillis LD, Lambrew CT, et al. Hemorrhagic events during therapy with recombinant tissue-type plasminogen activator, heparin, and aspirin for acute myocardial infarction: results of the Thrombolysis in Myocardial Infarction (TIMI), Phase II Trial. Ann Intern Med. 1991; 115: 256–265.[Abstract/Free Full Text]

32. Hosmer DW, Lemeshow S. Applied Logistic Regression. 2nd ed. New York, NY: John Wiley & Sons; 2000.

33. Arant CB, Wessel TR, Olson MB, Bairey Merz CN, Sopko G, Rogers WJ, Sharaf BL, Reis SE, Smith KM, Johnson BD, Handberg E, Mankad S, Pepine CJ. Hemoglobin level is an independent predictor for adverse cardiovascular outcomes in women undergoing evaluation for chest pain: results from the National Heart, Lung, and Blood Institute Women’s Ischemia Syndrome Evaluation Study. J Am Coll Cardiol. 2004; 43: 2009–2014.[Abstract/Free Full Text]

34. Gagnon DR, Zhang TJ, Brand FN, Kannel WB. Hematocrit and the risk of cardiovascular disease: the Framingham study: a 34-year follow-up. Am Heart J. 1994; 127: 674–682.[CrossRef][Medline] [Order article via Infotrieve]

35. Kershenovich S, Modiano M, Ewy GA. Markedly decreased coronary blood flow in secondary polycythemia. Am Heart J. 1992; 123: 521–523.[CrossRef][Medline] [Order article via Infotrieve]

36. Lowe GD, Forbes CD. Blood rheology and thrombosis. Clin Haematol. 1981; 10: 343–367.[Medline] [Order article via Infotrieve]

37. Dormandy JA, Hoare E, Colley J, Arrowsmith DE, Dormandy TL. Clinical, haemodynamic, rheological, and biochemical findings in 126 patients with intermittent claudication. BMJ. 1973; 4: 576–581.[Abstract/Free Full Text]

38. Smith KJ, Bleyer AJ, Little WC, Sane DC. The cardiovascular effects of erythropoietin. Cardiovasc Res. 2003; 59: 538–548.[Abstract/Free Full Text]

39. Ryan TJ, Antman EM, Brooks NH, Califf RM, Hillis LD, Hiratzka LF, Rapaport E, Riegel B, Russell RO, Smith EE III, Weaver WD, Gibbons RJ, Alpert JS, Eagle KA, Gardner TJ, Garson A Jr, Gregoratos G, Smith SC Jr. 1999 update: ACC/AHA guidelines for the management of patients with acute myocardial infarction: executive summary and recommendations: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction). Circulation. 1999; 100: 1016–1030.[Free Full Text]

40. Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, Jones RH, Kereiakes D, Kupersmith J, Levin TN, Pepine CJ, Schaeffer JW, Smith EE III, Steward DE, Theroux P. ACC/AHA guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina). 2002. American College of Cardiology Web site. Available at: http://www.acc.org/clinical/guidelines/unstable/unstable.pdf. Accessed August 6, 2004.

41. Hebert PC, Wells G, Blajchman MA, Marshall J, Martin C, Pagliarello G, Tweeddale M, Schweitzer I, Yetsir E, the Transfusion Requirements in Critical Care Investigators for the Canadian Critical Care Trials Group. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. N Engl J Med. 1999; 340: 409–417.[Abstract/Free Full Text]

42. Hebert PC, Yetisir E, Martin C, Blajchman MA, Wells G, Marshall J, Tweeddale M, Pagliarello G, Schweitzer I. Is a low transfusion threshold safe in critically ill patients with cardiovascular diseases? Crit Care Med. 2001; 29: 227–234.[CrossRef][Medline] [Order article via Infotrieve]

43. Rao SV, Jollis JG, Harrington RA, Granger CB, Newby LK, Armstrong PW, Moliterno DJ, Lindblad L, Pieper K, Topol EJ, Stamler JS, Califf RM. Relationship of blood transfusion and clinical outcomes in patients with acute coronary syndromes. JAMA. 2004; 292: 1555–1562.[Abstract/Free Full Text]




This article has been cited by other articles:


Home page
Am J EpidemiolHome page
P.-C. Chen, F.-C. Sung, K.-L. Chien, H.-C. Hsu, T.-C. Su, and Y.-T. Lee
Red Blood Cell Distribution Width and Risk of Cardiovascular Events and Mortality in a Community Cohort in Taiwan
Am. J. Epidemiol., December 14, 2009; (2009) kwp360v1.
[Abstract] [Full Text] [PDF]


