Question

The patient's history for update purposes

Patient A age 70. He is obese and 100% sedentary. He needs to do physical exercises, to lose weight, to decrease stress and to eat better (but he does not do that). He has diabetes: 25 years ago, he was diagnosed with diabetes type 2 and he has to take insulin.

Diet: He eats meat 3 times a day and does not eat dietary fiber.

Emotional: He is stressed and anxious, and works hard.

Parents: The mother and father died young because of complications of diabetes. Father: died at age 53 of myocardial infarction.

Symptoms now: shortness of breath, chest pain due to physical exertion (angina).

Has high blood pressure: 140/90. Never had hypertension before. His doctor prescribed for hypertension: Vasotec (enalapril).

He must take the following exams:

FSC: red blood cells, white blood cells and platelets

Lipid profile

Creatinine test

Uremia test (urine in the blood)

Electrolytes test (usually sodium or potassium or an acid-base imbalance)

Clearance of creatinine test

HbA1c test (also called glycated hemoglobin test, and glycohemoglobin)

Stress ECG test

Urine analysis

3 weeks later, the results:

Clearance of creatinine test show to us the GFR (Glomerular Filtration Rate) results:
GFR 55mL/min (normal: 90-125mL/min)

Lipid profile: low level HDL, high level LDL

Plasma creatinine level (creatinine test): 150 mmol/L (normal: 50-110 umol/L)

Uremia test : 8 mmol/L (N : 3 - 6,5 mmol/L)

Urine analysis: 120 mg/L of proteins (normal: < 80 mg/L)

Stress ECG test: Anomalies related to unstable angina

Doctor's conclusion: chronic renal insufficiency (CRI), unstable angina. Needs to do an emergency angiography.

Angiography test results: several atheroma plaques in the coronary arteries. He had to put four stents during the procedure.

He had to take these medicaments:

Clopidogrel (Plavix), Aspirine (acide salicylique, for 1 year), and Crestor (is a statine). And also, the insulin and Vasotec (énalapril).

Question F: What is the link with nutrition and alteroesclerose? What does the system renin angiotensin aldosterone do in this case and why is he involved in this case?

Answer 1

Atherosclerosis is formation of plagues in the inner lining of the blood vessel which results in the narrowing of blood vessel and makes heart to pump adequate blood. The atheroma is basically composed of lipids, calcium and fibrous connective tissue. The risk factors that lead to formation of atheroma are:

• high intake of saturated fats, trans fat, sugar, cholesterol and sodium
• sedentary lifestyle
• obesity,
• diabetes
• high blood pressure
• increased age
• family history of heart disorder
• smoking

Among these factors the Patient A is old age of 70, he is 100% sedentary, has diabetes, have family history of heart disorder,have high blood pressure and high lipids in blood. Thus this leads to development of angina the classic symptom in atherosclerosis.

• The saturated and trans fat along with cholesterol tend to build up the lipid levels in the blood. The dietary fats then contribute to formation of plaques by depositing on the walls of the arteries.
• Other important factor in nutrition is intake of adequate fiber. The fiber has a property to enhance the absorption all the excess cholesterol by the digestive tract.
• The intake of excessive sugar in diet is also harmful as its acidic in nature,inflammatory and messes with the arterial function. More over the high glycemic index is associated with high triglyceride levels that increases the risk of coronary artery disease.

The renin angiotensin aldosterone system is a hormone system that acts on multiple pathways primarily regulating blood pressure and fluid balance. The renin angiotensin aldosterone system is also found to be a promoter of atherosclerosis by its actions on vessels by promoting development of high blood pressure, insulin resistance, diabetes, obesity, vascular and systemic inflammation. The endothelial damage that occurs due to the oxidative stress creates imbalance in the vasoconstriction and vasodilation effects thereby increases the angiotensin 2 and decreases nitric oxide. This increase in angiotensin 2 enhances the vascular permeability via activation of vascular cell adhesion molecules, intercellular adhesion molecule and endothelial growth factor. Thereby the inflammatory process at the endothelial injury site and the adhesion of the lipids contribute to formation of artheroma.