Cardiovascular

Question 1

What is the endothelium , and what is it made up of?

Answer 1

• a monolayer of endothelial cells lining the blood interface throughout the CVS including cardiac chambers- critical to vascular health.
• The glycocalyx (GX), a carbohydrate-rich protective layer covering the ED, regulates permeability, controls NO production and acts as a mechanosensor of blood shear stress.

Question 2

key functions of the endothelium? What is the consequence of inflammation and ROS here?

Answer 2

• Role in fluid balance, host defence and selective movement of substances e.g., glucose and oxygen as has a semi permeable barrier
• Regulates vascular tone: Secretes vasodilators (e.g., NO) and vasoconstrictors (e.g., endothelin).
• Contains angiotensin-converting enzyme (ACE) ― plays a key role in regulating blood pressure.
• Angiogenesis: ED cells are the origin of all new blood vessels.
• Haemostasis: prevent platelet adherence/ coagulation
• Immune defence: deflect leukocyte adhesion and oppose local inflammation.

Inflammation= ↑ permeability, inflammatory cytokines and leukocyte adhesion, * Reduced vasodilator (NO, prostacyclin) molecules.
* Increased risk of thrombosis.

Question 3

What are vascular smooth muscle cells? location?
What happens under pathological conditions?

Answer 3

• Located in the tunica media and play a key role in vessel contraction and dilation (regulate blood circulation and pressure).
• maintain the integrity and elasticity of blood vessels whilst limiting immune cell infiltration.
• Under pathological conditions (e.g., inflammation, oxidative stress, telomere damage) VSMCs undergo phenotypic modulation, altering cell structure and function.
  (atherosclerosis and hypertension)- Increased inflammatory cytokines and extracellular matrix synthesis.
• Migration into the tunica intima and proliferation of VSMCs.

Question 4

What is the role of nitric oxide in CV health? how is it made?

Answer 4

• regulates vascular tone, reduces platelet aggregation and VSMC proliferation
• inhibits leukocyte adhesion and inflammatory cytokines, and opposes oxidation of LDLs.
• It is continuously generated from L-arginine by the ED enzyme eNOS.
• NO diffuses easily from the ED into VSMCs and the bloodstream, exerting its main physiological effects in large vessels.

Question 5

What are PPARs? and how do they impact CV health?

Answer 5

Peroxisome proliferator-activated receptors- nuclear transcription factors that control gene expression involved in adipogenesis, lipid and glucose metabolism, cellular proliferation and apoptosis.

• PPARs decrease inflammation and promote ED health.
• PPARα activation ↑ HDL-C, ↓TGs and inflammation and is anti- atherosclerotic.
  
  • PPAR-γ reduces blood glucose, fatty acids and insulin.

Question 6

Discuss CVD risk factors

Answer 6

• Family history: Offspring of parents with premature CVD = 60–75% risk increase.
• Genetics: MnSOD, NOS3, MTHFR and ACE gene polymorphisms.
• Ethnicity: South Asian or sub-Saharan African origin
• Gender: Risk is underestimated as women tend to experience more vague physical signs e.g., lightheaded with exertion
• Dyslipidaemia: ↑ total cholesterol ― ↑ LDL, VLDL, IDL, Lp(a), ↓ HDL; ↑ triglycerides.( sedentary lifestyle, excess alcohol, smoking, obesity, high saturated and trans fat, menopause.)
• Hypertension: CVD pathologies appear 5 years earlier
• Mitochondrial dysfunction: ATP is required to pump Ca ions out of myocardial cells, allows relaxation and maintains electrochemical gradient across myocardial cell membrane.
• Elevated homocysteine: Associated with LDL oxidation, monocyte adhesion and ED dysfunction. ↑ levels:
• Low folate and B12, (remethylation) vitamin B6 —converts homocysteine to cysteine in the methylation cycle.
• Genetic polymorphisms: MTHFR, FUT2, TCN impact B12 (all forms) absorption MTR, MTRR impact B12 activation (application of a methyl group).
• Thyroid hormones (TH): receptors are present in the myocardium and vascular tissue and changes can alter CV homeostasis.
• Inflammation: dyslipidaemia, dysbiosis and intestinal permeability, ROS, diabetes, excess adipose tissue and
  smoking.
• Obesity: Excess adipose tissue perpetuates inflammation -
  linked with ↑ endothelin-1 (ET-1), a potent vasoconstrictor peptide. Elevated ET-1 leads to fibrosis of VSMCs and ↑ ROS.
• Adiponectin, protecting against CVD, is decreased in obesity, also ↑ insulin sensitivity, thus low levels contribute to insulin resistance (IR).
• Obesity is associated with high levels of leptin, activates the SNS causing sodium retention, vasoconstriction & ↑ blood pressure.

