Elif Hande OZCAN CETIN, Kevser Gülcihan BALCI, Mehmet Serkan ÇETİN, Bahar TEKİN TAK, Firdevs Ayşenur EKİZLER, Mehmet ERDÖL, Fırat ÖZCAN, Özcan ÖZEKE, Serkan ÇAY, Ahmet TEMIZHAN, Serkan TOPALOĞLU, Dursun ARAS

Kalp yetersizliğinde yeni bir prognostik belirteç: Pik mitral regurgitasyon velositesinin sol ventrikül çıkış yolu velosite zaman integraline oranı

Amaç: Sistemik vaskuler rezistans (SVR), kalp yetersizliğinde risk tahmini ve tedavi klavuzluğunda kullanışlıdır. Pik mitral regurgitasyon velositesinin (MRV) sol ventrikül çıkış yolu velosite zaman integraline (LVOT VTI) oranının SVR ile pozitif yönde korele olduğu gösterilmiştir. Bu çalışmada düşük ejeksiyon fraksiyonlu kalp yetersizliği (DEF-KY) hastalarında MRV/LVOT VTI oranının bilinen prognostik belirteçlerle ilişkisi ve 1 yıllık ve uzun dönem birleşik son noktayi öngördürmedeki prognostik rolünü değerlendirmeyi amaçladık. Gereç ve Yöntemler: Prospektif olarak 72 DEF-KY hastası ve 10 sağlıklı kontrolü çalışmaya dahil ettik. Hastalar medyan 40.5 ay takip edildi. Birincil birileşik son nokta (BSN) mekanik dolaşım desteği, kalp transplantasyonu ve tüm nedenlere bağlı ölüm olarak tanımlandı. Bulgular: BSN(+) hastalarında daha yüksek MRV/LVOT VTI oranı saptandı (0.48±0.15 vs. 0.39±0.18 p=0.012). MRV/LVOT VTI oranı fonksiyonel sınıf (β=0.539, p=0<001), troponin I (β=0.415, p<0.001), serum BNP seviyesi (β=0.479, p<0.001), ve ürik asit düzeyi (β=0.235 p=0.018) ile pozitif yönde korele ve SEATTLE skor ile elde edilen yaşam beklentisi (β=-0.248, p=0.032) ile negatif korele izlendi. Diğer parametrelerle birlikte MRV / LVOT VTI oranındaki her 0,1 artış bir yıllık BSN riskini % 27 ve uzun dönem BSN riskini % 24,6 artırdı. Kaplan Meier analiziNDE MRV / LVOTVTI oranı ≥ 0.39 olan hastalarda diğerlerine göre uzun dönemde daha fazla BSN görüldü. Sonuç: MRV / LVOT VTI oranı diğer bilinen DEF-KY prognostik göstergeleri ile ilişkili olarak, kötü prognozun faydalı bir belirteci olarak görünmektedir

Anahtar Kelimeler:

sistemik vaskular rezistans, kalp yetersizliği, Pik mitral regurgitasyon velositesinin sol ventrikül çıkış yolu velosite zaman integraline oranı

A new prognostic marker in failing heart: Peak mitral regurgitation velocity to left ventricular outflow tract time velocity ıntegral ratio

