Mustafa Karabacak

Mean platelet volume is increased in patients with hypertensive crises

Abstract Platelets may be activated in hypertension (HT). Hypertensive crisis is an extreme phenotype of HT and HT-related thrombotic complications. We aimed to assess mean platelet volume (MPV) in patients with hypertensive crises. This study included 215 hypertensive urgency (HU) patients (84 male, mean age = 66 ± 15 years) and 60 hypertensive emergency (HE) patients (26 male, mean age = 68 ± 13 years), who were admitted to the emergency department with a diagnosis of hypertensive crises. Control group was composed of age- and sex-matched 39 normotensive patients. Blood samples were withdrawn for whole blood count and routine biochemical tests. Systolic blood pressure (BP) was significantly higher in the HE group than in the HU group (p < 0.001). Median mean platelet volume (MPV) was higher in the HE group compared with HU and control groups [9.5 (Interquartile range, IQR: 8.7–10.1), 8.4 (IQR: 7.7–9.1), and 8.3 (IQR: 7.7–8.7) fl, each p < 0.001, respectively). In linear regression analysis, systolic BP (β = 0.18, 95% confidence intervals (CI): 0.002–0.015, p = 0.007) and diabetes mellitus (β = 0.24, 95% CI: 0.28–0.95, p < 0.001) were independently associated with MPV levels. Our findings show that MPV can be elevated in patients with HE and HU. It can be independently associated with systolic BP and diabetes mellitus. These findings imply that platelet activation contribute to the pathogenesis of thrombotic complications in hypertensive crises.

The association between previous statin use and development of atrial fibrillation in patients presenting with acute coronary syndrome

AIMS To examine the association between statin use and the development of atrial fibrillation (AF) in patients presenting with acute coronary syndrome (ACS). METHODS From a total of 1000 patients presenting with ACS 241 were on and 759 were not on statin. An AF episode was accepted as endpoint. RESULTS The incidence of AF was less frequent in statin group compared to non-statin group (5% vs 10%, respectively, p=0.01). Independent predictors of AF were left atrial diameter, use of statin, age, hypertension, previous AF and use of angiotensin converting enzyme inhibitors or angiotensin receptor blockers. CONCLUSIONS In ACS patients, statin treatment was associated with lower incidence of AF.

Increased plasma monocyte chemoattractant protein-1 levels in patients with isolated low high-density lipoprotein cholesterol

Abstract Background. High-density lipoprotein cholesterol (HDL-C) inhibits inflammation associated with the development of atherosclerotic plaques. Monocyte chemoattractant protein-1 (MCP-1) contributes to the pathogenesis of atherosclerosis. The aim of this study was to evaluate the relationship between plasma MCP-1 levels and low HDL-C levels in patients without cardiovascular disease (CVD). Methods. This study included 55 patients with low HDL-C (≤ 35 mg/dL) and 33 age- and sex-matched control subjects with normal HDL-C (˃ 35 mg/dL). In addition to MCP-1 levels, laboratory parameters associated with inflammation such as neutrophil-lymphocyte ratio (NLR), uric acid and high sensitivity C-reactive protein (hs-CRP) were also evaluated. Results. HDL-C levels was significantly lower in study group compared to that of the control group (p < 0.001). MCP-1 were prominently higher in the low HDL-C group compared with those of the control group (p < 0.01). NLR, uric acid and hs-CRP levels were also higher in patients with low HDL-C than controls. Conclusion. These findings suggest that elevated plasma MCP-1 levels and inflammation status might be associated with the increased cardiovascular risk in patients with low HDL-C.

