Ilgın Karaca

Is inflammatory bowel disease a risk factor for early atherosclerosis

Objectives: Chronic inflammatory diseases are associated with an accelerated atherosclerotic process. Recent studies have discussed whether inflammatory bowel diseases (IBDs) can predict early atherosclerosis. We investigated this possibility. Methods: The study consisted of IBD cases (group 1, n = 40) and healthy persons (group 2, n = 40). The IBD group was selected so as not to have vascular disease or the presence of established major cardiovascular risk factors. Results: Group 1 cases showed a significant increase in carotid intima media thickness (cIMT; P = .01). Carotid artery stiffness was impaired in group 1 (P = .03) and high-sensitivity C-reactive protein (hsCRP), homeostasis model assessment of insulin resistance (HOMA-IR), and homocysteine (Hyc) were higher in group 1 patients (P = .02, P = .03, P = .05). Conclusions: Inflammatory bowel disease patients have an increased risk of early atherosclerosis as shown by greater values of cIMT, carotid artery stiffness, Hyc, hsCRP, and insulin resistance.

Are maximum P wave duration and P wave dispersion a marker of target organ damage in the hypertensive population

BackgroundHigh blood pressure, left ventricular hypertrophy and diastolic dysfunction may cause hemodynamic and morphological changes in the left atrium, consequently instability and heterogeneity in atrial conduction. This is seen as an increase in maximum P wave duration (Pmax) and P wave dispersion (PD) on the electrocardiogram (ECG). P wave dispersion on ECG has been encountered as a risk factor for atrial fibrillation (AF). The aim of this study is to examine whether PD and Pmax can be used as a non-invasive marker of target organ damage (LVH and diastolic dysfunction) in a hypertensive population.Material and methodsThe study registered a total of 120 cases (mean age 46.9 ± 10.6 years; 58 [48.3%] males and 62 [51.7%] females), of whom 60 were patients diagnosed as essential hypertension (group 1), and 60 were healthy individuals, who constituted the control group (group 2). Systolic and diastolic functions of all cases were evaluated by echocardiography, and maximum P wave duration (Pmax), and PD was calculated.ResultsMaximum P wave duration was 91.6 ± 10.2 ms in group 1, and 64 ± 10.2 ms in group 2 (p < 0.01), while PD was 56.1 ± 5.8 ms in group 1, and 30.3 ± 6.6 ms in group 2 (p < 0.01). Blood pressure, left atrium diameter, DT, IVRT, and E/A ratio, as well as left ventricular mass index increased markedly in group 1.ConclusionHigh blood pressure, LVH, diastolic dysfunction and increased left atrium diameter and volume shows parallelism in hypertensive cases. These physiopathological changes may cause different and heterogeneous atrial electrical conduction. This led to a marked increase in Pmax and PD in our cases. Thus, the results support the hypothesis that PD can be used as a non-invasive marker of target organ damage (LVH and LV diastolic dysfunction) in the hypertension population.

Strict fluid volume control and left ventricular hypertrophy in hypertensive patients on chronic haemodialysis: a cross-sectional study.

Left ventricular hypertrophy (LVH) is very common in haemodialysis patients. We measured left ventricular mass in three groups of haemodialysis patients: group A (n = 40) were normotensive and receiving a strict salt-restricted diet; group B (n = 23) were normotensive and receiving antihypertensive drugs; and group C (n = 43) were hypertensive despite anti-hypertensive drug treatment. The interdialytic weight gain in group B and group C was significantly higher than in group A; the mean left atrial index and left ventricular end-systolic and end-diastolic diameter indices were all higher in group B than in group A. The interventricular septum and posterior wall were significantly thicker in group B and group C than group A, resulting in a higher left ventricular mass index. Left ventricular systolic and diastolic function parameters were slightly better in group A than in the other groups. These results show that strict fluid volume control decreases blood pressure, reduces dilated cardiac compartments and corrects LVH more effectively than lowering blood pressure without correcting the volume overload.

Effect of Ongoing Inflammation in Rheumatoid Arthritis on P-Wave Dispersion:

It has been emphasized recently that there is a strong association between atrial fibrillation and inflammation. Rheumatoid arthritis (RA), characterized by ongoing inflammatory activity, can increase the risk of atrial arrhythmia. P-wave dispersion has been encountered as a risk factor for atrial fibrillation and the effect of inflammation on P-wave dispersion has not been studied thoroughly. The aim of this study was to examine the effect of ongoing inflammatory activity in RA on P-wave dispersion. The study comprised 82 patients diagnosed with RA and 41 healthy volunteers as controls. Systolic functions of all participants were evaluated by echocardiography. Maximum P-wave duration and dispersion were calculated and found to be significantly increased in the RA group compared with the healthy controls. These parameters were also significantly correlated with C-reactive protein levels. The findings of this study suggest that RA may be associated with increases in P-wave dispersion and maximum P-wave duration, and that this association may result from ongoing inflammation.

