Nawsad Saleh

Circulating endothelial and platelet derived microparticles reflect the size of myocardium at risk in patients with ST-elevation myocardial infarction.

OBJECTIVESnMicroparticles (MP) are small membrane vesicles, released from activated, damaged and apoptotic endothelial cells (EMP) or platelets (PMP) that may actively modulate inflammation, coagulation and vascular function. We tested the hypothesis that the number of circulating EMP or PMP in acute myocardial infarction correlates with the myocardium at risk (MaR) and infarct size (IS).nnnMETHODSnEMP were quantified in plasma samples of 36 patients (age: 63±10 years) with first time ST-elevation myocardial infarction (STEMI) using flow cytometry. EMP were defined as CD31(+)/CD42(-) MP and CD144(+) MP and PMP as CD31(+)/CD42(+) MP. MaR and IS was determined by cardiovascular magnetic resonance imaging one week after the index event.nnnRESULTSnPlasma levels of CD31(+)/CD42(-) EMP were 251.0±178.8/μl and CD144(+) 106.3±33.7/μl. PMP levels were 579.2±631.8/μl. MaR was 31.0±11.2% of the left ventricle and IS was 11.4±7.1% of the left ventricle. Patients with STEMI in the left anterior descending artery had higher levels of CD31(+)/CD42(-) EMP and PMP than those with other infarct-related arteries (p<0.05). The numbers of CD31(+)/CD42(-) EMP and PMP correlated to MaR, but not to IS.nnnCONCLUSIONSnCirculating EMP and PMP correlate to the size of MaR in patients with STEMI suggesting that they reflect the severity of the endothelial injury and platelet activation during myocardial ischemia.

Assessment of myocardium at risk with contrast enhanced steady-state free precession cine cardiovascular magnetic resonance compared to single-photon emission computed tomography

BackgroundFinal infarct size following coronary occlusion is determined by the duration of ischemia, the size of myocardium at risk (MaR) and reperfusion injury. The reference method for determining MaR, single-photon emission computed tomography (SPECT) before reperfusion, is impractical in an acute setting. The aim of the present study was to evaluate whether MaR can be determined from the contrast enhanced myocardium using steady-state free precession (SSFP) cine cardiovascular magnetic resonance (CMR) performed one week after the acute event in ST-elevation myocardial infarction (STEMI) patients with total coronary occlusion.ResultsSixteen patients with STEMI (age 64 ± 8 years) received intravenous 99 m-Tc immediately before primary percutaneous coronary intervention. SPECT was performed within four hours. MaR was defined as the non-perfused myocardial volume derived with SPECT. CMR was performed 7.8 ± 1.2 days after the myocardial infarction using a protocol in which the contrast agent was administered before acquisition of short-axis SSFP cines. MaR was evaluated as the contrast enhanced myocardial volume in the cines by two blinded observers. MaR determined from the enhanced region on cine CMR correlated significantly with that derived with SPECT (r2 = 0.78, p < 0.001). The difference in MaR determined by CMR and SPECT was 0.5 ± 5.1% (mean ± SD). The interobserver variability of contrast enhanced cine SSFP measurements was 1.6 ± 3.7% (mean ± SD) of the left ventricle wall volume.ConclusionsContrast enhanced SSFP cine CMR performed one week after acute infarction accurately depicts MaR prior to reperfusion in STEMI patients with total occlusion undergoing primary PCI. This suggests that a single CMR examination might be performed for determination of MaR and infarct size.

