Hakan Taşolar

Increased Platelet Distribution Width Is Associated With ST-Segment Elevation Myocardial Infarction and Thrombolysis Failure

We investigated 2 hypotheses: (1) a relationship between platelet indices and stable coronary artery disease (CAD) and acute ST-segment elevation myocardial infarction (STEMI) and (2) a relationship between platelet indices on admission and thrombolysis outcomes in patients with STEMI. A total of 260 patients were enrolled. The white blood cell (WBC) and platelet distribution width (PDW) were found to be increased in patients with STEMI (P for both < .001). White blood cell and PDW were independent predictors of acute STEMI. Mean platelet volume (MPV) and PDW were significantly higher in the thrombolysis failure group than in the thrombolysis success group (9.9 ± 1.8 vs 9.2 ± 1.5 fL, P = .021 and 17.7 ± 1.0 vs 16.4 ± 2.1 fL, P < .001, respectively). Mean platelet volume and PDW were independent predictors of thrombolysis failure. Patients with acute STEMI had higher PDW than did patients with stable CAD. In addition, higher PDW and MPV seem to correlate with thrombolysis failure in patients with STEMI.

Prediction of Coronary Artery Disease Severity Using CHADS2 and CHA2DS2-VASc Scores and a Newly Defined CHA2DS2-VASc-HS Score

As the CHADS2 and CHA2DS2-VASc scores include similar risk factors for the development of coronary artery disease (CAD), they may provide crucial information regarding the severity of coronary artery lesions and the risk of thromboembolism. To increase the likelihood of determining CAD severity, we formulated the CHA2DS2-VASc-HS score comprising hyperlipidemia and smoking in addition to the components of the CHA2DS2-VASc score and male instead of female gender. We aimed to investigate whether these 3 risk scores can be used to predict CAD severity. A total of 407 consecutive patients who underwent coronary angiography were enrolled in the study. Presence of >50% stenosis in a coronary artery was assessed as significant CAD. Of the patients, 87 had normal coronary angiograms and served as group 1. The remaining 320 patients with coronary stenosis were further classified into 2 groups according to CAD with stenosis of <50% or ≥50%: 123 patients with mild CAD as group 2 and 197 patients with severe CAD as group 3. The CHADS2, CHA2DS2-VASc, and CHA2DS2-VASc-HS scores were significantly different among the 3 groups. The CHADS2, CHA2DS2-VASc, and CHA2DS2-VASc-HS scores correlated significantly with the number of diseased vessels (r = 0.406, p <0.001; r = 0.308, p <0.001; and r = 0.533, p <0.001, respectively) and the Gensini score (r = 0.383, p <0.001; r = 0.300, p <0.001; and r = 0.500, p <0.001, respectively). The CHA2DS2-VASc-HS score was found to be the best scoring scheme to predict CAD severity in the area under the curve comparison of these scoring systems. For prediction of severe CAD, the cut-off value of CHA2DS2-VASc-HS score was >2 with a sensitivity of 85.2% and a specificity of 57.5% (area under the curve 0.802, 95% confidence interval 0.760 to 0.839, p <0.001). In conclusion, our findings suggest that the CHADS2, CHA2DS2-VASc, and especially CHA2DS2-VASc-HS scores could be considered predictive of the risk of severe CAD.

Effect of smoking on Tp-e interval, Tp-e/QT and Tp-e/QTc ratios as indices of ventricular arrhythmogenesis.

