Increased Platelet-leukocyte Aggregates Are Associated With Myocardial No-reflow in Patients With ST Elevation Myocardial Infarction.

OBJECTIVE: We aimed to investigate the association between platelet-leukocyte aggregates (PLA) levels on admission and the risk of myocardial no-reflow in patients with ST elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (PCI). METHODS: A total of 83 patients with STEMI undergoing primary PCI were included in the current study. Platelet-leukocyte conjugates (PLA), including platelet-monocyte aggregates (PMA), platelet-neutrophil aggregates (PNA) and platelet-lymphocyte aggregates were studied by flow cytometry in peripheral venous blood. No-reflow was defined as coronary blood flow grade thrombolysis in myocardial infarction ≤2 or thrombolysis in myocardial infarction 3 and myocardial blush grade ≤2. RESULTS: No-reflow was observed in 19 patients (22.9%). Compared with the reflow group, the level of PNA (76.5 ± 13.3) and PMA (90.3 ± 5.2) before PCI no-reflow group was significantly higher than that in normal reflow (P < 0.001). Using multiple logistic regression analysis, PNA (odds ratio [OR] = 1.179; 95% CI: 1.035-1.342; P = 0.013) and PMA (OR = 1.248; 95% CI: 1.040-1.498; P = 0.017) were found to be a significant predictor of no-reflow together with pain to balloon time (OR = 1.022; 95% CI: 1.002-1.041; P = 0.028), estimated glomerular filtration rate (OR = 1.311; 95% CI: 1.009-1.856; P = 0.047) and higher thrombus burden (OR = 0.061; 95% CI: 0.006-0.658; P = 0.021). Receiver operating characteristic curve analysis revealed that PNA (area under the curve = 0.881; 95% CI: 0.809-0.952; P < 0.001), PMA (area under the curve = 0.794; 95% CI: 0.699-0.889; P < 0.001) have important predictive value for the myocardial no-reflow. CONCLUSIONS: Our study indicated that preprocedural increased PLA levels display a significantly independent association with no-reflow phenomenon after PCI. Increased PLA levels may predict the development of no-reflow phenomenon in patients with STEMI who underwent PCI.

Association of lymphocyte-to-monocyte ratio with the no-reflow phenomenon in patients who underwent a primary percutaneous coronary intervention for ST-elevation myocardial infarction.

BACKGROUND: Recently, it has been shown that the lymphocyte-to-monocyte ratio (LMR) is a novel inflammatory marker. A decreased LMR is associated significantly with a high risk for vascular endpoints in patients with peripheral arterial disease. We aimed to investigate whether LMR on admission is associated with no-reflow after a primary percutaneous coronary intervention (PCI) in patients with ST-elevation myocardial infarction (STEMI). PATIENTS AND METHODS: A total of 857 patients (mean age 58.9±13.1 years, 75.6% men), who were admitted to our hospital for STEMI and undergoing primary PCI within 12 h of onset of symptoms, were recruited. LMR was calculated by dividing the lymphocyte count by the monocyte count. The patients were divided into two groups according to the postprocedural thrombolysis in myocardial infarction (TIMI) flows: no-reflow and normal-reflow. No-reflow was defined as a final TIMI flow of 2 or less or final TIMI flow of 3 with a myocardial blush grade of less than 2. RESULTS: Admission LMR levels were significantly lower in patients with no-reflow than in patients with normal-reflow (1.85±1.01 vs. 3.64±1.74, P<0.001). A receiver-operating characteristic analysis indicated that an LMR value of less than 2.292 and had a 76.3% sensitivity and a 72.5% specificity in predicting no-reflow. Multivariate analysis showed that LMR less than 2.292 [odds ratio (OR) 2.657, P=0.030], Killip class at least 2 at admission (OR 3.442, P=0.039), baseline infarct artery patency (OR 0.260, P=0.004), neutrophil count (OR 1.213, P=0.002), and total stent length (OR 1.059, P=0.001) were independent factors for predicting no-reflow. CONCLUSION: Our results suggested that LMR could be a simple and useful marker to predict high risk of patients for no-reflow in patients with STEMI who underwent primary PCI.

