Yalin Tolga Yaylali

Increased red blood cell deformability and decreased aggregation as potential adaptive mechanisms in the slow coronary flow phenomenon.

ObjectiveAt present, the precise pathophysiology of the slow coronary flow phenomenon (SCFP) is still unknown and there is no consensus as to how it should be treated. The rheological factors affect the clinical course of various cardiovascular diseases. We studied the intrinsic properties of blood in the SCFP. Materials and methodsTwenty-six SCFP patients who had angiographically confirmed SCFP, and had otherwise normal epicardial coronary arteries, were included in our study, as were 30 healthy individuals with normal results from arteriography. Red blood cell (RBC) deformability, aggregation, whole-blood viscosity at both native and standard (40%) hematocrit, and plasma viscosity were determined in each individual. The results were analyzed using a Mann–Whitney U-test, an unpaired t-test, and a &khgr;2-test, where appropriate. ResultsThe mean thrombolysis in myocardial infarction frame count was significantly higher in SCFP patients than in the controls. RBC deformability measured at five different shear rates was significantly higher in SCFP patients than in the controls. The RBC aggregation index was lower in SCFP patients. There were no statistically significant differences in RBC aggregation half-time (t1/2) and aggregation amplitude, whole-blood viscosity, and plasma viscosity between the two groups. ConclusionThe SCFP is associated with increased RBC deformability and decreased RBC aggregation. These hemorheological alterations, possibly also contributing factors in limiting the pathogenesis, can especially serve as beneficial adaptive mechanisms in the SCFP.

Dabigatran Versus Warfarin in Atrial Fibrillation: Multicenter Experience in Turkey.

Safety issues have been raised about dabigatran. We aimed to investigate the occurrence of safety outcomes in patients who had atrial fibrillation and a risk of stroke. We analyzed 439 patients prescribed dabigatran (n = 220) or warfarin (n = 219). Ischemic stroke occurred in 15 (6.8%) patients in the warfarin group versus 5 (5.2%) patients in the 110-mg group versus 1 (0.8%) patient in the 150-mg dabigatran group (P = .015). Intracranial hemorrhage occurred in 6 (2.7%) patients in the warfarin group versus 3 (2.4%) patients in the 150-mg dabigatran group (P = .104). Death from any cause occurred in 10 (4.6%) patients in the warfarin group versus 1 (1.0%) patient in the 110-mg dabigatran group (P = .005). Dabigatran was associated with less ischemic stroke and death from any cause than warfarin. Dabigatran may be a better option for stroke prophylaxis, where recommended monitoring with warfarin is suboptimal.

The effects of baseline heart rate recovery normality and exercise training protocol on heart rate recovery in patients with heart failure.

Objective: It is unclear which exercise training protocol yields superior heart rate recovery (HRR) improvement in heart failure (HF) patients. Whether baseline HRR normality plays a role in the improvement is unknown. We hypothesized that an exercise training protocol and baseline HRR normality would be factors in altering HRR in HF patients. Methods: In this prospective, randomized, controlled and 3 group parallel study, 41 stable HF patients were randomly assigned to 3-times-weekly training sessions for 12 weeks, consisting of i) 30 minutes of interval training (IT) (n=17, 63.7±8.8 years old) versus ii) 30 minutes of continuous training (CT) (n=13, 59.6±6.8 years old) versus iii) no training (CON) (n=11, 60.6±9.9 years old). Each patient had cardiopulmonary exercise testing before and after the training program. Maximum heart rates attained during the test and heart rates at 1 and 2 min (HRR1 and HRR2) during the recovery phase were recorded. Paired samples t-test or Wilcoxon signed-rank test was used for comparisons before and after training. One-way ANOVA or Kruskal-Wallis variance analysis was used for comparisons among groups. Results: HRR1 was unchanged after training. HRR2 improved in the IT group after training, and post-training HRR2 values were significantly faster in the IT group than in controls. Both HRR1 and HRR2 was significantly faster, irrespective of exercise protocol in patients with abnormal baseline values after training. Conclusion: HRR1 did not improve after training. HRR2 improved only in the IT group. Both HRRs in patients with abnormal baseline values improved after both exercise protocols. IT might be superior to CT in improving HRR2. Baseline HRR might play a role in its response to exercise.