P-Wave Dispersion in Panic Disorder

Background: P-wave dispersion (PWD) is defined as the difference between the maximum and the minimum P-wave (Pmax and Pmin, respectively) duration. Significant variation in cardiac atrial PWD has been correlated with changes in systemic autonomic tone such as during periods of anxiety. It is also known that the degree of PWD seen on 12-lead electrocardiogram (ECG) may be a predictor of susceptibility of the atrial myocardium to future atrial fibrillation (AF). Therefore, we firstly aimed to show an association between PWD and panic disorder, a state of high sympathetic tone. Methods: PWD was measured in 40 outpatients with panic disorder and in 40 physically and mentally healthy age- and gender-matched controls. In addition, the Panic Agoraphobia Scale (PAS) and the Hamilton Depression Rating Scale (HDRS) were scored concomitantly. Results: Both Pmax and Pmin were significantly higher than those of healthy controls. PWD was significantly greater in the panic disorder group than in the controls. As expected, the mean score on PAS was significantly higher for the panic disorder group than for the controls and correlated significantly with PWD. Heart rate (measured as RR intervals in milliseconds on electrocardiogram) did not differ significantly between the groups. Conclusions: The findings of the present study suggest that the disorder may be associated with an increase in PWD. This association may result from prolonged anxiety and increase in sympathetic modulation, which are main characteristics of panic disorder. PWD = P-wave dispersion; Pmax = maximum P-wave duration; Pmin = minimum P-wave duration; HRV = heart rate variability; AF = atrial fibrillation; ECG = electrocardiogram; PAS = The Panic Agoraphobia Scale; HDRS = Hamilton Depression Rating Scale; ANS = autonomic nervous system; DSM-IV = Diagnostic and Statistical Manual of Mental Disorders IV.

Early Effects of Treatment with Nebivolol and Quinapril on Endothelial Function in Patients with Hypertension

The objective of the present study was to compare the early effects of treatment with nebivolol and quinapril on the endothelial function in hypertensive patients. A total of 54 hypertensive patients was enrolled in the present study. One of the groups (n = 27) received quinapril 20 mg/day, and the other group (n = 27) received nebivolol 5 mg/day for a period of 4 weeks. The endothelial dysfunction was assessed using FMD (flow-mediated vasodilation) of the brachial arteries. The baseline characteristics of both groups were similar in age, gender, left venticular ejection fraction, left ventricular mass index, and body mass index. No significant difference was also found between the groups in the distribution of atherosclerotic risk factors as well as other echocardiographic, demographic, and biochemical measurements. Although the reduction of diastolic blood pressure was more pronounced in the nebivolol group after a 4-week treatment, the change in the systolic blood pressure was found to be similar in both treatment arms. Although a statistically nonsignificant increase was observed in flow-mediated vasodilation in the quinapril group (4.77% +/- 3.92%, 5.60% +/- 6.18%; p = .587), the increase in the post-treatment FMD was statistically significant in the nebivolol group (3.78% +/- 4.25%, 8.56% +/- 6.39%; p = .002). A significant change was observed in the resistive index value following flow-mediated vasodilation for both groups after treatment (p = .043; p = .027), whereas the change in the value of flow volume was significant only in the nebivolol group (p = .019).

The effect of long-term clopidogrel use on neointimal formation after percutaneous coronary intervention.

ObjectiveThe purpose of this study was to evaluate the long term effect of clopidogrel-based antiplatelet therapy on neointimal formation. MethodsThis study comprised 78 patients with typical stable angina pectoris or documented myocardial ischaemia, and with only one angiographic lesion in one native coronary artery undergoing successful stent implantation without predilatation with C-reactive protein levels ≤5 mg/l at 72 h after the procedure. All patients received dual antiplatelet therapy with 75 mg/day clopidogrel and 300 mg/day aspirin for four weeks. Clopidogrel was switched to isochronous placebo in half of the patients (n=39) at the end of the fourth week. This allocation was maintained for 20 weeks, and at week 24 of the study, coronary angiography and intravascular ultrasound imaging were performed again in all cases in order to evaluate the changes that had occurred in the in-stent neointimal formation; rates of restenosis were also recorded ResultsAt the end of the follow-up period, angiographic stenosis diameter and restenosis rates were smaller in the clopidogrel group than in the placebo group (23.3% versus 35.6%, p=0.05 and 5.12% versus 10.25%; p=0.03 respectively); the intravascular ultrasonographic neointimal cross sectional area was also smaller in the clopidogrel group (3.6±2.7 mm2 versus 5.2±2.5 mm2, p=0.03). ConclusionsLong-term clopidogrel administration significantly reduced neointimal formation at the stent site as well as reducing major clinical events in patients who did not develop high-risk systemic inflammatory response after percutaneous coronary intervention.

