A 50 years old (1) business executive (2) was leaving his office (3), when he developed severe chest (4) pain radiating to the left arm (5). He also had nausea (6) and breathlessness (7). He was immediately taken to the hospital where he was found to be overweight (8) and gave history of being hypertensive (9) and a smoker for past 25 years (10). His father had died of a heart attack at the age of 60 years (11).

On examination he was found to be dyspneic, was sweating profusely (12) and had a blood pressure of 90/50 mm of Hg (13).

His ECG showed acute ischemic changes (14).

Investigations:

Parameters	Patient	Reference Ranges
Total cholesterol	300 mg/dL	Normal: <200 mg/dL Borderline: 200-239 mg/dL High risk: >240 mg/dL
Triglycerides	250 mg/dL	Normal: <150 mg/dL Borderline: 150-199 mg/dL High risk: 200-499 mg/dL Very high risk: <500 mg/dL
LDL-Cholesterol	200 mg/dL	Desirable: 100-130 mg/dL Borderline: 131-159 mg/dL High risk: >160 mg/dL
HDL-Cholesterol	32 mg/dL	Normal: >55 mg/dL Borderline: 40-55 mg/dL High risk: <40 mg/dL
Creatine Kinase	400 U/L	Normal range: 25-195 U/L

Learning Objectives:

1.       Regulation of blood cholesterol and effects of diet and exercise on blood cholesterol levels.

2.       Metabolism of various lipoproteins and clinical significance of LDL-cholesterol.

3.       Pathogenesis of atherosclerosis and the factors affecting it.

4.       Various diseases due to atherosclerosis in the body.

1  Age:

Patient presents in late middle age. The protein formation decreases with age resulting in decreased elasticity and metabolism of tissue. Patients in this age group are screened for hypertension, cholesterol levels, colon cancers, prostatic cancers, eye etc.

LDL receptors are also decreased with age due to progressively decreasing protein turnover.

2         Occupation:

Business executives spend most of their time sitting on the chair. Most of the business executives use cars, elevators and planes while traveling and do not get enough exercise. Basically they have sedentary lifestyle. They are more prone to Cardiovascular diseases. They are commonly stressed trying to keep up with the dynamic market and meeting the demands of their clientele.

3         Activity:

Whenever a person gets up after sitting a while, his sympathetics are activated to keep the blood supply to brain constant. Sympathetics increase the heart rate and force of contraction. The heart is already overworked in patients suffering from hypertension and atherosclerosis. In such instances coronary artery can rapture or become more occluded producing ischemia and subsequently Myocardial infarction.

4         Chest Pain:

It may be due to Heart, lungs, intestinal, gall bladder or musculoskeletal damage. In this case it is ischemic in nature.

5         Spread of Pain:

Visceral afferent pain sensation is relayed near to interneurons receiving somatic afferents from same dermatomal segment. So pain from viscera are sometime seems to be radiating to somatic structures of same dermatome. Heart afferents run centrally in the middle and inferior cervical branches and especially in the thoracic cardiac branches of sympathetic trunk to enter spinal segments T1-T4/5, especially on the left side.T2 and/or T3’s lateral branches communicate with the medial cutaneous nerve of arm so that the pain from heart may be referred to medial side of left arm and/or left side of neck. Signals from one side may go through commissural fibers in spinal cord to other side as well.

In short, afferents from heart lie in proximity to afferents from medial arm and neck of left side, so the pain from heart is referred to these regions.

Heart is insensitive to heat, cold, cutting and touch. Pain ending are only stimulated when there is ischemia and accumulation of metabolites.

6         Nausea:

It is the realization of stimulation of vomiting centre or uncomfortable feeling in the upper GIT.  It may be due to overdistension, overexcitation or irritation of GIT or some metabolic disorder. Heart failure results in the sympathetic stimulation which can also cause vomiting or nausea.

7         Breathlessness:

Heart attack will lead to circulatory shock, which will prevent oxygenation and removal of carbon dioxide. Increased carbon dioxide concentration in body will stimulate the respiratory centre in medulla. This will give patient a feeling of dyspnea.

Dyspnea can be due to:

Abnormality of blood gases.

Amount of work respiratory muscles are performing.

State of mind.

8         Overweight:

It is calculated by BMI and waist circumference.

HOW TO DETERMINE YOUR BMI

Your BMI estimates how much you should weigh, based on your height. Here are the steps to calculate it:

• Multiply your weight in pounds by 703.
• Divide that answer by your height in inches.
• Divide that answer by your height in inches again.

