What is cardiovascular disease?
Cardiovascular disease (CVD) is the general term for blood vessel disease of the heart or body. CVD is the most common disease process in Western society and the financially well-off sections of developing countries. Blood vessel disease, called atherosclerosis, is the build up of atheroma or plaques in an artery, which leads to narrowing or complete blockage of the artery. Significant narrowing reduces the amount of arterial blood supply to an organ or body region and causes tissue hypoxia, reduced cell metabolism, and organ dysfunction.
In Australia, people in lower socioeconomic groups, Aboriginal and Torres Strait Islander people, and people living in remote locations, are more likely to be affected by CVD compared with the rest of the population.
There are five main types of CVD, which cause ischaemia or a lack of blood flow.
- Ischaemic heart disease of coronary artery disease can cause a myocardial infarction or heart attack.
- Cerebrovascular disease (of the brain) can cause a stroke or cerebral infarct.
- Peripheral artery disease of the arms and legs can cause claudication (calf pain with walking), distal tissue atrophy, and in severe cases gangrene.
- Renovascular disease affects blood flow to the kidneys and can cause renal failure.
- Aortic disease means atherosclerosis and narrowing of the main artery from the heart, the aorta. Atheroma can cause weakening of the wall of the aorta and aneurysmal dilation, which can rupture the artery causing fatal internal bleeding.
Atherosclerosis means the deposition of atheroma in the vessel wall of large and small arteries causing ischaemia, which means a lack of blood. Atheromatous plaques can contain a mixture of fat, cholesterol, blood cells, and fibrous tissue.
The overall death rate for cardiovascular disease has fallen by about 80% since the 1960s and continues to fall. Death rates from coronary heart disease, stroke, heart failure, rheumatic heart disease, and peripheral vascular disease, have all fallen markedly during the past 20 years. (Cardiovascular disease – Australian Facts 2011).
Cardiovascular disease facts and trends
- During 2007–08, approximately 3.5 million Australians had long-term CVD.
- Nearly 50,000 deaths were attributed to CVD in Australia in 2008 – more than any other disease group and 34% of the total.
- CVD was the main cause for 475,000 hospitalisations in 2007–08 and played a secondary role in a further 797,000.
- CVD accounted for about 18% of the overall burden of disease in Australia in 2003, with coronary heart disease and stroke contributing more than 80% of this burden.
- CVD remains the most expensive disease group in Australia, costing approximately $5.9 billion in 2004–05. Just over half of this money was from the cost of admitting patients to hospital for treatment.
How to treat cardiovascular disease
The aim of treating cardiovascular disease is to open the narrowed or blocked arteries that are causing symptoms and delay or prevent further arterial disease.
Treatment of cardiovascular disease combines changes to lifestyle factors that promote arteriosclerosis and prescribing medicines, in order to lower cholesterol and blood pressure.
A doctor may recommend prescription medicines that thin the blood or medication that lowers blood pressure, such as ACE inhibitors, angiotensin receptor blockers, calcium channel blockers and thiazide-like diuretics. Statins are used to lower lipid levels. Treatment depends on which part of the body is affected.
Surgical treatment of specific, significant arterial stenosis may be necessary to restore arterial blood flow. The invasiveness of the procedure varies according to the severity of the problem. For example, coronary artery triple bypass surgery (three arteries affected) is more invasive than balloon dilation of short segment stenosis in a single leg artery.
The goals of surgery are to improve blood flow, relieve symptoms and improve long-term survival. Surgical treatment of CVD may include:
- Coronary artery bypass grafting – reduces mortality compared with medical treatment alone, particularly in those with poor left ventricular function.
- Percutaneous transluminal coronary angioplasty (PTCA)
- Intracoronary stent – particularly useful for restenosis after PTCA
- Atherectomy – removal of atheromatous plaque
- Arterial bypass graft
- Endoluminal stent
Nutritional medicine treatment of cardiovascular disease
How do nutritional medicine specialists assess cardiovascular disease?
Clinical examination should focus on assessment of both cardiovascular and nutritional status.
