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European Heart Journal Advance Access originally published online on August 21, 2006
European Heart Journal 2006 27(21):2511-2515; doi:10.1093/eurheartj/ehl191
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Significance of total and differential leucocyte count in patients with acute myocardial infarction treated with primary coronary angioplasty

Matteo Mariani1,*, Raffaela Fetiveau1, Enrico Rossetti1, Arnaldo Poli1, Fabrizio Poletti1, Pietro Vandoni1, Maurizio D'Urbano1, Francesco Cafiero1, Giuseppe Mariani1, Catherine Klersy2 and Stefano De Servi1

1 Department of Cardiovascular Disease, Ospedale Civile di Legnano, Via Candiani, 2 Legnano, Milan, Italy
2 Scientific Direction, Policlinico San Matteo, Pavia, Italy

Received 12 July 2005; revised 19 July 2006; accepted 27 July 2006; online publish-ahead-of-print 21 August 2006.

* Corresponding author. Tel: +39 (0) 331 449513; fax: +39 (0) 331 449810. E-mail address: mat.mariani{at}tiscali.it

See page 2487 for the editorial comment on this article (doi:10.1093/eurheartj/ehl267)


    Abstract
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Aims The aim of this study was to correlate total and differential leucocyte (WBC) count with myocardial blush, peak CK levels, and left ventricular (LV) functional recovery at 6 months in 238 consecutive acute myocardial infarction (MI) patients treated with successful primary coronary angioplasty (PCI).

Methods and results Total and differential WBC counts were measured on admission and every 24 h for at least 4 days after PCI. ST-segment resolution and myocardial blush were evaluated immediately after successful primary PCI. LV functional recovery (defined as improvement involving at least two segments, or at least one segment, when only two were asynergic on the basal examination) was obtained through echocardiographic evaluation of LV wall motion at the baseline and at 6 months. Basal CK (P<0.001) and increased neutrophil levels (P<0.001) were the only independent factors related to peak CK, whereas neutrophils and monocytes peaks were related to ST-segment resolution as well as to myocardial blush grade (MBG) 2–3. MBG 2–3 and monocytes number (both as continuous values as well as percentile values) were the only variables independently associated with 6-month LV functional recovery.

Conclusion The present study shows that neutrophils and monocytes counts on the first days after acute MI treated with primary PCI are related to markers of effective myocardial reperfusion such as MBG 2–3 and ST-segment resolution. However, only monocytes and MBG are significantly and independently associated with contractile recovery of the infarcted area at 6 months.

Key Words: Leucocytes • Myocardial infarction • Inflammation


    Introduction
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Elevation of leukocytes (WBC) in acute myocardial infarction (MI) identifies a cohort of patients at increased risk for short- and long-term ischaemic complications and cardiac death.15 Leukocytosis has also been associated with reduced epicardial blood flow, thromboresistance, and an adverse outcome in patients treated with thrombolytic therapy for acute MI.6 In particular, peripheral monocytosis is related with left ventricular (LV) dysfunction and evolution to LV aneurysm suggesting a role of monocytes in the development of LV remodelling after reperfused acute MI.7 In contrast, an increased peripheral neutrophil count on admission in patients with acute MI has been significantly associated with the early development of congestive heart failure.8

Restoration of epicardial flow after acute MI does not necessarily lead to restoration of microvascular perfusion: for this reason, evaluation of microvascular perfusion has gained importance to predict recovery of LV contractility after acute MI.9,10 There are no data, however, relating the increase in total and differential leukocytes count with markers of effective myocardial reperfusion after primary coronary angioplasty (PCI) and evolution of LV function. Accordingly, the purpose of this study was to investigate the correlation between total and differential WBC count with microvascular reperfusion and 6-month LV functional recovery, assessed by changes in LV wall motion at echocardiography, in a large series of patients undergoing successful primary PCI for acute MI.


    Methods
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Study population
From September 1999 to May 2003, 325 consecutive patients with ST-segment elevation acute MI presenting within 12 h from symptom onset were treated with primary PCI in our catheterization laboratory. Patients with suboptimal angiographic result because of TIMI flow <3 (n=22), patients with chronic renal failure (creatinine ≥3 mg%), advanced liver diseases, malignancies, or concomitant infectious diseases (n=16) were excluded from the study. Moreover, 16 patients in whom the quality of coronary angiograms at the end of the primary PCI procedure did not allow adequate assessment of microvascular reperfusion, 10 patients in whom echocardiographic data were not available before primary PCI, and 15 patients with prior MI were excluded from the final analysis as well as 8 patients with left bundle branch block, which could not permit an accurate analysis of ST-segment elevation, were also excluded from the final analysis. The remaining 238 patients represent the study population.