Following are the reference ranges for BMI:

Underweight =     >18.5

Normal          =     18.5-24.9

Overweight  =     25-29.9

Obese            =     <30

9         Hypertensive:

Patient is labeled hypertensive when systolic pressure is constantly above 140 mm of Hg and diastolic pressure is constantly above 90 mm of Hg.

Hypertension leads to weakening and dilatation of arterial walls, leading to aneurysm and hemorrhage. It increases the chances of atherosclerosis by 60%.

10    Smoker:

Smokers are at an increased risk for lung cancer, chronic bronchitis , emphysema, myocardial infarction, systemic atherosclerosis, peptic ulcer disease and various forms of GIT and Respiratory tract cancers.

Smoking increases the chances of atherosclerosis by 200%.

11    Family History:

It is positive for acute myocardial infarction and familial hypercholesterolemia.

12    Sweating:

Sympathetics activate sweat gland.

13    Hypotensive:

Due to damage to some part of heart the heart is not able to pump blood effectively.

14    ECG:

In acute myocardial infarction current of injury appears. It is strongly positive In posterior wall infarction and negative in anterior wall infarction in lead V₂.

Investigations:

1         Total cholesterol:

It is increased. It may be due to decreased LDL receptors, increased dietary intake or genetic defects in lipoprotein metabolism. It may be raised secondarily to diabetes, primary hypothyroidism, nephritic syndrome, cholestasis and drugs (thiazide diuretics, loop diuretics β-blockers etc) etc.

2         Triglycerides:

Positive energy balance leads to conversion of carbohydrates into triglycerides. It is elevated in the genetic defects accompanying hypercholestrolemia. It may be increased secondarily to diabetes, nephrotic syndrome, smoking, insulin resistance etc.

3         LDL-Cholesterol:

Decreased uptake by liver will increase the quantity of the LDL in the plasma and its deposition in the arterial walls. It can also increase by increased production of apo-b₁₀₀.

4         HDL-Cholesterol:

HDL cholesterol is decreased by sedentary lifestyle, high lipid and carbohydrate diet, smoking, diabetes, drugs and genetic defects.

5         Creatine Kinase:

Creatine kinase (CK) is the enzyme found in skeletal and heart muscles. After acute myocardial infarction CK_MB isoenzyme form starts increasing in plasma after 4-8 hrs, peaks after 24hrs and return to baseline after 48-72 hrs.

Another marker for Cardiac injury is Cardiac Troponin I (TnI). It appears after 6 hours, peaks in 8-24 hrs and stays elevated for 3-10 days.

Learning Objectives:

1         Regulation of Blood Cholesterol levels and Effects of Diet and Exercise on the Cholesterol Levels:

Click here.

2         Metabolism of Lipoproteins and Clinical significance of LDL:

Lipponcot pg 227-237.

3         Pathogenesis of Atherosclerosis and Factors Affecting it:

Arteriosclerosis, hardening of arteries, arteriolosclerosis hardening of arterioles and atherosclerosis is hardening of the arteries by atheromatous plaques.

LDL not metabolized is oxidized by various oxidants in plasma and taken up by macrophage cells which become foam cells and get attached to arterial walls. The arterial wall becomes rough and thrombosis takes place, which may lead to embolism. This causes hardening of arterial walls and they become fragile, on slightly increased pressure they can rapture producing hemorrhage or blood clot can obstruct the flow to vital organs like heart and cause ischemia.

Fig 18.22 Lipponcott pg 235.

Following conditions increase atherosclerosis:

Modifiable:

1. Diabetes and impaired glucose tolerance.

2. High ‘bad’ cholesterol (LDL, VLDL).

3. Low good cholesterol (HDL).

4. High LDL/HDL ratio.

5. Tobacco smoking.

6. Hypertension.

7. Increased quantity of C-reactive proteins.

Non-Modifiable:

1. Old age.

2. Male.

3. Family history.

Lesser factors:

1. Obesity.

2. Sedentary lifestyle.

4              Various Diseases due to Atherosclerosis:

• Myocardial infarction
• Coronary arterial disease
• Peripheral artery disease
• Hypertension
• Renal disease

~A.D.

Reviwed by:

Dr. M.M.D

Acknowlegment:

Mr Sajjid who gave me this scenario.

Mr Hassaan who gave me a platform.

Disclaimer:

Author is not responsible for any injury especially brain damage or in common term ‘maghaz‘ that any individual browsing this article may experience.

Last words:

I would like to thank Mr Adnan for presenting previous scenario.Due some technical difficulties i was not able to do it.