The role of noninvasive cardiovascular testing, applied clinical nutrition and nutritional supplements in the prevention and treatment of coronary heart disease

Abstract

Numerous clinical trials suggest that we have reached a limit in our ability to decrease the incidence of coronary heart disease (CHD) and cardiovascular disease (CVD) utilizing the traditional diagnostic evaluation, prevention and treatment strategies for the top five cardiovascular risk factors of hypertension, diabetes mellitus, dyslipidemia, obesity and smoking. About 80% of heart disease (heart attacks, angina, coronary heart disease and congestive heart failure) can be prevented by optimal nutrition, optimal exercise, optimal weight and body composition, mild alcohol intake and avoiding smoking. Statistics show that approximately 50% of patients continue to have CHD or myocardial infarction (MI) despite presently defined 'normal' levels of the five risk factors listed above. This is often referred to as the 'CHD gap'. Novel and more accurate definitions and evaluations of these top five risk factors are required, such as 24 h ambulatory blood pressure (ABM) results, advanced lipid profiles, redefined fasting and 2 h dysglycemia parameters, a focus on visceral obesity and body composition and the effects of adipokines on cardiovascular risk. There are numerous traumatic insults from the environment that damage the cardiovascular system but there are only three finite vascular endothelial responses, which are inflammation, oxidative stress and immune vascular dysfunction. In addition, the concept of translational cardiovascular medicine is mandatory in order to correlate the myriad of CHD risk factors to the presence or absence of functional or structural damage to the vascular system, preclinical and clinical CHD. This can be accomplished by utilizing advanced and updated CV risk scoring systems, new and redefined CV risk factors and biomarkers, micronutrient testing, cardiovascular genetics, nutrigenomics, metabolomics, genetic expression testing and noninvasive cardiovascular testing.

Keywords: cardiovascular testing; coronary heart disease; nutrition; nutritional supplements.

Figure 1.

The pathogenesis of atherosclerotic plaque formation. An increase in LDL particles of small, dense size enter through the endothelial lining to the subintimal area where they are oxidized, taken up by macrophages and induce oxidative stress, inflammation, immune dysfunction and eventually form foam cells, fatty streaks and coronary artery plaques. LDL, low-density lipoprotein; HDL, high-density lipoprotein; Lp(a), lipoprotein a; RLP, remnant lipoprotein.

Figure 2.

Biochemical and biomechanical insults interact with vascular receptors, PRRs, NLRs, TLRs and caveolae, to induce the three finite responses of vascular inflammation, oxidative stress and vascular immune dysfunction which lead to endothelial dysfunction, and VSM and cardiac dysfunction, coronary heart disease, myocardial infarction and congestive heart failure. PRR, pattern recognition receptors; NLR, NOD-like receptors; NOD, nucleotide-binding oligomerization domain; TLR, toll-like receptor; VSMD, vascular smooth muscle dysfunction.

Figure 3.

Atherosclerosis progression. The earliest abnormality is endothelial dysfunction and loss of nitric oxide bioavailability. Then the IMT increases, followed by fatty streaks, atheroma, fibroatheroma and the complicated lesions with soft or hard plaque that may rupture and induce acute coronary thrombosis and myocardial infarction. IMT, intimal medial thickness.

Figure 4.

Progression of subintimal coronary atherosclerosis to obstructive coronary heart disease. In the earliest coronary lesion, there is minimal to no intracoronary luminal plaque formation. As the disease progresses, there is increased subintimal disease but the vascular lumen may still be normal in size on a coronary arteriogram. However, coronary computerized angiograms will demonstrate this extraluminal atheroma. Severe progression ensues with both severe extraluminal and intraluminal atheroma. CHD, coronary heart disease; MI, myocardial infarction.

Figure 5.

Coronary heart disease that is not detectable by angiogram (left) is evident using intravascular ultrasound (right). Note the arrow in the left which shows a 100% open lumen in the coronary artery but with intravascular ultrasound there is a large amount of subintimal atheroma present.