Primary angioplasty
Primary PCI was performed with conventional techniques and coronary stents were used without restrictions. The infarct-related artery was the only target of the procedure. Abciximab therapy was given by judgement of the operator and usually started during the procedure. Intra-aortic balloon pump was performed in case of haemodynamic instability. Primary PCI was considered successful when TIMI grade 3 coronary flow in the treated vessel, with a residual stenosis <20%, was achieved.

The angiographic images were acquired with a Toshiba DFP-2000A single-plane system at a cine rate of 25 frames/s. Basal TIMI flow and collateral circulation to the culprit vessel were evaluated on the first angiogram. Myocardial blush was graded, according to the dye density score proposed by van't Hof et al.11 in patients undergoing primary PCI: from 0 (no contrast density or abnormal persistence of contrast medium), to 3 (normal contrast density, relative to the dye density in uninvolved areas). Both TIMI flow and myocardial blush were graded on the angiograms immediately after primary PCI. Latero-lateral views for the left anterior descending coronary artery, right anterior oblique 45° views for the right coronary artery and latero-lateral or right anterior oblique 45° views for the circumflex artery were used in most cases. The duration of cine filming had to allow some filling of the venous system in order to evaluate the washout phase of contrast dye. To facilitate the subjective grading of myocardial blush grade (MBG), angiograms were digitized and a logarithmic non-magnified mask-mode background subtraction was applied to the image subset to eliminate non-contrast medium densities. The analysis was carried out by two experienced cardiologists who were blinded as to the patient's identity, electrocardiographic (ECG), and echocardiographic findings. TIMI flow grades were assessed as previously described.12

ECG analysis
A 12-lead ECG was recorded just before and at the end of the procedure. Analysis was done by one observer unaware of the clinical and angiographic data. As previously proposed, the sum of ST-segment elevation was measured manually 20 ms after the end of QRS complex from leads exploring the infarct area13 and its recovery after primary PCI was quantified as percentage of the value obtained from the basal ECG. ST-segment resolution was intended as a >50% reduction of the initial value.

WBC count and laboratory analysis
Total and differential WBC count were measured by an automated haematology analyzer (Coulter Gen-S) on admission and every 24 h for at least 4 days after primary PCI in all patients. Total CK was analyzed by a Roche/Hitachi system.

Echocardiographic analysis
A two-dimensional echocardiogram was performed using GE Vingmed System Five Performance instrument before primary PCI and 6 months thereafter, for the evaluation of LV wall motion score index (WMSI) and ejection fraction (EF). The analysis was carried out by two observers blinded to the clinical and angiographic data. Discrepancies were resolved by consensus. An LV WMSI was calculated on the model proposed by the American Society of Echocardiography.14 Accurate evaluation of the LV WMSI was performed by dividing the LV into 16 segments which was studied in the parasternal and subxiphoyd long- and short-axis, apical four-, three-, and two-chamber views. The following scoring system was used according to the recommendations of the American Society of Echocardiography: 1, normal or hyperkinetic; 2, hypokinetic; 3, akinetic; 4, dyskinetic. The WMSI was the sum of each segment score divided by the number of the segments—i.e. 16.14

Baseline images were used to assess the initial extent of LV dysfunction. Follow-up images were then paired with the corresponding baseline images and directly compared with random order of loops. When performing follow-up echocardiography, particular attention was paid to obtain the same echocardiographic views selected during baseline examination. Intraobserver and interobserver variability values in the evaluation of segmental myocardial function were 4% and 6%, respectively, which indicates the good reproducibility of the measurements.

A segment was considered to have functional improvement when systolic wall thickening and endocardial motion appeared in basally akinetic or dyskinetic segment or when normal or near-normal wall motion and thickening became apparent in a severely hypokinetic segment. Significant LV functional recovery was considered to have occurred when the improvement involved at least two segments, or at least one segment when only two were asynergic on the basal examination.

