Cancer Treatment Today » Heart Disease http://cancertreatmenttoday.org Knowledge is Power Thu, 26 Mar 2026 23:39:25 +0000 en-US hourly 1 Erythropoietin therapy for cardiomyopathy – pro http://cancertreatmenttoday.org/erythropoietin-therapy-for-cardiomyopathy-pro/ http://cancertreatmenttoday.org/erythropoietin-therapy-for-cardiomyopathy-pro/#comments Sun, 28 Oct 2012 03:36:52 +0000 M Levin, MD http://cancertreatmenttoday.org/?p=9645 Raising Hemoglobin levels is not always an unmitigated belssing. Studies in dialysis patients showed an increased risk of complications when Hb is raised above HB of 10-22.  Meta-analysis of reported randomized clincal trials(RCT)s conclude that normalization of hemoglobin with erythropoietin is harmful.

The connection between heart failure(HF) and Hb levels appears to exist but it is not certain that low Hb worsens heart failure. Three studies have looked at raising Hb in HF, one with transfusion and two with erythropietin and produced inconsistent results, with only one of them,  by Mancini et al, a randomized study, but it was a small study. 

Erythropoietin receptors are present in a variety of tissues, including the heart, and erythropoietin may have anti-inflammatory and antiapoptotic properties. Recently published studies have demonstrated that treatment with rHuEPO favorably attenuated ischemia-reperfusion injury in a mouse model. Whether these findings will have physiologic relevance in humans remains unknown, but they do suggest an additional potential mechanism for beneficial effects of erythropoietin treatment in human HF. On the other hand, higher Hb levels may increase the physiologic stress on the heart and increase hypertension and stroke. Several studies are ongoing . Clearly, routine adoption of erythropoietic agents to treat HF and cardiomyopathy is premature.

 

Robert N. Foley, Bryan M. Curtis, and Patrick S. ParfreyErythropoietin Therapy, Hemoglobin Targets, and Quality of Life in Healthy Hemodialysis Patients: A Randomized Trial Clin J Am Soc Nephrol. 2009 April; 4(4): 726–733
 
Mancini  D.M., Katz  S.D., Lamanca  J., Lamanca  J., Hudaihed  A., Androne  A.S.;  Effect of erythropoietin on exercise capacity in patients with moderate to severe chronic heart failure, Circulation 107 2003 294-299
 

Bohlius J, et al. Recombinant human erythropoesis stimulating agents and moratlity in patients

with cancer. A meta analysis of randomized trials. The Lancet,2009;373:1532.

Tonelli M, et al. Benefits and Harms of erythropoesis stimulating agents for anemia related to cancer: a metaanalysis. CMAJ,2009;180(11):e62-71.

Kotecha D, et al. Erythropoetin as a treatment of anemia in heart failure: systemic review of randomized trials. Am Heart J,2011;161(5):822.

Pfeffer MA, et al. A trial of darbepoetin alfa in type 2 diabetis and chronic kidney disease. N Engl J Med,2009;361:2019.

Skali H, et al. Stroke in patients with type 2 diabetes CKD, and anemia treated with darboepotin alpha. Circulation,2011;124:2903.

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]]> http://cancertreatmenttoday.org/erythropoietin-therapy-for-cardiomyopathy-pro/feed/ 0 Lipoprotein-associated phospholipase A2 – pro http://cancertreatmenttoday.org/heart-disease/ http://cancertreatmenttoday.org/heart-disease/#comments Tue, 19 Jun 2012 14:09:26 +0000 M Levin, MD http://cancertreatmenttoday.org/?page_id=443

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme that is produced by inflammatory cells, co-travels with circulating low-density lipoprotein (LDL), and hydrolyzes oxidized phospholipids in LDL. Its biological role has been controversial with initial reports purporting atheroprotective effects of Lp-PLA2 thought to be a consequence of degrading platelet-activating factor and removing polar phospholipids in modified LDL. Recent studies, however, focused on pro-inflammatory role of Lp-PLA2 mediated by products of the Lp-PLA2 reaction (lysophosphatidylcholine and oxidized nonesterified fatty acids). These bioactive lipid mediators, which are generated in lesion-prone vasculature and to a lesser extent in the circulation (eg, in electronegative LDL), are known to elicit several inflammatory responses. The proinflammatory action of Lp-PLA2 is also supported by a number of epidemiology studies suggesting that the circulating level of the enzyme is an independent predictor of cardiovascular events, despite some attenuation of the effect by inclusion of LDL, the primary carrier of Lp-PLA2, in the analysis.

Ascribing a role for Lp-PLA2, an enzyme that is produced by inflammatory cells, is transported on circulating LDL and hydrolyzes oxidized phospholipids in LDL, has been controversial. A growing number of epidemiological studies suggest that Lp-PLA2 is an independent predictor of cardiovascular events, despite some attenuation of this relationship by LDL, the primary carrier of Lp-PLA2. These observations strengthen the rationale to explore causal links between Lp-PLA2 and plaque vulnerability. The connection to cardiovascular diseae and Alzheimer’s remain unproven; neither are the effects of  interventions to reduce the level of this marker known. Empire considers this test to be be not medically necessary.

A.-L. Levonen, E. Vahakangas, J. K. Koponen, and S. Yla-Herttuala
Antioxidant Gene Therapy for Cardiovascular Disease: Current Status and Future Perspectives
Circulation, April 22, 2008; 117(16): 2142 – 2150.

W. Koenig
Cardiovascular Biomarkers: Added Value With an Integrated Approach?
Circulation, July 3, 2007; 116(1): 3 – 5.

A. Oldgren, S. K. James, A. Siegbahn, and L. Wallentin
Lipoprotein-associated phospholipase A2 does not predict mortality or new ischaemic events in acute coronary syndrome patients
Eur. Heart J., March 2, 2007; 28(6): 699 – 704.

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