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.

An unusual cause of mismanagement in an acute myocardial infarction case: pseudothrombocytopenia.

Thrombocytopenia determined by an automated counter may represent a benign, incidental finding in an asymptomatic patient or a potentially life-threatening disorder. Even if the low platelet count actually is a benign condition itself, in some conditions, any delay resulting from this condition consequently may be seriously hazardous. Low platelet count may alter the decision of heparin administration, which is an essential part of management during acute coronary syndromes. EDTA-dependent pseudothrombocytopenia (PTCP) is reported to have a prevalence of 0.1% in a general hospital; however, it is also reported that around 15% of the patients referred for a specialized center for isolated thrombocytopenia are actually cases of PTCP. In this report, we describe a patient with PTCP who could not receive reperfusion therapy during acute myocardial infarction because of the low platelet counts reported by an automated counter.

Hemodynamic collapse caused by a large unruptured aneurysm of the ascending aorta in an 18 year old.

Large aneurysms of the ascending aorta occasionally cause severe hemodynamic disturbance by compression. We describe the case of an 18-yr-old man who presented with dyspnea and developed hemodynamic collapse during computed tomography scanning. Computed tomography during resuscitation revealed that the aneurysm was compressing both the right pulmonary artery and the left bronchus. Emergency surgery was performed, but the patient died because of generalized cerebral infarction.

Anticalcifying nanoparticle antibody titer is an independent risk factor for coronary artery calcification.

BACKGROUND: Calcium phosphate deposition is present even in the early phases of the atherosclerotic plaque formation. Calcifying nanoparticles (CNPs), previously known as nanobacteria, have emerged as a potential causative agent for pathological calcification in human vasculature. This study investigates the relationship between the anti-CNPs antibody titers and the extent of coronary calcification. METHODS: A total of 197 consecutive patients undergoing multidetector computed tomography were enrolled in this study. The patients with coronary artery calcification (CAC; n=103) were included in the CAC group, and those without calcification (n=94) were determined as controls. The commercially available enzyme-linked immunosorbent assay kits were used to detect IgG antibodies against CNPs in serum samples. RESULTS: Mean titers of anti-CNPs antibodies were higher in individuals with CAC than in the control group (0.4 ± 0.4 vs. 0.19 ± 0.21U; P<0.0001). Multivariate logistic regression analysis revealed that high anti-CNPs antibody levels were an independent correlate of CAC in addition to conventional risk factors such as age, hypertension, diabetes mellitus, and low levels of high-density lipoprotein cholesterol. When the CAC scores were subcategorized: score 0, 1-100, 101-400, and more than 400, they still correlated significantly with the anti-CNPs antibody, especially in the group having CAC scores greater than 400 (P<0.0001). CONCLUSION: Anti-CNPs antibodies are an independent risk factor for CAC and the antibody levels correlate with CAC scores.

Does atorvastatin affect androgen levels in men in the era of very-low LDL targeting therapy?

BACKGROUND: An adequate pool of free intracellular cholesterol is essential for steroidogenesis in gonads and LDL is the major source of cholesterol used in this pathway. Effect of peripheral LDL on the synthesis of steroids is dose dependent and although LDL levels around 100 mg/dl is demonstrated to be safe in terms of steroidogenesis, effect of LDL levels <70 mg/dl with higher doses of statins on steroidogenesis remains controversial. MATERIAL AND METHODS: Androgen and gonadotropin levels are prospectively evaluated at baseline and after 12 weeks of treatment in 77 male coronary heart disease patients receiving high doses of atorvastatin (40-80 mg daily) targeting serum LDL levels <70 mg/dl and in 83 male coronary heart disease patients receiving regular doses of atorvastatin (10-20 mg daily) targeting serum LDL levels <100 mg/dl. RESULTS: At the end of the study, mean LDL levels of the high and regular dose atorvastatin groups were 77+/-9 mg/dl and 98+/-10 mg/dl respectively. After twelve weeks of treatment, there were no significant alterations in serum total testosterone, free testosterone, sex hormone binding globulin, luteinizing hormone and follicle stimulating hormone levels between two groups. CONCLUSION: High dose atorvastatin in order to reach serum LDL levels around 70 mg/dl seems to be as safe as regular doses in order to reach serum LDL levels around 100 mg/dl, in terms of gonadal steroidogenesis in men with coronary heart disease.

Direct stenting versus predilatation and stenting technique when using paclitaxel-eluting stents.