Statistical analysis
Data were reported as mean and standard deviation or median and 25th–75th percentiles for continuous variables and as absolute and relative frequencies for categorical variables. Baseline characteristics were compared between groups of patients with MBG 2–3 vs. patients with MBG 0–1, and between patients with significant {Sigma}STe recovery vs. those without. The Fisher's exact test was used to compare categorical variables. The Kruskal–Wallis test was used to compare continuous variables.

In order to assess primary endpoint (significant LV functional recovery defined as a binary variable) univariate and multivariate logistic regression was used. Odds ratios (OR) and their 95% confidence intervals (95% CI) were computed. The following potential predictors (all showing a P<0.1 at univariate analysis) were included: MBG 2–3, ST-segment resolution, diabetes, basal CK, peak CK, time of ischaemia, total WBC, neutrophils, and monocytes numbers. Collinearity was excluded by means of a correlation matrix between candidate predictors. Empirically, collinearity was excluded for R<0.5. Linearity of effect was assessed by means of likelihood ratio test by comparing a model in which the linearity assumption was checked by introducing the quartiles of the distribution of neutrophils and monocytes and a model in which the effect was considered to be linear. Total WBC, neutrophils, and monocytes were included in the analysis as continuous variables. A sensitivity analysis was performed by using the same variables dichotomized at the 25th, 50th, and 75th percentiles of their distribution. Calibration, discrimination, and goodness-of-fit [10] test were computed for model validation.

WBC peak, monocytes peak, neutrophils peak, ischaemic time, and basal CK were related to peak CK by linear regression model (after log-transformation of ischaemic time, basal CK, and peak CK to ensure a linear relationship with the continuous dependent variables). A linear regression model was also used to correlate a log-transformation of monocytes peak and neutrophils peak with clinical and laboratory variables. Linearity of effect was assessed as described earlier. No correction was applied for multiple tests. Stata 8 (StataCorp, College Station, TX, USA) was used for computation. A two-sided P-value <0.05 was considered statistically significant.


    Results
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
The clinical characteristics of the study population are shown in Table 1. The mean age was 62.4 years (range 38–88) and more than two-thirds of the patients were men. Anterior MI was present in about half of the patients (46%); the basal EF was 45.5±7.3% and LV WMSI was 1.49±0.25.


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Table 1 Clinical and angiographic variables in the study population

 
ST-segment resolution, myocardial blush, and total peak CK
ST-segment resolution occurred in 162 patients (68%). Patients with ST-segment resolution had a higher frequency of MBG 2–3 (P<0.001), a lower frequency of anterior MI (P<0.01), a lower peak CK (P=0.001), as well as lower neutrophils (P<0.05) and monocytes peaks (P<0.05). Patients with ST-segment resolution had also a better 6-month functional recovery than those without ST-segment resolution (P<0.05).

Shortly after successful PCI, a MBG 2–3 was found in 162 patients (68%), whereas 76 patients had grade 0–1 (32%). MBG 2–3 was related to lower basal CK (P<0.001) as well as peak CK (P<0.001), to a shorter ischaemic time (P<0.05), to lower total WBC (P<0.001), monocytes (P<0.001), and neutrophils peak (P<0.001). MBG 2–3 was also related to ST-segment resolution (P<0.001) and to a better 6-month functional recovery (P<0.001). Peak CK level was 2404+1955 U/L.

By multiple regression analysis, only admission CK (P<0.001) and neutrophils peak (P<0.001) were independently related to CK peak, whereas other variables including monocyte peak were not.

Total and differential WBC count
Median WBC peak was 11 395/mm3 (range 3100–26900); median neutrophils peak was 8345/mm3 (range 3770–22600), median monocytes peak was 890/mm3 (range 280–2400), and median lymphocytes peak was 2400/mm3 (range 300–12730).

The mean time from admission to the peak of WBC and neutrophils was 1±1 days, and to the peak of monocytes and lymphocytes was 2±1 days.

The correlation between total and differential WBC count with clinical and laboratory findings was assessed by means a linear regression model. Total WBC peak was associated with age (P=0.001), peak CK (P<0.001), multivessel coronary disease (P=0.0017), and inversely related to MBG 2–3 (P<0.001) as well as to 6-month LV functional recovery (P=0.013). Monocyte peak was associated with male gender (P=0.004) and peak CK (P=0.001), whereas it was inversely related to MBG 2–3 (P=0.000) as well as to 6-month LV functional recovery (P<0.001). Neutrophils peak was associated with anterior MI (P=0.026), basal (P<0.001) as well as peak CK (P<0.001), time of ischaemia (P=0.007), multivessel coronary disease (P=0.024), basal WMSI (P=0.020), basal EF(P=0.037), and inversely related to MBG 2–3 (P<0.001), ST-segment resolution (P=0.018), and to 6-month LV functional recovery (P<0.001). No relation was found between lymphocytes peak and any considered variable.

