PATIENT ENQUIRY

How to Treat Heart Disease


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What Is?
What is Heart Disease
How to Treat Heart Disease
Natural Treatments for Heart Disease

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 or atheroma, means a build up of fatty or calcific plaques along the arterial wall, which leads to narrowing or complete blockage. Significant narrowing reduces the amount of blood reaching an organ or body region and causes tissue ischaemia (lack of oxygen), reduced cell metabolism, and organ dysfunction

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 can lead to narrowing of the main artery, called the aorta, from the heart or an aortic aneurysm or ballooning of the aorta. Atheroma can cause weakening of the artery wall and ballooning of the artery, called an aneurysm, which can rupture the artery causing fatal internal bleeding.

Atherosclerosis means thedeposition of atheromain the vessel wall of large and small arteries causing ischaemia, which means a lack of blood. Atheromatous plaques can contain fat, cholesterol, blood cells and fibrous tissue.

Coronary artery disease means a build up of atheromatous plaque within the coronary arteries, which provide the heart muscle with oxygenated blood and nutrients. If significant ischaemia results, a myocardial infarction or heart attack results. The damaged heart muscle can stop pumping leading to heart failure.

  • During 2007–08, approximately 3.5 million Australians had a 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.

The overall death rate for CVD 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)

What is ischaemic heart disease?

What is ischaemic heart disease?

During 2011, ischaemic heart disease (IHD) killed at least 21,513 Australians (14% of all deaths). Approximately 380,000 Australians (1.7%) alive today have had a heart attack at some time.

Heart attacks, or myocardial infarcts, are the most common single cause of death. When athero¬matous plaque, also called arteriosclerosis, narrows or blocks the coronary arteries.

The primary initiator of atheroma in the arterial wall appears to be endothelial injury leading to increased adherence of monocytes and T-lymphocytes to the area. As plaque continues to build up over the years, localised thickening of the arterial wall reduces the artery lumen and can compromise blood flow.

IHD occurs when blood supply is insufficient for the oxygen demand of the muscle of the heart, called the myocardium. Symptoms include:

  • Chronic, progressive myocardial dysfunction resulting in limited exercise capacity, recurrent angina and congestive cardiac failure
  • Acute myocardial ischaemia that occurs as a result of either intra-arterial thrombosis or coronary artery spasm

What are the signs and symptoms of ischaemic heart disease?

Ischaemic heart disease (IHD) can develop over many years and symptoms may not occur until blockages of the heart arteries are severe and life-threatening. Exercise often brings on early symptoms because the heart works harder and pumps faster during exercise. However, symptoms can occur at rest. Sometimes a heart attack occurs without any apparent signs or symptoms.

IHD symptoms vary from person to person, but typical symptoms include:

  • Chest discomfort or pain called angina
  • Shortness of breath
  • Extreme fatigue with exertion
  • Pain in the shoulder or arm
  • Swelling of the feet

Women are more likely to experience other warning signs of a heart attack, including nausea, and back or jaw pain.

How can doctors diagnose ischaemic heart disease?

If a doctor suspects a person has ischaemic heart disease, also called coronary artery disease, he or she will listen to heart sounds, take a blood pressure, and arrange an ECG. However, referral to cardiologist who specialises in assessing and treating cardiac disease may be appropriate.

In order to make a diagnosis, a doctor assesses signs and symptoms, medical history, and risk factors. Based on this information, a doctor may order further tests to assess the heart including:

  • Electrocardiogram (ECG or EKG)
  • X-ray
  • Blood tests
  • Echocardiogram
  • Stress echo test
  • Nuclear heart scan/nuclear stress test
  • Cardiac CT
  • Magnetic resonance angiography (MRA), or
  • Cardiac angiography.
What is the cause of ischaemic heart disease?

What is the cause of ischaemic heart disease?

Ischaemic heart disease (IHD) is usually caused by a build-up of fatty deposits on the walls of the arteries that supply blood the myocardium (heart muscles), which need a steady supply of oxygen and nutrients to continuously pump blood from the heart chambers to the rest of the body.

IHD has been intensively researched during the past five decades and much is now known about what causes atheroma to form in coronary arteries.
The major risk factors are:

  • Age and gender(more than 45 years of age for men, and more than 55 years of age for women)
  • Family history
  • Elevated blood concentration of cholesterol (>7.7mmol/L), high LDL ‘bad’ cholesterol and low HDL ‘good’ cholesterol
  • Smoking
  • Hypertension – high blood pressure, and
  • Diabetes.

Other risk factors for IHD:

  • Obestity
  • Gout
  • Reduced hormone production (menopause in men and women)
  • Chronic inflammation
  • High levels of stress
  • Lack of exercise, and
  • Synthetic hormone replacement, such as the oral contraceptive pill and hormone replacement therapy.

Approximately 40% of people who suffer an acute myocardial infarction have none of these risk factors.

