Comparison of mean platelet volume values among different causes of pulmonary hypertension

Background: Pulmonary hypertension is caused by a heterogenous group of disorders with diverse pathophysiological mechanisms, with ultimate structural changes in the pulmonary vascular bed. Platelet activation plays an important role in the development of pulmonary arterial hypertension, while it is unknown whether it contributes to pathogenesis in other conditions. We aimed to investigate platelet activation in different causes of pulmonary hypertension by means of mean platelet volume measurement. Methods: A total of 67 patients with different causes of pulmonary hypertension, and 31 controls, were retrospectively reviewed. Patients with pulmonary hypertension were further grouped according to underlying disease, including pulmonary arterial hypertension, pulmonary hypertension due to left ventricular failure, and pulmonary hypertension due to chronic obstructive pulmonary disorder. All patients and controls&#8217; past medical data, admission echocardiograms and complete blood counts were reviewed. Results: Patients with pulmonary hypertension had higher mean platelet volume levels compared to healthy controls (8.77 &#177; 1.18 vs 7.89 &#177; 0.53; p < 0.001), and statistical significance was still present when pulmonary arterial hypertension patients were not included in the pulmonary hypertension group (8.59 &#177; 1.23 vs 7.89 &#177; 0.53; p < 0.001). Among patients with pulmonary hypertension, the pulmonary arterial hypertension group and the pulmonary hypertension due to left ventricular failure group had higher mean platelet volumes compared to healthy controls. Mean platelet volume did not correlate with pulmonary artery pressure. Conclusions: Our results indicate that mean platelet volume is not only elevated in pulmonary arterial hypertension, but also due to other causes of pulmonary hypertension. (Cardiol J 2012; 19, 2: 180&#8211;187

Assessment of Serum Sialic Acid and Oxidative Stress Parameters in Rheumatoid Arthritis Patients Receiving Anti-TNF-alpha and Conventional Therapies

Yilmaz, Gulsen/0000-0002-9630-3852;WOS: 000296178600005Objective: In this study, we aimed to evaluate sialic acid (SA) levels and oxidative stress parameters by measuring nitric oxide metabolites (NOx), thiobarbituric acid-reactive substances (TBARS) and thiol (SH) in rheumatoid arthritis (RA) patients treated with either conventional or anti-tumor necrosis factor-alpha (anti-TNF-alpha) therapy. Materials and Methods: Eighty-six RA patients and 20 healthy controls were enrolled in the study. All RA patients fulfilled the American College of Rheumatology (ACR) criteria for RA. Thirty patients were on anti-TNF-a therapy. The rest of the patients were either treated with two or three disease-modifying anti-rheumatic drugs. Health Assessment Questionnaire (HAQ) score and the Disease Activity Score 28 (DAS28) were calculated in all patients. NOx, TBARS, SA, and SH levels were measured in both patients and controls. Results: The SA levels were statistically higher in RA patients than in controls. We found increased levels of TBARS and NOx and decreased levels of SH in both groups, but these results were statistically insignificant. Spearman correlation analysis revealed positive correlation between serum TBARS levels and both NOx (r=0.322, p=0.001) and SA (r=0.242, p=0.017) levels. Conclusion: Our results confirm the role of SA in the pathogenesis of RA and its correlation with oxidative stress. Further studies on larger numbers of subjects and with longer treatment durations are needed to analyze the long-term effects of RA therapies on serum oxidative stress parameters. Turk J Phys Med Rehab 2010;56:182-5

Correction to: Comparison of 2D vena contracta area with 3D planimetric mitral valve area in rheumatoid mitral valve disease

Orijinal makaledeki bir hatadan kaynaklanan düzeltme.In the original publication of the article one co-author, A. Zencirci, was listed by mistake. Dr. A. Zencirci has not contributed to this article and therefore, the author list has been updated. The author name A. Zencirci has been removed. All authors have agreed to the updated author list. Correct order given in this article. The original article has been corrected

Comparison of 2D vena contracta area with 3D planimetric mitral valve area in rheumatoid mitral valve disease

Rheumatoid valve disease is a general health problem of developing countries, and it mainly affects after the age of 40. Assessment of the correct mitral valve area (MVA) is important for the treatment of rheumatoid valve disease. However, there are contradictions between the three-dimensional (3D) and two-dimensional (2D) methods. A measurement with 3D echocardiography is a more accurate method to measure the MVA. However, in centers without 3D echocardiography, there are some difficulties in the accurate measurement of the MVA. The aim of this study was to assess the value of 2D transesophageal echocardiography (TEE) mitral valve vena contracta area (VCA) in predicting the severity of rheumatoid mitral stenosis (RMS) by comparing 3D planimetry. A total of 24 patients (10 females and 14 males) who were diagnosed with mild/moderate/severe RMS with using pressure half time, mean transmitral gradient, and planimetry methods were included in this study. 3D images were acquired using the 3D zoom and full volume. 2D TEE VCA was measured at an angle of 140° and 60°, which was perpendicular to the former, with color Doppler and the VCA was measured with an ellipsoid area using mathematical formula. There was statistically significant relationship between the measurements of 2D VCA and 3D zoom mode MVA planimetry and MVA full measurements (MVA full volume) (p < 0.01). Calculation of the valvular area after measuring the mitral valve VCA with 2D TEE is a reliable method that is usable in centers without 3D echocardiography

