Coronary Artery Disease(CAD)

 Pathophysiology of CAD 

(Pathophysiology means a disease process

CAD means  coronary artery disease  where the arteries 

Supporting blood to the heart become narrowed or

Blocked due to a plaque( involves build up of fatty deposits

Of cholesterol and other substances within artery wall.)

Coronary artery disease is typically caused 

by atheromatous constriction of the vessel and subsequent blockage. From young adulthood onwards, early atheromatous plaque (derived from the Greek word; Athera - porridge and Oma - lump) is evident. A mature plaque comprises two components that are

 macrophages (also called big eaters)

 and smooth muscle cells, each of which belongs to a particular cell lineage [11]. The necrotic "foam cells"

 - monocyte-derived macrophages that move

 into the intima

(Inner lining  of blood vessels)

of  and absorb lipids - are the primary source

 of the lipid core. Smooth muscle cells

 migrate in the vascular wall from the media into the intima, where they multiply and change their phenotype (to create a fibrous capsule around the lipid core, forming the connective tissue matrix [11]. Calcification of the 

coronary arteries occurs in tandem with the progression of severe atherosclerosis( atherosclerosis is 

thickening or hardening of arteries caused by building of plaque in the inner lining

Of an artery)

 Risk factors

1 High cholesterol 

2Triglycerides 

3High BP

4Smoking

5Diabetes)

. Calcification usually begins as

 micro-nodules (0.5 to 15.0 μm) and later progress to larger calcium particles which form sheets like 

deposition (>3mm) in the arteries. 

These changes appear to take place concurrently

 with plaque evolution (Figure 1) [12]. Coronary artery stenosis of more than 50% or a reduction in the cross-sectional area by 80% usually leads to angina on exertion. Intimal damage causes thrombus development by causing denudation of the thrombogenic matrix or lipid pool. Occlusion is more complete in acute myocardial infarction than unstable angina, where arterial occlusion is frequently partial. Acute coronary events usually occur when a plaque ruptures and triggers the formation of a thrombus [11]. 

Figure 1. Coronary artery calcification.

Various factors have a role in the onset 

and advancement of calcification, 

which vary depending on the stage of plaque and the surrounding environment. Although

 it is usually associated with aging, various 

factors, including numerous associated risk factors that can accelerate the calcification in atheromatous plaques like environmental, genetic, family history, and lifestyle accounting for early CAD.

Ref

Cureus

. 2021 Dec Figure 1. Coronary artery calcificatiFigure 1

CT(12):e20149. doi: 10.7759/cureus.20149

Coronary Artery Calcium Score - A Reliable Indicator of Coronary Artery Disease?

Devarashetty Shreya 1,✉, Diana I Zamora 2, Gautami S Patel 3, Idan Grossmann 4, Kevin Rodriguez 5, Mridul Soni 6, Pranay K Joshi 7, Saawan C Patel 3, Ibrahim Sange 8,9

Editors: Alexander Muacevic, John R Adler

Targetibg Postprandial Hyperglycemia with Physical ACtivity

            Physical Inactivity   And

Excessive Postprandial Hyperglycemia

are major independent risk factors for Type 2diabetes and cardio

 vascular related moortality .

Current health policy guide lines recommend at leastat 150. Min of

Physical activity per week ,coupled with reduced daily sedentary 

Behavior by interrupting prolonged sitting with bouts of light activity in every30,min.

     Modern life style enforces physical inactivity through motorized transportation and     

and seated office working environments.

Plato wrote "Is s not the bodiily. Habit 

Spoiled by rest and ideal ness ,

but preserved for motion and excercise."

Global Burden of diseases injuries and risk

 factors.

   Sudy found low physical activity to be the 4th leading cause of 

Global mortality.

       In 2006 health survey for England found  that adults in the UK

Spend aprox imately 5 hours Per day  sitting in their spare time 

(Not Including  hours at paid work.)

Ref. Front Cardiovascular Medicine 2018 :July 18

Doi:10.3389 ,/fcrm2018 .00099

Thomas P.J Solamon

Frank K Eves

And

Mathew

J.Laye

Cancer log kill

Cancer log kill : Let us first know what is log eg 10 number log is 1 for 100 the log number 2 similarly for 1000 Log number 3 .
Now what is log kill it is hypothesis used in relation to capacity of chemotherapy in cancer killing  generally 2-3 .
What is the base ? Earliest dignosis of cancer is possible when cancer cells number is 10to the power of 9 wt of cancer cells is just 1gm .but with exponential growth it would be 10to the power of 12 weighing 1kg a critical stage .
Let us calculate the cancer log kill of patient with 10 to the power 9 even if cancer kill is log 3 the cancer cells would remain 10to the power of 6 and in the next cycle the cancer cells would be killed again 3log ie caccer cells would remain still 10 to the power of 3 .In next chemotherapy would kill almost all cancer cells except one

But cacer would not behave mathematically alone some new cancer cells would add to the remaining cacer cells some cancer cells would resist chemotherapy agents .
The above briefing helps to understand the need for multiple chemotherapy cycles.