Aim: Systemic vascular resistance (SVR) is useful for risk estimation and therapy guidance in HF. It has been shown that the ratio of peak mitral regurgitation velocity (MRV) to left ventricular outflow tract velocity-time integral (LVOT VTI) correlated positively with SVR. We aimed to assess the association of MRV/LVOT VTI ratio with established prognostic markers and its prognostic role for predicting one year and long term composite end-points in patients with HF and reduced ejection fraction (HFrEF).Material and Methods: We prospectively enrolled a total of 72 patients with HFrEF and 10 control subjects. Patients were followed up patients for median 40.5 months. Primary composite endpoint (CEP) was defined as any of these outcomes including requiring mechanical circulatory support, cardiac transplantation, and all-cause mortality.Results: CEP(+) patients had higher MRV/LVOT VTI ratio than others (0.48±0.15 vs. 0.39±0.18 p=0.012). MRV/LVOT VTI ratio was positively correlated with functional status (β=0.539, p=0<001), serum BNP level (β=0.479, p<0.001),troponin I (β=0.415, p<0.001), and Uric acid level (β=0.235 p=0.018) and negatively correlated with SEATTLE score derived life expectancy (β=-0.248, p=0.032). Adjusted with other parameters, every 0.1 increase in MRV/LVOT VTI ratio increased the one-year CEP risk by 37% and long-term CEP risk by 35%. In Kaplan Meier analysis, patients with MRV/LVOTVTI ratio ≥ 0.39 had more long-term CEP compared to others.Conclusion: MRV/LVOT VTI ratio seemed to be a useful predictor of poor prognosis associated with other established HF prognostic markers.

Keywords:

Systemic vascular resistance, Heart failure and reduced ejection fraction, peak mitral regurgitation velocity to left ventricular outflow tract velocity-time integral,

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1. Cotter G, Moshkovitz Y, Kaluski E et al. The role of cardiac power and systemic vascular resistance in the pathophysiology and diagnosis of patients with acute congestive heart failure. Eur J Heart Fail 2003; 5: 443–51.
2. Abbas AE, David Fortuin F, Patel B, Moreno CA, Schiller NB, Lester SJ. Noninvasive measurement of systemic vascular resistance using Doppler echocardiography. Journal of the American Society of Echocardiography 2004; 17: 834–8.
3. Kumar A, Parrillo JE. Shock: Classification, Pathophysiology, and Approach to Management. Critical Care Medicine 2008: 379–422.
4. Hatle L, Angelsen BA, Tromsdal A. Non-invasive estimation of pulmonary artery systolic pressure with Doppler ultrasound. Br Heart J 1981; 45: 157–65.
5. Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol 1990; 66: 493–6.
6. Yock PG, Popp RL. Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation 1984; 70: 657–62.
7. Ommen SR, Nishimura RA, Appleton CP et al. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: A comparative simultaneous Doppler-catheterization study. Circulation 2000; 102: 1788–94.
8. Levy WC, Mozaffarian D, Linker DT et al. The Seattle Heart Failure Model. Circulation 2006; 113: 1424–33.
9. Gardin JM, Adams DB, Douglas PS, Feigenbaum H, Forst DH, Fraser AG, et al. Recommendations for a standardized report for adult transthoracic echocardiography: A report from the American Society of Echocardiography’s Nomenclature and Standards Committee and Task Force for a Standardized Echocardiography Report. Journal of the American Society of Echocardiography 2002; 15: 275–90.
10. Stewart S, MacIntyre K, Hole DJ, Capewell S, McMurray JJ. More “malignant” than cancer? Five-year survival following a first admission for heart failure. Eur J Heart Fail 2001; 3: 315–22.
11. Hastillo A, Willis H, Hess M. The heart as a target organ of immune injury. Current Problems in Cardiology 1991; 16: 381–442.
12. James TN. Myocarditis and cardiomyopathy. N Engl J Med 1983; 308: 39–41.
13. Packer M. Neurohormonal interactions and adaptations in congestive heart failure. Circulation 1988; 77: 721–30.
14. Mancia G. Neurohumoral activation in congestive heart failure. Am Heart J 1990; 120: 1532–7.
15. Yancy CW, Jessup M, Bozkurt B et al. 2013 ACCF/AHA Guideline for the Management of Heart Failure. Circulation 2013;128.
16. Lund LH, Aaronson KD, Mancini DM. Validation of peak exercise oxygen consumption and the Heart Failure Survival Score for serial risk stratification in advanced heart failure. The American Journal of Cardiology 2005; 95: 734–41.
17. Kalogeropoulos AP, Georgiopoulou VV, Giamouzis G et al. Utility of the Seattle Heart Failure Model in Patients With Advanced Heart Failure. Journal of the American College of Cardiology 2009; 53: 334–42.