The incidence of ischemic heart disease increases exponentially with age.
Men have higher rates of IHD than women. Below 50 years of age, the rate of IHD in males approximates 3-4 times the rate of females, but after menopause there is an increase in the female incidence of IHD.

The prime risk factor is having a parent of the same sex who has suffered a myocardial infarction before 50 years of age.

The highest death rates from IHD occur in industrialised countries such as Northern Europe, Britain, USA, Australia and New Zealand. The lowest death rates occur in Japan, Mediterranean countries, and undeveloped hunter-gatherer societies.

Lifestyle factors, such as diet and level of physical activity, affect occurrence and this is reflected in the increase in IHD occurrence in migrants from low-risk to high-risk countries. A person whose cultural diet emphasises a high intake of vegetable fibre, complex carbohydrate, and monounsaturated oils or omega-3 fatty acids become ‘at risk’ for IHD when they adopt a western diet.

Certain racial or ethnic groups, including Australian Aboriginals, Samoans and other Pacific Islanders, and the Pima Indians of south-western USA and Mexico, have genes that make them more susceptible to IHD when exposed to western diets.

Contemporary genetic research suggests that human gene-related metabolism remains relatively fixed in a pattern that was developed to deal with a diet that is quite different to that currently found in Western society. Genetically speaking, humans today live in a nutritional environment that differs from that for which our genetic constitution was selected.

Today’s industrialised societies live on diets that generally consist of increased energy intake, saturated fat, omega-6 fatty acids, and trans fatty acids, with decreased energy expenditure, omega-3 fatty acids, complex carbohydrates, and fibre compared with diets before the age of industrialisation.

The current Western diet usually is deficient in omega-3 fatty acids, The ratio of omega-6 to omega-3 currently is between 20:1 to 14: 1, but centuries ago used to be 1:1.

Today we know that the interaction between genes and nutrients, along with other environmental factors, determine phenotype and the development of the individual. The rapid changes in our diet during the last 150 years have led to chronic diseases, such as atherosclerosis, high blood pressure, obesity, Type 2 diabetes, and many cancers.

How to prevent ischaemic heart disease

Certain types of heart disease, such as heart defects, can’t be prevented, but adequate, consistent changes to lifestyle will help prevent ischaemic heart disease.

A diet high in saturated fat, smoking, inadequate physical activity, and stress should be avoided, as they are the principal causes of IHD. Avoiding foods rich in saturated fats is important for lowering blood lipid levels and preventing arteriosclerosis. Adequate regular exercise is also essential. Cholesterol and hypertension should be kept under good control with diet and medical treatment as prescribed by a doctor.

Low to moderate alcohol consumption can protect a person against hypertension, ischaemic heart disease, stroke, and gallstones for some subgroups of the population. The cardiovascular health benefits of low to moderate alcohol consumption relates mainly to men 40 years of age or more and post-menopausal women.

For healthy men and women, drinking no more than two standard drinks on any day reduces your risk of harm from alcohol-related disease or injury over a lifetime. MORE>

How do doctors treat ischaemic heart disease?

Ischaemic heart disease (IHD) or coronary artery disease is the most common form of atheromatous disease. Sudden death is the first indication of IHD in up to 40% of cases. IHD can cause a heart attack, or myocardial infarction, which presents as acute chest pain and arrhythmia, with cardiovascular decompensation. A person with IHD may experience recurrent angina with effort or congestive cardiac failure, which presents as shortness of breath on exertion and fluid retention, with or without angina

The two vital treatment goals in myocardial infarction and angina are to improve coronary arterial circulation and prevent any progression of atheromatous disease.

Medical interventions to treat IHD include:

  • Thrombolytic therapyto dissolve thrombus, which must be performed within three hours of an acute infarction
  • Coronary angioplasty to expand artery narrowing with or without stent insertion
  • Coronary artery bypass surgery, to create a new blood vessel
  • Coronary artery vasodilationusing short acting glyceryl trinitrate and long-acting nitrate drugs
  • Beta-adrenergic blocking drugsto reduce myocardial oxygen demand, cardiac arrhythmia, andhypertension
  • Angiotensin-converting enzyme inhibitors (ACE inhibitors)to improve myocardial contractile function and reduce hypertension
  • Calcium-channel blocking drugsto stabilise myocardial contractility and improve coronary arterial perfusion, reduce occurrence of angina, and lower hypertension
  • HMGCoA reductase inhibitor drugs (statins) to reduce cholesterol synthesis and inhibit progression of atheromatous plaque, and
  • Platelet inhibitor drugs, such as aspirin, ticlopidine hydrochloride, dipyridamole, and abciximab (ReoPro) to inhibit platelet activation and aggregation, thereby reducing thrombogenesis and atheroma progression.

However, medical interventions seldom address the issue of revitalisation of damaged myocardium and, apart from the reportedly beneficial effect of ACE inhibitor drugs, their impact on long-term mortality remains questionable. Presumably, this lack of long-term benefit relates to progressive medication-induced alterations in cellular and systemic metabolism.