&#8216;Idiopathic&#8217; acute myocardial infarction in a young patient with noncompaction cardiomyopathy

Isolated left ventricular noncompaction (LVNC) is a rare hereditary cardiomyopathy characterized by prominent intraventricular trabeculations separated by deep intertrabecular recessus. While cardiac ischemia due to microvascular dysfunction is common in these patients, ST-segment elevation myocardial infarction (STEMI) is rare and usually seen as a consequence of coincidental coronary artery disease. We report the case of a 20 year-old male patient admitted to our emergency department with a complaint of squeezing chest pain who was subsequently diagnosed with STEMI according to electrocardiographic findings, although an emergent coronary angiogram demonstrated normal coronary arteries. Echocardiography revealed isolated LVNC, and the diagnosis was confirmed via magnetic resonance imaging. Repeat coronary catheterization with acetylcholine infusion and coronary flow reserve measurement failed to demonstrate vasospasm or microvascular dysfunction. As no apparent cause was found, this case was designated &#8216;idiopathic&#8217; myocardial infarction. Coronary thromboembolism due to stagnation of blood in the left ventricular cavity remained as the most probable mechanism underlying myocardial infarction

O volume plaquetário médio abaixo do normal está associado com extensão reduzida de doença arterial coronariana Lower than normal mean platelet volume is associated with reduced extent of coronary artery disease

FUNDAMENTO: A extensão da doença arterial coronariana aterosclerótica em pacientes com angina estável tem importantes implicações prognósticas e terapêuticas. Em modelos atuais de evolução de placas, os trombócitos desempenham um papel importante no crescimento de placas. O volume plaquetário médio é um marcador facilmente determinado, com evidência de correlação com a agregabilidade plaquetária in vitro, além de valores comprovadamente maiores após eventos vasculares agudos. OBJETIVO: No presente estudo, investigou-se a relação entre o volume plaquetário médio e a extensão angiográfica da doença arterial coronariana em pacientes com angina estável. MÉTODOS: Foram analisados prontuários, hemograma completo e dados angiográficos anteriores de 267 pacientes elegíveis com angina estável. A extensão angiográfica da doença arterial coronariana foi avaliada à luz de dados angiográficos, com o uso por um especialista do escore de Gensini em uma cardiologia invasiva. Os valores para o volume plaquetário médio foram obtidos a partir de hemogramas completos, obtidos um dia antes da angiografia. Com relação ao intervalo populacional para o volume plaquetário médio, os pacientes foram agrupados dentro (n = 176) e abaixo (n = 62) do referido intervalo. Foi realizada uma comparação entre grupos e uma análise correlacional. RESULTADOS: Não houve correlação linear entre o escore de Gensini total e o volume plaquetário médio (p = 0,29), ao passo que a contagem total de trombócitos apresentou correlação inversa com o volume plaquetário médio (p < 0,001, r = 0,41). Os pacientes com volume plaquetário médio abaixo do normal apresentaram um escore de Gensini (36,73 ± 32,5 vs. 45,63 ± 32,63; p = 0,023) e doença coronariana triarterial (18% VS. 36%; p = 0,007) significativamente inferiores se comparados com aqueles apresentando valores de volume plaquetário médio dentro dos intervalos populacionais. CONCLUSÃO: Nossas constatações não demonstraram nenhuma relação linear entre o volume plaquetário médio e a extensão da doença arterial coronariana, ao passo que os pacientes com volume plaquetário médio abaixo do normal apresentaram uma extensão reduzida da doença arterial coronariana.<br>BACKGROUND: Extent of atherosclerotic coronary artery disease in patients with stable angina has important prognostic and therapeutic implications. In current models of plaque evolution, thrombocytes play an important role in plaque growth. Mean platelet volume is a readily obtainable marker that was shown to correlate with platelet aggregability in vitro and increased values were demonstrated after acute vascular events. OBJECTIVE: In this study, we investigated the relationship of mean platelet volume and angiographic extent of coronary artery disease in patients with stable angina. METHODS: Past medical records, complete blood count and angiographic data of 267 eligible stable angina patients were reviewed. Angiographic extent of coronary artery disease was evaluated form angiographic data using Gensini score by an expert in invasive cardiology. Mean platelet volume values were obtained from complete blood counts that obtained one day before angiography. Patients were grouped as those within (n = 176) and lower than (n = 62) population-based range for mean platelet volume. Comparison between groups and correlation analysis was performed. RESULTS: There were no linear correlation between total Gensini score and mean platelet volume (p = 0.29), while total thrombocyte count was inversely correlated with mean platelet volume (p < 0.001; r = 0.41). Patients with lower than normal mean platelet volume had significantly lower Gensini score (36.73 ± 32.5 vs. 45.63 ± 32.63; p = 0.023) and three-vessel disease (18% vs. 36%; p = 0.007) compared with those mean platelet volume values within population-based ranges. CONCLUSION: Our findings show no linear relationship exists between mean platelet volume and extent of coronary artery disease, while patients with lower than normal mean platelet volume had reduced extent of coronary artery disease

