Increased Blood Volume Has Both Positive and Negative Impacts on Health

August 26, 2009

Scientists from the University of Heidelberg Hospital have discovered why thicker blood may simultaneously increase and decrease an individual’s risk for heart attack and stroke.

Scientists from the University of HeidelbergHospital have discovered why thicker blood may simultaneously increase and decrease an individual’s risk for heart attack and stroke.

Dr. Berend Isermann, consultant at Heidelberg University Hospital, Department of Internal Medicine I and Clinical Chemistry, and his team of researchers have found that, in mice with elevated fat levels and a genetic defect that increases clotting in the blood, larger plaques formed, but that the plaques were more stable, and “no vascular obstruction was observed, as the vascular wall expanded to adapt to the new situation,” according to the researchers. The identification of this genetic factor provides an explanation for why an increased blood volume may heighten the risk for heart attack and stroke while, at the same time, lowering that risk.

According to an abstract of the study, which was published in Circulation, in 2 mouse models with hyperlipidemia and genetically imposed hypercoagulability, “hypercoagulability resulted in larger plaques, but vascular stenosis was not enhanced secondary to positive vascular remodeling.”

“Our findings were made on mice, but they confirm the results of clinical studies on humans,” said Dr. Isermann. “In addition, in vitro studies show that human cells react similarly to mouse cells.”

In a contrary finding, the study results showed that the long-term use of anticoagulants (which, in the case of this study, was heparin) reversed the advantages of increased clotting. However, to try and preserve the positive impact of plaque stability, the researchers recommend “using anticoagulants that inhibit specific coagulation factors.”

“Here, we show a new function of the coagulation system, averting stenosis and plaque destabilization during de novo atherogenesis,” the researchers conclude in the Circulation abstract. “The in vivo and in vitro data establish that thrombin-induced signaling via protease-activated receptor-1, phospholipase-C{beta}, phosphoinositide 3-kinase, and nitric oxide in monocytes impairs monocyte transendothelial migration. This likely accounts for the reduced macrophage accumulation in plaques of hypercoagulable mice. Thus, in contrast to their role in unstable plaques or after vascular injury, hypercoagulability and thrombin convey a protective effect during de novo atherogenesis.”

Previous studies have shown that increased clotting is “detrimental” for plaque development.