Long-term impact of postconditioning on infarct size and left ventricular ejection fraction in patients with ST-elevation myocardial infarction

BackgroundIschemic postconditioning (PostC), reperfusion in brief cycles, is known to induce short-term reduction in infarct size in patients with ST elevation myocardial infarction (STEMI), especially among those with large myocardium at risk (MaR). The aim of the present study was to investigate the long-term effect of PostC on infarct size and left ventricular ejection fraction (LVEF).MethodsSixty-eight patients with a first STEMI were randomised to primary percutaneous coronary intervention (PCI) (nu2009=u200935) or PCI followed by PostC (nu2009=u200933). MaR was determined as abnormally contracting segments on left ventricular angiogram. Cardiac magnetic resonance was performed at 3 and 12xa0months for the determination of infarct size and LVEF.ResultsOverall there was no difference in infarct size expressed in percentage of MaR between patients randomised to the control (31%; 23, 41) and PostC (31%; 23, 43) groups at 12xa0months. Likewise there was no difference in LVEF between control (49%; 41, 55) and PostC (52%; 45, 55). In contrast, patients in the PostC group with MaR in the upper quartile had a significantly smaller infarct size (29%; 18, 38) than those in the control group (40%; 34, 48; pu2009<u20090.05) at 12xa0months. In these patients LVEF was higher in the PostC (47%; 43, 50) compared to the control group (38%; 34, 42; pu2009<u20090.01).ConclusionsIn this long-term follow-up study PostC did not reduce infarct size in relation to MaR or improved LVEF in the overall study population. However, the present data suggest that PostC exerts long-term beneficial effects in patients with large MaR thereby extending previously published short-term observations.Trial registrationKarolinska Clinical Trial Registration (http://www.kctr.se). Unique identifier: CT20080014

Effects of Myocardial Postconditioning on the Recruitment of Endothelial Progenitor Cells.

BACKGROUNDnIschemic postconditioning (PostC), brief repetitive cycles of ischemia and reperfusion during early reperfusion, is suggested to protect the myocardium in patients with stent thrombosis-elevation myocardial infarction (STEMI) by improved endothelial dysfunction and alteration of cytokine release. These mechanisms are also of importance for the recruitment of endothelial progenitor cells (EPC), an endogenous repair mechanism for re-endothelialization and neoangiogenesis. The aim of this study was to investigate the effect of PostC on recruitment of EPC.nnnMETHODSnEPC were analyzed in 20 patients with STEMI randomized to receive four cycles of PostC following percutaneous coronary intervention (PCI) or conventional PCI. Different subpopulations of EPC were quantified immediately and on day 4 using flow cytometry. Myocardium at risk, and infarct size was determined by cardiovascular magnetic resonance.nnnRESULTSnThere was no influence of PostC on the number of different EPC (CD34(+) , CD133(+) , CD34(+) CD133(+) , CD34(+) KDR(+) , CD34(-) CD133(+) KDR(+) , CD34(+) CD133(+) KDR(+) ). Left ventricular ejection fraction, myocardium at risk, and infarct size did not correlate to the mobilization of EPC. There was an inverse correlation between the symptom-to-balloon time and the mobilization of progenitor precursor cells (CD34(+) cells: R =-0.527, P = 0.02; CD133(+) cells: R =-0.624, P = 0.004; CD34(+) CD133(+) cells: R =-0.466, P = 0.04).nnnDISCUSSIONnIschemic PostC did not result in improved mobilization of EPC in STEMI patients. The recruitment of progenitor cells seems to be related to the duration of ischemia rather than the size of the ischemic myocardial area. More effort is needed to understand the changes of endothelial surface markers by PostC and their role in EPC recruitment and homing.

Femoral access-related complications during percutaneous transcatheter aortic valve implantation comparing single versus double Prostar XL device closure.

To evaluate the efficacy and safety of a double Prostar XL suture‐based closure technique compared to a conventional single Prostar XL technique in elective transcatheter aortic valve implantation (TAVI) via the common femoral artery.

Comparison of effects of a thrombin-based femoral artery closure device with those of a mechanical compression device on serum C-reactive protein and amyloid A after percutaneous coronary intervention

The present study evaluates whether the closing procedure of the femoral artery after percutaneous coronary intervention influences the degree of inflammation related to the procedure as measured by C-reactive protein (CRP) and serum amyloid A (SAA). A thrombin-based device (Duett sealing device) was compared with a mechanical compression device (FemoStop).

Platelet function and myocardial injury during percutaneous coronary intervention.

