Ayaktan pulmoner arteryel hipertansiyon hastalarında ortalama trombosit hacmi düzeyinin klinik sonlanımlar üzerine etkisi

GİRİŞ ve AMAÇ: Sağ kalp yetersizliği (KY) pulmoner arteryel hipertansiyon (PAH) hastalarında hastaneye yatışların ve ölümün başlıca nedenidir. Bu çalışmanın amacı; ayaktan PAH hastalarında Ortalama Trombosit Hacmi (OTH) ile KY nedenli hastaneye yatış ve mortalite arasındaki ilişkiyi değerlendirmekti. YÖNTEM ve GEREÇLER: Haziran 2011 ve Ağustos 2017 tarihleri arasında periyodik rutin kontolleri için spesifik PAH polikliniğimize başvurmuş 86 ayaktan PAH hastasından oluşan bir geriye dönük çalışma planladık. ROC analizine göre KY nedenli hastaneye yatışı öngördüren optimal OTH değeri > 8.4 fL olarak bulundu. Hastalar OTH > 8.4 fL ve OTH ≤ 8.4 fL olarak iki gruba ayrıldı. Olası öngördürücüler tek değişkenli ve çok değişkenli Cox regresyon analizi ile değerlendirildi. BULGULAR: Hastaların yaş ortalaması 50.8±11.6 idi. Ortalama takip süresi 27±13 aydı. OTH > 8.4 fL grubunda OTH ≤ 8.4 fL grubuna göre KY nedenli hastaneye yatış belirgin olarak daha fazlaydı (%73.0’e %12.2, p 8.4 fL olması ve vücut kitle indeksi ayaktan PAH hastalarında KY nedenli hastaneye yatış ile ilişkiliydi (p=0.009 ve p= 0.047, sırasıyla). Çok değişkenli analizde, OTH > 8.4 fL olması ayaktan PAH hastalarında KY nedenli hastaneye yatışların bağımsız güçlü bir öngördürüsü olarak bulundu (p=0.001, hazard ratio 7.639, 95% CI 2.414-24.178). TARTIŞMA ve SONUÇ: Ayaktan PAH hastalarında artmış OTH düzeyi ile KY nedenli hastaneye yatış arasındaki ilişki takiplerde yüksek riskli hastaları belirlemede kullanışlı olabilir.

Impact of the mean platelet volume level on clinical outcomes in outpatient patients with pulmonary arterial hypertension

INTRODUCTION: Right heart failure (HF) is main cause of death and rehospitalization in pulmonary arterial hypertension (PAH) patients. The aim of this study was to assess the relationship between mean platelet volume (MPV) with HFrelated hospitalization and mortality in outpatient PAH patientsMETHODS: We conducted a retrospective cohort study of 86PAH outpatients who admitted to our special PAH clinic for periodic routine controls between June 2011 and August 2017. According to the receiver-operating characteristic analysis, the optimal cut-off value of MPV to predict HF-related hospitalization was > 8.4 fL. Patients divided to two categories as MPV > 8.4 fL and MPV ≤ 8.4 fL groups. Potentialpredictors were evaluated in univariate and multivariate Coxregression analysis.RESULTS: The mean age of patients was 50.8±11.6 years.The mean follow-up was 27±13 months. HF-related hospitalization was found markedly higher in MPV > 8.4 fL group than MPV ≤ 8.4 fL group (73.0% vs. 12.2%, p 8.4 fL and BMI were associatedwith HF-related hospitalization in outpatient PAH patients (p=0.009 and p=0.047, respectively). In multivariate analysis, MPV > 8.4 fL was found a strong independent predictor of HF-related hospitalization in outpatient PAH patients (p=0.001, hazard ratio 7.639, 95% CI 2.414-24.178).DISCUSSION AND CONCLUSION: The relationship between increased MPV level and HF-related hospitalization in outpatient PAH patients may be useful to identfy high-risk patients in follow-up.

