Yucel Colkesen

Mean platelet volume is elevated during paroxysmal atrial fibrillation: a marker of increased platelet activation?

Paroxysmal atrial fibrillation might be a risk factor for stroke such as chronic atrial fibrillation. We examined the relation between mean platelet volume and paroxysmal atrial fibrillation to determine the effect of paroxysmal atrial fibrillation on the thrombotic state via elevated mean platelet volume. Mean platelet volume is a marker of platelet size, function, and activation. Increased mean platelet volume reflects active and large platelets that release more thromboxane A2 than smaller ones. We hypothesized that mean platelet volume is elevated in patients with paroxysmal atrial fibrillation. The study population comprised 103 consecutive patients who were detected to have paroxysmal atrial fibrillation by 24-h Holter monitoring and 87 control individuals with normal Holter monitoring. Mean platelet volume and inflammatory parameters were measured. Comprehensive clinical and echocardiographic data were collected. Patients with aortic and mitral stenosis, hyperthyroidism, hypothyroidism, malignancy, infection, and pregnancy were excluded from the study. Mean age of the patients was 63 ± 11 vs. 45 ± 14 years (P < 0.001) in paroxysmal atrial fibrillation and control groups, respectively. Fifty-seven patients (55%) in paroxysmal atrial fibrillation and 19 (21%) (P < 0.001) patients in control group were men. Mean platelet volume was significantly higher in the paroxysmal atrial fibrillation group when compared with control group (10.0 ± 2.0 vs. 8.3 ± 1.5 fl, respectively; P < 0.001). C-reactive protein (18.5 ± 28 vs. 3.8 ± 2 mg/l, respectively; P = 0.004) and erythrocyte sedimentation rate (21 ± 21 vs. 12 ± 7 mm/h, respectively; P = 0.01) were also higher in the paroxysmal atrial fibrillation group. There was no difference in white blood cell and platelet counts between groups. In a multivariate analysis, elevated mean platelet volume was associated with the occurrence of paroxysmal atrial fibrillation before and after adjustment for age and sex. Our results indicate that inflammatory markers such as C-reactive protein and erythrocyte sedimentation rate and the marker of platelet size and activity mean platelet volume are elevated in patients with paroxysmal atrial fibrillation.

Relation of Serum Parathyroid Hormone Level to Severity of Heart Failure

Increased parathyroid hormone (PTH) level is associated with all-cause mortality in patients with heart failure (HF). However its role for identifying advanced HF has not been previously studied. We aimed to investigate whether the assessment of serum PTH could enable clinicians to identify patients with advanced HF. One hundred fifty consecutive patients who visited our outpatient clinic with systolic HF were enrolled in the present study. Serum levels of PTH and brain natriuretic peptide (BNP) were measured across all New York Heart Association functional classes. Mean levels of PTH were 43 ± 19, 84 ± 56, 121 ± 47, and 161 ± 60 pg/ml in New York Heart Association functional classes I, II, III, and IV, respectively (p <0.001). In univariate analysis, body mass index, disease duration, PTH, BNP and hemoglobin levels, creatinine clearance, heart rate, systolic blood pressure, left ventricular ejection fraction, left ventricular diastolic diameter, left atrial size, presence of atrial fibrillation, and diuretic usage were found to be predictors of advanced HF. In multivariate logistic regression analysis, PTH level (hazard ratio 1.032, 95% confidence interval 1.003 to 1.062, p = 0.003) and body mass index (hazard ratio 0.542, 95% confidence interval 0.273 to 1.075, p = 0.079) were associated with advanced HF. Furthermore, serum PTH levels were correlated with BNP level and left ventricular ejection fraction (p <0.001 for the 2 comparisons). In receiver operator characteristics curve analysis, the optimal cut-off value of PTH to predict advanced HF was >96.4 pg/ml, with 93.3% sensitivity and 64.2% specificity. In conclusion, measurement of serum PTH could provide complementary information and a simple biomarker strategy to categorize patients with advanced HF based on increased PTH levels, allowing rapid risk stratification in these patients.

The role of mean platelet volume in predicting thrombotic events

Abstract Studies on platelet function have accelerated and gained popularity since the advent of novel treatment modalities and techniques on atherosclerotic vascular disease, such as antiplatelet drugs and stents. Today it is widely known that platelets exert a fundamental role in inflammation in addition to their long known role in homeostasis and thrombotic events. Interaction with endothelial cells and leukocytes mediates inflammation, contributes to atherogenesis and modulates immune activity. Platelet activation which is a central factor in many arterial disorders may be triggered by multiple pathways. Platelet activation is shown as forming a larger shape, aggregation and releasing various active contents. Mean platelet volume is a marker of platelet size, function and activation. Increased mean platelet volume is shown by active and large platelets that release more thromboxane A2 than smaller ones. The aim of this review is to determine whether early detection of platelet activation via increased mean platelet volume would help to recognize the pro-inflammatory state and administer appropriate and effective treatment properly. An easily detectable marker by using a prompt and functional technique would help our approach to inflammation caused by platelets.

