Tayfun Acil

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.

Acute Anterior Myocardial Infarction Following a Mild Nonpenetrating Chest Trauma A Case Report

Myocardial infarction in patients under age 45 years is a relatively unusual phenomenon; blunt chest trauma is one of the nonatherosclerotic mechanisms leading to acute myocardial infarc tion in young adults. The authors report a rare case of anterior myocardial infarction in a 22-year- old man following a mild nonpenetrating chest trauma whose left chest was elbowed during a soccer game.

Coronary lesion type, location, and characteristics of acute ST elevation myocardial infarction in young adults under 35 years of age.

ObjectiveIn the present study, we attempted to analyze the coronary artery lesion characteristics of acute ST elevation myocardial infarction (STEMI) in young patients (aged less than 35 years). MethodsWe retrospectively surveyed 25u2009038 coronary angiography procedures, which were carried out at The Baskent University Adana Hospital from 1998 to present, to discover acute STEMI in young patients. We studied clinical risk factors and angiographic characteristics in 42 consecutive patients who underwent primary coronary angiography for acute STEMI. Control group (n=42) had no history of coronary artery disease and had angiographically proven normal coronary arteries. All patients were under 35 years of age. Angiographic features for STEMI group were collected and both groups were compared for coronary risk factors. ResultsMale sex was more prevalent in acute STEMI group when compared with control participants (83 vs. 59%, respectively; P=0.01). A significant difference was found in cigarette smoking (62 vs. 36%, respectively; P=0.007) and family history (33 vs. 16%, respectively; P=0.03) between the two groups. No statistical significance was observed between the groups in terms of hypertension, diabetes mellitus, total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels. Mean high-density lipoprotein cholesterol level was 33±8u2009mg/dl in STEMI group and 39±12u2009mg/dl in control participants (P=0.02). Young patients with acute STEMI showed a preponderance of single-vessel disease (69%) and acute anterior STEMI (60%) owing to occluded left anterior descending artery (P<0.001). ConclusionWe observed risk factors such as family history, smoking, and low high-density lipoprotein cholesterol levels in young adults. Acute anterior STEMI owing to occluded left anterior descending artery was more frequent. Coronary atherosclerosis was characterized by higher presence of type B and proximal lesions. The handling selection was percutaneous coronary intervention in more than half of the patients.

Effects of short-term atorvastatin treatment on global fibrinolytic capacity, and sL-selectin and sFas levels in hyperlipidemic patients with coronary artery disease

BACKGROUNDnThe beneficial effects of HMG-CoA reductase inhibitors (statins) in patients with coronary artery disease (CAD) appear to be attributable not only to their lipid-lowering properties, but also to their therapeutic effects on the coagulation system, and anti-inflammatory effect. Furthermore, statins mitigate the apoptosis of vascular smooth muscle cells (VSMC) and macrophages in atherosclerotic plaques.nnnHYPOTHESISnThe purpose of this study was to evaluate the effects of short-term atorvastatin treatment on the fibrinolytic system and systemic inflammatory status, and on apoptosis in hyperlipidemic patients with CAD.nnnMETHODSnThe study population consisted of 36 hyperlipidemic patients (14 women and 22 men, mean age 53+/-9 years) with stable CAD, untreated with lipid-lowering medications. Serum lipoproteins, fibrinogen levels, sFas and sL-selectin, and global fibrinolytic capacity (GFC) were measured at baseline and after 12 weeks of treatment with atorvastatin, 10 mg/day.nnnRESULTSnAtorvastatin treatment decreased serum low-density lipoprotein (-39%, P=0.0001), total cholesterol (-32%, P=0.0001), and triglycerides (-22%, P=0.0001), and increased high-density lipoprotein (+13%, P=0.0001) at 12 weeks compared to baseline. These effects were associated with a decrease in plasma fibrinogen from 331+/-73 to 298+/-58 mg/dl (P=0.0001), and sL-selectin levels from 666+/-201 to 584+/-162 ng/ml (P=0.0001). sFas levels and GFC increased from 3754+/-1264 to 4873+/-1835 pg/ml and from 3.5+/-2.4 to 5.6+/-2.9 microg/ml, respectively (both P=0.0001).nnnCONCLUSIONSnThese results suggest that lipid lowering with atorvastatin therapy significantly increases GFC, decreases fibrinogen levels, and causes leukocyte deactivation. Our findings also suggest that atorvastatin treatment mitigates apoptosis of VSMC in the atherosclerotic plaque. These effects of atorvastatin may, in part, explain the early decrease in cardiovascular events observed in clinical trials of statins.

Patients with paroxysmal atrial fibrillation but not paroxysmal supraventricular tachycardia display evidence of platelet activation during arrhythmia.