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1. Othman 1.Pepe S, Marasco SF, Haas SJ, Sheeran FL, Krum H, Rosenfeldt FL. Coenzyme Q 10 in cardiovascular disease. Mitochondrion. 2007 Jun;7 Suppl: S154-67.
2. Molyneux SL, Florkowski CM, Lever M, George PM. Biological variation of coenzyme Q10. ClinChem 2005;51:455-7.
3. Turunen M, Olsson J, Dallner G. Metabolism and function of coenzyme Q,Biochimica et BiophysicaActa (BBA) - Biomembranes, Volume 1660, Issue 1-2, January 2004, Pages 171-99.
4. Crane FL ve ark. Biochemical Functions of Coenzyme Q10, Journal of the American College of Nutrition 2001; 20: 591-8.
5. Ito H, Nakajima T, Takikawa R, Hamada E, Iguchi M, Sugimoto T et al. Coenzyme Q10 attenuates cyanide activation of the ATP-sensitive K+ channel current in single cardiac myocytes of the guinea-pig. NaunynSchmiedebergs Arch Pharmacol. 1991;344:133-6.
6. Huynh K, Kiriazis H, Du XJ, Love JE, Jandeleit-Dahm KA, Forbes JM et al.Coenzyme Q10 attenuates diastolic dysfunctions, cardiomyocyte and cardiac fibrosis in the db/db mause model of tpe 2 diabetes. Diabetologia. 2012 May;55:1544-53.
7. Kumar A, Kaur H, Devi P, Mohan V (2009) Role of coenzyme Q10 (CoQ10) in cardiac disease, hypertension and Meniere-like syndrome. Pharmacol Ther 124:259-68
8. Langsjoen, P. H., & Folkers, K. (1993). Isolated diastolic dysfunction of the myocardium and its response to CoQ10 treatment. ClinInvestig 71(8 Suppl), S140-4
9. Langsjoen PH, Langsjoen A, Willis R, Folkers K. Treatment of hypertrophic cardiomyopathy with coenzyme Q10. Mol Aspects Med. 1997;18 Suppl:S145-51.
10. Rickham PP. Human Experimentation. Code of Ethics of the World Medical Association. Declaration of Helsinki. Br Med J.1964;2:177
11. Quiñones MA, Otto CM, Stoddard M, Waggoner A, Zoghbi WA; Doppler Quantification Task Force of the Nomenclature and Standards Committee of theAmerican Society of Echocardiography. Recommendations for quantification of Doppler echocardiography: a report from the Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of Echocardiography. J Am SocEchocardiogr. 2002 Feb;15:167-84.
12. Nagueh SF, Appleton CP, Gillebert TC, Marino PN, Oh JK, Smiseth OA et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echocardiogr. 2009 Feb;22:107-33.
13. Van Jaarsveld H, Potgeiter GM, Loschner A. Changes in NADH-coenzyme Q10 reductase (complex I) with autolysis in the rat heart as experimental model. Enzyme. 1986;35:206-14.
14. Folkers, K, Littarru G. P, Ho L, Runge T. M, Havanonda S, & Cooley D. (1970). Evidence for a deficiency of coenzyme Q10 in human heart disease. Int J VitamNutr Res 40, 380-90.
15. Mabuchi H, Nohara A, Kobayashi J, Kawashiri MA, Katsuda S, Inazu A et al; Hokuriku Lipid Research Group. Effects of CoQ10 supplementation on plasma lipoprotein lipid, CoQ10 and liver and muscle enzyme levels in hypercholesterolemic patients treated with atorvastatin: a randomized double-blind study. Atherosclerosis. 2007 Dec;195:182-9.
16. Hughes K, Lee BL, Feng X, Lee J, Ong CN. Coenzyme Q10 and differnces in coronary heart disease risk in Asian Indians and Chinese. Free RadicBiol Med. 2002 Jan 15;32:132-8.
17. Lagendijk J, Ubbink JB, Vermaak WJ. Measurement of the ratio between the reduced and oxidized forms of coenzyme Q10 in human plasma as a possible marker of oxidative stres. J Lipid Res 1996;37:67–75.
18. Yamashita S, Yamamoto Y. Simultaneous detection of ubiquinol and ubiquinone in human plasma as a marker of oxidative stres. Anal Biochem 1997;250:66-73.
19. Lagendijk J, Ubbink JB, Delport R, Vermaak WJ, Human JA. Ubiquinol/ubiquinon ratio as marker of oxidative stres in coronary artery disease. ResCommunMolPatholPharmacol. 1997 Jan;95:11-20.
20. Ruiz-Jiménez J, Priego-Capote F, MataGranados JM, Quesada JM, Luque de Castro MD. Determination of the ubiquinol-10 (coenzyme Q10) in human serum by liquid chromatography tandem mass spectrometry to evaluate the oxidative stress. J Chromatogr A. 2007 Dec 21;1175:242-8.
21. Miles MV, Horn PS, Morrison JA, Tang PH, DeGrauw T, Pesce AJ. Plazma CoQ10 refernce intervals, but not redox status, are affected by Gender and race in self-reported healthy adults. ClinChimActa 2003;332:123-32.
22. Miles MV, Horn PS, Tang PH, Morrison JA, Miles L, DeGrauw T et al. Age-related changes in plasma coenzyme Q10 concentrations and redox state in apparently healhy children and adults. ClinChimActa 2004;347:139-44.
23. Kumar A, Kaur H & Mohan V (2007). Coenzyme Q10 in isolated diastolic heart failure in hypertrophic cardiomyopathy (HCM). The 5th Conference of the International Coenzyme Q10 Association, Kobe Japan.
24. Ghirlanda G, Oradei A, Manto A, Lippa S, Uccioli L, Caputo S, et al. (1993). Evidence of plasma CoQ10-lowering effect by HMG-CoA reductase inhibitors: a double blind, placebocontrolled study. Clin Pharmocol J 33: 226-9.
25. Silver MA &Langsjoen PH (2003). Statin cardiomyopathy: a potential role for coenzyme Q10 therapy for statin induced changes in diastolic LV performance: description of a clinical protocol. Bio factors 18(1–4), 125-7.
26. Silver MA, Langsjoen PH, Szabo S, Patil H, Zelinger A. Effect of atorvastatin on left ventricular diastolic function and ability of coenzyme Q10 to reverse that dysfunction. Am J Cardiol. 2004 Nov 15;94:1306-10.
27. Chew GT, Watts GF, Davis TM, Stuckey BG, Beilin LJ, Thompson PL et al. Hemodynamic effects of fenofibrate and coenzyme Q10 in type 2 diabetics subjects with left ventricular diastolic dysfunctions. Diabetes Care. 2008 Aug;31:1502-9.