Zakir Lazoğlu

Increased Glycated Hemoglobin Level is Associated With SYNTAX Score II in Patients With Type 2 Diabetes Mellitus

SYNTAX score II (SS II) uses 2 anatomical and 6 clinical variables for the prediction of mortality after coronary artery bypass graft and percutaneous coronary intervention. The aim of this study was to investigate the relationship between glycated hemoglobin (HbA1c), fasting blood glucose (FBG), postprandial glucose (PPG), and SYNTAX Score (SS) and SS II in patients with type 2 diabetes mellitus and coronary artery disease (CAD). We enrolled 215 consecutive diabetic patients with stable angina pectoris who underwent coronary angiography. The SS II was calculated using a nomogram that was based on the findings of a previous study. There was a moderate correlation between HbA1c and SS (r = .396, P < .001), but there was a good correlation between HbA1c and SS II (r = .535, P < .001). There was also a weak correlation between FBG (r = .270, P = .001), PPG (r = .177, P = .027), and SS, but there was a weak–moderate correlation between FBG (r = .341, P < .001), PPG (r = .256, P = .001), and SS II. A better correlation has been detected between HbA1c and SS II compared to the correlation between HbA1c and SS.

The Paradox of Uric Acid in Cardiovascular Diseases

We read the article ‘‘Association Between Uric Acid and Coronary Collateral Circulation in Patients With Stable Coronary Artery Disease’’ by Uysal et al with interest. They investigated the association between serum uric acid (SUA) levels and development of coronary collateral (CC) vessels in patients with stable coronary artery disease (CAD). Higher levels of SUA were associated with poor CC vessels. We have some additional comments. There are some caveats including history of gout and coronary artery bypass grafting as exclusion criteria for no clear reasons, most importantly no control of current medication and a confounding difference in gender. The CC vessels are usually an adaptation to ischemia and shear stress, and they play a role in reducing infarct size, preserving left ventricular function, and increasing survival. The SUA levels are usually lower in premenopausal women compared with men. The SUA levels depend on several variables including dietary purine intake, fructose ingestion, the degradation of endogenous purines as well as renal and intestinal excretion of urate. Also, as the authors have mentioned, several drugs can influence SUA levels (eg, losartan and statins). Uric acid (UA) might have a protective effect against cardiovascular disease (CVD), but studies have reported associations with an increased risk of CAD, higher blood pressure, and adverse CVD risk profile. The Framingham Heart Study reported that UA was not a risk factor for CVD, and that clinical risk evaluation should only be based on the classic risk factors. Recently, Palmer et al investigated the association of plasma UA with CAD and hypertension using Mendelian randomization. They concluded that there is no evidence for a causal association, and that the apparent link is confounded by body weight. In the Multiple Risk Factor Intervention Trial, the association between hyperuricemia and CVD was weak and did not persist when the analysis was limited to men with hyperuricemia without a diagnosis of gout. Except an association with some neurological diseases, low SUA levels are not known cause of any disorder or disease. Questions waiting for answers include does lowering the SUA levels reduce CVD risk? What mechanisms may link SUA and CVD? These issues require well-designed prospective studies with hard end points, such as CVD mortality, myocardial infarction, and stroke. References

Comparison of the effects of metoprolol or carvedilol on serum gamma-glutamyltransferase and uric acid levels among patients with acute coronary syndrome without ST segment elevation

Objective: Serum gamma-glutamyltransferase (GGT) and uric acid levels measured in patients with acute coronary syndrome without ST segment elevation (NSTEMI) are important in diagnosis and in predicting the prognosis of the disease. There is a limited number of clinical studies investigating the effects of beta-blockers on GGT and uric acid levels in these patients. In our study, we aimed to investigate the effects of beta-blocker therapy on GGT and uric acid levels. Methods: We conducted a randomized, prospective clinical study. Hundred patients with NSTEMI were included in this study, and they were divided into two groups. Fifty patients were administered metoprolol succinate treatment (1 × 50 mg), whereas the remaining 50 patients were administered carvedilol treatment (2 × 12.5 mg). Thereafter, all of the patients underwent coronary angiography. Blood samples were taken at the time of admission, at the 1st month, and 3rd month to detect GGT and uric acid levels. Results: There was no statistically significant difference among the metoprolol or carvedilol groups in terms of the GGT levels measured at the baseline, 1st month, and 3rd month (p=0.904 and p=0.573, respectively). In addition, there was no statistically significant difference among the metoprolol or carvedilol groups in terms of uric acid levels measured at the baseline, 1st month, and 3rd month (p=0.601 and p=0.601, respectively). Conclusion: We found that GGT and uric acid levels did not show any change compared to the baseline values, with metoprolol and carvedilol treatment initiated in the early period in patients with NSTEMI.

A diagnostic dilemma: early repolarization syndrome associated with ventricular fibrillation.

An early repolarization (ER) pattern, characterized by J-point elevation, slurring of the terminal part of the QRS and ST-segment elevation, is a common finding on the 12-lead electrocardiogram. It has been suggested that J-point elevation, which was considered benign for many years, may play a critical role in the pathogenesis of idiopathic ventricular fibrillation (VF). Recent studies have shown that an ER pattern in inferior leads or inferolateral leads is associated with increased risk for life-threatening arrhythmias. We report the case of a 52-year-old man with no structural heart disease whose electrocardiogram showed type 2 ER pattern (with evidence of J-point and ST-segment elevation in electrocardiogram leads II, III, and aVF). The patient presented with VF.

PP-062 RELATION OF LEFT ATRIAL FUNCTIONS, P-TERMINAL FORCE AND INTERATRIAL BLOCK IN CHRONIC HAEMODIALYSIS PATIENTS

Objective: Metabolic syndrome (MS) is a cluster of risk factors leading to cardiometabolic diseases. The aim of the present study was to investigate the effect of MS on left atrial function, which is an important determinant of left ventricular filling. Methods: Left atrial (LA) volumes were measured echocardiographically in 32 MS patients and 32 age-sex matched controls. LA volumes were determined at the time of mitral valve opening (maximal, Vmax), at the onset of atrial systole (p wave at the electrocardiography, Vp) and at the mitral valve closure (minimal, Vmin) according to the biplane area-length method in apical 4-chamber and 2-chamber view. All volumes were corrected to the body surface area, and following left atrial emptying functions were calculated. LA passive emptying volume = Vmax−Vp, LA passive emptying fraction = LA passive emptying volume/Vmax. Conduit volume = LV stroke volume − (Vmax−Vmin), LA active emptying volume = Vp−Vmin, LA active emptying fraction = LA active emptying volume/Vp, LA total emptying volume = (Vmax−Vmin), LA total emptying fraction = LA total emptying volume/Vmax. Results: LA maximal volume and LA presystolic volume were significantly higher in MS patients than in controls (p< 0.001). But LA minimum volume was significantly lower in MS patients than in controls (p < 0.001). Although LA passive emptying volume (p < 0.03), LA passive emptying fraction (p < 0.001) and conduit volume (p < 0.001) were found to be significantly lower in MS patients than in controls, LA active emptying volume (p < 0.001) and LA active emptying fraction (p < 0.001) were significantly greater in MS patients than in controls. Conclusion: In our study, metabolic syndrome was associated with increased left atrial volume, decreased left atrial passive emptying function and increased pump function. Increased left atrial pump function represents a compensatory mechanism in patients with MS. Thus, these results underline the importance of maintaining a sinus rhythm in these patients.