What is the relationship between high blood pressure and inflammation?
High blood pressure and inflammation reinforce each other mutually, and higher inflammatory values in the blood mean a measurably greater risk of serious cardiovascular disease in people with high blood pressure. Have your blood pressure and CRP checked regularly, especially if you have other risk factors such as diabetes or excess weight.
Inflammation and high blood pressure reinforce each other in both directions. Inflammatory substances such as CRP, IL-6 and TNF-alpha (signalling molecules of the immune system) damage the inner lining of blood vessels, cause oxidative stress and activate the immune system in a way that drives blood pressure even higher. They also contribute to vascular remodelling and impaired kidney function, creating a vicious cycle.
Conversely, high blood pressure itself also fuels inflammation. The mechanical pressure on the heart is detected by proteins in the outer layer of heart cells, which attracts immune cells. These cause inflammation in the heart muscle and, ultimately, scar tissue formation. This explains a significant part of heart failure in which the pump itself still appears to be functioning normally.
In people with high blood pressure, higher levels of inflammatory markers in the blood are associated with a greater risk of death, both from cardiovascular disease and from other causes. CRP turns out to be the strongest predictor. These are associations, not proven causality, but they have been measured in large cohorts of tens of thousands of people.
The risk increases further when high blood pressure coincides with insulin resistance or obesity. Inflammatory markers then add an extra 1.2 to 1.8 times the risk of cardiovascular disease, although this additional risk diminishes at older ages.
The pulmonary vessels deserve separate attention: in pulmonary arterial hypertension, a serious form of elevated pressure specifically in the lung vessels, disrupted immune regulation plays a central role. Higher CRP levels here are associated with poorer survival and reduced walking capacity. Notably, obesity offers this group some protection against mortality, while at the same time raising CRP levels. That interplay is not yet fully understood.
Based on multiple observational cohorts (NHANES, UK Biobank, Shanghai), mechanistic research and association studies. No large randomised studies exist with breaking the inflammation-blood pressure cycle as a primary endpoint. Renal denervation as a treatment shows an unclear effect on inflammation.