Insulin resistance (IR): chronic hyperglycaemia leading to oxidative stress, inflammation and cellular damage.
* IR contributes to the lipid triad (high plasma TGs, low HDL, small dense LDLs) and dyslipidaemia, leading to atherosclerotic plaque formation. glucose is not cleared from the bloodstream increasing the risk of glycosylation reactions and the production
advanced glycation end products (AGEs).

-Smoking: ↑ oxidative stress (ROS react with NO to form harmful peroxynitrite) and lowers antioxidants (1 cigarette = 25 mg loss of vitamin C).

• Sedentary lifestyle: Exercise has a positive effect on lipid profile and blood pressure and ↑ insulin sensitivity and NO production.
• Chronic stress: May cause ED dysfunction especially in the presence of other risks e.g., smoking. Activates SNS and HPA-axis, ultimately ↑ inflammatory cytokines. ↑ heart rate and blood pressure through the SNS.
• Periodontal disease — ↑ systemic inflammation (↑ TNF, IL-1, IL-6, CRP) which impair vasodilation. Promotes endothelial
  dysfunction, arterial stiffness and ↑ fibrinogen (plaque formation).
• Heavy metals — induce oxidative stress, lipid peroxidation and inflammatory cytokines. Cadmium and lead compete with zinc. A zinc deficiency increases atherosclerosis risk.
• Melatonin deficiency — melatonin is a potent antioxidant with anti- hypertensive properties. It protects against coronary artery disease

Question 7

What are AGEs and by which two mechanisms do they exert their effects?

Answer 7

Advanced glycation end products (AGEs): Harmful compounds formed when protein or lipids becomes glycated after exposure to glucose.

1. Receptor-mediated: Bind to the cell receptor
   RAGE (ED, VSMCs and immune cells) increasing
   inflammatory cytokines and ROS via activation of NADPH oxidase, which activates NF-kB.
2. Non-receptor mediated: Increased EC matrix synthesis, trapping ED LDL and cross binding with collagen (vascular stiffening).

Question 8

What increases the risk of AGEs?

Answer 8

• advancing age. Renal accumulation of AGEs promotes kidney dysfunction.
• Polymorphisms of the AGER gene (encodes RAGE) c
• Diet (exogenous AGEs) contribute to overall AGE pool: High refined carbohydrates (sucrose, HFD), processed foods, meat and dairy.
• Cooking methods: High heat, grilling, roasting, searing / frying promote AGE formation.
• Smoking and sedentary lifestyles enhance AGE accumulation.

Question 9

How is the gut brain axis implicated in CVD?

Answer 9

• SCFAs produced by the microbiota, ↓ risk of metabolic endotoxemia by maintaining intestinal barrier integrity. SCFAs reduce serum lipids by inhibiting cholesterol synthesis or redirecting lipids to the liver.
• The gut microbiota play a role in cholesterol regulation by altering bile acids t
• Alterations in the gut microbiota can lead to
  an increase in harmful metabolites such as
  trimethylamine-N-oxide (TMAO) (endothelial dysfunction)

Question 10

Dietary considerations for CVD?

Answer 10

• High PRAL — foods rich in protein may induce low-grade metabolic acidosis, a risk factor
• Trans fats — promote dyslipidaemia (↑ LDL-C, TGLs, ↓ HDL-C), increase inflammation, contribute to ED dysfunction,
  encourage visceral adiposity and increase risk of IR.
• Fructose — promotes de novo lipogenesis, ↑ fatty acids-
  Palmitic acid ↑ expression of the receptor involved in the uptake of oxidised LDLs and is a major driver of atherosclerosis and CAD.
• Nutrient deficiencies (e.g., vitamin C, D, E, CoQ10, Mg).

Question 11

What are the main normal lipid profile markers?

Answer 11

: TC < 5 mmol / L,
non-HDL < 4 mmol / L
LDL-C < 3 mmol / L
HDL > 1 mmol / L (men) & > 1.2 mmol / L (women).
TG > 2.3 mmol / L
TC:HDL > 6 = higher risk for CVD.

Question 12

3 cardiovascular functional markers?