Takotsubo-syndrome presenting with supraventricular tachycardia, stroke, and thrombocytopenia

Takotsubo syndrome (TTS) is an increasingly reported reversible cardiomyopathy following profound emotional or physical stress. It has clinical presentation and electrocardiogram (ECG) findings mimicking an acute coronary syndrome. The precise pathophysiology and mechanisms of TTS remain unknown. Tachyarrhythmias in the formof ventricular tachycardia or fibrillation have been reported as a complication during the course of TTS [1]. To the best of our knowledge, no previous reports of supraventricular tachycardia (SVT) as an initial ECG finding and documented TTS have been published. We report a woman with TTS who presented with SVT and developed cardioembolic stroke and thrombocytopenia during its course. An 81-year-oldwomanwas brought to the emergency room for nausea, vomiting, shivering chills, profuse sweating, and deterioration of general condition with altered mental status. Shewas diagnosed hypertensive with no other history of heart disease. Her physical examination findings on the arrival were as follows: BP: 157/89 mmHg, P: 150/min, RR: 44/min, T: 36.8 °C, and bilateral rales at the bases. On admission, the ECG showed supraventricular tachycardia with an RBBB pattern (Fig. 1A). She was converted to a sinus rhythm with IV diltiazem and metoprolol. Post-conversion ECG showed a sinus tachycardia with dramatic ST-segment elevations in V2-6, a deformed QRS configuration, suggesting severe injury from proximal LAD occlusion (Fig. 1B).

The Association between Central Adiposity and Autonomic Dysfunction in Obesity

Objective: To determine the relationship between central adiposity parameters and autonomic nervous system (ANS) dysfunction. Subjects and Methods: The study included 114 obese individuals without any cardiovascular risk factors. Weight (in kg), height (in m), and waist circumference (WC; in cm) were measured and body mass index was calculated. Echocardiographic examination was performed to measure left ventricular mass and epicardial fat thickness (EFT). All the participants underwent an exercise test and electrophysiological evaluation using electromyography. Heart rate recovery (HRR) at 1-5 min, R-R interval variation at rest and during hyperventilation, and sympathetic skin response were measured. Pearsons correlation analysis was used. Multiple linear regression analysis was used to identify the factors associated with autonomic dysfunction. Results: The HRR at 1-5 min was negatively correlated with WC and age (WC-HRR1: r = -0.32; WC-HRR2: r = -0.31; WC-HRR3: r = -0.26; WC-HRR4: r = -0.23; WC-HRR5: r = -0.21; age-HRR2: r = -0.32; age-HRR3: r = -0.28; age-HRR4: r = -0.41; age-HRR5: r = -0.42). Age was the only independent predictor of reduced HRR at 1-5 min. In addition, WC predicted a reduced HRR at 3 min. There were no significant associations between central obesity and electrophysiological parameters. EFT was not associated with ANS dysfunction. Conclusion: In this study, central adiposity and aging were associated with ANS dysfunction in obese individuals. The WC could be a marker of ANS dysfunction in obese individuals without any cardiovascular risk factors. The HRR assessment at a later decay phase could be more valuable for evaluating ANS function than during early recovery.

Acute Serious Thrombocytopenia Associated with Intracoronary Tirofiban Use for Primary Angioplasty

Tirofiban, a specific glycoprotein IIb/IIIa inhibitor, may cause extensive thrombocytopenia with an incidence of 0.2% to 0.5%. We report the case of a 50-year-old man who developed thrombocytopenia after tirofiban use (both intracoronary and peripheral) over hours and the successful management of this complication after primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction.

Increased Plasma High-sensitivity C-reactive protein and Myeloperoxidase Levels May Predict Ischemia During Myocardial Perfusion Imaging in Slow Coronary Flow

BACKGROUND AND AIMS It is unclear whether changes in plasma levels of inflammatory markers could explain the link between ischemia and slow coronary flow (SCF). The aim of the study was to evaluate the plasma levels of high-sensitivity C-reactive protein (hsCRP), interleukin (IL)-6, and myeloperoxidase (MPO) during myocardial perfusion imaging (MPI) in SCF patients. METHODS The study population consisted of 53 SCF patients and 30 controls. Coronary flow rates were documented by TIMI frame count (TFC). Plasma levels of hsCRP, IL-6, MPO, and MPI were obtained in all participants. RESULTS hsCRP, IL-6 and MPO levels of SCF patients were higher than controls (hsCRP: 4.7 ± 2.5 vs. 1.7 ± 1.1 mg/L, p <0.001; IL-6: 8.2 ± 4.3 vs. 5.2 ± 2.1 pg/mL, p <0.001; and MPO: 75.9 ± 59.6 vs. 24.3 ± 16.7 ng/mL, p <0.001). Twenty-one SCF patients exhibited myocardial perfusion defect (MPD) on MPI. In SCF patients, the highest hsCRP, IL-6 and MPO levels were observed in patients with both MPD and three-vessel slow flow. Mean TFCs were positively correlated with plasma levels of hsCRP (r = 0.424, p = 0.002), IL-6 (r = 0.367, p = 0.007), MPO (r = 0.430, p = 0.001), and reversibility score (r = 0.671, p <0.001) in SCF patients. HsCRP and MPO were the independent variables, which predicted positive MPI results (hsCRP: OR, 2.176; 95% CI, 1.200-3.943; p = 0.010, MPO: OR, 1.026; 95% CI, 1.007-1.046; p = 0.008). CONCLUSIONS Inflammation may play a crucial role in both the pathogenesis and development of ischemia in SCF. Association of increased levels of inflammatory markers and ischemia suggests that endothelial inflammation may be largely responsible for clinical presentation. New combined treatment regimens should target endothelial activation and inflammation in SCF.

