Evaluation of Intravascular Hemolysis With Erythrocyte Creatine in Patients With Aortic Stenosis

Abstract

SummaryChronic intravascular hemolysis has been identified in patients with cardiac valve prostheses, but only a few case reports have evaluated intravascular hemolysis in patients with native valvular heart disease. To detect intravascular hemolysis in patients with aortic stenosis, erythrocyte creatine was evaluated with hemodynamic indices obtained by echocardiography.Erythrocyte creatine, a marker of erythrocyte age, was assayed in 30 patients with aortic stenosis and 10 aged matched healthy volunteers. Peak flow velocity of the aortic valve was determined by continuous-wave Doppler echocardiography. Twenty of 30 patients with aortic stenosis had high erythrocyte creatine levels (> 1.8 µmol/g Hb) and erythrocyte creatine was significantly higher as compared with control subjects (1.98 ± 0.49 versus 1.52 ± 0.19 µmol/g Hb, P = 0.007). Peak transvalvular pressure gradient ranged from 46 to 142 mmHg and peak flow velocity ranged from 3.40 to 5.95 m/second. Patients with aortic stenosis had a significantly lower erythrocyte count (387 ± 40 versus 436 ± 42 × 10 4 µL, P = 0.002) and hemoglobin (119 ± 11 versus 135 ± 11 g/L, P < 0.001) as compared with control subjects. Erythrocyte creatine had a fair correlation with peak flow velocity (r = 0.55, P = 0.002).In conclusion, intravascular hemolysis due to destruction of erythrocytes was detected in patients with moderate to severe aortic stenosis and the severity of intravascular hemolysis was related to valvular flow velocity of the aortic valve. (Int Heart J 2016; 57: 430-433)

Intravascular hemolysis in patients with mitral regurgitation: Evaluation by erythrocyte creatine

“…Several markers including fragmented red cell, reticulocyte, lactate dehydrogenase, indirect bilirubin, haptoglobin, and erythrocyte creatinine have been applied to estimate the severity of intravascular hemolysis [1][2][3][4][5][6][7][8][9][25][26][27]. Among these markers, lactate dehydrogenase has been widely used to estimate the severity of intravascular hemolysis, because close relation between lactate dehydrogenase and 51 Cr-labeling method has been demonstrated [2,25].…”

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Intravascular hemolysis has been reported in heart valve replacement with mechanical prostheses, stenotic valve diseases, hypertrophic cardiomyopathy, and pulmonary hypertension [1][2][3][4][5][6][7][8][9]. Even in cases of subclinical anemia, intravascular hemolysis due to destruction of erythrocytes remains to be evaluated.

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“…Red blood cell life span, measured by 51 Cr-labeling, has been used as a gold standard test to estimate the severity of intravascular hemolysis [1-3], but the 51 Cr-labeling method requires a prolonged examination period with series of blood drawn from the patient. In contrast to the 51 Cr-labeling method, measurement of erythrocyte creatine is simple, rapid, and economically favorable to determine the erythrocyte age by a single blood sample measurement [4,[7][8][9][10][11][12]. Intravascular hemolysis has been reported in patients with mitral regurgitation after incomplete mitral valve repair [13][14][15][16], but intravascular hemolysis in patients with mitral regurgitation with native valve has not been evaluated in detail.…”

Evaluation of Recombinant Human Erythropoietin Responsiveness by Erythrocyte Creatine in Haemodialysis Patients

“…An excellent correlation between erythrocyte creatine and direct measurement of red blood cell survival time by 51 Cr method has been reported [12,13]. In patients with normal erythropoietic capacity such as intravascular haemolysis and haemolytic anaemia, red cell production is accelerated in proportion to the amount of erythrocyte destruction, which lead to an increase in the young erythrocytes containing higher erythrocyte creatine levels [26][27][28][29]. In contrast, renal anaemia is mainly caused by decreased erythoropoietic capacity due to inadequate erythropoietin production and/or hypoesponsiveness to rHuEpo treatment [6,30].…”

Sildenafil Reduces the Risk of Thromboembolic Events in HeartMate II Patients with Low-Level Hemolysis and Significantly Improves the Pulmonary Circulation

“…11) Similar phenomena have been detected in patients with severe aortic stenosis. 12) Previous studies have demonstrated that fHb scavenges nitric oxide (NO) and reduces the bioavailability of NO during hemolysis, thus leading to endothelial dysfunction and platelet activation. 13,14) At the same time, elevated fHb interacts with the A1 and 2 domains of von Willebrand factor (vWF), which increases platelet adhesion to vWF.…”