Lower than Normal Mean Platelet Volume is Associated with Reduced Extent of Coronary Artery Disease

FUNDAMENTO: A extensão da doença arterial coronariana aterosclerótica em pacientes com angina estável tem importantes implicações prognósticas e terapêuticas. Em modelos atuais de evolução de placas, os trombócitos desempenham um papel importante no crescimento de placas. O volume plaquetário médio é um marcador facilmente determinado, com evidência de correlação com a agregabilidade plaquetária in vitro, além de valores comprovadamente maiores após eventos vasculares agudos. OBJETIVO: No presente estudo, investigou-se a relação entre o volume plaquetário médio e a extensão angiográfica da doença arterial coronariana em pacientes com angina estável. MÉTODOS: Foram analisados prontuários, hemograma completo e dados angiográficos anteriores de 267 pacientes elegíveis com angina estável. A extensão angiográfica da doença arterial coronariana foi avaliada à luz de dados angiográficos, com o uso por um especialista do escore de Gensini em uma cardiologia invasiva. Os valores para o volume plaquetário médio foram obtidos a partir de hemogramas completos, obtidos um dia antes da angiografia. Com relação ao intervalo populacional para o volume plaquetário médio, os pacientes foram agrupados dentro (n = 176) e abaixo (n = 62) do referido intervalo. Foi realizada uma comparação entre grupos e uma análise correlacional. RESULTADOS: Não houve correlação linear entre o escore de Gensini total e o volume plaquetário médio (p = 0,29), ao passo que a contagem total de trombócitos apresentou correlação inversa com o volume plaquetário médio (p < 0,001, r = 0,41). Os pacientes com volume plaquetário médio abaixo do normal apresentaram um escore de Gensini (36,73 ± 32,5 vs. 45,63 ± 32,63; p = 0,023) e doença coronariana triarterial (18% VS. 36%; p = 0,007) significativamente inferiores se comparados com aqueles apresentando valores de volume plaquetário médio dentro dos intervalos populacionais. CONCLUSÃO: Nossas constatações não demonstraram nenhuma relação linear entre o volume plaquetário médio e a extensão da doença arterial coronariana, ao passo que os pacientes com volume plaquetário médio abaixo do normal apresentaram uma extensão reduzida da doença arterial coronariana

Troponin and Anti-Troponin Autoantibody Levels in Patients with Ventricular Noncompaction

Ventricular hypertrabeculation/noncompaction is a morphologic and functional anomaly of myocardium characterized by prominent trabeculae accompanied by deep recessus. Dilated cardiomyopathy with left ventricular failure is observed in these patients, while the cause or pathophysiologic nature of this complication is not known. Anti-troponin antibodies are formed against circulating cardiac troponins after an acute coronary event or conditions associated with chronic myocyte necrosis, such as dilated cardiomyopathy. In present study, we aimed to investigate cardiac troponins and anti troponin autoantibodies in ventricular noncompaction/hypertrabeculation patients with/without reduced ejection fraction. A total of 50 patients with ventricular noncompaction and 23 healthy volunteers were included in this study. Noncompaction/hypertrabeculation was diagnosed with two-dimensional echocardiography using appropriate criteria. Depending on ejection fraction, patients were grouped into noncompaction with preserved EF (LVEF >50%, n = 24) and noncompaction with reduced EF (LVEF <35%, n = 26) groups. Troponin I, troponin T, anti-troponin I IgM and anti-troponin T IgM were measured with sandwich immunoassay method using a commercially available kit. Patients with noncompaction had significantly higher troponin I (28.98 +/- 9.21 ng/ml in NCNE group and 28.11 +/- 10.42 ng/ml in NCLE group), troponin T (22.17 +/- 6.97 pg/ml in NCNE group and 22.78 +/- 7.76 pg/ml in NCLE group) and antitroponin I IgM (1.92 +/- 0.43 mu g/ml in NCNE group and 1.79 +/- 0.36 mu g/ml in NCLE group) levels compared to control group, while antitroponin T IgM and IgG were only elevated in patients with noncompaction and reduced EF (15.81 +/- 6.52 mu g/ml for IgM and 16.46 +/- 6.25 mu g/ml for IgG). Elevated cardiac troponins and anti-troponin I autoantibodies were observed in patients with noncompaction preceding the decline in systolic function and could indicate ongoing myocardial damage in these patients