OBJECTIVE: To study the effects of chronic severe anemia on the aging heart. METHODS: We studied 41 elderly patients (mean age 69.8 yr, standard deviation [SD] 3.9 yr) suffering from chronic severe anemia (mean hemoglobin 6.3, SD 0.5 g/dL) with no history of cardiac disease, along with 63 healthy age- and sex-matched controls. Assessment included physical examination, electrocardiogram and Doppler echocardiography. RESULTS: Although heart rates were similar between patients and controls, arterial blood pressures were significantly lower in patients (mean pressure 92.7 mm Hg, SD 7.9, v. mean 102.1 mm Hg, SD 3.5; p < 0.001). No patient was found to have congestive heart failure. Patients with chronic anemia had larger diameters of the left (end-systolic 35.28, SD 4.20, v. 33.73, SD 2.08 mm, p < 0.05; end-diastolic 53.33, SD 4.55, v. 50.37, SD 2.10 mm, p < 0.001) and right ventricles (30.76, SD 3.98, v. 29.04, SD 2.04 mm; p < 0.05), and greater left-ventricular mass (277.64, SD 62.85, v. 212.91, SD 24.87 g; p < 0.001). Fractional shortening did not differ significantly (0.33, SD 0.04, v. 0.33, SD 0.03). The load-independent end-systolic index was lower in patients (2.67, SD 0.56, v. 3.87, SD 0.49 kdyn x m2/cm5; p < 0.001) along with end-systolic stress and total systemic resistance (p < 0.001) than controls, whereas the cardiac index was higher (4.31, SD 1.29, v. 2.73, SD 0.51 L/min/m2; p < 0.001). Differences between the 2 groups in diastolic function indices and pulmonary arterial pressures were not statistically significant. INTERPRETATION: Chronic severe anemia is well tolerated by the aging heart. Neither congestive heart failure nor clearly evident left-ventricular dysfunction were encountered. The heart exhibited an adaptive potential through remodelling by means of the Frank-Starling mechanism and afterload reduction. However, the lower end-systolic index in patients suggests that ventricular performance was marginally compromised. This state of high output was achieved mainly by increased stroke volume, with little contribution from heart rate.
OBJECTIVE: To study the effects of chronic severe anemia on the aging heart. METHODS: We studied 41 elderly patients (mean age 69.8 yr, standard deviation [SD] 3.9 yr) suffering from chronic severe anemia (mean hemoglobin 6.3, SD 0.5 g/dL) with no history of cardiac disease, along with 63 healthy age- and sex-matched controls. Assessment included physical examination, electrocardiogram and Doppler echocardiography. RESULTS: Although heart rates were similar between patients and controls, arterial blood pressures were significantly lower in patients (mean pressure 92.7 mm Hg, SD 7.9, v. mean 102.1 mm Hg, SD 3.5; p < 0.001). No patient was found to have congestive heart failure. Patients with chronic anemia had larger diameters of the left (end-systolic 35.28, SD 4.20, v. 33.73, SD 2.08 mm, p < 0.05; end-diastolic 53.33, SD 4.55, v. 50.37, SD 2.10 mm, p < 0.001) and right ventricles (30.76, SD 3.98, v. 29.04, SD 2.04 mm; p < 0.05), and greater left-ventricular mass (277.64, SD 62.85, v. 212.91, SD 24.87 g; p < 0.001). Fractional shortening did not differ significantly (0.33, SD 0.04, v. 0.33, SD 0.03). The load-independent end-systolic index was lower in patients (2.67, SD 0.56, v. 3.87, SD 0.49 kdyn x m2/cm5; p < 0.001) along with end-systolic stress and total systemic resistance (p < 0.001) than controls, whereas the cardiac index was higher (4.31, SD 1.29, v. 2.73, SD 0.51 L/min/m2; p < 0.001). Differences between the 2 groups in diastolic function indices and pulmonary arterial pressures were not statistically significant. INTERPRETATION: Chronic severe anemia is well tolerated by the aging heart. Neither congestive heart failure nor clearly evident left-ventricular dysfunction were encountered. The heart exhibited an adaptive potential through remodelling by means of the Frank-Starling mechanism and afterload reduction. However, the lower end-systolic index in patients suggests that ventricular performance was marginally compromised. This state of high output was achieved mainly by increased stroke volume, with little contribution from heart rate.
Authors: I Moyssakis; R Tzanetea; P Tsaftaridis; I Rombos; D P Papadopoulos; V Kalotychou; A Aessopos Journal: Postgrad Med J Date: 2005-11 Impact factor: 2.401
Authors: A I Triantafyllou; G P Vyssoulis; E A Karpanou; P L Karkalousos; E A Triantafyllou; A Aessopos; D T Farmakis Journal: J Hum Hypertens Date: 2013-10-24 Impact factor: 3.012
Authors: Donald S Silverberg; Dov Wexler; Adrian Iaina; Shoshana Steinbruch; Y Wollman; Doron Schwartz Journal: Int Urol Nephrol Date: 2006 Impact factor: 2.370
Authors: Jörg Stypmann; Markus A Engelen; Constanze Epping; Harold V M van Rijen; Peter Milberg; Christian Bruch; Günter Breithardt; Klaus Tiemann; Lars Eckardt Journal: Int J Cardiovasc Imaging Date: 2006-03-04 Impact factor: 2.357