Clinical and procedural predictors of suboptimal myocardial reperfusion in primary percutaneous coronary intervention

Abstract

Background Suboptimal myocardial perfusion in primary PCI is associated with increased infarct size, left ventricular (LV) dysfunction and higher mortality rates as compared as those with optimal myocardial perfusion. We identified clinical and procedural predictors of suboptimal myocardial reperfusion as judged by myocardial plush grade (MBG) in primary PCI. Methods and Results 100 patients with acute STEMI who underwent primary PCI were prospectively subjected to clinical, ECG, laboratory and angiographic evaluation. Patients were classified into: Optimal myocardial reperfusion group: (n=73) who had final MBG=3. Suboptimal myocardial reperfusion group: (n=27) who had persistent final MBG ≤ 2. Suboptimal myocardial reperfusion group had statistically significant little history of angina prior to MI 5 (18.5%) vs 44 (60.3%), little current aspirin intake 6(22%) vs 38 (52% ), increased blood sugar on admission (240 ± 101 mg/dl vs 171 ± 72 mg/dl), increased total leucocytic count on admission (12.1 ± 3.6 vs 10.2 ± 3.3) 103/mm3, longer reperfusion time (6.1 ± 2.8 vs 4.3 ± 2.1 h ), higher thrombus burden 12 (44.4 % ) vs 13 (17.8 %), higher predilatation pressure (16 ± 2.3 vs 14 ± 1.8 ATM), repeated balloon inflation during predilatation 24 (92.3 % ) vs 46 (69.7%) as compared optimal myocardial reperfusion group, (P < 0.05 for all). Conclusion Longer reperfusion time, repeated balloon inflations, high predilatation pressure> 15 ATM , high thrombus burden, neither history of angina nor aspirin intake prior to AMI, high total leucocytic count > 10103/mm3 and high blood glucose level > 160mg/dl were predictors for persistent suboptimal myocardial reperfusion in primary PCI.

No-reflow phenomenon in acute myocardial infarction: Relieve pressure from the procedure and focus attention to the patient

“…Interestingly, no lesion and pharmacological associations were documented. Recently, a study of Mahmoud et al [8] confirmed the importance of clinical and serological no-reflow predictors: among these, the authors described a high thrombus burden, a high total leucocytes count (>10,103/mm 3 ), a high blood glucose level (>160 mg/dl) and a delayed reperfusion. In conjunction, also some procedural variables (repeated balloon inflations and high predilatation pressure) were associated with the incidence of no-reflow.…”

Predictors of No-Reflow Phenomenon in Primary Percutaneous Coronary Intervention among Patients with Acute Myocardial Infarction

“…Analysis from a cohort of 781 PCI patients highlighted the prevalence of no-reflow among the elderly, those with significant thrombus burden, and cases with delayed (>4 hours) presentation post-symptom onset, emphasizing the absence of direct correlations with specific lesions or medication effects. Recent evidence also points to the importance of clinical and serological markers, including substantial thrombus Figure 1 Male Gender and No-Reflow load, elevated leukocyte count, high blood glucose levels, and delayed reperfusion, as predictors of no-reflow, alongside procedural factors like repeated balloon inflations and high predilatation pressure (19). The association of atrial fibrillation with a doubled risk of no-reflow in STEMI patients suggests potential preventative measures, such as strict glycemic control in diabetics and aggressive statin therapy for hyperlipidemia, to mitigate the risk of no-reflow.…”

A Clinical Score to Predict “Corrected Thrombolysis in Myocardial Infarction Frame Count” in Patients With ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

“…24-29,33 Ischemic time is another indicator for prognosis. 24,25,28,29,33 Prolonged ischemia is associated with microvascular damage, which is the main factor predisposing to impaired epicardial perfusion. 28,34 High serum cholesterol levels and DM were associated with impaired epicardial blood flow in previous studies.…”

“…28,34 High serum cholesterol levels and DM were associated with impaired epicardial blood flow in previous studies. 25,26 DM is known to be associated with endothelial dysfunction. 35 One of the underlying mechanisms of endothelial dysfunction in DM is the non-enzymatic glycation of proteins followed by altered redox potentials in the cells leading to increased inflammation.…”