AbstractBackground: Several studies have shown that inhibition of the glycoprotein IIb/IIIa receptor can reduce myocardial injury during percutaneous coronary intervention (PCI). The present study was performed to investigate platelet function, using a bedside diagnostic system, to test the hypothesis that patients with activated platelets have an increased risk for myocardial injury during PCI. Such information would be valuable to guide the PCI operator to whom he or she should give a glycoprotein IIb/IIIa inhibitor during and after the procedure.nMethods: 155 consecutive patients undergoing PCI were included in the study. 94 of the patients had stable angina pectoris and the remaining patients had unstable angina pectoris or ongoing myocardial infarction. Troponin T levels were measured in serum before PCI and at 6 am the day after PCI by an immunoassay. Platelet function was analyzed in arterial blood before PCI using the platelet function analyzer PFA-100® by Dade Behring.nResults: The platelet function analyzer PFA-100® could not discriminate between patients with or without myocardial injury during the procedure but between patients with or without acetyl salicylic acid.nConclusion: The platelet function analyzer PFA-100® cannot be used to guide the PCI operator to whom he or she should give a glycoprotein IIb/IIIa inhibitor but the results indicate that PFA-100® can be used to monitor platelet effects of ASA therapy.

A Path to Avoid during Transcatheter Aortic Valve Implantation: Case Report

Collateral pathways in vascular disease are important natural bypass conduits that protect against ischemia. Endovascular diagnostic and therapeutic procedures via peripheral access sites are performed frequently. This case report underlines the importance of being aware of collateral circulation in patients with chronic aortoiliac occlusive disease undergoing subclavian transcatheter aortic valve implantation to avoid acute limb ischemia. (©) RSNA, 2016.

The predictive value of inflammatory activity and markers of the adipo-insular axis on restenosis in patients with type 2 diabetes

Aims: Patients with type 2 diabetes (T2DM) have a high restenosis rate after percutaneous coronary intervention (PCI). This study investigated whether markers of inflammation and the adipo-insular axis associated with T2DM and poor metabolic control were able to predict restenosis after PCI in T2DM patients. Methods and results: The predictive value of traditional and non-traditional risk markers, including IL-1β, IL-6, TNF-α, hsCRP, interferon gamma, leptin, IGF-I, insulin, proinsulin and NT-proBNP, was investigated in 82 patients with T2DM. A re-angiography 6 months after the index percutaneous coronary intervention (PCI) revealed that 43% of the patients had a restenosis. In a multiple regression analysis, the only independent predictors of restenosis were fasting glucose before the PCI and previous myocardial infarction (odds ratio [OR] 1.44, 95% confidence interval [CI] 1.07—1.92; p = 0.015 and OR 8.00, 95% CI 2.49—25.67; p ≤ 0.001, respectively). None of the other markers remained as significant predictors. Conclusion: Fasting glucose prior to the PCI was an independent predictor of restenosis in patients with T2DM while analyses of a variety of markers related to inflammation and the adipo-insular axis did not add any further information.

Myocardium at risk with contrast enhanced SSFP compared to myocardial perfusion SPECT

Methods Sixteen patients with STEMI (age 64 ± 8 years) received intravenous 99 m-Tc immediately before primary percutaneous coronary intervention. A SPECT investigation was performed within four hours. MaR was defined as the non-perfused myocardial volume on SPECT. Magnetic resonance imaging (MRI) was performed 7.8 ± 1.2 days after the myocardial infarction using a protocol in which the contrast agent was administered before acquisition of short-axis cine images. MaR was evaluated as the contrast enhanced myocardial volume in cine SSFP by two blinded observers. Results MaR determined from the enhanced region on cine SSFP correlated significantly with that derived with SPECT (r2 = 0.78, p < 0.001). The difference in MaR determined by MRI and SPECT was 0.5 ± 5.1% (mean ± SD). The interobserver variability of contrast enhanced cine SSFP measurements was 1.6 ± 3.7% (mean ± SD) of the left ventricle wall volume Figures 1 and 2.