The effect of aspirin on mean platelet volume in patients with paroxysmal atrial fibrillation

Aspirin is one of the preferred therapies in the primary prevention of ischemic stroke in paroxysmal atrial fibrillation (PAF). Mean platelet volume (MPV) is a marker of platelet size and activation. Increased MPV reflects active and large platelets. The present observational study was designed to investigate whether aspirin treatment does affect MPV levels in patients with PAF. The study included 101 patients who were detected to have PAF by 24-hour Holter monitoring and divided into two groups based on aspirin treatment [ASA (+) and ASA (−)]. MPV was measured. Patients with aortic and mitral stenosis, hyperthyroidism, hypothyroidism, malignancy, infection, and pregnancy were excluded from the study. Of the 101 patients, 50 had no antiplatelet therapy and 51 had daily aspirin (100 mg) intake. Mean age of the patients was 66 ± 10 years and 35 (68%) were male in ASA (+) group. There was no difference in median levels of MPV (9.9 vs. 10.2 fl, respectively; p = 0.9) between groups. Both uni- and multivariate logistic regression analyses did not show an association between MPV and ASA use. Our results indicate that MPV as a predictive marker of platelet size and activity is not affected by aspirin use in patients with PAF.

Parathyroid hormone and heart failure: novel biomarker strategy.

Heart failure (HF) is a clinical syndrome featuring cardiac pump failure along with signs and symptoms arising from salt and water retention mediated by activated renin-angiotensin-aldosterone system (RAAS). In addition to this cardiorenal perspective, HF is accompanied by a systemic illness, especially in advanced stages characterized by oxidative stress in various tissues, causing damage to soft tissue and bone. Secondary hyperparathyroidism (SHPT) which is also considered to contribute this systemic illness is therefore prominent in advanced HF. SHPT in HF occurs as a result of RAAS activation, prominent hyperaldosteronism, loop diuretic usage and decreased calcitriol level, all of which results in calcium excretion. We review the evidence that high parathyroid hormone (PTH) is associated with advanced HF, as well as evidence that its associated with HF with preserved ejection fraction (HFPEF).

Relation of serum cortisol to delirium occurring after acute coronary syndromes

BACKGROUND Delirium can be associated with cardiac system disorders. Stress plays an important role in the pathogenesis of postoperative delirium. Cortisol is one of the most important stress hormones in humans. We aimed to investigate whether a relation exists between serum cortisol and the degree of delirium after acute coronary syndromes (ACS). METHODS We enrolled 52 consecutive patients who presented with ACS and were hospitalized in the coronary care unit. Patients were examined daily by a single psychiatrist, and delirium was diagnosed by using the Delirium Rating Scale (DSR). Blood samples were obtained at 6:00 am of the next morning after admission. RESULTS The mean age was 66 years (SD, ±6 years), and 52% were men. Delirium occurred in 25 patients (48%). The median score on the DRS was 17 for the delirious patients and 5 for the nondelirious. Median cortisol levels were significantly different between the delirium and nondelirium groups (13.9 vs 6.2 μg/dL; P < .01). There were significant correlations between the cortisol levels and the severity of the delirium based on DRS scores as well as between the cortisol levels and the presence of delirium (r = 0.65 and 0.74, respectively; P = .01). In a linear logistic regression model, cortisol predicted the occurrence of delirium (β = .81; P < .01). In receiver operating characteristics analysis, the optimal cutoff value of cortisol to predict delirium was 10.8 μg/dL, with 96% sensitivity and 89% specificity. CONCLUSION Delirium was common after ACS, and serum cortisol levels correlated with the degree of delirium and the risk of delirium.

Hemodynamic effects of left upper extremity arteriovenous fistula on ipsilateral internal mammary coronary artery bypass graft.

OBJECTIVE Arteriovenous fistula (AVF) in patients undergoing hemodialysis (HD) may cause coronary left internal mammary artery (IMA) steal. This phenomenon was demonstrated by few prospective studies with limited number of patients and case reports. We aimed to demonstrate with a relatively larger patient population that the AVF may cause ipsilateral IMA steal. METHODS We included 22 prospective patients undergoing HD who had left IMA to left anterior descending artery graft and left upper limb AVF. Right IMA was taken as control. Flows were assessed by using color Doppler ultrasonography. RESULTS The mean age was 57.8 ± 9 years. Statistically nonsignificant increases in AVF flow and decreases in left IMA flow were observed during HD compared with pre-HD. Moreover, fistula localization did not affect median left IMA flows (for peak systolic velocity [PSV] 43.7 versus 70 cm/s, respectively; p = 0.7, and for end diastolic velocity [EDV] 3.4 versus 6.5 cm/s, respectively; p = 0.7). We have not detected significant difference in left IMA flows during HD (median values of PSV 58.4 versus 68.4 cm/s, respectively; p = 0.1, and EDV 6.4 versus 4.4 cm/s, respectively; p = 0.08). Only three patients experienced dialysis-induced reduction of ipsilateral IMA flow that was accompanied by evidence of hypokinesia of the anterior left ventricular wall without clinical angina. CONCLUSIONS Hemodynamically affected left IMA flow by ipsilateral upper extremity AVF may cause steal phenomenon. Hemodynamic differences between left and right IMAs in patients undergoing HD via left wrist and brachial fistulae are limited.

