CVD1: Introduction and pathogenesis of CVD

Different forms of CVD

Prevalence of CVD

Major risk factors

Smoking: The chemicals inhaled while smoking causes damage to heart and blood vessels, increasing risk of developing atherosclerosis, or plaque buildup in the arteries.

Nutrition: A diet high in saturated, trans fat and cholesterol has been linked to CVD. LDL-cholesterol is the main risk factor for atherosclerosis. There are studies that suggest that omega-3 PUFAs have anti-thrombogenic properties, retard the growth of atherosclerotic plaque and promote nitric oxide-induced endothelial relaxation.

Trans fat (Trans Fatty Acids): TFAs increase total and LDL-cholesterol but reduces HDL levels.


Trans fat, primarily found in partially hydrogenated vegetable oils, is produced by the food industry to create solid fats from liquid oils


They are not synthesised in vitro and are not essential. Additionally, they are absorbed and incorporated in cellular membranes all over the body. They are catabolised and eventually disappear from the organism.

Gender: Males have higher risk of CVD

Age

Family history of hypercholesterolaemia (lack of LDL receptors), history of heart disease

Importance of endothelial function and blood pressure in CVD risk

Endothelial dysfunction is characterized by imbalanced vasodilation (widening of blood vessels) and vasoconstriction (narrowing of blood vessels), elevated ROS, pro-inflammatory factors and impaired nitric oxide synthesis.


Due to its tight specialised cell-to-cell junctions, the endothelium forms a barrier that selectively limits the movement of macromolecules


Activated endothelial cells may release various cytokines, chemokines, and growth factors that promote the proliferation, migration, and permeability of endothelial cells.


The endothelial cells with inflammatory phenotype cause inflammation in the blood vessels, resulting in endothelial dysfunction and following progression of CVD.

Diminished nitric oxide bioactivity may cause constriction of coronary arteries during exercise or during mental stress and contribute to provocation of myocardial ischemia in patients with coronary artery disease.


Additionally, diminished nitric oxide bioactivity may facilitate vascular inflammation that could lead to oxidation of lipoproteins and foam cell formation, the precursor of the atherosclerotic plaque.

Blood Pressure


High BP is a risk factor for atherosclerosis.


Enhanced vasoconstriction and remodeling of the arterial wall can contribute to the development of hypertension.


The excess strain and resulting damage from high blood pressure causes the coronary arteries slowly become narrowed from plaque.


There is increasing evidence that hypertension induces oxidative stress in the arterial wall. It has even been suggested that superoxide anions might trigger the development of hypertension in some models, presumably by inactivating endothelium-derived nitric oxide and thus mitigating this important vasodilator mechanism.

Stroke

Coronary heart disease

Peripheral vascular disease

angina (dull pain in the chest) - symptoms occur upon exertion, excitement or stress

acute myocardial infarction (heart attack)- prolonged ischaemia (restricted blood supply to tissues, leading to a decrease in oxygen and nutrients to the affected area) leads to death of heart muscle cells

Sudden localised loss of brain function which is either:

  1. Ischaemic (loss of blood supply, formation of clot)
  2. Emboli (clot formed in heart or other vessels and travels to brain)
  3. Haemorrhagic (rupture of arterial wall)

Aortic, iliac and leg arteries - usually co-exist with CHD
Major clinical manifestation is intermittent claudication - pain in leg muscles on walking

Iachaemic heart disease and stroke are the top 2 global cause of deaths (WHO). In Denmark, there are more than 1000 CHD death per 100,000 for males in 85+ age group.

The arteries of older adults have been exposed to the other risk factors (e.g., high cholesterol, hypertension, and smoking) for a longer period of time.

Dietary fibre has also shown some promise in terms of lowering LDL-cholesterol effects. Fibre improves lipid profile, blood glucose levels, and can lower BP. All of which reduces risk of CVD.


Dietary fibre grabs on to fats and cholesterol in the small intestines so that it's excreted instead of absorbed into the bloodstream. Reduces the amount of bile salts reabsorbed from the intestine. The body then needs to make more bile salts and uses cholesterol to do this. therefore, lowering cholesterol levels.