Answer 12

• Lp-PLA 2: Enzyme produced by monocytes, macrophages, T-cells. Upregulated in atherosclerotic plaques and vascular inflammation.
• hsCRP: Inhibits NO and e-NOS and is involved in plaque deposition. Low risk: < 1.0 mg / L. High risk: > 3.0 mg / L.
• MPO: Released by macrophages and measures the body’s response to damaged arterial walls. High MPO is associated with inflammation / oxidative stress and a poor prognosis. Exacerbated by high BP, obesity and smoking. Low=<470 pmol/L, high ≥ 540 pmol/L.

Question 13

What are some key nutrients to support CV health?

Answer 13

Vitamin C 500–1000 mg 3 x daily
* Downregulates NADPH oxidase, key source of ROS in the vascular wall.
* Upregulates endothelial NO synthase
* Lowers tendency for platelet aggregation.

Vitamin E 400–800 iu / day
* Mixed tocotrienols and tocopherols — along with vitamin C protects the endothelium from ROS and supports NO synthesis.
* ↓ oxidation of LDL-C and deposition in arterial walls.
* Inhibits platelet aggregation and ↓ clotting factors to support healthy blood viscosity.

Vitamin D 600–1000 iu / day
* Modulates NO synthesis and influences cells involved in atherogenesis e.g., ED, VSMCs, monocytes and cardiac myocytes.
* Modulates RAAS and lowers BP.

Omega-3 fatty acids 3–6 g / day
* Improves lipid and lipoprotein profiles.
* Involved in the synthesis of key regulators of inflammation, vasodilation and platelet aggregation.
* EPA stabilises cellular membranes
* DHA supports membrane fluidity.

Magnesium Glycinate/ taurate) 500–800 mg / day
* Through regulation of ion transporters e.g., potassium and calcium channels, modulates neuronal excitation, intracardiac conduction and myocardial contraction.
* Helps regulate vascular tone and stabilise heart rhythm.

Co-enzyme Q10 60–300 mg / day
* Protects against endothelial dysfunction and reduces LDL oxidation (↓ atherosclerosis risk).
* Increases superoxide dismutase activity, which preserves the activity of NO (↓ risk of high BP).
* Supports mitochondrial health and production of ATP.

Question 14

2 herbs to support cardiovascular health?

Answer 14

Hawthorn 1,000–1,500 mg
* Cardiac tonic; strengthens and improves vascular elasticity, has ACE-inhibiting actions (↓ BP).
* Hawthorn reduces ET-1 and increases NO levels, hence having vasodilatory effects.
* Antioxidant (e.g., ↑ SOD), anti-inflammatory (inhibits NF-κB).

Garlic 2–5 g fresh bulb /day
* Antihypertensive effects by stimulating NO production in ED cells.
Lowers homocysteine CVD risk.
* Decreases arterial calcification (stiffness).
* Reduces LDL cholesterol and LDL oxidation.
* Enhances glutathione and SOD.
* Protects against abnormal platelet aggregation.

Question 15

How can stress management, exercise and a plant based diet improve CVD?

Answer 15

1) regular physical activity and exercise significantly reduces CVD risk :
– Leads to a more favourable lipoprotein profile; ↓ TGs.
– Improves insulin sensitivity, and insulin signaling in the vascular endothelium, activating eNOS, which ↑ NO synthesis.
– net reduction in blood pressure at rest

2) diaphragmatic breathing exercises, humming, singing to promote parasympathetic activity. Include herbal teas to relieve stress e.g., chamomile, passionflower, lemon balm, lime flower tea.

3) Plant-based and Mediterranean-style diets are
associated with significantly reduced CVD risk
↓ inflammatory mediators, ROS and
RNS; reduced adiposity and
risk of thrombosis; ↑ SCFA production, improved
insulin sensitivity, ↑ adiponectin and improved ED function.

Question 16

Which drugs used for CVD can add to nutrient depletion?

Answer 16

• Statins: Block HMG CoA-reductase ↓ coenzyme Q10 synthesis.
• Cholestyramine (↓ cholesterol): A bile acid sequestrant.
  ↓ absorption of fat-soluble vitamins and beta-carotene.
• Loop and thiazide diuretics: ↑ potassium, calcium, thiamine and zinc (thiazide) excretion.
• ACE inhibitors: Bind with zinc preventing utilisation by the body.
• Beta-blockers: ↓ melatonin production by inhibiting
  adrenergic beta1 receptors; block the biological
  pathway of CoQ10-dependent enzymes.

