How Does Smoking Increase Cardiovascular Disease - Essay Example

How Does Smoking increase Cardiovascular Disease Contents Contents 2 3 INTRODUCTION 4 LITERATURE REVIEW 5 FUTURE DIRECTIONS 8 works cited 10 ABSTRACT It has been proven to the satisfaction of the general medical community that there is a strong correlation between smoking and cardiovascular (and other) diseases. This article reviews some of the studies which take this reasoning further, parsing different sub-populations, and attempting to understand various elements of smoking and smoking cessation. Some of the articles cited demonstrate how patients who quit smoking can see an improvement in their outcomes. Smoking is highly addictive, which makes it difficult for many to cease smoking. This article reviews literature which demonstrates that reduction in smoking can also have beneficial effects on cardiovascular disease. In order to demonstrate the highly-addictive properties of smoking, one study followed a cohort of men who were diagnosed with an acute, largely fatal, disease diagnosis, and others who were diagnosed with chronic, smoking-related illness. While there was some reduction in smoking, and some cessation, this behavior was not universal. This article reviews further research that is needed in order to better tailor findings about smoking and cardiovascular (and other vascular) disease, in order to understand how it correlates to specific genomic types, and to better predict who might be most susceptible to heart disease. INTRODUCTION There is no more medical debate about whether smoking causes cardiovascular and other diseases. Despite the nearly-unanimous verdict of the medical community, the persistence of smoking behaviors requires a better understanding of who is most susceptible, and how smoking exactly affects health. Much of the research in the past has concentrated on "all-or-nothing" verdicts: non-smokers versus smokers. In fact, there are many smokers who may decide, on the basis of personal diagnoses, to reduce their smoking rather than quit altogether. New research has established that smoking reduction may have some advantages as compared to continuing to smoke at previous rates. The entire science of genomics offers, in conjunction with new clinical studies, the opportunity to better track who is susceptible and who is less likely to contract smoking-related illnesses. New diagnostic techniques may offer the opportunity to track smoking-related illnesses more exactly, giving physicians new ways of identifying and tracking the course of smoking-related illnesses. LITERATURE REVIEW The evidence that smoking is related to heart disease has existed for several decades. Recent work has attempted to better understand the mechanisms by which smoking influences heart disease, and to vary the types of smoking exposure in order to determine degree of severity of cardiovascular damage and the amount and timing of smoking. According to Terry Martin, there are no "easy" or lighter ways to prevent the deleterious effect of smoking (Martin). Low-tar cigarettes are no better than regular cigarettes. In a useful overview of literature, Martin cites the National Cancer Institute's recent study which concludes that even light cigarettes "provide no benefit to smokers' health." The Journal of the American College of Cardiology (JACC) concluded that, while smoking increases the chances of contracting heart disease, smoking cessation can lengthen one's quality of life-years, but not to the same extent as if one had not smoked at all (Iso). This study, which was performed on Asians, found that the best benefits to reduction of heart disease occurred 10-14 years after cessation. Note that the Japanese population studied generally has a much lower rate of heart disease than Caucasians or African-Americans. One should be cautious, therefore, in tying these results to those expected with different populations. That there is a link is indisputable. For example, an article in the "Journal of Behavioral Medicine" in 2005 recounts the study of smokers from age 51 to 61, with longitudinal 2-year follow-up visits over 6 years (Falba). This study was interesting in that it analyzed the behavior of patients who received a new diagnosis of acute and/or chronic disease. The underlying hypothesis is that, if one is faced with an illness which may be life-threatening, one may be more inclined to stop smoking. The research found that smokers uniformly cut their smoking or eliminated it, with two exceptions: those with lung cancer diagnoses (which have a 5 year survival rate below 10%) tended to quit smoking less than others, while those with a diagnosis of CHF (congestive heart failure) or similar heart problems tended to quit smoking more than the average. While the author does not advance a reason for these two outlying results, the reason may be due in part to the acute and deadly nature of lung cancer (i.e. "if I'm going to die anyway"), while the heart patient realizes that his/her smoking cessation can have a positive effect on their lifespan and quality of life years. A recent article, for example, measures the impacts of stress on heart rate and catecholamine production (Robinson). Chatecholaminergic compounds have been related to inflammatory response and increased stress. The underlying hypothesis was that active smokers should have increased chatecholamine response as well as increased heart rates, indicating that the subjects who smoke are likely to see higher "spikes" during stressful periods than non-smokers. It was especially interesting to see that those who are smokers, but are 'deprived,' (i.e. are not currently smoking), showed a similar result to those who were not smokers to begin with. It is understandable in an industry which spends billions of dollars on advertising and public image that there have been challenges, sometimes sponsored by the tobacco industry, to the preponderance of evidence that smoking can create or exacerbate heart disease. A study by a British group analyzes some of the statistical problems in studies related to smoking and heart disease, particularly in applying the results to a small area (Law). While primarily concerned with statistics, such as Bayesian and spatial modeling, the method does introduce some clinically useful