Direct stenting without predilatation is a well-defined, feasible method with bare metal stents. Direct stenting has also been shown to be safe and feasible with drug-eluting stents, however, there is much less evidence with this type of device when compared with bare metal stents. Three hundred and sixty-four coronary lesions in 257 consecutive patients (mean age, 57.4 +/- 9.8 years; 63 women) who had undergone elective stenting either with or without predilatation via a paclitaxel-eluting stent between March 2003 and March 2006 were retrospectively analyzed. Quantitative coronary angiography analysis was compared between the two groups of procedures; stenting with predilatation and direct stenting. All procedures were uneventful. No deaths occurred during the follow-up period. Direct stenting when compared with the predilatation technique, significantly decreased both procedure time (32.1 +/- 17.9 minute versus 41.2 +/- 18.6 minute, P < 0.0001) and fluoroscopy time (10.6 +/- 7.8 minute versus 15.5 +/- 7.6 minute, P < 0.0001). There was no difference in quantitative analysis parameters of coronary angiography during follow-up or the rates of stent thrombosis and restenosis. Direct stenting seems to be as feasible and safe as conventional predilatation and stenting in selected cases. Direct stenting seems to decrease procedural time and radiation exposure without any negative effect on quantitative analysis parameters of coronary angiography with approximately a one-year follow-up period.

Altered autonomic neural control of the cardiovascular system in patients with polycystic ovary syndrome.

PURPOSE: Polycystic ovary syndrome (PCOS) is frequently accompanied by the presence of cardiovascular risk factors. It has also been recognized that there is a significant relationship between the autonomic nervous system and adverse cardiac events. Heart rate recovery (HRR) after exercise is a marker of parasympathetic activity and attenuation of this parameter has been shown to be associated with increased cardiac mortality. A delayed recovery of systolic blood pressure (SBP) after peak exercise has been found to have diagnostic value and might reflect sympathetic hyperactivity. The analysis of variations in heart rate has also been used to determine the balance between sympathetic and vagal nerve activities in the heart. Our objective was to determine HRR, the SBP response to exercise and heart rate variability (HRV) in patients with PCOS. METHODS: The study population consisted of 26 untreated patients with PCOS and 24 healthy controls who were matched with respect to age, body mass index and physical activity. All subjects underwent symptom-limited exercise tolerance test according to a modified Bruce protocol. Following peak exercise, subjects walked a 2-min cool-down period. Heart rate recovery was calculated as the difference between heart rate at peak exercise and heart rate at the relevant minute of recovery. Blood pressure recovery indexes were determined by dividing the systolic blood pressure at 1, 2 and 3 min in recovery to the systolic blood pressure at peak exercise. RESULTS: HRR at 1 min (HRR1) of the patients with PCOS were significantly lower than that of controls (20+/-4 vs 28+/-8 bpm, p<0.0001). Although, resting SBP of the two groups were similar (117+/-7 vs 117+/-10 mmHg, p=0.663), the SBP of the patients with PCOS at peak exercise were significantly higher when compared to controls (172+/-12 vs 156+/-14 mmHg, p<0.0001). In addition, the SBP of the patients with PCOS remained significantly elevated when compared to controls at the first, second and third minute of recovery (168+/-13 vs 148+/-15 mmHg, 162+/-13 vs 136+/-16 mmHg, 152+/-17 vs 127+/-15 mmHg, respectively, p<0.0001 for all three). The SBP recovery index at 2 and 3 min of the patients with PCOS were significantly higher than that of controls (0.93+/-0.04 vs 0.87+/-0.07, p<0.0001 and 0.87+/-0.07 vs 0.82+/-0.09, p=0.017, respectively). Both time domain and frequency domain parameters of patients with PCOS were significantly lower than that of controls. CONCLUSION: This study shows that the patients with PCOS have attenuated HRR1, exaggerated SBP response to exercise which is delayed to recover and a depressed HRV. These findings might also suggest alterations in autonomic neurol control of the cardiovascular system in this disorder.

Simvastatin improves the attenuated heart rate recovery of type 2 diabetics.

Heart rate recovery at 1min (HRR1) is a strong predictor of all-cause mortality. The effects of statins on the autonomic nervous system may account for their beneficial effects in survival. Our aim was to determine if statin therapy improves heart rate recovery in hypercholesterolemic patients with type 2 diabetes mellitus. Thirty type 2 diabetic patients without known coronary artery disease and low density lipoprotein cholesterol>100mg/dl and 30 age and sex matched non-diabetic controls were included in a prospective study. Patients with diabetes were treated with simvastatin 40mg/day for 1 year. No lipid-lowering therapy was administered to the control group. Exercise testing with 2min cool-down period was performed at baseline, 6, 12 weeks and at 1 year. The diabetics had significantly lower HRR1 compared with non-diabetics at baseline (19.2+/-5.4bpm versus 24.2+/-4bpm, p<0.0001). Simvastatin therapy significantly improved HRR1 after 12 weeks compared to baseline (19.2+/-5.4bpm versus 24+/-5bpm, p<0.0001) and this improvement remained significant at 1 year (26+/-4.4bpm, p<0.0001 compared to baseline). HRR1 did not change in the control group (p=0.39 by ANOVA). This study demonstrates that treatment with simvastatin might improve the attenuated heart rate recovery of diabetic subjects. In patients with diabetes, the mortality benefit provided by statins might involve their effects on the autonomic nervous system.