Ramazan Topsakal

Platelet activation and inflammatory response in patients with non-dipper hypertension

OBJECTIVE Non-dipper hypertensives had about three times the risk of atherosclerotic events than hypertensives whose blood pressure was >10% lower at night compared to daytime (dippers). Platelet activation and inflammatory response may derive from most atherosclerotic events. Mean platelet volume (MPV) is a determinant of platelet activation and high sensitive C-reactive protein (hs-CRP) is the best candidate assay to identify and monitor the inflammatory response. We aimed to determine whether MPV and hs-CRP levels are elevated in non-dipper patients compared to dippers and healthy controls. In addition, we tried to find out if MPV and CRP are related to each other or not in non-dipper hypertensives. METHOD The total 126 patients study group included 86 patients with hypertension and 40 healthy subjects (16 male, mean age; 51+/-4) as control. Ambulatory blood pressure monitoring was performed for all patients. Hypertensive patients were divided into two groups; 46 dipper patients (18 male, mean age; 50+/-9) and 40 non-dipper patients (17 male, mean age; 53+/-11). Clinical baseline characteristics were similar between groups. We measured mean platelet volume in a blood sample collected in EDTA tubes and high-sensitive CRP was measured by using BN2 model nephlometer. RESULTS Non-dipper patients demonstrated higher levels of MPV compared to dippers and normotensives (9.72+/-0.52 fl vs 9.38+/-0.33 fl and 8.92+/-0.42 fl, p<0.05, respectively). High-sensitive CRP levels were also significantly higher in non-dippers compared to dippers and normotensives (4.9+/-1.7mg/l vs 3.8+/-1.5mg/l and 2.7+/-0.8mg/l, p<0.05, respectively). There was significant positive correlation between MPV and CRP levels (p=0.002, r=0.482) in non-dipper hypertensives. CONCLUSION Our results suggest that patients with non-dipping tend to have increased platelet activation and inflammatory response. Increased platelet activation and inflammatory response could contribute to increase the atherosclerotic risk in non-dipper patients compared to dippers.

Preload Dependence of Doppler Tissue Imaging Derived Indexes of Left Ventricular Diastolic Function

Doppler tissue imaging (DTI) has been proposed as a tool for the evaluation of diastolic function. Controversy exists regarding whether DTI measurements are influenced by preload. Changes in the circulating volume associated with hemodialysis result in preload reduction. To determine the influence of preload reduction on DTI and standard pulsed‐Doppler transmitral diastolic velocities, 30 patients (mean age 41 ± 14) with chronic renal insufficiency without overt heart disease were studied by DTI and standard pulsed Doppler before and after hemodialysis. From the apical window, DTI sample volume was placed at the lateral and septal mitral annulus and at the midsegment of lateral and septal myocardial wall of the left ventricle. Peak early diastolic annular and myocardial, and peak late diastolic annular and myocardial velocities were measured. Transmitral peak early and late diastolic velocities were also recorded by standard pulsed Doppler. The peak velocity of early diastolic mitral flow decreased from 100 ± 30 to 85 ± 34 cm/s (P < 0.001) after hemodialysis. Hemodialysis elicited marked reduction in early diastolic lateral mitral annular and midlateral myocardial velocities (6.9 ± 3.2 to 6.3 ± 2.9 cm/s, P < 0.04 and 6.7 ± 0.3 to 5.5 ± 2 cm/s, P < 0.001, respectively). Early diastolic, septal mitral annular, and midseptal myocardial velocities were also significantly decreased (5.8 ± 2.8 to 4.6 ± 2 cm/s, P < 0.006 and 6.2 ± 2 to 5.1 ± 1 cm/s, P < 0.008, respectively). Late diastolic mitral annular and myocardial velocities did not change. It is concluded that early diastolic mitral annular and myocardial velocities are affected by acute preload reduction. It is necessary to consider preload when diastolic function is assessed by DTI.

