MSN Home  |  My MSN  |  Hotmail
Sign in to Windows Live ID Web Search:   
go to MSNGroups 
Free Forum Hosting
Important Announcement Important Announcement
The MSN Groups service will close in February 2009. You can move your group to Multiply, MSN’s partner for online groups. Learn More 
What's New
  Ask Joel  
  Prior Questions  
  Who is Joel?  
  Joel's Library  
  No Medical Advice  
  Joel's Videos  
General : Clogged arteries  
 Message 1 of 3 in Discussion 
From: Joel  (Original Message)Sent: 1/1/2006 12:16 PM
Hi Joel,

I was reading some articles on the why quit web site and I wanted to know about the arteries. I know now that nicotine in the blood causes stored fat to be released every time a puff is inhaled. My question
Do the arteries become unclogged over time? After never having a puff again.


First  Previous  2-3 of 3  Next  Last 
 Message 2 of 3 in Discussion 
From: JoelSent: 1/1/2006 12:21 PM
Hello Anthony:
We had a similar question posed a few days ago in the string Question regarding arteries. The replies there talks about the reduction in death rates that occurs after quitting. Hope this helps answer your concerns.

 Message 3 of 3 in Discussion 
From: JoelSent: 1/1/2006 12:29 PM
From: John (Gold)  (Original Message) Sent: 6/7/2003 7:45 AM
Clot, Inflammation Factors
 Higher in Smokers
Fri Jun 6, 5:23 PM ET
By Linda Carroll

NEW YORK (Reuters Health) - Cigarette smokers have higher blood levels of three clotting and inflammation factors that have been linked to a clot.jpg (27809 bytes)greater risk of heart disease, a new study shows.

A heart expert unaffiliated with the study said that the new results may help explain why smokers are at higher risk of having heart attacks -- and why that risk diminishes fairly quickly after a smoker quits.

"It's been clear for a while that smoking is a risk factor for heart disease," Dr. Daniel J. Rader, director of preventive cardiology at the University of Pennsylvania School of Medicine in Philadelphia, said in an interview. "But there's still a big question as to why smoking is a risk factor."

In the new study, which included more than 17,000 smokers, non-smokers and former smokers, current smokers had the highest levels of C-reactive protein, fibrinogen and homocysteine.

Former smokers had only slightly elevated levels of all three markers compared to non-smokers, according to the report published this week in the Annals of Internal Medicine.

The study, conducted by Dr. Lydia A. Bazzano, of the Tulane University School of Public Health and Tropical Medicine in New Orleans, and colleagues, included participants in the National Health and Nutrition Examination Study (NHANES).

The study may help explain why the risk of heart disease and heart attack go down quickly after a smoker kicks the habit, Rader said.

"If smoking promoted atherosclerosis, you would expect that if someone smoked for 20 years that the elevated risk would still persist," Rader explained. "So that suggests that the impact of smoking is not so much on plaque buildup itself but on factors that promote plaque rupture."

A heart attack occurs when fatty plaques inside arteries rupture and the body forms a clot to help repair the damage, Rader explained. If any of the clots make their way to the heart's arteries, they can block blood flow to the organ.

Fibrinogen and C-reactive protein are both related to inflammation, Rader said.

"And that's definitely a key component of plaque rupture," he added. "Fibrinogen and homocysteine are key components in the development of (clots)."

There are other, more important, markers of clots, Rader noted. And, he added, "It would have been a more complete study if those other markers had also been measured."

Still, the new study underscores the importance of quitting smoking to protect the heart, Rader said.

"It's a little known fact that in ex-smokers the risk of heart disease goes back to baseline within about two years, as compared to lung cancer, for which the markedly increased risk remains at least a couple of decades after a smoker quits," he said.

SOURCE: Annals of Internal Medicine 2003;138:891-899.

Copyright © 2003 Reuters Limited. All rights reserved

Annals of Interal Medicine 2003;138:891-899

June 3, 2003   Volume 138, Number 11

Relationship between Cigarette Smoking and Novel Risk Factors for Cardiovascular Disease in the United States

Lydia A. Bazzano, MD, PhD; Jiang He, MD, PhD; Paul Muntner, PhD; Suma Vupputuri, PhD; and Paul K. Whelton, MD, MSc

Background:  Few studies have examined the relationship between cigarette smoking and novel risk factors for cardiovascular disease in a general population or have included a biochemical marker of current smoking.

Objective:  To examine the relationship between cigarette smoking and serum C-reactive protein, fibrinogen, and homocysteine levels.

Design:  Cross-sectional study.

Setting:  The U.S. general population.

Patients:  4187 current smokers, 4791 former smokers, and 8375 never-smokers 18 years of age or older who participated in the Third National Health and Nutrition Examination Survey conducted between 1988 and 1994.

Measurements:  Serum C-reactive protein levels were categorized as detectable (2.2 to 9.9 mg/L) or clinically elevated (10 mg/L), and fibrinogen and homocysteine levels were defined as elevated if in the 85th percentile or greater (11.1 μmol/L and 12.7 mmol/L, respectively).

Results:  After adjustment for traditional cardiovascular disease risk factors, cigarette smoking was related to elevated levels of C-reactive protein, fibrinogen, and homocysteine. Compared with never smoking cigarettes, self-reported current cigarette smoking was associated with a C-reactive protein level in the detectable (odds ratio, 1.66 [95% CI, 1.40 to 1.97]; P < 0.001) or clinically elevated (odds ratio, 1.98 [CI, 1.57 to 2.51]; P < 0.001) ranges, with elevated levels of fibrinogen (odds ratio, 2.15 [CI, 1.65 to 2.80]; P < 0.001) and homocysteine (odds ratio, 2.10 [CI, 1.62 to 2.74]; P < 0.001). There were positive and significant dose–response relationships between measures of cigarette smoking (cigarettes per day, pack-years, and serum cotinine levels) and elevated levels of novel risk factors.

Conclusions:  These findings suggest that inflammation and hyperhomocysteinemia may be important mechanisms by which smoking promotes atherosclerotic disease.

Ann Intern Med. 2003;138:891?97.

Cardiovascular disease is the leading cause of death worldwide (1). In the United States, cardiovascular death accounted for approximately 40% (958 775) of all deaths in 1999 (2). Cigarette smoking is a major modifiable risk factor for cardiovascular disease, including coronary heart disease, stroke, peripheral vascular disease, and congestive heart failure (3, 4). In 1990, an estimated 20% of deaths from cardiovascular disease could be attributed to cigarette smoking in the United States (5).

The relationship between cigarette smoking and many established risk factors for cardiovascular disease has been studied. Cigarette smoking has been associated with higher serum levels of cholesterol, coronary vasomotor reactivity, platelet aggregation, and a prothombotic state (6-9). However, few data are available on the relationship between cigarette smoking and newly emerging risk factors for cardiovascular disease (10-13). We used the large sample size and representative nature of the Third National Health and Nutrition Examination Survey (NHANES III) to examine the relationship between cigarette smoking status and novel risk factors for cardiovascular disease, including serum C-reactive protein, fibrinogen, and homocysteine levels.

Related Freedom Threads: