Can high-sensitive troponin levels within the normal range predict positivity in treadmill test?

BACKGROUND: This study aimed to determine whether a high level of high-sensitivity troponin T (hsTnT) predicts a positive treadmill test in patients with suspected stable ischemic heart disease (SIHD). METHODS: In all, 366 patients with suspected SIHD were included in the study. We measured the serum hsTnT levels before the treadmill test. The treadmill test was performed according to the Bruce protocol. RESULTS: Of the 366 patients, 97 had positive treadmill tests. The hsTnT levels were significantly higher in the positive group than in the negative group. In the binary logistic regression analysis, hsTnT, pretest probability, metabolic equivalents (METs), target heart rate (THR) percentage, and Duke treadmill score (DTS) were independent predictors of a positive treadmill test [hsTnT odds ratio (OR): 2.178, P < 0.001; pretest probability OR: 1.036, P = 0.007; METs OR: 0.755, P = 0.008; THR OR: 0.773, P < 0.001; DTS OR: 2.661, P = 0.012]. In the receiver operating characteristic (ROC) curve analysis, the area under the curve (AUC) value of the model with the combined parameters of hsTnT, pretest probability, METs, THR, and DTS was statistically significant in predicting a positive treadmill test [combined model AUC: 0.945 (0.922-0.968), P < 0.001]. CONCLUSIONS: In sum, high pretest hsTnT levels predicted a positive treadmill test in patients with suspected SIHD. Analysis of the hsTnT levels before the treadmill test can increase the sensitivity and specificity of the treadmill test. The methods for measuring hsTnT levels are cheap and easily accessible and can be used before the treadmill test in patients with suspected SIHD.

Q fever endocarditis: is it always subacute or chronic?

Q fever is a zoonotic disease caused by Coxiella burnetii, an obligate intracellular bacterium, which cannot be grown using routine blood culture methods. Although C. burnetii is reported to be the causative agent in approximately 50% of blood culture-negative infective endocarditis cases in developed countries, the incidence in Turkey is yet to be defined. The clinical course of Q fever endocarditis is generally subacute and chronic; the disease may be present for years with only subtle symptoms and no vegetation visible on echocardiography while the bacteria gradually destroy the heart valves. This is the case of the successful treatment of a young man with Q fever endocarditis that had an acute clinical course. In 1 month, he developed New York Heart Association class IV heart failure and a large, 3-cm vegetation was observed on an echocardiogram.

Predictors of left ventricle ejection fraction and early in-hospital mortality in patients with ST-segment elevation myocardial infarction: Single-center data from a tertiary referral university hospital in Istanbul.

BACKGROUND: Little is known about the management and mortality rates of ST-segment elevation myocardial infarction patients in developing countries. In this study, to expose independent predictors of early (24 h) in-hospital mortality and ejection fraction, we report our experience with 362 ST-segment elevation myocardial infarction patients admitted to the Istanbul Medical Faculty, Istanbul University, a tertiary referral university hospital, and treated with primary percutaneous intervention. METHODS: This is a retrospective study that enrolled all patients (362) admitted with ST-segment elevation myocardial infarction to Department of Cardiology, Istanbul Medical Faculty, Istanbul University, between January 2015 and December 2016. The clinical characteristics of patients were collected retrospectively from medical chart review. Collected data were analyzed using IBM SPSS Statistics (version 21). RESULTS: In the forward stepwise logistic regression analysis, target vessel diameter (p = 0.001), systolic blood pressure (p < 0.001), and troponin T levels (p = 0.007) were independent predictors for early in-hospital mortality, while target vessel diameter (p = 0.03), troponin T level (p < 0.001), heart rate (p = 0.001), and chest pain (p = 0.001) duration were the independent predictors for ejection fraction of 50% and above. CONCLUSION: Our study is one of the few studies to investigate the predictors of early in-hospital mortality among patients hospitalized with ST-segment elevation myocardial infarction in a tertiary referral university hospital in a developing country. The identified predictors for mortality (including left ventricle ejection fraction and troponin T levels), left ventricle ejection fraction (including troponin T level, chest pain duration), and heart rate are consistent with what has been described in large registries in the United States and Europe.

Galectin-3: A Novel Biomarker Predicts Sudden Cardiac Death in Hypertrophic Cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy is a primary cardiac disease characterized by left ventricular hypertrophy, myocyte hypertrophy and irregularities and interstitial fibrosis in the absence of any cardiac or systemic diseases and may lead to sudden cardiac death (SCD). Galectin-3 is a ß-galactoside-binding lectin that has been associated with cardiac fibrosis and inflammation. In this study, we aimed to investigate the relationship between serum galectin-3 levels and the criteria for 5-year sudden death risk, recently defined in the European Society of Cardiology guidelines (2014), in patients with hypertrophic cardiomyopathy. MATERIALS AND METHODS: A total of 52 hypertrophic cardiomyopathy patients were enrolled in the study. Patients were questioned for sudden death risk predictors as outlined in the 2014 European Society of Cardiology guideline. A standardized clinical evaluation was carried out on the basis of previously described prognostic variables to calculate the 5-year risk of SCD. Blood samples were taken from all patients to measure serum galectin-3 levels. A statistical significance level of P < 0.05 was accepted in all tests. RESULTS: We found that there was a significant correlation between the estimated 5-year risk of SCD and serum levels of galectin-3. CONCLUSIONS: Galectin-3 may be an inexpensive and easily accessible parameter to predict arrhythmia risk. In addition, it can be used to determine antiarrhythmic prophylaxis as a predictor of an arrhythmia storm in implantable cardioverter defibrillator-implanted patients who are not available for magnetic resonance imaging.

Endocan: a novel biomarker associated with well-developed coronary collateral circulation in patients with stable angina and chronic total occlusion.

Angiogenesis and arteriogenesis have a crucial role in the formation of coronary collateral vessels. It has been shown that endocan and vascular cell adhesion molecule-1 (VCAM-1) are potential angiogenetic factors. We investigated the relationship between serum endocan levels and grade of coronary collaterals, and also the correlation of endocan levels with serum VCAM-1 levels. Patients with stable angina and at least one total coronary occlusion at invasive coronary angiography were included in our study. Collateral degree was graded according to Rentrop and Cohen's classification. Patients who had grade 0 or 1 collateral vessels were included in the poorly-developed collateral group, and those with grade 2 or 3 coronary collateral vessels were included in the well-developed collateral group. Serum endocan and VCAM-1 levels were significantly higher in the well-developed collateral group (436.6 ± 213.3 ng/mL vs. 216.1 ± 78.5 ng/mL, p < .001; 11.02 ± 6.58 ng/mL vs. 6.78 ± 1.14 ng/mL, p < .001, respectively). In a logistic regression analysis, only serum endocan level remained as an independent predictor for good collateral development. In the ROC curve analysis, 282 ng/mL endocan level had an a 82 % sensitivity and 86 % specificity for prediction of the well-developed collateral group. Higher endocan level was related to better coronary collateral development. In the event that these results are confirmed in further studies, endocan may be considered as an anti-ischemic treatment strategy in order to improve collateral development.

Doppler-derived strain imaging detects left ventricular systolic dysfunction in children with Turner syndrome.

OBJECTIVES: Children with Turner syndrome (TS) are at increased risk of cardiovascular disease (CVD), but associations with subclinical CVD are not well-characterized. The purpose of this study was to assess myocardial function using strain imaging (SI) by echocardiography in children with TS and without known CVD. METHODS: The study included 48 children with TS aged 4-16 years and 20 healthy control children. Children with TS were excluded if they had a cardiac malformation, a decreased left ventricular (LV) systolic function, or any chronic disease. Each child had an echocardiographic examination with conventional echocardiography and one-dimensional longitudinal strain (1DST) echocardiography. RESULTS: Septal and lateral systolic strain (S) and strain rate (SR) values, which are indicative of longitudinal myocardial function, were significantly decreased in TS patients. However, LV ejection fraction (LVEF) and LV fractional shortening (LVFS) was not significantly different between groups. LV mass index (LVMi), interventricular septum (IVS) thickness, LV posterior wall (LVPW) thickness, and left atrial (LA) diameter index were significantly higher in TS children compared to controls. Peak transmitral flow velocity in late diastole (peak A) was significantly higher, whereas peak transmitral flow velocity in early diastole (peak E), deceleration time (DT), and the ratio of early to late diastolic filling were significantly lower, in TS patients. CONCLUSION: Reduced LV systolic S and SR in children with TS may indicate early myocardial dysfunction before any detectable change in LVEF.

Effect of carvedilol on silent anthracycline-induced cardiotoxicity assessed by strain imaging: A prospective randomized controlled study with six-month follow-up.

BACKGROUND: The use of antracycline (ANT) in breast cancer has been associated with adverse cardiac events. Two-dimensional (2D) strain imaging (SI) can provide a more sensitive measure of altered left ventricular (LV) systolic function. We aimed to evaluate the preventive effect of carvedilol administration assessed by SI in a patient with breast cancer treated with ANT. METHODS: Patients receiving ANT were randomly assigned to the carvedilol- or placebo-receiving group. Each received an echocardiographic examination with conventional 2D echocardiography, pulsed tissue Doppler, and 2D SI prior to and 6 months post ANT treatment. RESULTS: During the 6-month follow-up period there were no patient deaths or interrupted chemotherapy treatments due to doxorubicin-induced cardiotoxicity. Both left ventricular ejection fraction (LVEF) and fractional shortening (FS) were within normal limits for all patients before and after ANT therapy. EF, FS and LV dimensions were measured using M-mode echocardiography and found to be similar in both groups before and after ANT therapy. The mean EF, FS, and LV echocardiograph baseline and control dimensions were similar in both groups after 6 months. Though baseline SI parameters were similar between the groups, there was a significant decrease in LV basal septal and basal lateral peak systolic strain in the control group compared to the carvedilol group. CONCLUSIONS: These results indicate that carvedilol has a protective effect against the cardiotoxicity induced by ANT.

Impact of vitamin D insufficiency on the epicardial coronary flow velocity and endothelial function.

OBJECTIVE: Increasing evidence suggests a relationship between vitamin D (VD) insufficiency and cardiovascular disease. The present study evaluated the effect of VD insufficiency on epicardial coronary flow rate, subclinical atherosclerosis, and endothelial function. METHODS: The present study was cross-sectional and observational. We enrolled 222 consecutive patients who had undergone coronary angiography for suspected ischemic heart disease and were found to have normal or near-normal coronary arteries. Thereafter, 25(OH)D3 levels were measured and the coronary flow rate was assessed using the thrombolysis in myocardial infarction frame count. Slow coronary flow (SCF) was defined as a thrombolysis in myocardial infarction frame count greater than 27/frame. Endothelial function was assessed by brachial artery flow-mediated dilatation. Carotid intima-media thickness, an indicator of subclinical atherosclerosis, was measured using B-mode ultrasonography. RESULTS: The mean level of 25(OH)D3 was 31.8 ng/ml, and 47% (n=106) of the patients had insufficient 25(OH)D levels (<30 ng/ml). Baseline characteristics were similar between VD-insufficient and VD-sufficient groups. The incidence of SCF was significantly higher in the VD-insufficient group than in patients with sufficient VD (relative risk=3.5, 95% confidence interval=1.1-10.5, P=0.01). After adjusting for cardiovascular disease risk factors, VD insufficiency was independently associated with SCF. The linear regression analysis showed that VD insufficiency was correlated independently with % flow-mediated dilatation (ß=0.424, P<0.001) and carotid intima-media thickness (ß=0.43, P<0.001). CONCLUSION: A strong association was found between VD insufficiency and the SCF phenomenon. In addition, VD insufficiency was associated with endothelial dysfunction and subclinical atherosclerosis. We believe that further studies are required to clarify the role of VD in patients with SCF.

Relationship Between Brachial Artery Flow-Mediated Dilation, Carotid Artery Intima-Media Thickness and Coronary Flow Reserve in Patients With Coronary Artery Disease.

BACKGROUND: The aim of this study was to assess the relationship between brachial artery flow mediated dilation (FMD), carotid artery intima-media thickness (IMT) and coronary flow reserve (CFR) in patients with coronary artery disease (CAD). METHODS: Fifty patients with coronary artery disease, except left anterior descending artery (LAD), who showed no cardiac symptoms and 45 control subjects underwent assessment of brachial artery FMD, carotid artery intima-media thickness by high-resolution ultrasound. In addition, transthoracic second harmonic Doppler echocardiography was used to measure CFR. RESULTS: All of the parameters were found to be correlated with each other. CFR correlated with brachial artery FMD (r = 0.232, P < 0.05) and with carotid IMT (r = -0.403, P < 0.001). Carotid IMT correlated with brachial artery FMD (r = -0.211, P < 0.05). CONCLUSION: Transthoracic CFR correlated with well-established noninvasive predictors of atherosclerosis and we suggest that it can be used as a surrogate for coronary atherosclerosis.

Nebivolol prevents remodeling in a rat myocardial infarction model: an echocardiographic study.

OBJECTIVE: Ventricular remodeling (VR) which develops after myocardial infarction (MI) plays an important role in progressive left ventricular dysfunction. We aimed to investigate the role of nebivolol treatment on VR after a MI in a rat ischemia-reperfusion model. METHODS: Rats were divided into 3 groups of 12 each: sham operated (sham-control), MI-induced (MI-control) and nebivolol treated (MI-nebivolol). Left ventricular (LV) diameters, volumes, and diastolic filling parameters were evaluated by echocardiography. On the 28th day, after recording the systemic and LV pressures and determining the plasma nitric oxide (NO) and peroxynitrite (ONOO-) levels , animals were sacrificed and heart, body and LV weights (HW, BW, LVW) were measured and infarct sizes were determined. Results were evaluated statistically by ANOVA for repeated measurements 3x3 factorial design with post-hoc Bonferroni test. RESULTS: After MI, while VR (an increase in LV diameters and volumes associated with a decrease in EF, FS and posterior wall thickness change (LWPc) was significant in MI-control rats (p<0.05 for; all comparisons) these changes were significantly less in MI-nebivolol group (p=0.08 and p=0.06 for EF and FS respectively). LV end diastolic pressure (LVEDP) was lower (p<0.005) and Delta+/- dp/dt's (p<0.05) were higher in MI-nebivolol group compared to MI-control animals. Although infarct sizes were similar in MI-induced groups (p=0.79); LVW/HW and HW/BW's were significantly greater in the MI-control group compared to sham-control (p<0.01 for all comparisons), these changes were not statistically significant in MI-nebivolol group. The increase in plasma NO and ONOO- levels were also prevented with nebivolol. CONCLUSION: Nebivolol therapy reduced the effects of VR in rats after MI. These beneficial effects were not related to its heart rate and blood pressure reducing effects. Nitric oxide regulatory action of this compound may contribute these beneficial effects on VR developed after MI.

No association of the TLR2 gene Arg753Gln polymorphism with rheumatic heart disease and Behçet's disease.

Behçet's disease (BD) is a multisystem inflammatory disorder of unknown etiology, and infections with different microorganisms including streptococci have been claimed as triggers of inflammatory attacks in BD pathogenesis. Toll-like receptor 2 (TLR2) has been known to recognize several microbial antigens including that of streptococci, and TLR2 gene Arg753Gln polymorphism has been reported to be strongly associated with acute rheumatic fever with an odds ratio of 100. This study aimed to investigate the TLR2 gene Arg753Gln polymorphism in a group of patients with BD and rheumatic heart disease (RHD) and to analyze the role of genotyping errors resulting from duplicated gene segments. The study group consisted of 211 patients with BD, 95 patients with RHD, and 94 matched Turkish healthy controls. Because of the duplicated exon 3 in 23-kb upstream of the TLR2 gene, genotyping for the Arg753Gln polymorphism with polymerase chain reaction-restriction fragment length polymorphism method was carried out using a new set of primers and PstI restriction enzyme. TLR2 gene Gln753 allele was observed in two of 211 (1.0%) patients with BD, five of 95 (5.3%) patients with RHD, and two of 94 (2.1%) healthy controls. All patients and controls were found to be heterozygous for Arg753Gln polymorphism, except one patient with BD, who was homozygous for Gln753. Although a slight increase of heterozygosity was noted in patients with RHD, no statistically significant difference was observed in the distribution of Arg753Gln polymorphism in BD and RHD compared to healthy controls. In conclusion, TLR2 gene Arg753Gln polymorphism is not associated with BD nor with RHD; and a duplicated region of the TLR2 exon 3 located 23-kb upstream of the polymorphic region may explain contradictory association findings described so far.

Intraaortic balloon occlusion during refractory cardiac arrest. A case report.

Despite recent advances in its management, the outcome from cardiac arrest is often poor despite appropriate cardiopulmonary resuscitation (CPR). The coronary perfusion pressure (CPP) achieved during CPR is associated with successful return of spontaneous circulation (ROSC). Continuous balloon occlusion of the descending aorta is an experimental method that can occlude the 'unnecessary' part of the circulation, thus diverting generated pressure and blood flow to the heart and brain. We present a case report with a patient unresponsive to standard CPR in which constant intraaortic balloon occlusion achieved ROSC and successful survival.

The effects of nebivolol on apoptosis in a rat infarct model.

BACKGROUND: In the present study, nitric oxide (NO) was investigated to see if it mediated effects of nebivolol on apoptosis in the rat myocardial infarction (MI) model. METHODS AND RESULTS: Rats were divided into 3 groups: sham operated (sham-control), MI-induced (MI-control) and nebivolol treated (MI-nebivolol). The initial dose of nebivolol was administrated intravenously (iv) within 10 min of post-MI reperfusion and continued orally for 28 days. NO mediated effects of nebivolol were assessed either in the early (2(nd) day) or sub-acute (28(th) day) period of MI by histologic, hemodynamic and biologic studies. Left ventricular (LV) pressure changes were prevented with nebivolol (the increase in LV end-diastolic pressure and the decrease in maximum rise and fall rate of LV pressure (+dp/dt and -dp/dt) was significantly less in MI-nebivolol). Total and regional apoptotic indexes were significantly lower in the MI-nebivolol group (10.2 vs 7.1%, respectively on the 2(nd) day; p=0.004). Although plasma nitrite/nitrate, cyclic guanylate cyclase and peroxynitrite concentrations were high both in MI-control and MI-nebivolol groups on the 2(nd) day, these concentrations were decreased to the basal value on the 28(th) day in the MI-nebivolol group. CONCLUSION: As a result, nebivolol treatment (initially by iv within 10 min of reperfusion and continued orally) reduced the myocardial apoptosis after MI. This beneficial effect of nebivolol is mediated by NO regulation.

Improvement of endothelial dysfunction with simvastatin in patients with autosomal dominant polycystic kidney disease.

Cardiovascular problems are a major cause of morbidity and mortality in patients with autosomal dominant polycystic kidney disease (ADPKD). Endothelial dysfunction (ED), which is an early manifestation of vascular injury, has been shown in patients with ADPKD. Statins have a beneficial effect in the reversal of ED. The aim of this study was to investigate the effects of a statin, simvastatin, on ED in patients with ADPKD. Sixteen patients with ADPKD having well-preserved renal function were included in the study. Endothelial function of the brachial artery was evaluated by using high-resolution vascular ultrasound. Endothelial-dependent dilatation (EDD) was expressed as the percentage change in the brachial artery diameter from baseline to reactive hyperemia. After the baseline evaluations of EDDs, patients were started treatment with simvastatin at a dose of 40 mg/day and were treated for six months. EDDs were recalculated after one and six months of therapy. Interleukin-6 (IL-6) and high-sensitivity C-reactive protein were also measured as markers of inflammation. Baseline EDD was 11.3 +/- 6.9% in patients with ADPKD. After one month of simvastatin treatment, EDD increased significantly to 14.6 +/- 4.6 % (P = 0.016 versus baseline). Endothelial-dependent dilatation further increased significantly to 18.9 +/- 7.5 % (P = 0.011 versus baseline, P = 0.048 versus first month) after six months of therapy. There was also a significant decrease in the level of IL-6 from 21.6 +/- 21.7 pg/mL to 9.1 +/- 3.5 pg/mL (P= 0.002). Six months of simvastatin therapy resulted in a significant improvement of ED in patients with ADPKD. This finding may be in part related to the pleiotropic effects of simvastatin.

Clinical relevance of aspirin resistance in patients with stable coronary artery disease: a prospective follow-up study (PROSPECTAR).

Aspirin resistance may increase the risk of major adverse cardiac events (MACE) more than threefold in patients with stable coronary artery disease (CAD). This study aimed to determine the prevalence of aspirin resistance in patients with stable CAD, the role of aspirin resistance on outcome in the follow-up, and the effect of clopidogrel therapy in MACE prevention in aspirin-resistant individuals. We detected the prevalence of aspirin resistance in 234 patients with stable CAD. Platelet function was determined by PFA-100 with collagen and/or epinephrine and collagen and/or ADP cartridges. The mean follow-up time was 20.6 +/- 6.9 months. The primary endpoints of the study were occurrence of myocardial infarction, unstable angina, stroke and cardiac death. Of patients, 22.2% (n = 52) were aspirin resistant by PFA-100. During follow-up, MACE occurred in eight patients (15.4%) with aspirin resistance and in 20 patients (11.0%) with aspirin-sensitive platelet aggregation (P = 0.269). MACE increased in aspirin-resistant patients after termination of clopidogrel therapy. Eleven patients experienced MACE after cessation of clopidogrel therapy (P < 0.001). The MACE risk in patients with stable CAD having detected aspirin resistance was similar compared with patients having aspirin-sensitive platelet aggregation by PFA-100. The MACE prevalence increased during follow-up, however, just after cessation of clopidogrel therapy.