The mean platelet volume in patients with non-dipper hypertension compared to dippers and normotensives

Abstract Objectives. Increased platelet activation plays an important role in the development of atherosclerosis. Mean platelet volume (MPV) is a determinant of platelet activation. In our study, we aimed to determine whether MPV levels are elevated in non-dipper patients compared with dippers and healthy controls. In addition, we tried to find out if MPV levels are correlated with blood pressure measurements in hypertensive patients. Methods. This cross-sectional study included 56 hypertensive patients; 27 age- and sex-matched healthy volunteers were enrolled to study as a control subjects. Ambulatory blood pressure monitoring was performed for all patients. Hypertensive patients were divided into two groups: 28 dipper patients (10 male, mean age 51 ±8 years) and 28 non-dipper patients (11 male, mean age 53±10 years). MPV was measured in a blood sample collected in EDTA tubes and was also used for whole blood counts in all patients. Results. In non-dipper patients, 24-h systolic blood pressure (141.5±10.21 vs 132.3±7.7 mmHg, p<0.001), 24-h diastolic blood pressure (88.2±8.5 vs 81.0±8.2 mmHg, p<0.01) and 24-h average blood pressure (105.7±8.5 vs 97.7±7.4 mmHg, p<0.001) are significantly higher than dippers. Whereas daytime measurements were similar between dippers and non-dippers, there was a significant difference between each group during night-time measurements (night-time systolic 137.1 ±11.0 vs 120.2±8.0 mmHg, p<0.001; night-time diastolic 85.3±8.0 vs 72.8±7.9 mmHg, p<0.001). Non-dipper patients (9.61 ±0.42 fl) demonstrated higher levels of MPV compared with dippers (9.24±0.35 fl) and normotensives (8.87±0.33 fl) (p<0.001 and p<0.001, respectively). There was significant correlation between MPV and ambulatory diastolic and systolic blood pressure in non-dipper hypertensives. Conclusion. Our results suggest that MPV, a determinant of platelet activation, has a positively correlation with blood pressure and elevated in non-dipper compared with dippers and controls. Increased platelet activation could contribute to increase the atherosclerotic risk in non-dipper patients compared with dippers.

Effects of Calcium Treatment on QT Interval and QT Dispersion in Hypocalcemia

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The relationship between Helicobacter pylori IgG titre and coronary atherosclerosis.

Objectives — The role of Helicobacter pylori (HP) in the progression of atherosclerosis is con-troversial.We investigated the relation between HP IgG antibody titres and severity and intensity of coronary atherosclerosis and also clinical presentation of coronary artery disease (CAD). Methods — The patient group consisted of 353 patients with angiographically proven CAD, which contains 3 different subgroups: 163 patients with myocardial infarction (MI), 106 patients with unstable angina (USAP) and 84 patients with stable angina (SAP). Control group included 163 subjects with angiographically proven normal coronary arteries. Helicobacter pylori IgG antibody titres were measured by an enzyme immunoassay method in all patients. Gensini and Extent scores were used to evaluate the angiographic severity and extent of atherosclerosis. C-reactive protein levels were measured by Behring nephelometry system kits. Results — Seropositivity rates for HP were similar between groups (82.7% in the patient group and 86.6% in the control group (P > 0.05)). Also HP-IgG levels were similar among the MI, USAP and SAP groups. No significant correlation was observed between CRP levels and HP-IgG level titres. There was no significant correlation between HP-IgG level (r = 0.086, P = 0.2) and Gensini score but a significant poor correlation was observed between HP-IgG level and Extent score (r = + 0.156, P = 0.03). Conclusions — Helicobacter pylori IgG titres do not play an important role in the presentation of CAD and do not increase systemic inflammatory response. However, Helicobacter pylori IgG antibody titres may be correlated with the extent of CAD.