Treatments for ischaemic heart disease include lifestyle changes, medicines, and medical procedures.

Treatment goals aim to relieve symptoms and reduce a person’s risk factors to delay or even prevent further atherosclerosis. Surgical treatment can widen or bypass occluded arteries, while medication can lower the risk of blood clots and prevent complications of IHD.

Nutritional medicine treatment of cardiovascular disease

An effective, integrated dietary and nutritional program improves myocardial cellular metabolism, cardiovascular function, general health An effective, integrated dietary and nutritional program improves myocardial cellular metabolism, cardiovascular function, general health status, and long-term mortality. Nutritional therapy needs to be integrated with medical interventions, with a focus on improvement of clearly identified metabolic mechanisms. Keeping your heart healthy will also have other health benefits, and help reduce your risk of stroke and dementia.

An integrated diet and nutrient supplement program, tailored to individual nutrient needs, is crucial to optimise myo¬cardial function and cardiovascular integrity. This program is based on detailed assessment of a person’s nutritional and metabolic status, including medical treatment.

You can take action to prevent of delay coronary artery disease by reducing the number or risk factors that apply to you. If you smoke, it’s time to quit. Make time for regular physical exercise. Change to a healthy diet that includes a variety of fruits and vegetables.

Thorough clinical history

A thorough history, dating back to infancy, including a detailed family history, should be taken with particular emphasis on the following:

  • Current symptoms of cardiovascular disease, including: ischaemic pain (angina at rest or with effort, referred cardiac pain in neck, shoulder or epigastrium and peripheral claudication); exercise tolerance and symptoms of cardiac failure; palpitations and cardiac arrhythmias; hypertensive symptoms; cerebrovascular insufficiency (transient episodes of dizziness, fainting, confusion, disorientation, paraesthesia and paresis).
  • Family history of heart disease, diabetes, obesity and hypertension may be related to a genetic susceptibility to insulin resistance and/or abnormalities of lipoprotein or homocysteine metabolism and would strongly suggest appropriate tests for this condition, which will have a strong influence on the type of diet required.
  • History of recurrent respiratory tract, gastrointestinal symptoms or overt allergic disease may indicate the presence of previously unidentified food sensitivity and/or a chronic infectious process with intracellular organisms such as Mycoplasma, Chlamydia, rickettsiae or viruses. These patients would require thorough testing of immunological function including: IgE and IgG allergy testing; measurement of gluten anti-bodies; estimation of high-sensitivity C-reactive protein (CRP) and cytokine levels, such as interleukin-2 and interleukin-6; serology or preferably PCR (polymerase-chain reaction) testing for infectious organisms.
  • Recurrent antibiotic therapy or an episode of intensive antibiotic therapy may indicate the presence of bowel dysbiosis, particularly if easy bruising is present with unduly compromised hepatic detoxification, thereby reducing tissue glutathione and CoQ10 capacity and increasing demand for antioxidants such as ascorbate, Vitamin E and selenium.
  • Current or past smoking – cigarette smoking undoubtedly contributes to development of CHD. Importantly, regular smoking of marijuana is equally as detrimental as cigarettes, excess alcohol consumption and long-term drug use (prescribed medications included).
  • A history of chronic stress-reactions and/or depression may relate to long-term high nutrient demand that induces tissue insufficiency.
  • Current exercise – frequency, intensity and duration and exercise capacity.

Dietary history look for:

  • High-level consumption of saturated fats and/or low-level consumption of seafood may indicate omega-3-FA insufficiency and blood lipid abnormalities
  • Low consumption of fruit, vegetables and whole grains (dietary fibre) may suggest inadequate cholesterol excretion with or without adequate fat absorption; may suggest bowel dysbiosis; inadequate antioxidant intake (ascorbate, Vitamin E and flavonoids); increased insulin response to dietary carbohydrates (hyperinsulinaemia).
  • High level consumption of processed foods may suggest an excessive intake of: refined carbohydrates, exacerbating insulin responses and contributing to insulin resistance; hydrogenated/saturated fats, contributing to adverse blood lipid metabolism; high dietary salt/potassium ratio and a corresponding low intake of: dietary fibre; antioxidants and other vitamins; essential fatty acids; magnesium and zinc.
  • Physical examination and nutritional assessment

    A thorough physical and examination and nutritional assessment is important. 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 men or 0.8 in women.
    • Body composition – a lean weight less than 85% of the minimum weight for height may suggest a protein depletion state secondary to inadequate dietary intake, impaired digestion or impaired protein synthesis due to B6/zinc insufficiency or low anabolic hormone status.
    • Signs of essential fatty acid 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.
    Laboratory investigations in the natural treatment of heart disease.

    Laboratory investigations in the natural treatment of heart 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-fatty acid.

    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 dietary carbo¬hyd¬rate intake should be reduced and 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.