Question 17

Define systolic and diastolic blood pressure
Signs and symptoms of hypertension?

Answer 17

systolic BP is the pressure blood exerts on arterial walls when the heart contracts and diastolic BP is the pressure when the heart relaxes
Fatigue, headache, dizziness, visual disturbance. However, is often asymptomatic

Question 18

What are the three types of hypertension?

Answer 18

Essential [or primary] (95%) ― no specific underlying medical cause. Drivers include vascular resistance (due to vasoconstriction, atherosclerosis, loss of blood vessel elasticity, increased blood viscosity), obesity, stress and anxiety, smoking, high salt intake.

• Secondary hypertension (5%) ― due to diseases of the kidneys, adrenals, thyroid, diabetes.
• Malignant hypertension is pressure
  above 180/120, which risks damaging organs, e.g., kidneys (medical emergency).

Question 19

What are some causes and risk factors of hypertension?

Answer 19

(consider all those for CVD)

-Genetic
* Obesity (especially ↑ abdominal adiposity) — activates the RAAS causing vasoconstriction and water retention.

• Excess alcohol — ↓ the baroreceptor reflex (ability to
  respond to BP changes) by interacting with receptors in
  the brain stem; ↑ sympathetic outflow ↑ heart rate and BP; stimulates the ED to release vasoconstrictors, activates the RAAS.
• Stress — ↑ SNS activity causing vasoconstriction. High cortisol↑ the potent vasoconstrictor ET-1; activates the RAAS.
• Nutritional deficiencies — especially magnesium (vasodilates), potassium (↑ urinary excretion of sodium, ↓ blood volume).
• High table salt intake and / or low potassium.
• Inactivity — associated with higher HR, increased cardiac contractility and greater force on the arteries.
• Smoking — damages endothelium; nicotine constricts blood vessels and increases heart rate.
• Drugs — NSAIDs, corticosteroids, decongestants can ↑ BP.
• Raised uric acid — stimulates the RAGE pathway, which increases NF-KB and disrupts eNOS activity. It exacerbates endothelial insulin resistance and lowers
  NO, whilst also upregulating genes that code for components of the RAAS (increasing BP).

Question 20

What is the natural approach to hypertension?

Answer 20

Adapt the Natural Approach to CVD.
Increase potassium / sodium ratio >3:1:
* Include fresh fruit and vegetables (high potassium / sodium ratio)-, encourages vasodilation reduces sensitivity to angiotensin II and lowers SNS activity.
* Lowers NADPH oxidase, decreasing ROS in the vascular wall.
* Restrict sodium intake to 1.5g / day.
-Also focus on lowering uric acid levels

DASH Diet:
- fresh vegetables and fruits, legumes, nuts, seeds, whole grains, fish, lean meat and low-fat dairy and limits saturated fats and salt. PUFA / MUFA are preferred. Sodium is restricted.

• ACE inhibitory peptides: Naturally-occurring ACE
  inhibitory peptides can be found in spirulina, mushrooms, spinach, hemp seeds, walnuts and bitter melon seeds.
  act like a decoy encouraging ACE to react with peptides, reducing vasoconstriction via angiotensin II.
• Optimise sleep: melatonin is associated with anti-hypertensive effects through GABA stimulation, angiotensin-II inhibition and increases in NO.
• Optimise weight; include aerobic and resistance exercise;
  Start gently and gradually ↑ CV fitness.
• Stress management: Essential
  – Diaphragmatic breathing: Shown to decrease systolic and diastolic BP, heart rate and anxiety,
  – Earthing: (Walking barefoot on grass or sand) improves heart rate variability, lowers night-time cortisol and
  promotes a parasympathetic state.

Question 21

Herbs recommended for hypertension?

Answer 21

• Thetraditional‘C.A.T.’formula:Equalparts dried herbs infused, 1 cup 2–3 x daily.
  – Crataegus spp. [hawthorn] (cardiotonic, hypotensive).
  – Achillea millefolium [yarrow] (diuretic, hypotensive).
  – Tilia europea [lime flower] (nervine relaxant, diuretic, anti-hyperlipidaemic).

Question 22

What is atherosclerosis and how is it formed?

Answer 22

• narrowing and hardening of large and medium arteries, which reduces blood flow.
• Increased permeability facilitates entry of LDL into the intima. LDL becomes ‘trapped’ within the vessel wall and is oxidised to mLDL.
• mLDL recruit leukocytes expressing high levels of pro-inflammatory cytokines. Also trigger cytokine release from ED and VSMC cells.
• Macrophages consume lipoproteins to form foam cells, along with cellular debris and inflammation drives plaque formation.
• A cap is formed over the plaque to wall off the plaque from blood.