BACKGROUNDnSmoking may lead to ventricular arrhythmias and sudden cardiac death via altering ventricular recovery time dispersion indices such as QT interval and QT dispersion (QTd). The Tp-e/QT and Tp-e/QTc ratios are also known as predictors of ventricular arrhythmogenesis. The aim of this study was to evaluate the relationship between cigarette smoking and ventricular repolarisation dispersion using these novel electrocardiographic parameters.nnnMETHODSnOne hundred and twenty-one chronic smokers and 70 age- and sex-matched non-smoker controls were included in our study. The Tp-e interval and Tp-e/QT ratio were measured by 12-lead electrocardiogram, and corrected for heart rate.nnnRESULTSnQTd (34.2 ± 8.4, 27.2 ± 10.4, P<0.001) and corrected QTd (37.3 ± 8.9, 29.8 ± 11.2, P<0.001) were significantly increased in the smokers compared to the non-smoker control group. The Tp-e interval (76.5 ± 6.3, 70.3 ± 6.8, P<0.001), cTp-e interval (83.5 ± 8.0, 77.1 ± 8.7, P<0.001), Tp-e/QT (0.20 ± 0.03, 0.19 ± 0.02, P<0.001) and Tp-e/QTc ratios (0.19 ± 0.02, 0.17 ± 0.02, P<0.001) were increased in the patient group when compared to the controls. Significant positive correlations were also found between the level of smoking with the cTp-e interval (r=0.836, P<0.001), and Tp-e/QT (r=0.714, P<0.001) and Tp-e/QTc ratios (r=0.448, P<0.001).nnnCONCLUSIONnWe found in our study that cTp-e interval, Tp-e/QT and Tp-e/QTc ratios were increased in smokers and significantly correlated to the amount of smoking.

Is atrial fibrillation a risk factor for contrast-induced nephropathy in patients with ST-elevation myocardial infarction?

BACKGROUNDnContrast-induced nephropathy (CIN) is an iatrogenic problem in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). Atrial fibrillation (AF) may also contribute to impaired kidney function. Several factors may contribute to the development of CIN. In patients with STEMI, concomitant AF is associated with higher in-hospital/follow-up mortality and morbidity. Therefore, we aimed to investigate the relationship between AF and CIN developments.nnnMETHODSnIn this study, 650 consecutive STEMI patients treated with PPCI were enrolled. Patients with AF at admission who did not achieve a sinus rhythm during 48h after hospitalization were defined as AF patients. CIN was defined by an increase in serum creatinine by >25% or 0.5mg/dL within 72h following contrast media exposure.nnnRESULTSnOur patients were divided into two groups based on whether they had AF, and although warfarin usage was different, the other parameters were similar between the groups. When our patients were grouped according to CIN development [group 1: CIN (+), group 2: CIN (-)], creatinine levels prior to PPCI (p=0.020), estimated glomerular filtration rate (eGFR) prior to PPCI (p<0.001), left ventricular ejection fraction (LVEF) (p=0.011), AF (p<0.001), and warfarin usage (p=0.016) were different between the two groups. We also performed multivariate logistic regression analyses and found that AF [odds ratio (OR), 6.945; 95% confidence interval (CI), 2.789-17.293; p<0.001], eGFR (OR, 0.973; 95% CI, 0.957-0.989; p=0.001), and LVEF (OR, 0.963; 95% CI, 0.935-0.991; p=0.010) independently predicted CIN development in patients with STEMI.nnnCONCLUSIONSnThe risk factors for CIN are multifactorial and identifying high-risk patients is the most important step for prevention. In addition to traditional risk factors, AF can contribute to CIN development in patients with STEMI.

Endothelial nitric oxide synthase levels and their response to exercise in patients with slow coronary flow

Summary Background Endothelial dysfunction plays a key role in the aetiopathogenesis of slow coronary flow (SCF) even if there is no obstructive epicardial lesion. Reduced plasma levels of endothelial nitric oxide synthase (eNOS) are an important indicator of endothelial dysfunction. We aimed to determine plasma levels of eNOS and their relationship with exercise in patients with SCF. Methods Twenty-two patients with SCF in at least one coronary artery and 17 healthy individuals were included in this study. The TIMI frame count method was used to determine SCF. Plasma levels of eNOS before and after effort were determined in the patient and control groups. Results Basal eNOS levels in the patient group were lower than in the control group (p = 0.040), and plasma eNOS levels after exercise decreased more significantly in the patient group compared to the control group (p = 0.002). Median decreases of eNOS in response to exercise were higher in the SCF group than in the control group (p < 0.001), and the decrease observed in the control group was not statistically significant (p = 0.35). There were significantly negative correlations between TIMI frame count and plasma levels of eNOS at baseline and after exercise (r = –0.51, p = 0.015, r = –0.58, p = 0.005, respectively). Moreover, there was also a positive correlation between the rate–pressure product and plasma levels of eNOS after exercise in patients with SCF (r = 0.494, p = 0.019). Conclusion Our findings indicate an important pathophysiological relationship between the severity of SCF in which endothelial dysfunction plays a role in its pathogenesis and the level of circulating plasma levels of eNOS.

The association of serum albumin with coronary slow flow

SummaryBackgroundA number of inflammatory markers such as high-sensitivity C-reactive protein (Hs-CRP), interleukin-6 (IL-6), and fibrinogen have been shown to be associated with coronary slow flow (CSF). Our aim was to investigate the relationship between albumin, a long-acting negative acute-phase protein, and CSF.MethodsA total of 106 patients with angiographically proven slow coronary flow and 57 control subjects with normal coronary flow were included in the study. Serum levels of Hs-CRP and albumin were measured. CSF was defined by Thrombolysis In Myocardial Infarction (TIMI) frame count (TFC) method.ResultsSerum albumin (s-albumin) was significantly lower in the CSF group (3.79u2009±u20090.3 vs 4.17u2009±u20090.3, pu2009<u20090.001), whereas Hs-CRP level was significantly higher in the CSF group compared with the controls (1.22u2009±u20090.79 vs 0.76u2009±u20090.44, pu2009<u20090.001). S-albumin and Hs-CRP were correlated with the mean TFC in the whole study population (r=u2009−u20090.574, pu2009<u20090.001; ru2009=u20090.376, pu2009<u20090.001, respectively). Hs-CRP and low s-albumin were found to be significant predictors of CSF in the multivariate analysis. The comparison of receiver-operating characteristics curves for s-albumin and Hs-CRP demonstrated that s-albumin was the strongest predictor of CSF.ConclusionsWe found that s-albumin levels decreased and Hs-CRP levels increased in patients with CSF. S-albumin was also found to have superior predictive value than Hs-CRP for diagnosing CSF. S-albumin, an inexpensive and easily measurable laboratory variable, may be a useful predictor of CSF, especially when other reasons which alter its serum levels were excluded.ZusammenfassungGrundlagenVon mehreren Entzündungsmarkern, wie hochsensitivem C-reaktiven Protein (hs-CRP), Interleukin-6 (IL-6) und Fibrinogen konnte gezeigt werden, dass sie mit langsamem koronarem Durchfluss („coronary slow flow“, CSF) vergesellschaftet sind. Ziel unserer Studie war es, zu prüfen, ob ein Zusammenhang zwischen Albumin, einem lang-wirksamen negativen Akutphasenprotein und CSF besteht.MethodikInsgesamt wurden 106 Patienten mit angiographisch nachgewiesenem CSF und 57 Kontrollen mit normalem Koronarfluss in die Studie aufgenommen. Die Serumkonzentrationen von hs-CRP und Albumin wurden gemessen. CSF wurde durch die TIMI (Thrombolysis In Myocardial Infarction) Frame Count (TFC) Methode erhoben.ErgebnisseDas Serum Albumin war in der Gruppe mit CSF im Vergleich zur Kontrolle signifikant erniedrigt (3,79u2009±u20090,3 vs 4,17u2009±u20090,3, pu2009<u20090,001) – die hs-CRP Konzentrationen dahingegen signifikant erhöht (1,22u2009±u20090,79 vs 0,76u2009±u20090,44, pu2009<u20090,001). Serum Albumin und hs-CRP waren in der Gesamtpopulation mit dem mittleren TFC korrelieret (r=u2009−u20090,574, pu2009<u20090,001; ru2009= 0,376, pu2009<u20090,001, respektive). In der Multivarianzanalyse zeigte sich, dass hs-CRP und niedriges Serum Albumin signifikante Prädiktoren eines CSF sind. Der Vergleich der ROC Analysen für hs CRP und Serum Albumin ergab, dass das Serum Albumin der stärkste Prädiktor eines CSF war.SchlussfolgerungenBei unseren Patienten mit CSF waren die Serum Albumin-Konzentrationen erniedrigt und die hs-CRP Werte erhöht. Das Serum Albumin war in unseren Händen der bessere Prädiktor als das hs-CRP für einen CSF. Serum Albumin ist ein billiger und leicht messbarer Laborparameter, der – nach Ausschluss anderer Albumin beeinflussender Faktoren - ein nützlicher Prädiktor für einen CSF sein kann.

atrial electromechanical coupling intervals in pregnant subjects

Summary Objective The aim of this study was to evaluate atrial conduction abnormalities obtained by tissue Doppler imaging (TDI) and electrocardiogram analysis in pregnant subjects. Methods A total of 30 pregnant subjects (28 ± 4 years) and 30 controls (28 ± 3 years) were included. Systolic and diastolic left ventricular (LV) function was measured using conventional echocardiography and TDI. Inter-atrial, intra-atrial and intra-left atrial electromechanical coupling (PA) intervals were measured with TDI. P-wave dispersion (PD) was calculated from a 12-lead electrocardiogram. Results Atrial electromechanical coupling at the septal and left lateral mitral annulus (PA septal, PA lateral) was significantly prolonged in pregnant subjects (62.1 ± 2.7 vs 55.3 ± 3.2 ms, p < 0.001; 45.7 ± 2.5 vs 43.1 ± 2.7 ms, p < 0.001, respectively). Inter-atrial (PA lateral – PA tricuspid), intra-atrial (PA septum – PA tricuspid) and intra-left atrial (PA lateral – PA septum) electromechanical coupling intervals, maximum P-wave (Pmax) duration and PD were significantly longer in the pregnant subjects (26.4 ± 4.0 vs 20.2 ± 3.6 ms, p < 0.001; 10.0 ± 2.0 vs 8.0 ± 2.6 ms, p = 0.002; 16.4 ± 3.3 vs 12.2 ± 3.0 ms, p < 0.001; 103.1 ± 5.4 vs 96.8 ± 7.4 ms, p < 0.001; 50.7 ± 6.8 vs 41.6 ± 5.5 ms, p < 0.001, respectively). We found a significant positive correlation between inter-atrial and intra-left atrial electromechanical coupling intervals and Pmax (r = 0.282, p = 0.029, r = 0.378, p = 0.003, respectively). Conclusion This study showed that atrial electromechanical coupling intervals and PD, which are predictors of AF, were longer in pregnant subjects and this may cause an increased risk of AF in pregnancy.

Is the level of resistin appropriate for predicting atrial fibrillation

We read the paper entitled ‘‘Increased level of resistin predicts development of atrial fibrillation’’ by Ozcan et al. [1] with interest. These authors stated that plasma resistin and the high sensitivity C-reactive protein levels were the only independent predictors of atrial fibrillation (AF) and that elevated levels of plasma resistin were related to the paroxysmal AF group and the persistent AF group, but not to the permanent AF group. Although several risk factors have been identified for the development of AF, the pathogenesis is multifactorial and not totally understood. Different factors are included in this selfperpetuating process such as volume and/or pressure overload in the heart, fibrosis, oxidative stress, and inflammation. Since cardiac inflammatory disorders such as myocarditis, pericarditis, and postperiocardiotomy syndrome frequently are accompanied by AF, clinicians concentrate upon the idea that AF is closely associated with inflammation according to these clinical observations [2]. Previously, inflammatory markers have been assessed in the cardiac tissue, intracardiac blood, and peripheral blood in patients with AF. Furthermore, in one study, higher C-reactive protein (CRP) and interleukin-6 levels were detected in the left atrium than in the coronary sinus during AF and the authors concluded that there appears to be intracardiac sequestration of inflammatory cytokines, potentially pointing to an important mechanism of atrial remodeling [3]. However, if the blood samples of this study had been collected from left atrium or coronary sinus, results different from that study could have been obtained, and especially the atrial inflammation could be more accurately evaluated. The authors also stated that the permanent AF was associated with higher levels of CRP than paroxysmal AF, implying that CRP levels may be related to the burden of AF, but the same thing is not valid for resistin levels. The reason for these results may be due to the small number of patients included in the study as well as drug usage. Namely, circulating resistin levels are found to be decreased by the anti-diabetic drug rosiglitazone [4]. Moreover, reduced circulating resistin levels after rosiglitazone treatment have been reported by Moore et al. [5]. If the detailed history of drug usage of the patient population had been questioned, different results might have been obtained. Furthermore, inflammation appears to play an important role in the development of thromboembolic complications associated with AF. The relationship between inflammation and AF-related thromboembolism was supported by the observation in which interleukin-6 and CRP are markedly elevated in patients with dilated left atrium and an inadequately functioning left atrial appendage. Moreover, CRP has also been shown to be correlated

