How atherosclerosis will cause aortic aneurysm ??

how it will cause aneurysm ,,, in the same time it causing thicking of the wall of the aorta ???

The build up of plaque caused by atherosclerosis makes the arteries less elastic. Imagine a balloon that has been blown up too many times...it doesn't go back to its original shape over time. Consequently, the arteries do not expand and contract as easily each time the heart beats and pushes a torrent of blood through the artery...including the aorta. Over time a combination of the weakening and hardening makes the aorta more prone to cracking and ultimately breaking. Again using my balloon analogy...now you have a weakened balloon and as it gets older and more brittle, it is more likely to break.

an aneurysm is a weak spot in the blood vessle wall,,,,,,, if im thinking right,,,,,,,,, ur either born with them,,,,,,,,,, or u never have them at all

I read the thickened artery slows the blood and the result is a sort of bubble in front of the blocked place from stretching out the artery. If that bubble ruptures it isn't good. Like a baloon that is weakened from stretching it out.

My dad died from a coronary heart attack, caused by arteriosclerosis (same thing) 10 yrs ago this July. Basically the walls of ur arteries thicken with fat and cholesterol (which turns into plaque) making it harder for the blood to travel through. My dad was on blood thinners and had 2 surgeries to have arteries that travel from the heart to the leg replaced with plastic-like tubing. He completely changed his diet and walked several times a day to help take the numbness and cold feeling out of his legs and feet. In the end, the plaque eventually loosened and travelled to his heart causing a coronary. There was no warning signs that he was going to die, he just went to bed and never woke up! This is hereditary, so if it's present in ur family, make sure u get tested often.

Here are a couple sites that helped me to understand how this disease works.

http://www.nlm.nih.gov/medlineplus/ency/...
http://www.mayoclinic.com/health/arterio...

here is what wikipedia says about it..

the first link says "The physical change in the aortic diameter can occur secondary to an intrinsic defect in the protein construction of the aortic wall, trauma, infection, or due to progressive destruction of aortic proteins by enzymes"
http://en.wikipedia.org/wiki/Aortic_aneu...

Abdominal aortic aneurysms may have a genetic component..
http://en.wikipedia.org/wiki/Abdominal_a...

AORTIC ANEURYSM PATHOLOGY.
The physical change in the aortic diameter can occur secondary to an intrinsic defect in the protein construction of the aortic wall, trauma, infection, or due to progressive destruction of aortic proteins by enzymes is called Aneurysm.
BACKGROUND: To test whether deficiency in endothelial nitric oxide synthase (eNOS) affects atherosclerosis development, we compared lesion formation in apolipoprotein E (apoE)/eNOS-double knockout (DKO) and apoE-knockout (KO) control animals. METHODS AND RESULTS: After 16 weeks of "Western-type" diet, apoE/eNOS-DKO males and females showed significant increases in lesion area of 93.6% and 59.2% compared with apoE-KO mice. All apoE/eNOS-DKO animals studied developed peripheral coronary arteriosclerosis, associated with perivascular and myocardial fibrosis, whereas none of the apoE-KO mice did. Transthoracic echocardiography showed a significantly increased left ventricular wall thickness and decreased fractional shortening in DKO animals. Mean arterial pressure was increased in DKO mice and was comparable in degree to eNOS-KO animals. Male DKO animals developed atherosclerotic abdominal aneurysms and aortic dissection. CONCLUSIONS: eNOS deficiency increases atherosclerosis in Western-type diet-fed apoE-KO animals and introduces coronary disease and an array of cardiovascular complications, including spontaneous aortic aneurysm and dissection. This phenotype constitutes the first murine model to demonstrate distal coronary arteriosclerosis associated with evidence of myocardial ischemia, infarction, and heart failure. Hypertrophy and reduced left ventricular function cannot be explained by increased blood pressure alone, because eNOS-KO animals do not develop these complications.