Question 23

How does endothelial dysfunction cause/ precede atheroscorosis?

Answer 23

1) Damage to the protective glycocalyx layer of the endothelium is driven by inflammation, oxidative stress, oxidised LDLs, hyperglyceamia and endotoxaemia

2) this leads to altered regulation of inflammatory
cytokines, eicosanoids and compounds that promote clotting risk.

3) Upregulation of chemo-attractant molecules promotes migration of phagocytic and inflammatory immune cells into blood vessels.

• Disturbs NO metabolism ↑ hypertension risk increases shear stress worsening endothelial dysfunctionplaque development.

Question 24

How does inflammation play a critical role in the
genesis, progression, and manifestation of atherosclerotic disease?

Answer 24

ED dysfunction, subintimal cholesterol accumulation and monocyte / T-cell recruitment drives the inflammatory response.

• Monocytes become resident macrophages in the sub-endothelial space and form ‘inflammasomes’ releasing inflammatory cytokines which activate IL-6 and enhance the inflammatory cascade in the vessel walls.
• Inflammation thins the fibrous plaque cap leading to instability and rupture.
• Pro-inflammatory cytokines differentiate VSMC into osteoblast-like cells increasing plaque calcification.

Question 25

How is dyslipidaemia implicated in the aetiology of atherosclerosis?

Answer 25

dyslipidaemia is a significant risk factor marked by:

– ↑ total cholesterol — ↑ LDL, VLDL, IDL, Lp(a), ↓ HDL; ↑ TGs.

TGs are hydrophobic and must combine with lipoproteins to travel in plasma. In a similar manner to oxidised LDLs, TG-rich lipoproteins (e.g., VLDLs and VLDL remnants) are
prone to endothelial accumulation and uptake by foam cells and are strongly linked with endothelial dysfunction.

High TGs are also linked with low HDLs

Question 26

Natural ways to promote a healthy lipid profile in atherosclerosis?

Answer 26

• Avoid high saturated fat
• Increase omega-3 FAs and MUFAs: E.g., avocado, unrefined olive oil.
  -Regular EVOO consumption reduces LDL-C and oxidised LDLs, and improves post-prandial glycaemic profiles.
• EVOO polyphenols oleocanthal and oleacein have antioxidant and anti-inflammatory effects (↓ markers including CRP and IL-6).
• Red yeast rice (2400–4800 mg / day) ― contains monacolin K, an inhibitor of cholesterol synthesis via HMG CoA reductase.

-Increase dietary fibre (30–35 g / day):
* Soluble fibre associated with a decrease in TC and LDL-C.

• Include dietary sources of beta-glucans (soluble + insoluble fibre) e.g., oats, mushrooms, seaweed, barley. Interact
  with lipids and biliary salts in the bowel and
  lower LDL-C, non-HDL-cholesterol and
  
  • Are also a source of SCFAs — decrease liver
    cholesterol synthesis and increase bile excretion, and modulate immune function.

Question 27

How would you naturally support endothelial health and vasodilation?

Answer 27

• Hawthorn berries, bilberry, blueberries and blackcurrants are antioxidant and support blood vessel integrity and tone.
• Lower ET-1 levels: Enhance citrus flavonoids, quercetin, epicatechins, garlic, olive oil, ginkgo, folate, blackcurrant.
• Beetroot juice 200ml a day contains inorganic nitrates that convert to NO in the body. Also ↓ homocysteine ― contains betaine- re-methylates homocysteine to methionine.
  • L-theanine ↑ NO production in ED cells through eNOS phosphorylation (green tea is a key source).

Reduce homocysteine:
* B6, folate and B12 (supplement methylfolate and methylcobalamin supplementation), TMG (3 g twice daily).

Lower fibrinogen levels:
* increases blood viscosity, stimulating fibrin formation and increasing platelet aggregation.
* Mediterranean-style diets promote healthy levels. Garlic reduces fibrinogen, ↑ fibrinolytic activity (also ↓ atherogenicity of LDLs).
* Mild to moderate exercise reduces fibrinogen levels.

• Sauna: ↑ circulation and arterial vasodilation. Avoid in unstable angina / recent MI and hypertension.
• Dry skin brushing: Supports circulation and lymphatic function, increases toxin elimination.