Cardiovascular assessment includes recording of pulse rate, pulse rhythm and blood pressure, peripheral perfusion, arterial murmurs (bruits are indicative of widespread arteriosclerosis) and cardiac pump inadequacy (cardiac failure).
Nutritional assessment focuses on:
- Overweight and obesity – increased BMI indicates increased risk of insulin resistance, particularly when the umbilical:hip ratio exceeds 0.9 in males or 0.8 in females.
- Body composition – a lean weight less than 85% of the minimum weight for height may suggest a protein depletion state secondary to a) inadequate dietary intake, b) impaired digestion and/or c) impaired protein synthesis due to B6/zinc insufficiency and/or low anabolic hormone status.
- Signs of EFA imbalance and antioxidant insufficiency.
- Signs suggestive of mild or early nutrient inadequacy, e.g. Vitamin B6, zinc, magnesium, calcium etc., and
- Signs suggestive of food reactivity, impaired digestion and bowel dysbiosis.
The goal in treating cardiovascular disease using nutritional medicine is to reduce the damage to artery walls and delay or prevent the development of arterial disease, which can narrow, even occlude, small blood vessels.
Laboratory Investigations for cardiovascular disease
Laboratory investigation should be used to provide further data that is crucial to the understanding of a patient’s metabolic requirements.
Blood lipid analysis:
- Elevated LDL-cholesterol suggests that saturated and trans fatty acid intake may be excessive and dietary intake of antioxidants, omega-3-FA, phytosterols and fibre inadequate.
- Reduced HDL-cholesterol suggests impaired hepatic cholesterol clearance that may be associated with insulin resistance, EFA imbalance and/or increased metabolic requirement for niacin and taurine (taurine synthesis is Vitamin B6 dependant).
- Elevated triglyceride level (VLDL) may be indicative of excessive intake of refined carbohydrates and saturated fats, insulin resistance and/or inadequate intake of omega-3-FA. It may also indicate an increase need for niacin, pantethine, chromium and/or vanadium.
- Elevated Lp(a) above 0.3 g/L suggests an increased need for ascorbate and niacin.
Apo E phenotype has a substantial influence on an individual’s response to dietary change in fat and carbohydrate intake. Patients with the Apo E-4 allele respond well to a low fat, high (60%) carbohydrate diet, whereas this type of diet will reduce HDL-cholesterol and increase triglycerides in those people with Apo E-3/2 phenotype. As this later phenotype is more common, Apo E phenotype testing is helpful in determining the basic diet type required.
Serum fibrinogen, ferritin and high-sensitivity CRP are acute-phase reactants and elevated levels are predictive of increased cardiovascular risk. Raised levels may indicate the presence of a low-grade inflammatory process and/or hepatic fatty infiltration secondary to insulin resistance. If ferritin level is markedly raised, haemochromatosis must be excluded by further testing. Elevated fibrinogen levels suggest an increased need for Vitamin E, ascorbate, quercetin and omega-3-FA.
Blood/serum urea, creatinine, urate and serum albumin may be useful in evaluating protein status with low U/C ratio and albumin indicative of protein depletion. In the majority of IHD patients, protein depletion may be due to low anabolic hormone production and appropriate hormone testing is advisable (DHEA, androstenedione, free testosterone, progesterone and oestrogen).
Insulin resistance and hyperinsulinaemia should be excluded by a 3-hour glucose tolerance test, with 30 minute sampling and measurement of both glucose and insulin levels – a peak insulin rise eight-fold above the fasting level or above 100mU/L indicates hyperinsulinaemia and strongly suggests insulin resistance is present. Insulin resistance indicates an increased need for antioxidants, omega-3-FAs and possibly also chromium and vanadium.
Elevation of glycated-Hb (HbA1c) above 5.5% indicates that protein glycation is increased, which suggests that a) dietary carbo¬hyd¬rate intake should be reduced and b) Vitamin E intake should be increased together with other plant-derived antioxidants.
Elevated serum homocysteine above 15mmol/L indicates impaired homocysteine metabolism and indicates a greater need for folic acid, Vitamin B6 and betaine. As endothelial damage may occur at lower levels, between 9–15 mmol/L, several practitioners suggest that folate and B6 supplementation should be commenced even with homocysteine levels in this range.