To accurately evaluate the molecular environment underlying cardiovascular disease (CVD), it's necessary to assess various biomarkers that influence the synergistic dynamics of this multifactorial process. These markers provide insight into interrelated CVD mechanisms such as inflammation, accumulation of fatty deposits, the function and integrity of the endothelium (the inner layer of cells lining blood vessel walls), glucose/insulin response, blood clotting function, and other important factors.

The role of serum cholesterol levels in the development and progression of heart disease has been well-established by research over the last forty years: the higher the serum cholesterol, the more frequently associated heart disease is found.1-4 More specifically, elevated serum levels of LDL, the "bad" cholesterol, are established as a major cause of coronary heart disease.5-8 Conversely, high levels of HDL, good cholesterol, can reduce the likelihood of developing coronary heart disease by as much as 50%.9 But cholesterol is only one part of the clinical picture.

Recent breakthroughs in molecular research have revealed other biochemical mechanisms that play a crucial role in the development of CVD. High levels of the amino acid homocysteine, for example, have been correlated with mechanisms related to artery damage and blood clotting.10 One study found that men with extremely high homocysteine levels were three times more likely to have a heart attack, and that this increased occurrence was independent of their blood lipid levels.11 Homocysteine levels can rise due to nutritional deficiencies and inborn errors of metabolism.

Fibrinogen is a blood protein that the body depends on for proper clotting, to prevent bleeding to death in response to injury. But if fibrinogen levels become too high, from stress, obesity, inflammation, aging, or other causes, this substance can play a key role in artery disease by restricting blood flow, accelerating plaque deposits, and promoting damage to arteries.12-16

Analyzing specific components of fatty cholesterol provides added insight into cardiovascular health. One of these components, lipoprotein(a), has been called the most important genetic factor associated with early atherosclerosis and coronary artery disease.17 Other constituents, such as apo A-1 and apo-B are also important. Researchers from one Mayo Clinic study argued that specific apolipoprotein components of cholesterol—particularly A-1 and A-2–may be considerably better markers than cholesterol itself.18 Researchers from Johns Hopkins asserted that apo A-1 and apo-B were better indicators of premature coronary atherosclerosis than markers such as LDL cholesterol.19

Increasingly, attention has been focused on inflammation as a driving force in the process of heart disease. Two separate studies recently published in the New England Journal of Medicine report that plasma C-reactive protein (CRP), a marker for systemic inflammation, is a strong predictor of heart attack and stroke. In one study, men with the highest CRP values had three times the incidence of myocardial infarction and two times the incidence of ischemic stroke. Significantly, these relationships remained steady over long periods, and were independent of other lipid and non-lipid factors, including smoking.20 Another analysis evaluated biomarkers of inflammation in over 28,000 healthy postmenopausal women and found that C-reactive protein was the most predictive marker for future cardiac events such as heart attacks. Women with the highest CRP levels had a greater than fourfold risk of experiencing a cardiac event compared to those with the lowest levels.21

All these biomarkers can exert a combined effect on cardiovascular disease that is even greater than the sum of their individual parts. For this reason, assessing these markers together is crucial.

Comprehensive Cardiovascular Assessment is an advanced analysis of biochemical CVD markers that includes powerful new independent factors influenced by heredity, nutrition, and inflammation, as well as classic lipid markers, a cardiovascular index, and 2 computed ratios.

