Borghi and Cicero’s monograph sets an example for what is called translational research, which aims to speed the application of research findings from the basic science laboratory to the bedside or clinic. Since the Framingham Heart Study, hypercholesterolemia and hypertension have been linked epidemiologically as major risk factors for coronary heart disease. At various times, the two risk factors have also been linked together in syndromes such as dyslipidemic hypertension, syndrome X, and most recently, the metabolic syndrome. In patients with the metabolic syndrome, low-density lipoprotein cholesterol (LDL-C) remains the primary target, with triglycerides and non-high-density lipoprotein cholesterol (HDL-C) as secondary targets. It is speculated that insulin resistance may represent the common factor in the metabolic syndrome; however, HDL-C, triglycerides, and blood pressure each plays a contributing role in the definition of the metabolic syndrome.
As Borghi and Cicero argue, blood pressure and cholesterol are linked at the basic science level through the renin-angiotensin system (RAS), endothelial dysfunction, and LDL-C oxidation. In a mouse model, statins have been shown to decrease atherosclerosis when the RAS is stimulated [1]. At the clinical level, hypertensive patients benefit greatly from statin treatment, largely due to the fact that they are at high cardiovascular risk because of the interdependence of hypertension and hypercholesterolemia. These risk factors frequently coexist in the same individual.
It is of interest that when hypertension exists on a background of very low levels of LDL-C, as in China and Japan 30 years ago, stroke was very common, but coronary heart disease was not [2]. Thus, in the presence of hypertension, coronary heart disease requires a sufficiently high level of LDL-C to promote the development of atherosclerotic plaques. In addition, in a study of African Americans with PCSK9 gene mutations and decreased levels of LDL-C, coronary heart disease was very rare, even in the presence of hypertension, diabetes, or smoking [3].
With this monograph, Borghi and Cicero have provided a valuable reference and service by calling attention to the interaction of hypertension and hypercholesterolemia on both basic science and clinical levels.

 

REFERENCES

1. van der Hoorn JW, Kleemann R, Havekes LM, Kooistra T, Princen HM, Jukema JW. Olmesartan and pravastatin additively reduce development of atherosclerosis in APOE*3Leiden transgenic mice. J Hypertens 2007;25(12):2454-2462.

2. Chen Z, Peto R, Collins R, MacMahon S, Lu J, Li W. Serum cholesterol concentration and coronary heart disease in population with low cholesterol concentrations. BMJ 1991;303(6797):276-282.

3. Cohen JC, Boerwinkle E, Mosley TH Jr, Hobbs HH. Sequence variations in PCSK9, low LDL, and protection against coronary heart disease. N Engl J Med 2006;354(12):1264-1272.