Question 28

Nutrients for atherosclorosis

Answer 28

1) L-citrulline 500–3000 mg / day
* NO is synthesised from L-arginine by eNOS.
* Arginase in intestinal enterocytes ↓ the availability of oral L-arginine supplementation. L-citrulline is not affected by arginase and skips First Pass Metabolism before conversion to arginine so enhances both arginine and NO bioavailability.
* Renal arginine regulates BP, blocks formation of endothelin, ↓ renal sodium reabsorption and is a potent antioxidant.

2) Pantothenic acid 300 mg x 3 daily
* Metabolised to cystamine-SH. Reduces
TC, LDL, Apo-B, TG and increases HDL
* Reduces lipid deposition, oxidation and fatty streak formation.

3) Niacin (B3) 500–3000 mg daily
* reduces TC, LDL, Apo-B, LDL-P, TGs and VLDL.
* Also shown to decrease fibrinogen.
* Note: Can cause niacin flush, GI disturbance.

4) Omega-3 3000–5000 mg / day.
* Reduces TG, VLDL, LDL-P and chylomicron remnants. Uniquely reduces Lp-PLA 2.
* Anti-inflammatory, anti-thrombotic, lowers BP, heart rate and IR. PPAR-α agonist.
* Reduces CVD progression and stabilises plaques.

5) Pycogenol (pine bark extract) 100–200 mg / day
* Flavonoid, antioxidant, anti-inflammatory, anti-thrombotic.
* Enhances NO and ED function, reduces BP and Hs-CRP.
* ↓ myeloperoxidase ― an enzyme secreted from macrophages that ↑ oxidation of lipoproteins i
* reduces foam cell formation in atherosclerosis.

6) Lycopene
25 mg / day
* Anti-oxidant. Suppresses intestinal cholesterol absorption. Lowers TC, LDL-C, inflammation and increases HDL-C.
* Activates PPAR-γ.

7) Citrus Bergamia 500-1000 mg/ day.
* Natural source of flavonoids, e.g., naringin, hesperidin, neohesperidin and neoeriocitrin.
* Lowers LDL and TGs. Increases PPAR activation.
* Reduces ROS, oxidised LDL, balances blood glucose and reduces weight.
* Improves serum glucose via AMPK and GLUT 4 receptor.
Globe artichoke
Dietary + 1–2 g / day powdered
* Reduces serum LDL, TC and TGs.
* Regulates lipid metabolism, increases bile production, is antioxidant and hepatoprotective.

Question 29

What is Ischaemic heart disease? How does it happen?

Answer 29

an imbalance between myocardial oxygen supply and demand, associated with inadequate arterial supply via the coronary arteries, commonly caused by atherosclerosis. includes angina and myocardial infarction

• Atheroma and too much vasoconstriction reduce blood vessel lumen size and coronary blood flow. When oxygen demand > oxygen supply, myocardial hypoxia, accumulation of waste metabolites and ischaemia ensues.

Question 30

What are the two types of angina with signs and symptoms?

Answer 30

chest pain caused by insufficient supply of oxygenated blood supply to the myocardium by the coronary arteries.

1) Stable angina: Predictable transient chest pain during exertion or emotional stress. Ischaemia resolves once oxygen balance is restored.

2) Unstable angina: Unpredictable / occurs at rest.
Plaque disruption initiates platelet aggregation, thrombus formation and vasoconstriction.

Stable angina signs / symptoms: Constricting chest pain
(can radiate to the neck, L shoulder / arm and jaw), worsened
by exertion, relieved by rest. SOB, sweating, nausea

Question 31

3 causes and risk factors of angina?

Answer 31

Normal CVD risk factors plus:

• Cigarette smoking ― linked to endothelial dysfunction,
  coronary artery spasm, vessel wall injury, oxidative stress, elevates fibrinogen, platelet activation and inflammation.
• Vitamin D deficiency ― correlation with chronic angina.
  Improves endothelial function by signalling for the transcription of eNOS; modulates the RAAS to lower BP.
• Family history of premature IHD is a strong risk factor for angina

Question 32

How does prolonged ischaemia lead to a myocardial infarction?

Answer 32

• Prolonged ischaemia leads to myocardial necrosis. - Ischaemic myocardial cells release adenosine
  and lactate onto nerve endings causing pain.
• Infarcted areas produce scar tissue. The remaining tissue hypertrophies and can result in cardiac dysfunction and heart failure.