References:
1 Martin MJ, Hulley SB, Browner WS, Kuller LH, Wentworth D. Serum cholesterol, blood pressure and mortality: implications from a cohort of 361,662 men. Lancet 1986;2(8513):933-6.
2 Kannel WB. Range of serum cholesterol values in the population developing coronary artery disease. Am J Cardiol 1995;76(9):69C-77C.
3 Castelli WP, Anderson K, Wilson PW, Levy D. Lipids and risk of coronary heart disease. The Framingham Study. Ann Epidemiol 1992;2:23-8.
4 Wong ND, Wilson PW, Kannel WB. Serum cholesterol as a prognostic factor after myocardial infarction: The Framingham Study. Ann Intern Med 1991;115(9):687-93.
5 Consensus Conference. Lowering blood cholesterol to prevent heart disease. JAMA 1985;253:2080-2086.
6 La Rosa JC, Hunninghake D, Bush D, Criqui MH, Getz GS, Gotto AM Jr, et al. The cholesterol facts. A summary of the evidence relating dietary fats, serum cholesterol, and coronary heart disease. Circulation 1990;81:1721-1733.
7 Frick MH, Elo O, Haapo K, Heinonen OP, Heinsalmi P, Helo P, et al. Helsinki heart study: primary prevention trial with gemfibrozil in middle-aged men with dyslipidemia. Safety of treatment, changes in risk factors, and incidence of coronary heart disase. N Engl J Med 1987;317:1237 1245.
8 Lipid Research Clinics Program: The Lipid Research Clinics Coronary Primary Prevention Trial Results. I. Reduction in incidence of coronary heart disease. JAMA 1984;251:351-364.
9 Gordon T, Castelli WP, Hjortland MC, Kannel WB, Dawber TR: High density lipoprotein as a protective factor against coronary heart disease. The Framingham Study. Am J Med 1977;62:707-714.
10 Ross R. Factors influencing atherogenesis. In: Hurst JW, Schlant RC, Rackley CE, Sonnenblick EH, Wenger NK, editors. The heart, arteries, and veins. New York: McGraw-Hill, 1990:877-923.
11 Stampfer MJ, Malinow MR, Willet WC, Newcomer LM, Upson B, Ullmann D, et al. A prospective study of plasma homocyst(e)ine and risk of myocardial infarction in US physicians. JAMA 1992;268(7):877-881.
12 Caen JP, Soria J, Collet JP, Soria C. Fibrinogen, a vascular risk factor. Bull Acad Natl Med 1993;177(8):1433-41.
13 Juhan-Vague I, Pyke SD, Alessi MC, Jespersen J, Haverkate F, Thompson SG. Fibrinolytic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. Circulation 1996;94(9):2057-63.
14 Lau CS, McLaren M, Mackay I, Belch JJ. Baseline plasma fibrinolysis and its correlation with clinical manifestations in patients with Raynaud's phenomenon. Ann Rheum 1993;52(6):443-8.
15 Levenson J, Giral P, Razavian M, Gariepy J, Simon A. Fibrinogen and silent atherosclerosis in subjects with cardiovascular risk factors. Arterioscler Thromb Vasc Biol 1995;15(9):1263-8.
16 Giannasi G, Ferrari S, Galetta F. Fibrinogen as a cardiovascular risk factor. Minerva Cardioangiol 1995;43(5):169-75.
17 Doetsch K, Roheim PS, Thompson JJ. Human lipoprotein(a) quantified by 'capture' ELISA. Ann Clin Lab Sci 1991;21(3):216-218.
18 Kottke BA, Zinsmeister AR, Holmes DR Jr, Kneller RW, Hallaway BJ, Mao SJ. Apolipoproteins and coronary artery disease. Mayo Clinic Proc 1986;61:1.
19 Kwiterovich PO Jr, Coresh J, Smith HH, Bachorik PS, Derby CA, Perason TA. Comparison of the plasma levels of apolipoproteins B and A-1, and other risk factors in men and women with premature coronary artery disease. AM J Cardiol 1992;69(12):1015-21.

20 Ridker PM, Cushman M, Stampher MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336(14):973-9.

21 Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. New Engl J Med 2000 ; 342 (12): 836-43.

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Dr. Rispoli, Ph.D., L.Ac. has had a clinical practice for over 20 years. Her programs work because she is so thorough in testing and providing a nutritional approach. Remember that the body can heal itself if given the proper nutrients.

The information herein is not intended as diagnosis, treatment or a cure. Should you have a medical condition please seek the advice of your medical doctor.