Increased ventricular pacing threshold levels in patients with high serum uric acid levels

BACKGROUNDnPermanent cardiac pacemakers (PCM) are accepted as the most effective treatment for symptomatic bradyarrhythmias. Serum uric acid (UA) levels are associated with various inflammatory markers, oxidative stress, and endothelial dysfunction. This study aimed to investigate the association between serum UA and ventricular pacing threshold (VPT) levels in patients who underwent permanent pacemaker implantation.nnnMATERIALS AND METHODSnWe retrospectively analyzed a total of 198 patients who underwent PCM implantation for indications such as symptomatic bradycardia without a reversible etiology and high-degree and complete atrioventricular block.nnnRESULTSnVPT values were found to correlate with serum UA levels (r=0.591, p<0.001), high sensitivity C-reactive protein (hs-CRP) levels (r=0.505, p<0.001), and ventricular impedance (r=0.220, p=0.016). The serum UA levels and hs-CRP levels were also correlated (r=0.691, p<0.001). To identify independent risk factors for VPT values, a multivariate linear regression model was conducted, and serum UA levels (β=0.361, p=0.001), hs-CRP levels (β=0.277, p=0.012), and impedance values (β=0.207, p=0.011) were found to be independent risk factors for VPT.nnnCONCLUSIONnIn the present study, VPT values at the time of implantation and at the 30th day were increased in patients with high serum UA levels. To further extend the life of pacemakers, as well as other factors that affect threshold values, serum UA levels should be noted.

Prediction of no-reflow and major adverse cardiovascular events with a new scoring system in STEMI patients

BACKGROUNDnNo-reflow is associated with a poor prognosis in STEMI patients. There are many factors and mechanisms that contribute to the development of no-reflow, including age, reperfusion time, a high thrombus burden, Killip class, long stent use, ejection fraction ≤40, and a high Syntax score. In this study, we aimed to evaluate the parameters associated with no-reflow prediction by creating a new scoring system.nnnMETHODSnThe study included 515 consecutive STEMI patients who underwent PCI; 632 STEMI patients who had undergone PCI in another center were included in the external validation of the scoring system. The correlations between 1-year major adverse cardiac events and low/high risk score were assessed.nnnRESULTSnIn this study, seven independent variables were used to build a risk score for predicting no-reflow. The predictors of no-reflow are age, EF ≤40, SS ≥22, stent length ≥20, thrombus grade ≥4, Killip class ≥3, and pain-balloon time ≥4u2009h. In the derivation group, the optimal threshold score for predicting no-reflow was >10, with a 75% sensitivity and 77.7% specificity (Area under the curve (AUC)u2009=u20090.809, 95%CI: 0.772-0.842, Pu2009<u20090.001). In the validation group, AUC was 0.793 (95%CI: 0.760-0.824, Pu2009<u20090.001).nnnCONCLUSIONnThis new score, which can be calculated in STEMI patients before PCI and used to predict no-reflow in STEMI patients, may help physicians to estimate the development of no-reflow in the pre-PCI period.