Short-term effects of fluvastatin therapy on plasma interleukin-10 levels in patients with chronic heart failure.

BackgroundExperimental data demonstrated that inflammatory mediators, such as pro-inflammatory and anti-inflammatory cytokines and their receptors might have important role in the development and the progression of heart failure (HF). Statins were shown to downregulate inflammatory cytokines in HF. Interleukin (IL)-10 is one of the most important anti-inflammatory cytokines. The effect of statin therapy on plasma IL-10 levels is not known in patients with HF. We conducted this study to investigate the effects of fluvastatin therapy on plasma IL-10 cytokine concentration in patients with HF. MethodsA total of 29 patients with ischemic HF were included in this prospective uncontrolled study. Patients were assigned to fluvastatin (80 mg/day) after baseline examinations. Determination of biochemical parameters including lipids, IL-10, and tumor necrosis factor-&agr; were performed at baseline and 12 weeks after the initiation of fluvastatin therapy. All participants also underwent symptom-limited exercise tolerance test at baseline and 12 weeks, and heart rate recovery (HRR) was calculated. ResultsA significant elevation in the plasma levels of IL-10 after 12 weeks of fluvastatin treatment (4.8±1.0 vs. 6.5±1.3 pg/ml, P=0.002) was observed. Plasma tumor necrosis factor-&agr; levels were significantly decreased after fluvastatin therapy (6.3±2.3 vs. 4.8±1.4 pg/ml, P=0.003). Fluvastatin therapy significantly improved HRR at 1 min after 12 weeks compared with baseline (19±7 vs. 24±9 bpm, P<0.001). A positive correlation between the change in the levels of IL-10 and the change in HRR at 1 min (r=0.57, P<0.001) was observed. ConclusionFluvastatin therapy might lead to an increase in plasma IL-10 levels and an associated improvement in vagal tonus as assessed by HRR at 1 min in patients with HF. These findings might partly explain the possible benefit observed in statin trials.

Transcatheter aortic valve implantation in a patient with bicuspid aortic stenosis and a borderline-sized annulus

Bicuspid aortic valve (BAV) is currently considered an exclusion criterion for transcatheter aortic valve implantation (TAVI). The risk of adverse aortic events such as incomplete sealing, severe paravalvular regurgitation or dislocation due to elliptic shape and asymmetric calcifications in annulus are higher in TAVI. In this case report, we detailed a case of successful trans-femoral TAVI in a 51-year old male with BAV and its management without in-hospital and 30-day complications. The challenge in this case was the patients anatomy with a 27-mm annulus for balloon expandable device. The applied strategy was balloon sizing and overdilating the 29-mm stented valve with additional volume that obviated re-ballooning. Trans-femoral TAVI was performed uneventfully under fluoroscopic and transoesophageal echocardiography guidance. A multidetector computed tomography (MDCT) evaluation at 1 month did not show device dislodgement or any other complications. Evidence for evaluation post-TAVI is not sufficient in BAV. We believe patients with BAV should undergo a comprehensive assessment after TAVI including MDCT evaluation.

Evaluation of coronary artery-saphenous vein composite grafts: the aortic no-touch technique.

We retrospectively compared the results of conventional coronary artery bypass grafting (CABG) performed on patients who showed no preoperative evidence of serious atherosclerosis of the ascending aorta with the results of the aortic no-touch technique (using coronary artery-saphenous vein composite grafts) on CABG patients who did show such evidence. From 2003 through 2012, 3,152 consecutive patients underwent isolated primary CABG at our hospital. We chose 360 for the current study. The study group (n=120) comprised patients who had undergone operation via the aortic no-touch technique. Propensity-score-matching (1:2) was used to select the control group of 240 patients who had undergone conventional CABG. Early and late survival rates, reintervention-free survival rates, and freedom from cardiac death were compared. Early and late mortality rates were similar in the study and control groups (P=0.19 vs P=0.29, respectively), as were cardiac-related death (2.5% vs 2.1%, respectively; P=0.53) and overall death (8.3% vs 7.9%, respectively; P=0.51). Overall survival rates were 91.7% vs 92.1% and freedom-from-cardiac-death rates were 97.4% vs 97.5% (P=0.71 vs P=0.78, respectively; mean follow-up period, 5.27 ± 2.51 yr). Reintervention-free survival rates were also similar (96.7% vs 98.8%, respectively; P=0.2). As a result of the similar rates of early and late survival, reintervention-free survival, and freedom from cardiac death, we conclude that the aortic no-touch technique with composite grafts might be a reasonable option in patients who have atherosclerotic ascending aorta that cannot be clamped.