The neutrophil to lymphocyte ratio was associated with impaired myocardial perfusion and long term adverse outcome in patients with ST-elevated myocardial infarction undergoing primary coronary intervention.

OBJECTIVES: In the present study we aimed to reveal any probable correlation between neutrophil-to-lymphocyte ratio (N/L ratio) and the occurrence of no-reflow, along with assessment of the prognostic value of N/L ratio in patients with ST-segment elevation myocardial infarction (STEMI). BACKGROUND: The N/L ratio stands practically for the balance between neutrophil and lymphocyte counts in the body, which can also be utilized as an index for systemic inflammatory status. METHODS: In our study, we included 204 consecutive patients suffering from STEMI who underwent primary percutaneous coronary intervention (PCI). Patients with STEMI were assigned into distinct tertiles based on their N/L ratios on admission. No-reflow encountered following PCI was evaluated through both angiography [Thrombolysis in Myocardial Infarction (TIMI) flow and myocardial blush grade (MBG)] and electrocardiography (as ST-segment resolution). RESULTS: Patients featured with no ST-resolution were documented to have displayed significantly higher N/L ratio on admission compared to those with intermediate or complete ST-segment resolution. The number of the patients characterized with no-reflow, evident both angiographically (TIMI flow ≤ 2 or TIMI flow 3 with final myocardial bush grade ≤ 2 after PCI) and electrocardiographically (ST-resolution <30%), was encountered to depict increments throughout successive N/L ratio tertiles. Moreover, the same also held true for three-year mortality rates across the tertile groups (9% vs. 15% vs. 35%, p < 0.01). Multivariable logistic regression analysis disclosed that N/L ratio on admission stood for a significant indicator for long-term mortality in patients with no-reflow phenomenon detected with MBG. Elevated N/L ratio on admission was also found to be a significant indicator for three-year mortality and major adverse cardiac events. CONCLUSIONS: In patients with STEMI who underwent primary PCI, elevated N/L ratios on admission were revealed to be correlated with both no-reflow phenomenon and long-term prognosis.

Clinical analysis of the risk factors of slow coronary flow.

Slow coronary flow (SCF) phenomenon is a coronary microvascular disorder characterized by the delayed passage of contrast in the absence of obstructive epicardial coronary disease, and is an important clinical entity because it may be the cause of precordial pain when the body is at rest and/or during exercise. Although clinical and pathological features of SCF have been previously described, its etiopathogenesis remains unclear. The present study aims to investigate the risk factors of slow coronary flow, in order to provide the foundation for further exploration of potential mechanisms of SCF. A total of 47 consecutive patients with documented slow coronary flow, and 33 patients with normal coronary flow--as defined by TIMI frame count (TFC)--were recruited for this study. Clinical information was collected, and biochemical indicators including high-sensitivity C-reactive protein (hs-CRP), and a marker of systemic inflammation were detected. Logistic regression analysis was performed for statistical analysis. SCF patients had a higher level of serum uric acid (323.2 ± 79.3 vs. 282.8 ± 82.4 µmol/l, p = 0.03), 2-h postprandial blood glucose (8.6 ± 2.7 vs. 7.5 ± 1.8 mmol/l, p = 0.04), platelet count (165.9 ± 51.6 × 10(3) vs. 127.0 ± 32.0 × 10(3) cells/µl, p = 0.0003) and hs-CRP (3.4 ± 0.8 vs. 2.0 ± 0.9 mg/l, p < 0.0001) than those of patients in the control group. No marked differences in other variables were observed between the two groups. Logistic regression showed serum uric acid level (χ(2) = 3.84, ß = 0.007, p = 0.049), 2-h postprandial blood glucose (χ(2) = 5.02, ß = 0.277, p = 0.025) and blood platelet count (χ(2) = 12.16, ß = 0.026, p = 0.001) were independent predictors of SCF. When hs-CRP was included in the multivariate model, hs-CRP (χ(2) = 21.19, ß = 1.90, p < 0.0001) was the only independent predictor of SCF. These findings suggested that an elevation of serum uric acid level, 2-h postprandial blood glucose, and blood platelet count might be the causes of SCF, and inflammation was likely to be implicated in the causal pathway leading to SCF.