Coronary flow reserve after L-thyroxine therapy in Hashimoto's thyroiditis patients with subclinical and overt hypothyroidism.

BACKGROUND/AIMS: Overt and subclinical hypothyroidism are reported to be associated with increased cardiovascular disease risk. We have used coronary flow reserve (CFR) measurement by trans-thoracic Doppler echocardiography (TTDE) to determine coronary microvascular function in Hashimoto's thyroiditis patients with overt and subclinical hypothyroidism and to evaluate effects of L-thyroxine replacement on coronary endothelial function. METHODS: In total, 10 overt hypothyroid patients, 10 subclinical hypothyroid patients, and 10 controls were enrolled. FT4, TSH, anti-thyroid antibodies, lipid profile, insulin, glucose, HOMA-IR, physical parameters, and CFR measured by TTDE were recorded before and after 6 months of L: -thyroxine replacement in all groups. RESULTS: CFR values of all hypothyroid patients at baseline were significantly lower than those in controls. After L: -thyroxine, CFR increased significantly in overt and subclinical hypothyroidism with respect to the baseline measurements (P < 0.05). When baseline and second measurements were evaluated collectively for patients and controls, CFR was positively correlated with FT4 levels (r = 0.31, P = 0.01) and negatively correlated with TSH and HOMA-IR (r = -0.38, P = 0.002 and r = -0.42, P < 0.001, respectively). CONCLUSION: Subclinical as well as overt hypothyroid patients have impaired coronary microvascular function which improved after L: -thyroxine therapy. Treatment of Hashimoto's thyroiditis patients with subclinical hypothyroidism should be considered to improve cardiovascular disease risk.

Association of haematological indices with the degree of microvascular injury in patients with acute anterior wall myocardial infarction treated with primary percutaneous coronary intervention.

BACKGROUND: In acute myocardial infarction (AMI), increased neutrophil count has been associated with more severe coronary artery disease and larger infarct size. Increased mean platelet volume (MPV) is also associated with poor clinical outcome and impaired angiographic reperfusion in patients with AMI. However, the associations of neutrophil count and MPV with the indices of tissue level reperfusion were not fully elucidated. AIM: To elucidate the relationship between baseline neutrophil count and MPV on presentation and microvascular injury in patients with anterior AMI treated with primary percutaneous coronary intervention (pPCI). METHODS: 41 patients with anterior wall AMI treated successfully with pPCI were included. The leucocyte count, neutrophil count and MPV were obtained on admission, and the percentage of neutrophils was calculated. After PCI thrombolysis in myocardial infarction, grade 3 flow was established in all patients. The coronary flow velocity pattern (diastolic deceleration time (DDT)) was examined with transthoracic echocardiography and measured intracoronary pressures with fibreoptic pressure-temperature sensor-tipped guidewire in the left anterior descending artery within 48 h after pPCI. Thermodilution-derived coronary flow reserve (CFR) was calculated. Index of microvascular resistance (IMR) was defined as simultaneously measured distal coronary pressure divided by the inverse of the thermodilution-derived hyperaemic mean transit time. Subsequently, a short compliant balloon was placed in the stented segment and inflated to measure coronary wedge pressure (CWP). RESULTS: Higher neutrophil counts were strongly associated with higher IMR (r = 0.86, p<0.001), lower CFR (r = -0.60, p<0.001), shorter DDT (r = -0.73, p<0.001) and higher CWP (r = 0.73, p<0.001). Likewise, there were significant correlations among the percentage of neutrophils and CFR (r = -0.34, p = 0.02), IMR (r = 0.46, p = 0.002), DDT (r = -0.36, p = 0.01) and CWP (r = 0.49, p = 0.001). Relationships among leucocyte count and IMR (r = 0.38, p = 0.01), CFR (r = -0.33, p = 0.03), DDT (r = -0.36, p = 0.01) and CWP (r = 0.32, p = 0.026) were slightly significant. Higher neutrophil count remained independently associated with indices of microvascular perfusion in multivariable models controlling for age, smoking habits and time to treatment. Also, higher MPV on admission was strongly associated with higher IMR (r = 0.89, p<0.001), steeper DDT (r = -0.64, p<0.001), lower CFR (r = -0.43, p = 0.004) and higher CWP (r = 0.77, p<0.001). CONCLUSION: Absolute and relative neutrophilia and higher MPV on admission were independently associated with impaired microvascular perfusion in patients with anterior AMI treated with pPCI. It is possible that neutrophilia and high MPV are simple surrogate markers of worse microvascular injury in patients with AMI.