Clinical outcome and 6-month functional recovery
At 6 months there were seven new MI and one death, whereas 16 patients had recurrent angina. A new revascularization procedure was performed in 54 patients [48 patients had a new PCI and 6 patients underwent coronary artery bypass grafts (CABG)]. Echocardiograms at 6 months was performed in all the 237 patients alive at that time.

LV functional recovery was detected in 154 patients (66%) at the echocardiographic control performed 6 months after the acute event.

At univariate analysis, basal CK as well as peak CK, time of ischemia, MBG 2–3, diabetes, Killip class >1, ST-segment resolution, total and differential leukocytes count were significantly associated with 6-month LV functional recovery, both in the model using continuous values of total and differential leukocytes count, as well as in the model using the 25th and 50th percentile values.

By multiple regression analysis, including all these variables, MBG 2–3, CK peak, diabetes, ischaemic time, and monocytes number were associated with 6-month LV functional recovery both in the model using continuous values of total and differential leukocytes count, as well as in the model using the 25th and 50th percentile values (Table 2).


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Table 2 Variables associated with significant 6-month LV functional recovery

 
Number of patients with LV functional recovery according to quartiles of monocyte values are shown in Figure 1. Figure 2 shows the relation between quartiles of monocytes values and 6-month EF.


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Figure 1 Number of patients with LV functional recovery at 6-months was inversely related to monocyte count in the acute MI phase.

 

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Figure 2 Inverse relation between EF at 6-months and monocytes count quartiles.

 

    Discussion
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
The main and original finding of this study is that the differential WBC count on the first few days after acute MI is associated with the recovery of LV function in patients treated with primary PCI. Indeed, neutrophils and monocytes peak values were related to CK release, effectiveness of reperfusion and LV functional recovery, all important determinants of infarct size and final derangement of myocardial contractility.

Clinical outcome after acute MI is not only associated with restoration of coronary flow in the epicardial artery, but also with microvascular flow in the myocardium.15 In 25–50% of cases, despite a rapid and sustained flow through a previously occluded epicardial coronary artery, lack of microvascular reperfusion (no-reflow phenomenon) may still be observed. The no-reflow phenomenon is associated with unfavourable LV remodelling and poor clinical prognosis.1518 A new method of assessing myocardial perfusion on final angiograms after primary PCI is the MBG developed by van't Hoff et al. who have demonstrated an association between impaired myocardial perfusion, assessed by MBG, and early and late mortality.11,19 We also showed that integrated analysis of myocardial blush and ST-segment resolution allows a real-time grading of microvascular reperfusion of the infarct area and predicts the time course and magnitude of LV functional recovery.20 In the present study, an MBG 2–3, found in two-thirds of patients, was the most powerful predictor of 6-month LV functional recovery confirming the reliability of this method in assessing the evolution of LV function after acute MI.9,10

In acute MI, increased leukocyte count is a common finding that reflects the infiltration of WBC into the necrotic myocardial tissue.2123 Neutrophils are the first leukocytes to be found in the damaged myocardial area and are removed from myocardial tissue after phagocytosing the debris. In contrast, monocytes migrate from capillaries to extravascular space and are transformed into macrophages and outnumber neutrophils 2–3 days after the acute episode. Macrophage-secreted cytokines stimulate fibroblast proliferation, collagen production, and promote monocytosis. Several studies have suggested that leukocytes count at initial examination of patients with acute MI predicts outcome in both short-term and long-term follow-up.15 Increased neutrophil count on hospital admission in patients with acute MI is significantly associated with early development of congestive heart failure,8 whereas peripheral monocytosis after acute MI is associated with LV dysfunction and evolution to LV aneurysm.7 Recently, Kirtane et al.24 showed that higher neutrophil counts correlate with reduced epicardial patency after thrombolysis and with a longer corrected TIMI frame count, suggesting an association between neutrophilia and impaired microvascular perfusion, possibly as a result of neutrophil-mediated microvascular plugging and reduced coronary vasodilator reserve as described in animal models of ischaemia-reperfusion.25

