Association between kaolin-induced maximum amplitude and slow-flow/no-reflow in ST elevation myocardial infarction patients treated with primary percutaneous coronary intervention

Highlights

• Kaolin-induced maximum amplitude was associated with the risk of slow flow/no-reflow in ST-segment elevation myocardial patients who were treated with percutaneous coronary intervention.

• Kaolin-induced maximum amplitude and slow flow/no-reflow both predicted the long-term cardiovascular events risk.

• A high kaolin-induced maximum amplitude level was associated with a significantly increased risk of ischemia events only in ST-segment elevation myocardial patients with slow-flow/no-reflow.

Abstract

Background

ST-segment elevation myocardial infarction (STEMI) patients with a high thrombus burden have a relatively high slow-flow/no-reflow risk. However, the association between kaolin-induced maximum amplitude (MA_thrombin) and slow-flow/no-reflow has been scarcely explored.

Methods

STEMI patients treated with primary percutaneous coronary intervention (PCI) were retrospectively enrolled from January 2015 to December 2019 at China-Japan Friendship Hospital. MA_thrombin levels were measured using thromboelastography before the PCI procedure. The patients were divided into two groups according to thrombolysis in myocardial infarction (TIMI) flow grade after primary PCI: the normal flow group (TIMI flow grade = 3) and slow-flow/no-reflow (TIMI flow grade ≤ 2). The logistic regression model and restricted cubic spline regression (RCS) were used to analyze the predictive value of MA_thrombin for slow-flow/no-reflow. All patients were followed up after discharge and observed the adverse cardiovascular events between the two groups.

Results

A total of 690 patients were enrolled, with 108(15.7%) having slow-flow/no-reflow. The multivariate logistic regression model analysis showed that MA_thrombin level was an independent risk factor for slow-flow/no-reflow. The RCS analysis showed a nonlinear relationship between MA_thrombin levels and slow-flow/no-reflow. The cut-off value of MA_thrombin levels for predicting slow-flow/no-reflow was 68 mm. During a median follow-up time of 4.4 years, slow-flow/no-reflow (hazard ratio 1.93, 95% confidence interval 1.27–2.93, P = 0.002) and MA_thrombin levels (hazard ratio 1.06, 95% confidence interval 1.03–1.08, P < 0.001) were independent risk factors for predicting the long-term of adverse clinical cardiovascular events.

Conclusion

MA_thrombin was an independent risk factor for predicting slow-flow/ no-reflow in STEMI patients who underwent primary PCI.

Introduction

Although the relative incidence of ST elevation myocardial infarction (STEMI) is decreasing, the mortality is still high if patients do not receive immediate treatment [1]. Current guidelines recommend that patients with STEMI receive primary percutaneous coronary intervention (PCI) to re-open the culprit vessel, which can reduce infarct size and improve clinical prognosis [2,3]. However, 10–50% of patients fail to achieve adequate myocardial tissue reperfusion despite an open infarct-related artery [[4], [5], [6]]. This phenomenon was termed slow-flow or no-reflow [6]. STEMI patients with slow-flow/no-reflow have a two-fold higher risk of 5-year mortality than patients with normal flow [2]. Though some dealing with attempts to prevent or alleviate the slow-flow or no-reflow phenomenon have been reported, there is no consensus on how to deal with slow-flow or no-reflow [[7], [8], [9]]. Therefore, exploring the factors that predict the occurrence of slow-flow/no-reflow in patients with STEMI is helpful in adopting early risk stratification and identifying high-risk patients.

The underlying mechanisms of slow-flow/no-reflow are the structural disruption and dysfunction of coronary microcirculation, including the edema of endothelial and myocardial cells, platelet-leukocyte aggregation, microembolization, and impaired microvascular vasomotion [6]. During revascularization procedures, the iatrogenic or spontaneous rupture of an atherosclerotic plaque can be embolized into the coronary microcirculation if the blood flow is restored [10]. Therefore, the intrinsic hemostatic properties may influence the risk of slow-flow/no-reflow, and thrombus aspiration can reduce the occurrence of no-reflow in STEMI patients who undergo PCI [11]. The proper assessment of biological thrombus burden indicators may lower the risk of slow-flow/no-reflow. Previous studies reported that plasma d-dimer and fibrinogen concentrations were elevated in STEMI patients with no-reflow [12,13]. However, these levels were influenced by age and infection status [14]. Studies of the predictive role of d-dimer or fibrinogen in coronary no-reflow have been inconsistent [11,[15], [16], [17]].

The blood coagulation process involves multiple elements, such as platelets, procoagulants, anticoagulants, and fibrinolytic factors. A comprehensive evaluation of the impact of these components on thrombosis will aid in reducing the occurrence of slow blood flow/no-reflow in patients with STEMI. Thromboelastography (TEG) is a whole-blood assay that reveals the dynamic viscoelastic properties of blood clot generation [18]. Kaolin-induced maximum amplitude (MA_thrombin) represents the maximum platelet-fibrin clot strength, which is influenced by platelet count, platelet function, and fibrinogen. MA_thrombin can be used as a biological indicator of the severity of thrombus burden and predict the risk of ischemic events [19,20]. The present study investigated the predictive value of MA_thrombin for slow-flow/no-reflow and clinical prognosis in STEMI patients who underwent primary PCI.