Microvascular obstruction after percutaneous coronary intervention

Lee, Chi‐Hang; Tse, Hung‐Fat

doi:10.1002/ccd.22234

Cited by 16 publications

(13 citation statements)

References 24 publications

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“…Importantly, factors which are known to impact on the development of MVO such as the presence of comorbid conditions, antiplatelet and anticoagulant therapy and MI size were not significantly different between the two treatment groups. MVO results in poor myocardial perfusion despite epicardial coronary artery revascularisation, and its development has been attributed to a variety of factors including distal embolisation, endothelial dysfunction, leucocyte migration and plugging and platelet aggregation 13. The mechanism underlying the increased incidence of MVO following PPCI in the rhEPOβ-treated group in our study is unknown but may be attributed to the increased platelet reactivity and the prothrombotic effects which have been described with rhEPO therapy in healthy subjects and a number of different disease states 14 15.…”

Section: Discussionmentioning

confidence: 99%

Effect of erythropoietin as an adjunct to primary percutaneous coronary intervention: a randomised controlled clinical trial

Ludman

Yellon

Hasleton

et al. 2011

Heart

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Objective The acute administration of high-dose erythropoietin (EPO) on reperfusing ischaemic myocardium has been reported to halve myocardial infarct (MI) size in preclinical studies, but its effect in ST elevation myocardial infarction patients undergoing primary percutaneous coronary intervention (PPCI) remains unknown. We investigated whether high-dose EPO administered as an adjunct to PPCI reduces MI size. Design Double-blinded, randomised, placebo-controlled. Setting Single tertiary cardiac centre. Patients Fifty-one ST elevation myocardial infarction patients undergoing PPCI. Interventions Patients were randomly assigned to receive either a single intravenous bolus of EPO (50 000 IU) prior to PPCI with a further bolus given 24 h later (n¼26) or placebo (n¼25). Main outcome measures MI size measured by 24 h area under the curve troponin T and cardiac magnetic resonance imaging performed on day 2 and at 4 months. Results EPO treatment failed to reduce MI size (troponin T area under the curve: 114.6678 mg/ml EPO vs 100.8668 mg/ml placebo; infarct mass by cardiac magnetic resonance: 33616 g EPO vs 25616 g placebo; both p>0.05). Unexpectedly, EPO treatment doubled the incidence of microvascular obstruction (82% EPO vs 47% placebo; p¼0.02) and significantly increased indexed left ventricular (LV) end-diastolic volumes (84610 ml/m 2 EPO vs 73613 ml/m 2 placebo; p¼0.003), indexed LV end-systolic volumes (4169 ml/m 2 EPO vs 35611 ml/m 2 placebo; p¼0.035) and indexed myocardial mass (89616 g/m 2 EPO vs 79611 g/m 2 placebo; p¼0.03). At 4 months, there were no significant differences between groups. Conclusions High-dose EPO administered as an adjunct to PPCI failed to reduce MI size. In fact, EPO treatment was associated with an increased incidence of microvascular obstruction, LV dilatation and increased LV mass. Clinical Trial Registration Information http://public. ukcrn.org.uk/search/StudyDetail.aspx?StudyID¼4058 Unique Identifier¼Study ID 4058.

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Section: Discussionmentioning

confidence: 99%

Effect of erythropoietin as an adjunct to primary percutaneous coronary intervention: a randomised controlled clinical trial

Ludman

Yellon

Hasleton

et al. 2011

Heart

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“…Clinicians must therefore rely considerably on cardiac biomarkers. However, this is not without difficulties, as a definite cut-off value for prognostic significance has not been established for the present sensitive cardiac biomarkers, and the nature of the association between elevated biomarkers after PCI and prognosis is still under discussion [ 2 , 3 , 15 – 21 ]. The question is whether increased all-cause mortality is caused by acute PCI-related myocardial necrosis or whether the elevations of biomarkers is due to diffuse cTn release functioning as a general indicator of increased risk.…”

Section: Discussionmentioning

confidence: 99%

Incidence and impact on prognosis of peri-procedural myocardial infarction in 2760 elective patients with stable angina pectoris in a historical prospective follow-up study