Question 33

What is a myocardial infarction and what are the two types?

Answer 33

MI = an acute blockage of a coronary artery usually due to a thrombus, resulting in the death of myocardial tissue.

1) ST-Segment Elevation MI (STEMI) = full occlusion (severe).
2) Non-ST-Elevation MI (NSTEMI) = partial occlusion.

Question 34

What are some signs/ symptoms, complications of MI and what is the allopathic approach?

Answer 34

Severe prolonged crushing retrosternal chest pain. Pain radiates to the left shoulder, jaw / neck or arms. Sweating, cool / clammy skin. Feeling of ‘impending doom’. Dyspnoea
Nausea, vomiting, weakness.

• Complications: Arrhythmias, heart failure, cardiogenic shock, death.
• Diagnosis: ECG findings then Fibrinolysis,
  O2 therapy, morphine, nitrates, beta blockers, aspirin for acute management.

Question 35

Which nutrients can be used for IHD?

Answer 35

1) L-carnitine 1000 mg x 2 daily
* Improves FA utilisation and myocardial ATP production, prevents the production of toxic FA metabolites which would normally impair myocardial contractility.

2) Magnesium 200 to 400 mg x 3 daily
* deficiency produces coronary artery spasms.
helps with smooth muscle contraction.

3) Hawthorn (Crataegus spp.) 1,000–1,500 mg
* Its flavonoids have been shown to inhibit the enzyme 3’,5’-cyclic-AMP, responsible for dilating the coronary arteries.

4) CoQ10 100 to 300 (if on statins) mg daily
* Increases eNOS and NO, improves ED function and vascular elasticity.
* Exerts anti-inflammatory effects – lowers TNF-α and IL-6.

5) L-arginine 1000 to 2000 mg x 3 daily
* Promotes vasodilation by increasing NO.
* Increases SOD levels, reduces lipid peroxidation and xanthine oxidase activity (reducing uric
acid formation)

6) Ginkgo biloba 60–120 mg / day.
* Enhances microcirculation and tissue
perfusion (antagonises ‘platelet activating factor’ by blocking receptors). Scavenges ROS

Question 36

What is heart failure with signs/symptoms/ complications and allopathic approach?

Answer 36

a syndrome in which the heart is impaired as a pump ― failing to supply sufficient blood flow.

• Breathlessness, nocturnal dyspnoea, fluid retention , fatigue, exercise intolerance, lightheadedness, syncope, tachycardia.
• Complications: Atrial fibrillation, ventricular arrhythmias, CKD, sudden cardiac death.
• Allopathic approach: Digoxin (a synthetic form of digitoxin, that increases the force of myocardial
  contraction), diuretics, calcium channel blockers, ACE-inhibitors

Question 37

What are some causes and risk factors of heart failure?

Answer 37

• Results from various CV conditions ― e.g., IHD, hypertension, AF, cardiomyopathy, LVF, pulmonary hypertension, heart valve abnormalities.
• smoking (leads to LV hypertrophy and systolic dysfunction); raised homocysteine; sedentary etc.
• Co-morbidities (so causes of each apply) ― e.g., CKD, anaemia, T2DM, thyrotoxicosis, hypothyroidism, COPD all impair functional status and prognosis of HF.

– CKD causes a chronic proinflammatory state that can
result in atherosclerotic lesions and myocardial fibrosis.

• IR ― IR ↓ myocardial glucose utilisation and ↑ FFA oxidation
  ↑ myocardial oxygen consumption and the generation of ROS. This impairs cardiac contractibility by changing sarcoplasmic reticular calcium stores and ↑ mitochondrial dysfunction.
• Obesity ― alters cardiac structure, promotes endothelial dysfunction, contributes to IR and ↑ inflammatory cytokines.
• Nutrient deficiencies ― CoQ10 (normally ↓ ROS and ↑ NO), vitamin D (normally ↓ inflammatory cytokines and ↑ calcium absorption etc.),
  t

Question 38

Nutrients for heart failure

Answer 38

1) CoQ10 300–400 mg daily.
* Cardiac myocytes contain >3500 mitochondria / cell
and require the highest levels of ATP activity. CoQ10
is essential in the ETC and is a powerful antioxidant.

2) D-ribose 5–15 g daily
* Has been shown to regenerate low myocardial ATP and improves ventricular function following ischaemia.

3) Magnesium 400–800 mg daily (citrate)
* Critical for ATP. When deficient increases RAAS (increasing BP), predisposes to low K and may worsen cardiac contractility, increase vasoconstriction and deplete cardiac energy stores.