Effects of substitutive therapy on right ventricular systolic and diastolic functions in patients with idiopathic hypogonadotropic hypogonadism

Background: There have been controversial studies evaluating ventricular functions in patients with idiopathic hypogonadotropic hypogonadism (IHH). A recent study has demonstrated that low serum testosterone levels are associated with increased cardiovascular mortality. Aim: We aimed to investigate ventricular functions by standard echocardiography and examine the effects of substitutive therapy on right ventricular (RV) functions in patients with IHH by means of pulsed wave tissue Doppler imaging (PWTDI). Methods: Twenty-three patients with IHH and 31 controls were evaluated by standard echocardiography and PWTDI. Isovolumic acceleration (IVA), myocardial systolic wave (Sm) velocity, myocardial precontraction time (PCTm), and PCTm to contraction time (CTm) ratio were determined as systolic indices. Myocardial relaxation time (RTm), early (Em) velocity, late (Am) velocity, and Em to Am ratio were determined as diastolic indices. Results: Peak pulmonary artery pressure (PAP) was significantly higher in control subjects (p=0.008). IVA and Sm values were similar in patients and controls. Em, Am velocities, and their ratios did not differ. PCTm was significantly longer (p=0.001 ) and PCTm to CTm ratio was significantly higher in patients (p=0.001). These parameters also decreased after replacement therapy, albeit not statistically significantly (p>0.05). PAP was significantly higher after substitutive therapy (p=0.009). Conclusions: Ventricular functions are normal in patients with IHH. Substitutive therapy has no effects on RV functions. However, substitutive therapy may increase PAP in small amounts, which has no immediate clinical implication with short-term use.

Decreased plasma adiponectin concentrations in patients with syndrome X

Objective — The levels of adiponectin, an anti-atherogenic protein, are decreased in patients with coronary artery disease. Syndrome X is associated with endothelial dysfunction, which is a key feature in the evolution of atherosclerosis.We sought to determine whether serum adiponectin levels are decreased in patients with syndrome X. Methods — Twenty-three syndrome X patients (14 men, 9 women) who presented with stable angina pectoris, had a positive non-invasive stress test or an abnormal myocardial perfusion scintigraphy single photon emission computed tomography (MPS SPECT) and a normal coronary angiogram, were included in our study, as were 17 asymptomatic healthy subjects (13 men, 4 women) with normal results from non-invasive stress testing. The serum adiponectin levels and lipid profiles of the patients and control subjects were determined with venous samples collected after a 12-hour fast. The results were analysed by a Mann Whitney U test. Results — Mean age (54.1 ± 11.8 y in patients and 59.8 ± 9.6 y in control subjects, P > 0.05) and body mass index (28.0 ± 3.3 in patients and 27.1 ± 4.2 in control subjects, P > 0.05) did not differ between the two groups. Adiponectin levels in patients with syndrome X (1.5 ± 1.1 mg/dl) were significantly lower than those in the control group (5.3 ± 2.9 mg/dl, P < 0.0001). Serum total cholesterol (TCHOL), triglyceride (TG), LDL, and HDL-cholesterol levels did not differ between the two groups (P > 0.05). Conclusion — Serum adiponectin levels were lower in patients with syndrome X, and these low adiponectin concentrations may cause endothelial dysfunction.Thus, patients with a marked drop in adiponectin levels may be considered at high risk for future coronary events and may therefore benefit from additional pharmacological treatment.

Hemorheological dysfunction in cardiac syndrome X

Abstract Background: Cardiac syndrome X (CSX) is often described as angina or angina-like chest pain with a normal coronary arteriogram, yet the underlying pathophysiological mechanisms have not been fully elucidated. The aim of the current study was to determine alterations in blood rheology (erythrocyte aggregation and deformability, plasma viscosity – PV) in patients with CSX. Methods: The study comprised 26 CSX patients (55.77 ± 12.33 years) and 37 age- and sex-matched (56.32 ± 11.98 years) healthy controls. Erythrocyte aggregation and deformability were measured by an ektacytometer and PV with a rotational viscometer. Results: Erythrocyte deformability measured at 1.69 and 3.00 Pa was lower in the CSX patients compared to the controls (p = .0001 and .017, respectively). Erythrocyte aggregation index (AI) (72.758 ± 7.65 vs. 66.483 ± 6.63, p = .002) and PV measured at a shear rate of 375 s−1 (1.932 ± 0.225 vs. 1.725 ± 0.331, p = .019) were significantly higher in patients with CSX. When AI, RDW and erythrocyte deformability measured at 1.69 Pa were evaluated together, it was observed that the increase in AI and RDW augments the risk of having CSX (OR: 1.2 and 2.65, respectively), while the rise in deformability decreases this risk (OR = 0.02). Conclusions: Hemorheological impairments are associated with CSX.