Home page
Eur Heart JHome page
E. M. Jolic{oelig}ur, W. W. O'Neill, A. Hellkamp, C. W. Hamm, D. R. Holmes Jr., H. R. Al-Khalidi, M. R. Patel, F. J. Van de Werf, K. Pieper, P. W. Armstrong, et al.
Transfusion and mortality in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention
Eur. Heart J., November 1, 2009; 30(21): 2575 - 2583.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
E. S. van Hattum, A. Algra, J. A. Lawson, B. C. Eikelboom, F. L. Moll, and M. J.D. Tangelder
Bleeding Increases the Risk of Ischemic Events in Patients With Peripheral Arterial Disease
Circulation, October 20, 2009; 120(16): 1569 - 1576.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
A. H.M. van Straten, M. A. Soliman Hamad, A. J. van Zundert, E. J. Martens, J. P.A.M. Schonberger, and A. M. de Wolf
Preoperative Hemoglobin Level as a Predictor of Survival After Coronary Artery Bypass Grafting: A Comparison With the Matched General Population
Circulation, July 14, 2009; 120(2): 118 - 125.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll Cardiol IntvHome page
E. Nikolsky, R. Mehran, H. M. Sadeghi, C. L. Grines, D. A. Cox, E. Garcia, J. E. Tcheng, J. J. Griffin, G. Guagliumi, T. Stuckey, et al.
Prognostic Impact of Blood Transfusion After Primary Angioplasty for Acute Myocardial Infarction: Analysis From the CADILLAC (Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications) Trial
J. Am. Coll. Cardiol. Intv., July 1, 2009; 2(7): 624 - 632.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
B. J. Doyle, C. S. Rihal, D. A. Gastineau, and D. R. Holmes Jr
Bleeding, blood transfusion, and increased mortality after percutaneous coronary intervention implications for contemporary practice.
J. Am. Coll. Cardiol., June 2, 2009; 53(22): 2019 - 2027.
[Abstract] [Full Text] [PDF]


Home page
Eur Heart JHome page
S. D. Anker, A. Voors, D. Okonko, A. L. Clark, M. K. James, S. von Haehling, J. Kjekshus, P. Ponikowski, K. Dickstein, and for the OPTIMAAL Investigators
Prevalence, incidence, and prognostic value of anaemia in patients after an acute myocardial infarction: data from the OPTIMAAL trial
Eur. Heart J., June 1, 2009; 30(11): 1331 - 1339.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll Cardiol IntvHome page
S. Koul and D. J. Moliterno
Bare-Metal Versus Drug-Eluting Stent Placement Among Patients Presenting With Anemia
J. Am. Coll. Cardiol. Intv., April 1, 2009; 2(4): 337 - 338.
[Full Text] [PDF]


Home page
J. Am. Soc. Nephrol.Home page
K. Kalantar-Zadeh and G. R. Aronoff
Hemoglobin Variability in Anemia of Chronic Kidney Disease
J. Am. Soc. Nephrol., March 1, 2009; 20(3): 479 - 487.
[Abstract] [Full Text] [PDF]


Home page
ANGIOLOGYHome page
E. D. Pagourelias, C. Koumaras, A. I. Kakafika, K. Tziomalos, P. G. Zorou, V. G. Athyros, and A. Karagiannis
Cardiorenal Anemia Syndrome: Do Erythropoietin and Iron Therapy Have a Place in the Treatment of Heart Failure?
Angiology, February 1, 2009; 60(1): 74 - 81.
[Abstract] [PDF]


Home page
J Am Coll Cardiol IntvHome page
M. H. Shishehbor, S. Madhwal, V. Rajagopal, A. Hsu, P. Kelly, H. S. Gurm, S. R. Kapadia, M. S. Lauer, and E. J. Topol
Impact of Blood Transfusion on Short- and Long-Term Mortality in Patients With ST-Segment Elevation Myocardial Infarction
J. Am. Coll. Cardiol. Intv., January 1, 2009; 2(1): 46 - 53.
[Abstract] [Full Text] [PDF]


Home page
ESC Textbook of Cardiovascular MedicineHome page
C. W. Hamm, H. Möllmann, J.-P. Bassand, and F. van de Werf
CHAPTER 16 Acute Coronary Syndromes
ESC Textbook of Cardiovascular Medicine, January 1, 2009; 2(1): med-9780199566990-chapter - med-9780199566990-chapter.
[Abstract] [Full Text] [PDF]


Home page
Anesth. Analg.Home page
G. M. T. Hare, A. K. Y. Tsui, A. T. McLaren, T. E. Ragoonanan, J. Yu, and C. D. Mazer
Anemia and Cerebral Outcomes: Many Questions, Fewer Answers
Anesth. Analg., October 1, 2008; 107(4): 1356 - 1370.
[Abstract] [Full Text] [PDF]


Home page
Eur J EchocardiogrHome page
M. Richardson-Lobbedez, S. Marechaux, C. Bauters, J. Darchis, J. L. Auffray, J. J. Bauchart, J. M. Aubert, T. H. LeJemtel, M. Lesenne, E. Van Belle, et al.
Prognostic importance of tissue Doppler-derived diastolic function in patients presenting with acute coronary syndrome: a bedside echocardiographic study
Eur J Echocardiogr, September 1, 2008; 9(5): 594 - 598.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
I. S. Anand
Anemia and Chronic Heart Failure: Implications and Treatment Options
J. Am. Coll. Cardiol., August 12, 2008; 52(7): 501 - 511.
[Abstract] [Full Text] [PDF]


