Hemorrhagic and vascular complications are rarely seen during TRC. However, majority of these complications could be managed conservatively without a requirement for surgical reconstruction.
Objective. The most important step in the treatment of ST elevation myocardial infarction is to sustain myocardial blood supply as soon as possible. The two main treatment methods used today to provide myocardial reperfusion are thrombolytic therapy and percutaneous coronary intervention. In our study, reperfusion arrhythmias were investigated as if they are indicators of coronary artery patency or ongoing ischemia after revascularization. Methods. 151 patients with a diagnosis of acute ST elevation myocardial infarction were investigated. 54 patients underwent primary percutaneous coronary intervention and 97 patients were treated with thrombolytic therapy. The frequency of reperfusion arrythmias following revascularization procedures in the first 48 hours after admission was examined. The relation between reperfusion arrhythmias, ST segment regression, coronary artery patency, and infarct related artery documented by angiography were analyzed. Results. There was no statistically significant difference between the two groups in the frequency of reperfusion arrhythmias (P = 0.355). Although angiographic vessel patency was higher in patients undergoing percutaneous coronary intervention, there was no significant difference between the patency rates of each group with and without reperfusion arrythmias. Conclusion. Our study suggests that recorded arrhythmias following different revascularization procedures in acute ST elevation myocardial infarction may not always indicate vessel patency and reperfusion. Ongoing vascular occlusion and ischemia may lead to various arrhythmias which may not be distinguished from reperfusion arrhythmias.
Objective: Patients with resistant hypertension are at increased risk for cardiovascular events. Mean platelet volume (MPV) is an accepted biomarker of platelet activation and considered as a risk factor for cardiovascular disease. The aim of this study was to determine whether MPV levels are higher in resistant hypertensive (RHTN) patients than in controlled hypertensive (CHTN) patients and healthy normotensive controls.
Materials and Methods
Results:The mean platelet volume levels were significantly higher in RHTN group than in the CHTN and normotensive groups (p<0.001). In correlation analysis office systolic and diastolic blood pressure was positively correlated with MPV.
Conclusion:Our study demonstrated that MPV, as an important indicator of platelet activation, was statistically higher in RHTN patients than in CHTN and in normotensive subjects. Elevated MPV levels may help to determine a high risk group for atherosclerosis in RHTN patients. Bulgular: Dirençli hipertansif grupta ortalama trombosit hacmi kontrollü hipertansif ve normotansif gruba göre istatistiksel olarak anlamlı olarak yüksek saptanmıştır (p<0,001). Korelasyon analizinde ofis sistolik ve diastoliktansiyonları ortalama trombosit hacmiyle pozitif korelasyon göstermekteydi.
KeywordsSonuç: Çalışmamızda trombosit aktivasyonunun önemli belirteci olan ortalama trombosit hacmi dirençli hipertansif hastalarda diğer gruplara gore anlamlı olarak yüksek saptanmıştır. Artmış ortalama trombosit hacminin dirençli hipertansif hastalarda atheroskleroz açısından yük-sek riskli olanları değerlendirmede kullanılabileceği düşünülmektedir.Anahtar Kelimeler: Dirençli hipertansion, ortalama trombosit hacmi, kontrollü hipertansiyon
The present study aimed to evaluate the late-term changes in radial artery luminal diameter (RAD) and vasodilatation response following transradial catheterization (TRC). TRC-inducing trauma to radial artery intima may trigger chronic phase vascular changes and lead to anatomical and functional impairment. There is controversial data whether the impairment persists or repairs later. Fifty-six consecutive patients undergoing TRC were enrolled prospectively. Baseline RAD, flow-mediated dilatation (FMD) and nitroglycerin-mediated dilatation (NMD) of the radial artery at the access site were measured before TRC by high-resolution ultrasound. Six months later; RAD, FMD and NMD were measured again at the same access site. RAD at the sixth month was reduced compared with pre-procedural measurements (2.85 ± 0.44 versus 2.74 ± 0.42 mm, p = 0.0001).The average FMD decreased to 5.66 ± 5.87 %, which was significantly lower than the observed pre-procedural FMD (9.45 ± 5.01 %) 6 months after TRC (p = 0.0001). Likewise, the average NMD at the sixth month was reduced compared with pre-procedural NMD (9.52 ± 6.77 versus 6.64 ± 6.51 %, p = 0.018). Logistic regression analysis indicated that pre-procedural radial artery diameter to sheath size ratio was the independent predictor of NMD reduction (95 % confidence interval, β = -9.74, p = 0.024). TRC may lead to a significant luminal diameter reduction and impairment of vasodilatation response in the radial artery at late term.
Objectives: Although heparin is highly effective in reducing the rate of radial artery occlusion after transradial catheterization, the optimal heparin dose is still controversial. The aim of this study was to evaluate the efficacy and safety of two different heparin doses during transradial coronary angiography. Methods: 490 consecutive patients undergoing transradial coronary angiography were prospectively enrolled into this double-blind randomized trial. A total of 202 patients enrolled in the low-dose (LD; 2,500 U of heparin) group and 202 patients enrolled in the high-dose (HD; 5,000 U of heparin) group were included in the final analysis. The primary endpoint of the study was radial artery occlusion. Bleeding and hematomas were the secondary outcome measures. Results: At day 7, radial artery occlusion occurred in 5.9% of the patients in the LD group and in 5.4% of the patients in the HD group (p = 0.83). Bleeding during deflation of the transradial band occurred in 6.4% of the patients in the LD group and in 18.3% of the patients in the HD group; the difference was statistically significant (p < 0.001). Higher-dose heparin was found to be an independent predictor of bleeding (p = 0.007). Conclusion: A lower dose of heparin (i.e. 2,500 U) decreases bleeding during transradial band deflation without an increase in radial artery occlusion.
Platelet volume is a marker of platelet function and activation. An elevated mean platelet volume (MPV) is associated with acute coronary syndromes (ACS). Recurrent cardiovascular events were found to be higher in patients with aspirin resistance. In this study, we investigated the effect of MPV on prognosis of patients with and without aspirin resistance by PFA-100 in settings of non-ST-segment elevated ACS. Two hundred and twenty patients with ACS were followed for an average of 14.86 +/- 5.93 months for the occurrence of death, myocardial infarction (MI) and revascularization. Aspirin effect on platelet function was assessed by PFA-100. According to MPV value and aspirin resistance status, patients were divided into four groups. Group 4 (with an elevated MPV and aspirin resistance) was significantly associated with worse prognosis for composite endpoint (death, MI and revascularization), death and MI (for all, log-rank P < 0.0001). Multivariate analysis showed that presence of an elevated MPV and aspirin resistance was an independent predictor of composite endpoint [hazard ratio 8.21, 95% confidence interval (CI) 3.48-19.35, P < 0.0001], death (hazard ratio 5.48, 95% CI 1.62-18.53, P = 0.006) and MI (hazard ratio 4.44, 95% CI 1.57-12.58, P = 0.005). Presence of an elevated MPV and aspirin resistance was significantly associated with death, MI and the composite endpoint, due to the lack of beneficial effect of aspirin on activated platelets. Patients with ACS, especially in the presence of an elevated MPV may benefit from the evaluation of aspirin resistance for risk stratification.
The results of this study suggest that a high sCD40L level at admission is associated with increased in-hospital and 1-year all-cause mortality rates in patients with STEMI undergoing primary PCI.
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