Christensen

Huang

Torp‐Pedersen

et al. 2016

BMC Cardiovasc Disord

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BackgroundThe clinical significance of myocardial infarction related to treatment with percutaneous coronary intervention (PCI) has been subject of great discussion. This subject has been studied for many years using different definitions of peri-procedural myocardial infarction and different biomarkers, the results have varied greatly depending on methods and time of the study. This study was to determine the incidence and prognostic significance of elevated cardiac biomarkers after elective PCI in patients with stable angina pectoris using the current cut-off set by the Third Universal Definition of Myocardial Infarction and current biomarkers.MethodsWe performed a historical prospective follow-up study of all patients with stable angina pectoris who underwent elective PCI at Aalborg University Hospital, Denmark from January 1st 2000 to December 31st 2012. We stratified patients according to peak post-PCI troponin T (cTnT) and Creatine Kinase MB mass (CK-MBmass).ResultsFollow-up for time to all-cause mortality was mean 5.8 years and total 15,891 years and mean 3.7 years and total 10,160 years for the combined endpoint of all-cause mortality and new onset heart failure. During the follow up period 399 of 2760 patients died (14.5 %) and 1095 (39.7 %) suffered the combined endpoint. Post-PCI concentration of cTnT and CK-MBmass was elevated above the defined cut-off in 419 patients (15.2 %) and 113 patients (4.1 %) respectively. There was no statistically significant difference between the groups in stratified analysis of the hazard rates by time regarding all-cause mortality for cTnT nor CK-MBmass. Regarding the combined endpoint the results were ambiguous. The results were unchanged in multivariable analyses that included age and gender.ConclusionThe incidence of elevated biomarkers after elective PCI in patients with stable angina pectoris using the defined cut-off (>5 x URL) was 15.2 % using cTnT and 4.1 % using CK-MBmass. The independent prognostic value for both cardiac biomarkers of any cut-off showed no statistical significance for all-cause mortality, whereas the combined endpoint (all-cause mortality or new-onset heart failure) were ambiguous in both short- and long-term follow-up.

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“…However, impaired angiographic reflow is seen on some patients' angiographies despite opening up the epicardial coronary vessels in the setting of pPCI. This phenomenon is called no-reflow and is a predictor of poor outcomes [2]. The no-reflow phenomenon may be caused by multiple factors that eventually lead to distal microvascular obstruction and endothelial dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Association of monocyte count on admission with angiographic no-reflow after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction

et al. 2016

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A b s t r a c t Background:The no-reflow phenomenon during primary percutaneous coronary intervention (pPCI) in patients with ST-elevation myocardial infarction (STEMI) can lead to poor outcomes. It has been shown that the monocytes may be involved in the pathogenesis of coronary artery disease and associated with high risk of myocardial infarction. Aim:To assess the relation between admission monocyte count and angiographic no-reflow after pPCI. Methods:A total of 236 patients with acute STEMI, who underwent pPCI, were enrolled. The patients were divided into two groups (no-reflow and normal reflow) based on post-pPCI Thrombolysis in Myocardial Infarction (TIMI) flow grade. No reflow was defined as TIMI flow grades ≤ 2, and normal reflow was defined as TIMI 3 flow grade. The monocyte count and other laboratory parameters were measured on admission before pPCI. Conclusions:Monocyte count on admission and low haemoglobin concentration were independent clinical predictors of no-reflow following pPCI in patients with STEMI. Our findings suggest that admission monocyte count may be available for early risk stratification of no-reflow after pPCI and might allow the improvement of strategies to prevent this phenomenon.

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Microvascular obstruction after percutaneous coronary intervention

Cited by 16 publications

References 24 publications

Effect of erythropoietin as an adjunct to primary percutaneous coronary intervention: a randomised controlled clinical trial

Effect of erythropoietin as an adjunct to primary percutaneous coronary intervention: a randomised controlled clinical trial

Incidence and impact on prognosis of peri-procedural myocardial infarction in 2760 elective patients with stable angina pectoris in a historical prospective follow-up study

Association of monocyte count on admission with angiographic no-reflow after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction

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