It is well known that chronic atrial fibrillation (CAF) and paroxysmal atrial fibrillation (PAF) are associated with a hypercoagulable state. However, pathological hemostatic changes during the paroxysmal supraventricular tachycardia (PSVT) have not yet been elucidated. To determine platelet activity in patients with PSVT, PAF and CAF, we examined the levels of β-thromboglobulin (BTG) and platelet factor 4 (PF4) during tachyarrhythmia attacks. We measured the levels of BTG and PF4, as an index of platelet activation in 15 patients with PAF (9 men, mean age 45 ± 11), and 14 patients with PSVT (8 men, mean age 40 ± 10). Levels were compared to 22 age and sex-matched healthy controls in sinus rhythm and with 25 patients with CAF (16 men, mean age 51 ± 12). Blood samples were taken during arrhythmia and 24 hours after conversion to sinus rhythm. Patients taking medications or have clinical conditions that may affect the BTG and PF4 levels were excluded. In patients with PAF, BTG and PF4 levels were significantly higher than in controls (u2009p<0.009, and p = 0.002, respectively), and in patients with PSVT (u2009p<0.04, and p = 0.009, respectively), however, BTG and PF4 levels were significantly lower than CAF patients (u2009p = 0.002, and p = 0.02, respectively). Moreover, BTG and PF4 levels were significantly decreased 24 hours after conversion to sinus rhythm (u2009p<0.0001, and p = 0.004, respectively). Although BTG and PF4 levels in patients with PSVT were significantly lower than in patients with PAF (u2009p = 0.04, and p = 0.009, respectively) and CAF (u2009p = 0.0001, and p = 0.0001, respectively), BTG and PF4 levels were similar to controls and did not change significantly after recovery to sinus rhythm (u2009p = NS for all). These results indicate that there was no platelet activation in patients with PSVT during tachyarrhythmia but significantly increased platelet activity in PAF and CAF patients. There was a significant decrement of the platelet activity to a level of control subjects twenty-four hours after cardioversion of PAF.

Coronary artery dissection during pregnancy.

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Tumor necrosis factor-α polymorphism in Turkish patients with dilated cardiomyopathy

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What is the optimal evaluation time of the QT dispersion after acute myocardial infarction for the risk stratification

Tumor necrosis factora (TNF-a) is a proinflammatory cytokine with pleiotropic biological effects. Numerous studies have indicated a role of TNFa in the pathophysiology of congestive heart failure w1–4x. Since genetic polymorphisms in the TNF locus were known to be related to several autoimmune, infectious, and neoplastic diseases w5x, the association between TNFa gene polymorphism and dilated cardiomyopathy (DCM) was also studiedw6–8x. However, the results obtained were contradictory. Studies done in patients with different ethnic origins yielded contrasting results w6,7x.

Thrombosis involving the major veins with heterozygote factor V Leiden mutation as the only risk factor.

The sequential changes of the corrected QT dispersion (QTcD) were studied in 136 patients 1 day to 30 days after a transmural acute myocardial infarction (AMI) to investigate the optimal measurement time of QT dispersion for risk stratification. The study group included 136 patients (89 men; mean age, 57 ±10 years) with transmural AMI who were treated with throm bolytics (Tr+ group, n = 73) or not (Tr- group, n = 63) and 65 healthy controls (43 men; mean age, 56 ±7 years). Fourteen patients in whom ventricular tachycardia (VT), ventricular fibrilla tion (VF), or sudden cardiac death developed during the 30-day period were also evaluated as major cardiac arrhythmia (MCA) group. ECGs were obtained for each patient on days 1, 3, 5, 10, 15, and 30 after AMI. QTc dispersion in patients with AMI (for every period of QTcD after MI) was significantly more prolonged than in normal controls (49.3 ± 16.3 ms) (p < 0.001). QTcD was significantly greater in patients without thrombolytics than in patients with thrombolytics for every period (days 1, 3, 5, 10, 15, and 30) of QTcD after MI (p < 0.001). The mean of QTcD was significantly greater in patients with MCA than in patients without MCA group for every period (days 1, 3, 5, 10, 15, and 30) of QTcD after MI (p < 0.05). Maximal QTcD was seen on day 10 (p < 0.05 1st vs day 10 for each group) after myocardial infarction, and then reached a plateau for an each group. The ideal time to measure the QTD for risk stratification is at least 10 days after AMI.

Prognostic value of tissue Doppler imaging in patients with chronic congestive heart failure

A 27-year-old man was admitted to our hospital with the complaints of swelling of his face and lower limbs. Echocardiography showed minimal pericardial effusion accom panied by disordered diastolic function. Cardiac catheterization was performed to rule out constrictive pericarditis. Normal pressure tracings of the right heart rule out constrictive peri carditis, however, a narrowing of the inferior vena cava was observed. Venographies of the inferior and superior vena cavae showed extensive thrombotic involvement of these great veins. Protein C, protein S, anticardiolipin antibodies, fibrinogen, an tithrombin-III, activated protein C resistance, and factor V lev els were in normal limits. Heterozygosity for factor V Leiden mutation was detected. We conclude that factor V Leiden mu tation can cause extensive thrombotic involvement of major veins and should be considered in idiopathic thrombosis of them.