Mahmut Şahin

Is galectin-3 a biomarker, a player-or both-in the presence of coronary atherosclerosis?

Atherosclerosis is a complex process mediated by leukocytes, macrophages and various inflammatory markers. Galectin-3 is secreted by activated macrophages and is involved in cardiac fibrosis, cardiac remodeling, and inflammation. The present study aimed to determine the relationship between the presence and severity of coronary artery disease (CAD) and serum galectin-3 levels. The study included 82 patients with CAD confirmed via coronary angiography and 82 healthy participants as control group. Angiographic CAD was defined as ≥50% luminal diameter stenosis of at least one major epicardial coronary artery. The severity of CAD was determined by the Gensini score; and the serum galectin-3 levels were measured via ELISA. Serum galectin-3 levels were significantly higher in the patient group with CAD than in the control group (12.96±4.92 vs 5.52±1.9 ng/mL, p<0.001). In the correlation analysis, serum galectin-3 showed significant correlation with the Gensini score (r=0.715, p<0.001), number of diseased vessels (r=0.752, p<0.001) and serum hs-CRP level (r=0.607, p<0.001). In addition, multivariate logistic regression analysis showed that the serum galectin-3 levels were significant and independent predictors of the presence of angiographic CAD (OR=3.933, 95% CI 2.395 to 6.457; p<0.001). In the present study, the serum galectin-3 levels were higher in the patients with CAD than in healthy controls. Also, serum galectin-3 levels showed a significant positive correlation with the severity of CAD. An increased serum galectin-3 level may be considered an important activator and a marker of the atherosclerotic inflammatory process in CAD.

Serum Neutrophil Gelatinase-Associated Lipocalin Levels and Aortic Stiffness in Noncritical Coronary Artery Disease

Aim: The aim of this study was to establish the degree of aortic stiffness and levels of neutrophil gelatinase-associated lipocalin (NGAL) in patients with stable ischemic heart disease. Materials and Methods: Patients who were found to have stable, noncritical lesions on coronary angiography were included in the study [noncritical coronary artery disease (CAD)]. The control group consisted of those patients who had similar risk profiles and metabolic parameters without atherosclerosis on angiography. Results: A total of 101 patients were included in the study of which 56 had noncritical CAD. Whereas the aortic strain (9.11 ± 3.4 vs. 14.01 ± 4.1%, p < 0.001) and aortic distensibility (3.98 ± 1.9 10-6 cm2/dyn vs. 6.33 ± 2.3 10-6 cm2/dyn, p < 0.001) were lower in the noncritical CAD group, the aortic stiffness index was higher (6.34 ± 3.9 vs. 3.37 ± 2.4, p < 0.001) as compared to controls. Serum NGAL levels were higher in the noncritical CAD group (79.29 ± 38.8 vs. 48.05 ± 21.4 ng/ml, p < 0.001). NGAL levels were negatively correlated with aortic strain (p < 0.01, r = 0.57) and distensibility (p < 0.001, r = 0.62), but positively correlated with the aortic stiffness index (p < 0.001, r = 0.72). Conclusion: We show that in patients with noncritical CAD, the degree of aortic stiffness and NGAL levels are higher. These markers can be used as tools for further risk stratification of patients with noncritical CAD.

Apical hypertrophic cardiomyopathy: a case of slow flow in lad and malign ventricular arrhythmia

The coronary slow flow phenomenon is an angiographic finding characterized by delayed distal vessel opacification in the absence of epicardial coronary artery disease. Patients often present with acute coronary syndrome. Histopathologic studies have revealed the existence of fibromuscular hyperplasia and myofibrilar hypertrophy. Apical hypertrophic cardiomyopathy is a benign progressive form of hypertrophic cardiomyopathy, that is rarely observed in western communities. It remains commonly asymptomatic until advanced ages. Syncope, arrhythmia or sudden death may be the first symptom. We report a case of slow coronary arterial flow in a 71-year-old male patient with apical hypertrophic cardiomyopathy who experienced chest pain and sudden cardiac arrest due to ventricular arrhythmia.

Highlights from ACC.17 scientific sessions

The ACC 2017 meeting was held in Washington D.C. between March 17 and 19, 2017. Although the meeting had an overall scientific impact, it was partly affected by the travel bans of colleagues from some countries. Herein, we discuss some highlights of the meeting. The most striking aspect of ACC 2017 was the presentation of plenty of late-breaking clinical trials. The most striking among all was “FOURIER” trial in which Turkish scientists had also participated (1). Evolocumab therapy resulted in 59% further reduction of LDL cholesterol compared to standard care. The FOURIER trial shows that evolocumab, which is a fully human monoclonal antibody against PCSK9, causes a significant reduction of 15% in the primary end-points of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization; in addition, it also causes a significant reduction of 20% in some secondary end-points of cardiovascular death, myocardial infarction, or stroke. Notably, the benefit was driven by reductions in the incidence of nonfatal AMI, stroke, and coronary revascularization, but the incidence of cardiovascular (CV) death remained similar in both groups. However, it is important to note that cost issues were of concern even in the USA. The bococizumab trial (SPIRE) was also presented in the same session (2). As we all know, bococizumab trial was halted prematurely by the sponsor company Pfizer because of the high incidence of antidrug antibodies after a median follow-up of 10 months. Pfizer decided to publish data transparently both in the meeting and also in the journal. In contrast to the overall positive result of the evolocumab trial, bococizumab did not result in a decreased rate of major cardiovascular outcomes in the predefined lower-risk group, despite an overall 56% decrease of LDL cholesterol from the baseline. Of note, in the higher-risk group, major cardiovascular events significantly decreased by 21%. Injection-site reactions were common in the bococizumab group (10.4%). Furthermore, at 1 year, 48% patients who received bococizumab had detectable antidrug antibodies after 3 months (3). This resulted in an attenuation of the decrease in LDL cholesterol levels. All these findings may be related to humanized characteristic of bococizumab, in contrast to fully human antibodies, evolocumab and alirocumab. ACC 2017 has provided the participants the opportunity of joining the announcement of the low-awaited results of SURTAVI trial, which was simultaneously published in the New England Journal of Medicine (NEJM) (4). Transcatheter aortic-valve replacement (TAVR) is a guideline-recommended alternative to surgery in patients with severe aortic stenosis who are at high surgical risk. However, outcomes among patients with aortic stenosis who are at intermediate surgical risk are not known. In this trial, 1660 patients with aortic stenosis and with intermediate surgical risk were randomized into TAVR and surgery groups (864 versus 796 patients consecutively). The primary end point, which was a composite of death from any cause or disabling stroke at 24 months, was noted to be 12.6% in the TAVR group and 14.0% in the surgery group (noninferiority). Of note, TAVR resulted in lower mean gradients and larger aortic-valve areas than surgery, apart from lower rates of acute kidney injury and atrial fibrillation, at a cost of higher rates of residual aortic regurgitation and pacemaker requirement. Along with this finding, ACC/AHA Valvular Heart Disease Guidelines Update was released with the following Class-IIa recommendation: “TAVR is a reasonable alternative to surgical AVR for symptomatic patients with severe AS (Stage D) and an intermediate surgical risk” (5). The same update also added a Class-IB (derived from nonrandomized studies) recommendation for mechanical prosthetic valve thrombosis as “Urgent initial treatment with either slow-infusion low-dose fibrinolytic therapy or emergency surgery is recommended for patients with a thrombosed left-sided mechanical prosthetic heart valve presenting with symptoms of valve obstruction” up on data, coming from members of Turkish Society of Cardiology (5). Rivaroxaban or ASPIRIN for Extended Treatment of Venous Thromboembolism (EINSTEIN CHOICE) trial was also presented at ACC 2017 and simultaneously published in NEJM (6). The trial aimed to compare the efficacy and safety of once-daily rivaroxaban (doses of 20 or 10 mg) with aspirin (dose of 100 mg) for extended therapy in patients with venous thromboembolism after primary anticoagulant therapy for 6–12 months. A total of 3396 patients were randomized to rivaroxaban 20 mg (n=1121), rivaroxaban 10 mg (n=1136), and aspirin 100 mg (n=1139) groups and followed up for almost 1 year. The primary efficacy outcome was symptomatic recurrent fatal or nonfatal venous thromboembolism, which occurred in 1.5% patients with rivaroxaban 20 mg, in 1.2% patients with rivaroxaban 10 mg, and 4.4% patients with aspirin (hazard ratio for rivaroxaban 20 mg vs. aspirin, 0.34; hazard ratio for rivaroxaban 10 mg vs. aspirin, 0.26; p<0.001 for both comparisons). Major bleeding was 0.5% in the rivaroxaban 20 Highlights from ACC.17 scientific sessions

Effect of routine postdilatation on final coronary blood flow in primary percutaneous coronary intervention patients without angiographic stent expansion problems

Inadequate expansion of coronary stents is associated with stent thrombosis in early stage and with stent restenosis in later stages. Postdilatation (postD) performed using non-compliant balloons improves stent expansion. However, use of this ballooning strategy in primary percutaneous coronary intervention (PPCI) has not been evaluated adequately. Patients who presented with ST segment elevation myocardial infarction (STEMI) and underwent PPCI were included in the present study. Patients were randomized into two groups as those for whom postD was performed (n=62) and those for whom postD was not performed (n=62). Coronary blood flow was evaluated using the thrombolysis in myocardial infarction (TIMI) flow and TIMI frame count (TFC). Total of 124 patients with STEMI were included in the study. There was no difference with respect to baseline TIMI flow, culprit coronary artery and MI localization. However, slow-reflow rate (14.5% vs 35.5%, p=0.007) and final corrected TFC (28.9±16.9 vs 37.0±23.1, p=0.028) were significantly higher in the postD group. Multivariate regression analysis showed postD as an independent variable for slow reflow (OR 11.566, 95% CI 1.633 to 81.908, p=0.014). In our study, routine postD during PPCI was found to be associated with an increased risk of slow reflow in patients without angiographic stent expansion problems.