In our study, low monocytes and neutrophils count were significantly related to MBG and ST-segment resolution, which are reliable markers of effective myocardial reperfusion after primary PCI, indicating that neutrophils and monocytes rise after acute MI is dependent on microvascular function and may be used as a non-invasive marker of failed or incomplete myocardial reperfusion. Our data confirm those reported by Kirtane et al.,24 who found a relation between high neutrophil count and impaired microvascular perfusion. Monocyte count, however, was not included in that analysis, therefore the relative importance of all cellular components of WBC count was not assessed in that study. In keeping with those findings, we also observed that peak CK was positively correlated with neutrophil count, whereas we did not find any relation of peak CK with monocyte count. In contrast, only monocyte count together with MBG was significantly and independently associated with LV functional recovery at 6 months, whereas neutrophil count was not. Therefore, our data seem to suggest that different pathogenetic mechanisms are involved in the rise of neutrophils and monocytes in acute MI treated by primary PCI.

From our data it is not clear if a high monocyte count is a cause or an effect of the pathophysiological process that leads to impairment of myocardial perfusion following primary PCI. It must be noticed, however, that the multiple regression analysis showed that monocyte count was associated with late functional recovery of the infarcted area independent of MBG, suggesting that monocytosis per se may have a negative action on contractile recovery of the infarcted area. It is possible that monocyte-secreted cytokines would have a direct toxic effect on damaged but still viable myocardial cells, hampering their functional recovery and favouring collagen synthesis.

In conclusion, the present study shows that neutrophil and monocyte counts on the first days after acute MI treated with successful primary PCI are related to markers of effective myocardial reperfusion such as MBG and ST-segment resolution. However, only monocyte number and MBG are significantly and independently associated with the contractile recovery of the infarcted area at 6 months.

Conflict of interest: none declared.