Relationship between platelet indices and spontaneous echo contrast in patients with mitral stenosis

AIMS To determine the association of platelet indices with spontaneous echo contrast (SEC) in patients with mitral stenosis. METHODS AND RESULTS A total of 232 consecutive patients with mitral stenosis who undergoing mitral balloon valvuloplasty were enrolled to the study. Patients were divided into two groups according to the formation of SEC in the left atrium. Group 1: mitral stenosis complicated with SEC; Group 2: mitral stenosis without SEC. Transthoracic echocardiography and transoesophageal echocardiography were performed for each patient. Complete blood counting parameters were measured and all routine biochemical tests were performed. There were 133 patients (mean age 42 ± 11 and 74% female) in the SEC(-) group and 99 patients (mean age 45 ± 10 and 64% female) in the SEC(+) group. Plateletcrit (0.25 ± 0.06 vs. 0.27 ± 0.07, P = 0.043) and mean platelet volume (MPV) levels (9.4 ± 1.1 vs. 10.4 ± 1.2, P < 0.001) were significantly higher in the SEC(+) group. When we divided the SEC(+) patients into four subgroups according to previously reported criteria, MPV levels increased to correlate with the degree of SEC (P < 0.001). At multivariate analysis, MPV levels [odds ratio (OR) 2.365, 95% confidence interval (CI) 1.720-3.251; P < 0.001] and PCT levels (OR 2.699, 95% CI 1.584-4.598; P= 0.033) are independent risk factors of SEC in patients with mitral stenosis. CONCLUSION In patients with mitral stenosis, cheaply and easily measurable platelet indices including MPV and PCT levels are associated with the presence of SEC and are independent risk factors of SEC.

Colour tissue Doppler echocardiographic evaluation of right ventricular function in patients with right ventricular infarction.

Objective: This study was undertaken to determine right ventricular (RV) function as assessed by colour Doppler tissue imaging (DTI) in patients with RV infarction. Methods: During the study period, 35 patients were evaluated: 14 patients had an inferior myocardial infarction (MI) with RV infarction and 21 patients had an inferior MI without RV involvement. Twenty age-matched healthy subjects served as controls. The diagnosis of RV infarction was defined by ST segment elevation >0.1 mV in lead V4R. Systolic and early and late diastolic velocities were acquired from the apical four-chamber view at the lateral tricuspid annulus, the septal side of the tricuspid annulus and the RV free mid-wall using colour DTI. Results: Systolic and early diastolic velocities at the lateral tricuspid annulus were significantly reduced in patients with inferior MI with RV infarction compared with those in healthy individuals (7.8 ± 1 vs. 11 ± 2 cm/s, p < 0.002) and patients with inferior MI without RV infarction (7.8 ± 1 vs. 10 ± 1 cm/s, p < 0.002). The late diastolic lateral annular velocity did not differ between the groups. Systolic and early diastolic RV free wall velocities were also significantly decreased in patients with RV infarction compared with those in healthy individuals (7 ± 1 vs. 8.7 ± 1 cm/s, p < 0.01; 6.3 ± 2 vs. 8.7 ± 2 cm/s, p < 0.05, respectively) and patients with inferior MI without RV infarction (7 ± 1 vs. 9 ± 2 cm/s, p < 0.01; 6.3 ± 2 vs. 8.3 ± 2 cm/s, p < 0.05, respectively). Conclusion: The evaluation of tricuspid annular and RV free wall velocities using colour DTI provides a rapid and noninvasive tool for assessing RV function in patients with RV infarction.

Does Serum Bilirubin Level on Admission Predict TIMI Flow Grade and In-Hospital MACE in Patients With STEMI Undergoing Primary PCI

We evaluated the association of total bilirubin with post-percutaneous coronary intervention (PCI) coronary blood flow and in-hospital major adverse cardiac events (MACEs) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary PCI. A total of 536 consecutive patients with STEMI (male 79%, mean age = 59.9 ± 12.6 years) admitted within 6 hours from symptom onset were enrolled. Patients were divided into 2 groups based on the thrombolysis in myocardial infarction (MI) flow grade. In-stent thrombosis, nonfatal MI, and in-hospital mortality were significantly higher in no-reflow group (P = .007, P = .002, and P < .001, respectively). On multivariate regression, the total bilirubin levels remained independent predictors of no-reflow (odds ratio [OR] 1.586, 95% confidence interval [CI] 1.02-2.47; P = .042) and in-hospital MACE (OR 1.399, 95% CI 1.053-1.857; P = .020). Serum bilirubin levels were independently associated with no-reflow and in-hospital MACE in patients with STEMI undergoing primary PCI.