Cardiovascular diseases and vehicle driving: The proposal of Turkish Society of Cardiology 2016

The rate of traffic accidents due to medical causes is unknown. Based on data from Canada and the United States, cardiovascular conditions account for less than 5% of commercial vehicle accidents. European data shows that about 0.1% of reportable road accidents maybe attributed to medical conditions, of which 10-25% is due to cardiac events. Driving guidelines and regulations in cardiovascular diseases are of importance, not only for protecting the health of the patients but also for protection of the community. Therefore, our aim as the Turkish Society of Cardiology is to provide a guide for cardiologists that addresses this important issue, and reports a consensus on medical standards for drivers with cardiovascular disorders.

Evaluation of inhomogeneities of repolarization in patients with psoriasis vulgaris

Introduction The arrhythmia potential has not been investigated adequately in psoriatic patients. In this study, we assessed the ventricular repolarization dispersion, using the Tp-e interval and the Tp-e/QT ratio, and investigated the association with inflammation. Material and methods Seventy-one psoriasis vulgaris patients and 70 age- and gender-matched healthy individuals were enrolled in the study. The severity of the disease was calculated using Psoriasis Area and Severity Index scoring. The QTd was defined as the difference between the maximum and minimum QT intervals. The Tp-e interval was defined as the interval from the peak of the T wave to the end of the T wave. The Tp-e interval was corrected for heart rate. The Tp-e/QT ratio was calculated using these measurements. Results There were no significant differences between the groups with respect to basal clinical and laboratory characteristics (p > 0.05). The Tp-e interval, the corrected Tp-e interval (cTp-e) and the Tp-e/QT ratio were also significantly higher in psoriasis patients compared to the control group (78.5 ±8.0 ms vs. 71.4 ±7.6 ms, p < 0.001, 86.3 ±13.2 ms vs. 77.6 ±9.0 ms, p < 0.001 and 0.21 ±0.02 vs. 0.19 ±0.02, p < 0.001 respectively). A significant correlation was detected between the cTp-e time and the Tp-e/QT ratio and the PASI score in the group of psoriatic patients (r = 0.51, p < 0.001; r = 0.59, p < 0.001, respectively). Conclusions In our study, we detected a significant increase in the Tp-e interval and the Tp-e/QT ratio in patients with psoriasis vulgaris. The Tp-e interval and the Tp-e/QT ratio may be predictors for ventricular arrhythmias in patients with psoriasis vulgaris.

The relationship between coronary slow flow phenomenon and urotensin-II: A prospective and controlled study

Objective: The underlying mechanism of coronary slow flow (CSF) has not yet been clarified, although many studies have been conducted to understand its pathophysiology. In this study, we investigated the role of a very potent vasoconstrictor, urotensin-II (UII), in the pathophysiology of CSF. This prospective and controlled investigation aimed to evaluate the association between CSF and serum levels of UII. Methods: Our study included 32 patients with slow flow in any coronary artery and 32 patients with normal coronary arteries. Coronary flow was calculated using the Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC) method, and CSF was defined as TFC ≥39 for the left anterior descending artery, TFC ≥27 for the circumflex coronary artery, and TFC ≥24 for the right coronary artery. UII levels in blood samples obtained from both groups were measured by enzyme-linked immunosorbent assay (ELISA) method. Results: UII levels were significantly higher in the CSF group than in the control group [122 pg/mL (71-831), 95 pg/mL (21-635), respectively; p<0.001]. High-density lipoprotein (HDL) levels were lower in the CSF group, and leukocyte counts were significantly higher. A positive correlation between UII and mean TFC (r=0.524, p=0.002) was found in the CSF group. The multivariate logistic regression analysis determined that UII, HDL, and cigarette smoking were independent indicators in predicting CSF (OR=1.010, 95% confidence interval 1.002-1014, p=0.019; OR=0.927, 95% confidence interval 0.869-0.988, p=0.019; OR=5.755, 95% confidence interval 1.272-26.041, p=0.021, respectively). Conclusion: Serum UII levels were found to be significantly higher in the CSF group, suggesting that UII may be one of the underlying factors in the pathogenesis of CSF