    References
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Modan B, Shor S, Shani M. (1975) Acute myocardial infarction: prognostic value of white blood cell count and blood glucose level. JAMA 233:266–267.[Abstract]
  2. Burr ML, Holliday RM, Fehily AM, Whitehead PJ. (1992) Haematological prognostic indices after myocardial infarction: evidence from the Diet and Reinfarction Trial (DART). Eur Heart J 13:166–170.[Abstract/Free Full Text]
  3. Cannon CP, McCabe CH, Wilcox RG, Bentley JH, Braunwald E. (2001) Association of white blood cell count with increased mortality in acute myocardial infarction and unstable angina. Am J Cardiol 87:636–639.[CrossRef][ISI][Medline]
  4. Furmann MI, Becker RC, Yarzebski J, Savegeau J, Gore JM, Golgberg RJ. (1996) Effect of elevated leukocyte count on in-hospital mortality following acute myocardial infarction. Am J Cardiol 78:945–948.[CrossRef][ISI][Medline]
  5. Pellizzon GG, Dixon SR, Gregg W, Cox DA, Mattos L, Boura JA, Grines LL, Addala S, O'Neill WW, Grines CL. for the Stent PAMI Investigators. (2003) Relation of admission white blood cell count to long-term outcomes after primary coronary angioplasty for acute myocardial infarction. Am J Cardiol 91:729–731.[CrossRef][ISI][Medline]
  6. Barron HV, Cannon CP, Murphy SA, Braunwald E, Gibson CM. (2000) Association between white blood cell count, epicardial blood flow, myocardial perfusion and clinical outcomes in the setting of acute myocardial infarction. A Thrombolysis in Myocardial Infarction 10 Substudy. Circulation 102:2329–2334.[Abstract/Free Full Text]
  7. Maekawa Y, Anzai T, Yoshikawa T, Asakura Y, Takahashi T, Ishikawa S, Mitamura H, Ogawa S. (2002) Prognostic significance of peripheral monocytosis after reperfused acute myocardial infarction: a possible role for left ventricular remodeling. J Am Coll Cardiol 39:241–246.[Abstract/Free Full Text]
  8. Kyne L, Hausdorff JM, Knight E, Dukas L, Azhar G, Wie JY. (2000) Neutrophilia and congestive heart failure after acute myocardial infarction. Am Heart J 139:94–100.[ISI][Medline]
  9. Gibson CM. (2003) Has my patient achieved adequate myocardial reperfusion? Circulation 108:504–507.[Free Full Text]
  10. Gibson CM and Schömig A. (2004) Coronary and myocardial angiography: angiographic assessment of both epicardial and myocardial perfusion. Circulation 109:3096–3105.[Free Full Text]
  11. van't Hof AWJ, Liem A, Suryapranata H, Zijlstra F. (1998) Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction: myocardial blush grade. Circulation 97:2302–2306.[Abstract/Free Full Text]
  12. The TIMI study group. (1985) The thrombolysis in myocardial infarction (TIMI) trial: phase I findings. N Engl J Med 312:932–936.[Medline]
  13. Claeys MJ, Bosmans J, Veenstra L, Jorens P, De Raedt H, Vrints CJ. (1999) Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction. Circulation 99:1972–1977.[Abstract/Free Full Text]
  14. Schiller NB, Shah PM, Crawford M, De Maria A, Devereux R, Feigenbaum H, Gutgesell H, Reichek N, Sahn D, Schnittger I, Silverman LH, Tajik AJ. (1989) Recommendations for quantitation of left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Sub-committee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardigr 2:358–367.
  15. Gibson CM, Cannon CP, Murphy SA, Marble SJ, Barron HV, Braunwald E. TIMI Study Group. (2002) Relationship of the TIMI myocardial perfusion grades, flow grades, frame count, and percutaneous coronary intervention to long-term outcomes after thrombolytic administration in acute myocardial infarction. Circulation 105:1909–1913.[Abstract/Free Full Text]
  16. Ito H, Maruyama A, Iwakura K, Takiuchi S, Masuyama T, Hori M, Higashino J, Fujii K, Minamino T. (1996) Clinical implication of the ‘no reflow’ phenomenon: a predictor of complication and left ventricular remodelling in reperfused anterior wall myocardial infarction. Circulation 93:223–228.[Abstract/Free Full Text]
  17. Sakuma T, Hayashi Y, Sumii K, Imazu M, Yamakido M. (1998) Prediction of short and intermediate-term prognosis of patients with acute myocardial infarction using myocardial contrast echocardiography one day after recanalization. J Am Coll Cardiol 32:890–897.[Abstract/Free Full Text]
  18. Bolognese L, Carrabba N, Parodi G, Santoro GM, Buonamici P, Cerisano G, Antoniucci D. (2004) Impact of microvascular dysfunction on left ventricular remodeling and long-term clinical outcome after primary coronary angioplasty for acute myocardial infarction. Circulation 109:1121–1126.[Abstract/Free Full Text]
  19. Haager PK, Christott P, Heussen N, Lepper W, Hanrath P, Hoffmann R. (2003) Prediction of clinical outcome after mechanical revascularization in acute myocardial infarction by markers of myocardial reperfusion. J Am Coll Cardiol 41:532–538.[Abstract/Free Full Text]
  20. Poli A, Fetiveau R, Vandoni P, Del Rosso G, D'Urbano M, Seveso G, Cafiero F, De Servi S. (2002) Integrated analysis of myocardial blush and ST-segment elevation recovery after successful primary angioplasty. Real-time grading of microvascular reperfusion and prediction of early and late recovery of left ventricular function. Circulation 106:313–318.[Abstract/Free Full Text]
  21. Mallory GK, White PD, Salcedo-Salgar J. (1939) The speed of healing of myocardial infarction. A study of the pathologic anatomy in 72 cases. Am Heart J 18:647–671.[CrossRef][ISI]
  22. Fishbein MC, Maclean D, Maroko PR. (1978) The histopathologic evolution of myocardial infarction. Chest 73:843–849.[Free Full Text]
  23. Factor SM and Bache RG. (1994) Pathophysiology of myocardial ischemia. In Schlant RC (Ed.). The Heart 8th ed. (McGraw-Hill, New York, USA) pp. 1033–1053.
  24. Kirtane AJ, Bui A, Murphy SA, Barron HV, Gibson CM. (2004) Association of peripheral neutrophilia with adverse angiographic outcomes in ST-elevation myocardial infarction. Am J Cardiol 93:532–536.[CrossRef][ISI][Medline]
  25. Kloner RA, Giacomelli F, Alker KJ, Hale SL, Matthews R, Bellows S. (1991) Influx of neutrophils into the walls of large epicardial coronary arteries in response to ischemia/reperfusion. Circulation 84:1758–1772.[Abstract/Free Full Text]

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