ideas. For example, they suggest that the amount of cigarettes that one smokes, and how that volume of smoking changes over time, has been under-studied. Could it be, as in the Falba article, that those who diminish but don't completely stop their smoking have some health benefits By grouping heavy smokers with light smokers in most studies, there may be some useful clinical information which is being lost. Smoking behavior starts early in life, with many smokers starting in their early teens. If one puts off smoking to a later age, the deleterious effects may be put off for some time. According to an article in "Clinician Reviews," early starts to smoking can exacerbate conditions, such as high blood pressure, which can result in a higher chance of heart disease in later life. This study, called "CARDIA," or Coronary Artery Risk Development in Young Adults, studied white and African-American men, with starting ages ranging from 18 to 30. These men were followed for 15 years, with regular measurement of heart disease indicators, including blood pressure, lipids and serum glucose levels. The study used two CT scans after 15 years to look for coronary artery calcium, which the authors assert can be indicative of underlying coronary artery disease. The authors do not prove their assertion that CAC is directly linked to heart disease, which is a matter of dispute, due to the poor resolution and indirect nature of the measure. The evidence seems to be that calcium scoring alone is a poor predictor, except in extreme cases (Greenland). Despite this indirect and disputed link to heart disease, it did appear that calcium scores were higher for cigarette smokers, and the more one smoked, the higher the scores. In addition, other markers, such as HDL/LDL ratio, serum glucose levels and other serum levels climbed with more smoking as well. The article concludes that unmodified smoking habits early in life can lead to higher chances of heart disease later in life. FUTURE DIRECTIONS While there is a substantial body of literature demonstrating the link between cardiovascular disease and smoking, there are several areas which require further research in order to establish the true danger for individuals and specific populations. In particular, it would be helpful to know why all smokers don't contract cardiovascular disease, or why the course of the disease doesn't proceed at the same rate. Although 1/3 of smokers contract and die of related diseases, particularly heart disease and strokes, why is it that 2/3rds of such subjects do not die of smoking-related diseases It could be that the nature of "smoking related diseases" should be widened, to include other diseases or causative elements which may prove less direct. For example, there is a good deal of evidence that generalized inflammation can lead to vulnerable plaque, and so-called "silent" heart attacks which claim 1/3rd of all acute myocardial infarction deaths. If cigarettes are associated with such inflammation, that may be a reason for the connection, and incorporate more heart-attack victims due to smoking than previously thought. The current work in genetic diagnostics and testing help to pinpoint those who have higher susceptibilities to certain diseases. It could be that our genes, or the environment to which they were subjected, are primary causative factors in conjunction with smoking. That is, some people are more susceptible than others to the deleterious effects of smoking due to their genetic predisposition. The exact amount of smoking has not been adequately studied: that is, how many cigarettes smoked may have a correlation to the degree of cardiovascular and other diseases. Is a 10-cigarette per day habit less deleterious than a 20- or 30-cigarette per day habit What is the correlation between the number of cigarettes and the course of a disease While it is understandable that one uses CT scans and calcium scoring to predict the effects on coronary arteries, future techniques of non-invasive measurement need to be perfected in order to develop a more direct picture of susceptibility to vascular disease. Calcium scoring, as outlined here, is an indirect and far-from-perfect indicator of future cardiovascular disease. As MRI and CT machines improve their resolution and ability to differentiate tissue, lesions and composition, they will make it easier for scientists to track the progression of vessel occlusion. In addition, other vessels need to be tracked: stroke and peripheral vascular disease claims many lives, and may also be related to smoking. Until better diagnostic tools come along, it will be difficult to have an accurate whole-body scan which ties directly to a patient's risks of vascular disease throughout the body. Finally, the "gross" effects of smoking are correlated through population studies. As our genetic testing tools become more refined, we may be able to understand exactly which components of smoke affect which DNA and protein synthesis at the cellular level, and how those effects differ from person to person. Perhaps the future will allow us to develop a susceptibility score for each individual-giving some a 'green card' which would allow them to smoke with little or no consequences, while giving a 'red card' to those who are in greater danger of acquiring diseases due to smoking. works cited Falba, T. "Health events and the smoking cessation of middle aged Americans." Journal of Behavioral Medicine (2005): n.p. Greenland, P., LaBree, L., Azen, S. P., Doherty, T. M. and Detrano, R. C. "Coronary Artery Calcium Score Combined With Framingham Score for Risk Prediction in Asymptomatic Individuals." JAMA (2004): 210-215. Iso, H. et al. "Smoking Cessation and Mortality from Cardiovascular Disease among Japanese Men and Women." American Journal of Epidemiology (2005): 170-179. Law, J. Haining, R., Maheswaran, R. and Pearson, T. "Analyzing the relationship between smoking and coronary heart disease at the small area level: a Bayesian approach to spatial modeling." Geographical Analysis (2006): 140. Martin, T. "Are Light Cigarettes Better for You" 2007. Smoking Cessation. 28 November 2007 . Robinson, J. D. and Cinciripini, P. M. "The effects of stress and smoking on catecholaminergic and cardiovascular response." Behavioral medicine (2006): 13. Read More