Home page
HeartHome page
A J Chase, E B Fretz, W P Warburton, W P Klinke, R G Carere, D Pi, B Berry, and J D Hilton
Association of the arterial access site at angioplasty with transfusion and mortality: the M.O.R.T.A.L study (Mortality benefit Of Reduced Transfusion after percutaneous coronary intervention via the Arm or Leg)
Heart, August 1, 2008; 94(8): 1019 - 1025.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
W. C. Levy
Anemia in heart failure: marker or mediator of adverse prognosis?
J. Am. Coll. Cardiol., February 5, 2008; 51(5): 577 - 578.
[Full Text] [PDF]


Home page
CirculationHome page
K. Karkouti, D. N. Wijeysundera, W. S. Beattie, and for the Reducing Bleeding in Cardiac Surgery (RBC)
Risk Associated With Preoperative Anemia in Cardiac Surgery: A Multicenter Cohort Study
Circulation, January 29, 2008; 117(4): 478 - 484.
[Abstract] [Full Text] [PDF]


Home page
Eur Heart JHome page
Authors/Task Force Members, J.-P. Bassand, C. W. Hamm, D. Ardissino, E. Boersma, A. Budaj, F. Fernandez-Aviles, K. A.A. Fox, D. Hasdai, E. M. Ohman, et al.
Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes: The Task Force for the Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of the European Society of Cardiology
Eur. Heart J., July 1, 2007; 28(13): 1598 - 1660.
[Full Text] [PDF]


Home page
Eur Heart JHome page
D. Aronson, M. Suleiman, Y. Agmon, A. Suleiman, M. Blich, M. Kapeliovich, R. Beyar, W. Markiewicz, and H. Hammerman
Changes in haemoglobin levels during hospital course and long-term outcome after acute myocardial infarction
Eur. Heart J., June 1, 2007; 28(11): 1289 - 1296.
[Abstract] [Full Text] [PDF]


Home page
Eur Heart JHome page
J.-P. Bassand
Impact of anaemia, bleeding, and transfusions in acute coronary syndromes: a shift in the paradigm
Eur. Heart J., June 1, 2007; 28(11): 1273 - 1274.
[Full Text] [PDF]


Home page
Eur Heart JHome page
S. V. Rao, J. A. Eikelboom, C. B. Granger, R. A. Harrington, R. M. Califf, and J.-P. Bassand
Bleeding and blood transfusion issues in patients with non-ST-segment elevation acute coronary syndromes
Eur. Heart J., May 2, 2007; 28(10): 1193 - 1204.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
F. Andreotti, G. Coluzzi, and F. Crea
Letter by Andreotti et al Regarding Article, "Hemoglobin Level, Chronic Kidney Disease, and the Risks of Death and Hospitalization in Adults With Chronic Heart Failure: The Anemia in Chronic Heart Failure: Outcomes and Resource Utilization (ANCHOR) Study"
Circulation, March 6, 2007; 115(9): e313 - e313.
[Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
G. J. Murphy and G. D. Angelini
Indications for Blood Transfusion in Cardiac Surgery
Ann. Thorac. Surg., December 1, 2006; 82(6): 2323 - 2334.
[Abstract] [Full Text] [PDF]


Home page
Eur J Heart FailHome page
N. Valeur, O. W. Nielsen, J. J.V. McMurray, C. Torp-Pedersen, L. Kober, and TRACE Study Group
Anaemia is an independent predictor of mortality in patients with left ventricular systolic dysfunction following acute myocardial infarction
Eur J Heart Fail, October 1, 2006; 8(6): 577 - 584.
[Abstract] [Full Text] [PDF]


Home page
Eur Heart J SupplHome page
J. W. Eikelboom and J. Hirsh
Bleeding and management of bleeding
Eur. Heart J. Suppl., October 1, 2006; 8(suppl_G): G38 - G45.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
J. W. Eikelboom, S. R. Mehta, S. S. Anand, C. Xie, K. A.A. Fox, and S. Yusuf
Adverse Impact of Bleeding on Prognosis in Patients With Acute Coronary Syndromes
Circulation, August 22, 2006; 114(8): 774 - 782.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
X. Yang, K. P. Alexander, A. Y. Chen, M. T. Roe, R. G. Brindis, S. V. Rao, W. B. Gibler, E. M. Ohman, E. D. Peterson, and for the CRUSADE Investigators
The Implications of Blood Transfusions for Patients With Non-ST-Segment Elevation Acute Coronary Syndromes: Results From the CRUSADE National Quality Improvement Initiative
J. Am. Coll. Cardiol., October 18, 2005; 46(8): 1490 - 1495.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
111/16/2042    most recent
01.CIR.0000162477.70955.5Fv1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sabatine, M. S.
Right arrow Articles by Braunwald, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sabatine, M. S.
Right arrow Articles by Braunwald, E.
Related Collections
Right arrow Acute coronary syndromes