Oxidative Stress Status Increase in Patients with Nonischemic Heart Failure

Objective: It was the aim of this study to investigate the serum oxidative stress level in nonischemic patients with heart failure (HF). Subjects and Methods: The study included 37 patients who presented to the Department of Cardiology, Suleyman Demirel University, Isparta, Turkey, with a diagnosis of asymptomatic HF (New York Heart Association class I-II). The patients had a left ventricular (LV) ejection fraction (EF) of ≤40% and normal coronary arteries or nonsignificant stenosis (stenosis <40%). In addition, 30 age- and sex-matched normal patients were selected as the control group. Clinical and laboratory characteristics presumed to be associated with oxidative stress were evaluated. Results: Demographic characteristics were comparable. However, creatinine and potassium levels were higher in the HF than in the control group. Total oxidative status [2.42 μmol H2O2 Eq/l (range 0.74-5.86) vs. 1.81 μmol H2O2 Eq/l (range 0.42-3.45); p < 0.01], oxidative stress index [2.24 (range 0.63-5.33) vs. 1.53 (range 0.28-2.51); p < 0.01] and uric acid (6.1 ± 1.8 vs. 4.4 ± 1.1 mg/dl; p < 0.01) levels were significantly higher in the HF than in the control group. The total antioxidant capacity was similar in both groups [1.22 mmol Trolox Eq/l (range 0.61-1.99) vs. 1.18 mmol Trolox Eq/l (range 0.82-1.80); p = 0.77]. The γ-glutamyltransferase levels were also comparable in both groups [32 U/l (range 11-106) vs. 23 U/l (range 11-72); p = 0.10]. Conclusion: The oxidative stress levels were higher in HF patients, and hence, oxidative stress may play an important role in poor prognosis of HF. Therefore, antioxidant treatment might be reasonable.

The effect of pretreatment with renin-angiotensin-aldosterone system blockers on cardioversion success and acute recurrence of atrial fibrillation

Background:  Renin‐angiotensin‐aldosterone system (RAS) may be activated during atrial fibrillation (AF). It is unclear whether RAS inhibition may facilitate cardioversion from AF and may prevent acute recurrence of AF (ARAF). We thus investigated the effect of pretreatment with RAS blockers on cardioversion success and ARAF in patients with AF scheduled for elective cardioversion.

Comparison of the effects of carvedilol and nebivolol on diastolic functions of the left ventricle in patients with non-ischemic heart failure

BACKGROUND We investigated whether carvediolol or nebiovolol with vasodilator properties will produce different effects on diastolic function of the left ventricle (LV) in heart failure (HF) with low ejection fraction (EF). METHODS Sixty-one non-ischemic HF patients with EF ≤40% randomly received carvedilol (n = 31, 16 male) or nebivolol (n = 30, 19 male). Clinical and echocardiographic evaluations were performed at baseline, 3 and 6 months after therapy. Mitral inflow velocities (E and A waves), deceleration time of E wave (DT), isovolumetric relaxation time (IVRT), mitral annular velocities (Ea and Aa waves) were evaluated. Mitral E/A and E/Ea ratios were calculated. RESULTS In carvediolol and nebivolol groups, mitral E/A ratio (from 1.08 ± 0.31 to 0.87 ± 0.30 vs. from 0.98 ± 0.20 to 0.80 ± 0.20, p = 0.30) and IVRT (from 108 ± 13 to 94 ± 10 ms vs. from 107 ± 22 to 92 ± 10 ms, p = 0.25) similarly decreased while DT prolonged (from 184 ± 40 to 218 ± 42 ms vs. from 193 ± 37 to 222 ± 36 ms, p = 0.71). Also, E/Ea ratio significantly decreased in each group (p = 0.01), but it was lower in nebivolol group than carvedilol group at 6 months (10.2 ± 2 vs. 11.8 ± 2, p = 0.01). Carvediolol and nebivolol reduced similarly N-terminal pro-B type natriuretic peptide level (from 666 to 137 vs. 661 to 123 pg/dL, p = 0.41, respectively) and improved functional capacity (p > 0.05). CONCLUSIONS At 6 month follow-up, carvedilol and nebivolol appear to similarly improve LV diastolic functions in non-ischemic HF patients.

Mean Platelet Volume in Patients With Carbon Monoxide Poisoning

Carbon monoxide (CO) poisoning is frequent and can lead to high morbidity and mortality. Some studies have indicated increased platelet activation and aggregation in CO poisoning. Thus, we investigated mean platelet volume (MPV), an indicator of platelet activation, in patients with CO poisoning. We included 193 (117 women) patients who presented with a diagnosis of CO poisoning between June 2011 and March 2013. Control group was composed of 39 (15 women) patients. Troponin and creatine kinase MB levels were significantly higher in the CO poisoning group. Platelet counts were significantly higher in patients with CO poisoning (281 ± 76 vs 248 ± 65 × 109, respectively; P = .01). Similarly, MPV was significantly higher in the CO poisoning group (8.9 ± 0.8 vs 7.9 ± 0.9 fL, respectively; P < .001). Elevated MPV values may indicate that patients with CO poisoning have a higher risk of thromboembolic and cardiovascular complications due to platelet activation.

Is signal peptide-CUB-EGF domain-containing protein1 a diagnostic biomarker in patients with hypertensive crises

BACKGROUND Platelet activation might play a significant role in the pathophysiology of cardiovascular and cerebrovascular events in hypertension (HT). Signal peptide-CUB-EGF domain-containing protein1 (SCUBE1), an indicator of platelet activation, is increased in HT. The aim of this study was to investigate the SCUBE1 in patients with hypertensive crises. METHODS This study included 33 hypertensive urgency (HU) and 39 hypertensive emergency (HI) patients admitted to our emergency department with a diagnosis of hypertensive crisis. Platelet activation was evaluated with biochemical markers such as SCUBE1, soluble CD40L (sCD40L), mean platelet volume, and platelet count. RESULTS The SCUBE1 values of the HE patients were significantly higher than other groups (1.09 ± 0.49, 0.71 ± 0.23 and 0.37 ± 0.02 ng/dl, respectively; p <  0.01). The sCD40L values were higher in the hypertensive crises compared with the control group (4.16 ± 1.82, 3.41 ± 1.76 and 1.76 ± 0.68 ng/ml, respectively; p <  0.01). More importantly, SCUBE1 had high sensitivity and specificity in the detection of target organ damage. CONCLUSION In present study showed that SCUBE1 was significantly higher in HE patients. In addition, sCD40L level, presence of diabetes, and systolic blood pressure were independently associated with increased SCUBE1. According to our results, SCUBE1 might be a diagnostic biomarker in hypertensive crisis patients.

Effect of previous statin use on the incidence of sustained ventricular tachycardia and ventricular fibrillation in patients presenting with acute coronary syndrome.

OBJECTIVE Recent studies suggest that statins have anti-arrhythmic effects. The aim of this study was to evaluate the effects of statins on sustained ventricular tachycardia or ventricular fibrillation (S-VT or VF) in patients presenting with acute coronary syndrome (ACS). METHODS The population of this study consisted of consecutive patients admitted to coronary care unit. It was an observational case-controlled retrospective analysis performed on prospective cohort. From a total of 1000 patients presenting with ACS, 241 were on and 759 were not on statin. Patient demographics, clinical characteristics and previous medical treatment including statins were recorded. A S-VT or VF episode during hospitalization was accepted as endpoint. Multiple logistic regression model was performed which considered the occurrence of S-VT or VF as the response variable. RESULTS Sustained VT or VF occurred in 3.3% of patients in statin group and in 9% of patients in non-statin group. Univariate positive predictors of S-VT or VF were ST elevation myocardial infarction as clinical presentation, smoking and thrombolysis; univariate negative predictors of S-VT or VF were ejection fraction, use of acetylsalicylic acid before hospitalization, use of statin before hospitalization, initiation of clopidogrel at the hospital and normal coronary arteries. In the multiple logistic regression analysis, the only independent predictor of S-VT or VF was ejection fraction (OR 0.96; 95% CI 0.93 to 0.99; p=0.005). CONCLUSION Our results indicate that, although the incidence of S-VT/VF was significantly lower in patients with ACS and previous statin use; statin use is not an independent predictor of the occurrence of S-VT or VF in patients presenting with ACS.

Influence of statin therapy on circadian variation of acute myocardial infarction.

OBJECTIVE Strong evidence has suggested that there is a circadian periodicity of acute coronary event. Beta-blockers, aspirin and angiotensin-converting enzyme inhibitors decrease the rate of acute myocardial infarction (AMI) and blunt the peak incidence in the morning. However, such effect has not been evaluated for statins. Accordingly, the present study aimed to evaluate the influence of statin therapy on circadian variation of AMI. METHODS This retrospective study consisted of 451 consecutive patients with acute ST segment elevation AMI. The patients were divided into two group based on prior statin usage. In statistical analysis t test, Chi-square test and Mann Whitney U test were used for comparison of groups. We used harmonic regression models to evaluate the circadian variation of onset of MI symptoms in patients receiving statin and patients not receiving statin. RESULTS In all study participants, the highest incidence of AMI was between 6.00 and 12.00; the odds ratio was 1.34 (95% CI 1.20 to 1.46, p=0.001). In the non-statin group, the highest incidence of AMI occurred between 0:00 A.M. and 06.00. There was still a peak incidence between 6.00 A.M. and noon in the statin therapy receiving group; the odds ratio was 1.61 (95% CI 1.34 to 1.80, p=0.001). Accordingly, there was no statistical difference between the statin and non-statin groups regarding circadian variation of AMI. Prior usage of statin did not blunt the peak incidence of AMI in the morning. CONCLUSION Prior usage of statin does not seem to play a role in the circadian periodicity of AMI.