The role of aspirin resistance on outcome in patients with acute coronary syndrome and the effect of clopidogrel therapy in the prevention of major cardiovascular events.

BACKGROUND: Aspirin resistance may increase up to more then threefold the risk of major cardiovascular events (MACE) in patients with stable coronary artery disease. AIM: The aim of our study was to determine; the prevalence of aspirin resistance in patients with acute coronary syndromes, the role of aspirin resistance on outcome in the follow-up and the effect of clopidogrel therapy in the prevention of MACE in aspirin resistant subjects. MATERIAL AND METHODS: We detected the prevelance of aspirin resistance in 105 patients with acute coronary syndrome. Platelet functions were analyzed in Platelet Function Analyzer (PFA)-100 (Dade Behring, Germany) with collagen and/or epinephrine (Col/Epi) and collagen and/or ADP (Col/ADP) cartridges. Primary end points of the study were myocardial infarction, unstable angina, cardiac death. RESULTS: 19% (n = 20) of patients were aspirin resistant by PFA-100. In the follow-up, MACE occured in 9 patients (45%) with aspirin resistance and in 10 patients (11.7%) with aspirin sensitive platelet aggregation (p = 0.001). Multivariate analysis showed that aspirin resistance was an independant predictor of MACE. The prevalence of MACE in patients who were on clopidogrel treatment for 12 months were lower compared to those who were on a clopidogrel treatment for the first six months (p = 0.040). CONCLUSIONS: We determined that the MACE risk in patients with acute coronary syndromes having detected aspirin resistance, was higher at statistically significant levels compared to patients having aspirin sensitive platelet aggregation. Our results showed that aspirin resistance, was an independant predictor of MACE in patients with acute coronary syndrome.

Effects of percutaneous coronary thrombectomy with the X-sizer catheter on epicardial flow and microvascular function in acute coronary syndromes.

During percutaneous coronary intervention, slow coronary flow and distal embolization are still important problems, especially in cases with intracoronary thrombus. The aim of this study was to learn the effectiveness and early term results of thrombectomy with the X-SIZER catheter system in acute coronary syndrome. Twenty-nine patients (22 [76%] men; 55.9 +/- 11.1 years) with acute coronary syndrome and intracoronary thrombus detected in coronary angiography were included into the study. X-sizer thrombectomy was applied to 14 of the patients, and conventional percutaneous transluminal coronary angioplasty (PTCA) was applied to the others. Baseline characteristics were similar in both groups. Mean thrombolysis in myocardial infarction (TIMI) flow increased from 0.8 +/- 0.9 to 2.4 +/- 0.6 in X-sizer-treated patients (p<0.001) and TIMI 3 flow was maintained in 71.4% of the patients. Similary, mean TIMI flow increased from 0.36 +/- 0.81 to 2.73 +/- 0.47 in conventional PTCA-treated patients (p<0.001) and TIMI 3 flow was maintained in 73% of the patients (NS). Mean myocardial blush grade (MBG) increased from 0.7 +/- 0.7 to 2.6 +/- 0.6 in X-sizer-treated patients (p<0.001) and from 0.27 +/- 0.65 to 2.36 +/- 0.67 in the conventional PTCA-treated patients (p<0.001). Postprocedural MBG 3 was obtained in 64.3% of X-Sizer-treated patients and in 45% of controls. Although microvascular function in the thrombectomy-applied patients was found better, there was no significant difference between the two groups. Furthermore it was detected that the use of tirofiban yielded no additional improvement in epicardial and microvascular flow. In acute coronary syndromes, use of X-sizer in addition to primary percutaneous coronary interventions is a safe and relatively effective method in the prevention of distal embolization.