4) Thiamine B1 100–200 mg daily
* coenzyme in energy-producing reactions — fuelling myocardial contraction. Note: CVD drugs e.g., diuretics cause a B1 deficiency.

5) L-carnitine 2000–3000 mg daily
* Facilitates the transfer of fatty acids across mitochondrial membranes to initiate beta-oxidation. The heart uses free fatty acids as its main energy source!

6) Hawthorn (Crataegus spp.) 1,000–1,500 mg
* vasodilatory effects on the coronary arteries and potent antioxidant properties. Increases NO.

Question 39

Signs, symptoms, complications of varicose veins

Answer 39

Visible vein dilation; aching, burning, throbbing, heaviness. Worse for prolonged standing and at the end of the day.
* Complications: ↑ venous pressure = fluid leakage into surrounding tissues (‘varicose eczema’). Slow healing varicose ulcers.

Question 40

Causes and risk factors of varicose veins?

Answer 40

• Increased abdominal pressure ― constipation, obesity, pregnancy, childbirth and post-labour, ascites.
• Inherited valve defects ― an absence of some valves or faulty valves.
• Cigarette smoking (= hypoxia, which results in endothelial damage, vessel wall inflammation and a loss of elasticity).
• Being sedentary (increasing venous pressure).
• Lack of dietary connective tissue support, e.g.,
  low vitamin C (increases type I collagen synthesis),
  low bioflavonoids (support connective tissue integrity).
• Portal hypertension ― increased portal
  vein pressure e.g., due to liver cirrhosis and heart failure.
• Increased blood viscosity and stagnation ― dehydration, liver congestion, sedentary lifestyle.
• Structural ― e.g., poor diaphragm motion (consider causes such as stress, asthma etc.), weak pelvic floor (consider pregnancy).Dilated veins are associated with a decrease in collagen and elastin content.

Question 41

Natural approach to varicose veins/ haemorrhoids?

Answer 41

1) CNM Naturopathic Diet. Reduce inflammation, increase blood flow and speed up repair of damaged veins / valves. Correct root causes!

2) Vitamin C-rich foods (to support collagen synthesis).
3) Bioflavonoids such as rutin, proanthocyanidins and anthocyanins which improve the integrity of ground substance and the vascular system, whilst also acting as antioxidants. Food source examples: buckwheat (highest source of rutin) grapes,
apples, cranberry, blueberry, figs, blackcurrants, capers, asparagus, green tea.

3) garlic, onions, ginger, cayenne enhance fibrinolytic activity

4) Optimise liver function —Fibre-rich plant foods: Reduce venous pressure with defecation. Ground flaxseed, or psyllium husk (15–30 g / day). See detox lecture.

5) Raise feet above heart (20 mins / day) — reduces blood pooling and improves venous return.

6) Reduce weight: Address cause and exercise!
Exercise sitting (rotate ankles). Avoid prolonged standing.

7) Support stockings esp. if standing for prolonged periods is unavoidable. Elevate the legs periodically.

8) Topical application of astringent herbs: Horse chestnut
witch hazel, yarrow

9) Support Spleen Qi: tea with equal parts cinnamon, ginger, and tangerine peel stimulates Qi and blood circulation.
* Resolve Blood stasis by reducing stress and exercising frequently.
* Include foods that disperse stagnant blood, e.g., chives, leeks.
* Include blood-nourishing dark leafy greens, beetroot

Question 42

Nutrients for varicose veins/ heammorhoids?

Answer 42

1) Vitamin C with bioflavonoids 1.5–2 g through the day
* Support connective tissue integrity ― increases collagen synthesis

2) Horse chestnut 400 mg (seed) daily for 3 months.
* ↑ venous tone by ↑ the production of prostaglandin F2, which regulates the contractile action of veins, and inhibits the catabolism of venous tissue mucopolysaccharides.
* Inhibits enzymes that destroy venous structures, e.g., collagenase, hyaluronidase, and elastase,

3) Gotu kola 500 mg x 2 daily
* Contains triterpenic acids that have supportive effects on connective tissue.
* Stimulates glycosaminoglycan and collagen synthesis, which supports vein structure and improves blood flow.

4) Butcher’s broom (Ruscus aculeatus) 300–500 mg x 2 daily
* Vasoconstrictive and astringent (its ruscogenin content has anti-elastase activity, which ↓ the diameter of veins).