Effects of chronic obstructive pulmonary disease on coronary atherosclerosis

The chronic systemic inflammation and oxidative stress are important features in chronic obstructive pulmonary disease (COPD). Atherosclerosis is accepted as an inflammatory disease. Both local and systemic inflammation and oxidative stress negatively affect the atherosclerotic process. Metabolic alterations, systemic inflammation, and neurohormonal activation frequently occur in patients with COPD. However, the impact of COPD on intensity and severity of atherosclerosis and morphology of stenotic lesions in patients with established coronary artery disease by coronary angiography is unknown. Eighty-eight patients who were diagnosed with COPD disease were enrolled in the study. Eighty-two patients without any pulmonary disease were included in the control group. Coronary angiography and blood gases analysis were performed in all patients. Gensini score and Extent score were used to evaluate the intensity and severity of atherosclerosis. Lesion morphologies were defined in all patients. The mean number of affected coronary arteries was 2.5 ± 0.6 in the COPD group and 2.1 ± 0.7 in the control group (P = 0.004). The mean Extent score was 37 ± 16 in the COPD group and 23 ± 11 in the control group (P = 0.001). The Gensini score in the COPD group was significantly higher than that in the control group (respectively 10.9 ± 6.3 vs 6.6 ± 4.1, P = 0.01). The number of critical lesions, and type B and C lesions were higher in the COPD group. Multivariate analysis demonstrated that COPD was independently predictive for Gensini score (odds ratio 1.371; 95% confidence interval 1.682–9.228; P = 0.002) and Extent score (odds ratio 1.648; 95% confidence interval 2.023–13.339; P = 0.001). Severity and intensity of atherosclerosis increases in COPD and atherosclerotic lesions have worse morphological properties in COPD.

Effects of nebivolol therapy on endothelial functions in cardiac syndrome X.

Endothelial dysfunction is major pathophysiologic mechanism in cardiac syndrome X (CSX), which causes a decrease in plasma nitrite oxide (NO) levels. It was demonstrated that nebivolol improves endothelial function and increases NO release. Despite this pathophysiologic relation, the effect of nebivolol therapy on endothelial function in patients with CSX is unknown. The aim of this study is to evaluate the effect of nebivolol on patients in CSX. Thirty-eight patients who were diagnosed with CSX were prospectively enrolled in the study. The treatment group consisted of 20 patients and the control group consisted of 18 patients. An oral 5-mg dose of nebivolol was given daily and maintained for 4 weeks in the treatment group. Ultrasonographic parameters (brachial artery flow-mediated dilatation [FMD], brachial artery lumen diameters) and inflammatory markers (high-sensitivity C-reactive protein [hsCRP], von Willebrand factor [vWf], and fibrinogen) were measured at baseline and end of the 4 weeks. Brachial baseline lumen diameter, brachial lumen diameter after reactive hyperemia, and FMD were 4.61 ± 0.49 mm, 4.87 ± 0.53 mm, and 5.6% ± 2.3% at baseline. After the nebivolol therapy, there was a significant increase in both brachial artery baseline lumen diameter and lumen diameter after reactive hyperemia (P < 0.001 and P = 0.002). However, there was no significant change in FMD (5.6% ± 2.2% vs 5.3% ± 2.1%, P not significant). Levels of hsCRP, vWf, and fibrinogen were significantly decreased (hsCRP: 3.4 ± 0.49 mg/dl vs 2.97 ± 0.74 mg/dl, P = 0.001; vWf: 107 ± 62 vs 86 ± 58, P = 0.004; fibrinogen: 341 ± 89 mg/dl vs 299 ± 87 mg/ dl, P = 0.01) in the treatment group. Nebivolol therapy may have a favorable effect on endothelial function in CSX. Further studies are needed to confirm the clinical significance of nebivolol therapy in CSX.