Adiponectin levels in coronary artery ectasia

Etiopathogenesis of coronary artery ectasia (CAE), which is defi ned as abnormal dilatation of a segment of the coronary artery to 1.5 times of an adjacent normal coronary artery segment, is unclear. However, it is speculated that CAE develops in the atherosclerosis process through degeneration of coronary artery media layer. Our objective in this study is to compare levels of adiponectin between cases with CAE and normal coronary anatomy, and to examine whether adiponectin plays a role in CAE etiopathogenesis. The study registered a total of 66 cases, consisting of CAE cases (group 1, n = 36) and cases with normal coronary anatomy (group 2, n = 30). Taking coronary artery diameters of the control group cases as the reference, patients with abnormal segments 1.5 times larger than the adjacent segments were accepted as CAE. Serum adiponectin levels were 4.31 ± 2.02 µg/ml in group 1 and 6.73 ± 4.0 µg/ml in group 2 (P = 0.02). High-sensitivity Creactive protein was 4.8 ± 3.8 mg/l in group 1 and 3.6 ± 3.4 mg/l in group 2 (P > 0.05). There was a negative correlation between ectatic coronary artery diameter and plasma adiponectin level (P = 0.03; r = −0.339). It was known that adiponectin levels dropped in atherosclerotic heart disease. In this study we found low plasma adiponectin levels in acquired CAE, attributed to atherosclerosis. Therefore, we think that adiponectin might be playing a role in etiopathogenesis and progression of CAE. This in turn may indicate that hypo-adiponectinemia may be useful in revealing a realized risk in CAE. However, larger, randomized, multicenter studies are required to examine the role of adiponectin in the development of CAE.

The effect of interventional treatment in acute myocardial infarction on ST resolution: a comparison of coronary angioplasty with excimer laser angioplasty.

The treatment methods for acute myocardial infarction (MI) have started to change in the new millennium. Myocardial perfusion (ST-segment resolution) is the target rather than achieving TIMI-III flow in the infarct-related artery. In this study the authors compared the effect of percutaneous transluminal coronary angioplasty (PTCA) and excimer laser angioplasty (ELCA), which was accepted as one of the thrombolysis methods, on ST-segment resolution. A stent was applied after ELCA to 36 patients (4 women, 32 men; mean age 50.44 ±9.8 years) in group I and a stent was applied after balloon angioplasty to 44 patients (5 women, 39 men; mean age 50.77 ±12.2 years) in group II. Fisher’s exact test was used in the analysis of data, and p<0.05 was accepted as significant. There was no difference between the groups with respect to symptom duration, time to angioplasty, risk factors, infarct localization, stent diameter, and length. TIMI-III flow was achieved in 33 patients (92%) in group I and in 40 patients (91%) in group II. There was no statistical difference in TIMI flow between the groups. In group I, complete ST resolution was observed in 75% (27/36) of the patients, partial resolution in 22% (8/36), and resolution was unsuccessful in 3% (1/36). In group II, complete, partial, and unsuccessful ST resolution were 41% (18/44), 45% (20/44), and 14% (6/44), respectively. The mean ST resolution was 82.78 ±11.8% in group I and 66.36 ±10% in group II (p=0.001). ST segment resolution, which is a good predictor of tissue perfusion, was higher with ELCA than with balloon angioplasty. These findings should be supported by large randomized studies.

Predictive value of C-reactive protein in patients with unstable angina pectoris undergoing coronary artery stent implantation.

In-stent restenosis is a major problem following coronary stent implantation, and inflammation plays an active role. We evaluated the effectiveness of the inflammatory marker C-reactive protein (CRP) as a predictor of in-stent restenosis after successful stent implantation, in 86 patients with unstable angina pectoris. Plasma CRP was measured in all patients before the procedure, and at 48-72 h and 1, 2 and 3 months post-procedure. An angiographic loss of 50% at follow-up was accepted as in-stent restenosis. We found negative and positive predictive values of the pre-procedural plasma CRP for determining 6-month in-stent restenosis of 34% and 61%, respectively. We also found a strong correlation between the 3-month post-procedural CRP value and 6-month in-stent restenosis; the negative and positive predictive values being 8% and 76%, respectively. In conclusion, we showed that a plasma CRP value > 3 mg/l in the third month after coronary stent implantation was a strong predictor of angiographic in-stent restenosis.