Smoking and Cardiovascular Diseases

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Smoking and Cardiovascular Diseases

Introduction

Cigarette smoking still remains a critical health hazard and continues to cause significant effects to cardiovascular morbidity and mortality. The CDC observes that tobacco use continues to be the single largest source of death and disease that can be prevented in the United States. It has been noted that cigarette smoking is responsible for over 480, 000 deaths annually and 41000 of these deaths result from passive smoking (CDC, 2016). Diseases arising from smoking in the US were found to cost over $300 billion in medical care costs and reducing the overall productivity of the population.  By 2015, it was estimated that about 15.1% on the total US population were smokers with 75.7% of these being daily smokers and 24.3% smoking some days (CDC, 2016). Cigarette smoking exposure occurs in two forms: active and passive smoking. Whichever the form of exposure, it is considered as a predisposing factor to cardiovascular disorders. It has been observed that the toxic component in cigarette smoke is responsible for increased inflammation, thrombosis, and oxidation of low-density lipoprotein cholesterol (Ambrose, 2004). This paper will be developed to analyze the relationship between smoking and cardiovascular disease.

Clinical Symptoms

Cigarette smoking acts as an independent risk factor but is also found to have multiplicative interaction with other risk factors for heart diseases thereby escalating the risk factors. Cigarette smoking has also been observed to be the cause of peripheral arterial disease, aortic aneurysm, CHD, and cerebrovascular disease (CDC, 2010).  The general means by which smoking results to cardiovascular disease is the development of atherosclerotic changes through the reduction in the size of the vascular lumen and the induction of hypercoagulable state. This has been known to escalate the risk of acute thrombosis.

Cigarette smoking is normally considered in two phases: the tar phase and the gas phase. The tar phase includes the material trapped when the smoke is channeled through the Cambridge glass-fiber and retained and is of size greater than 0.1 um. The gas phase includes the material that passes through the filter. The cigarette smoke breathed in from the tobacco from the active smoker’s mouth is referred to as the mainstream smoke while the smoke from the burning ends of cigarette is referred to as the side stream smoke. The mainstream smoke is made up of 8% tar and 92% gaseous constitutes.

Cigarette smoking exposes an individual to various clinical atherosclerotic syndromes, not limited to stable angina, acute coronary syndromes, sudden death, and stram. Atherosclerosis was found to arise and expand in the form of vasomotor dysfunction, inflammation, and modification of lipids. The vasomotor dysfunction is the main and first noticeable manifestation of atherosclerotic changes in a vessel. This was found to manifest in both the active and passive smoke exposure. Cigarette smoke is said to impair the endothelium-dependent vasodilation in the major vascular beds including the coronary and brachial arteries (Ambrose, 2004). The nitric oxide levels affected by cigarette smoke have been found to be the main cause of the vasodilator functioning in the endothelium.  The effect of this to the endothelial cells is the alteration of the expression and engagement of the endothelial Nitric Oxide synthase enzyme. The nitric oxide serves a role of vaso-regulatory molecule, regulates inflammation, leukocyte adhesion, platelet activation, and thrombosis. This means that the alteration of Nitric oxide biosynthesis corresponds to the initiation and progression of atherosclerosis and thrombotic ailments (Ambrose, 2004).

Lipid metabolism is affected by tobacco smoke components, specifically nicotine. Through this, the tobacco smoke has been noted to promote atherosclerosis. Smoking causes significant elevated levels of the cholesterol level and the triglycerides. Smoking further reduces the serum concentrations of high-density lipoprotein which is known to provide a protective buffer against the development if atherosclerosis. The smoking-induced shifts in the lipid metabolism combined with the destruction of vascular endothelium causes increased chances of atherosclerosis in smokers.

Cigarette smoking has been known to contribute an inflammatory response which has been noted to be a contributor to the atherosclerosis, a cardiovascular disorder. Cigarette smoke has been associated with increments in the levels of multiple inflammatory markers such as C-reactive protein, interleukin, and tumor necrosis. Cigarette smoking leads to the activation of pro-atherogenic molecules causing changes in the cell to cell interactions (Ambrose, 2004).

Smoking was found to induce the adherence of platelets and macrophages which causes the development of a procoagulant and inflammatory environment. The macrophages takes up the oxidized lipoproteins sourced from the oxidative modifications and transdifferentiate into the foam cells. On top of direct physical damage to endothelial cells, smoking is known to induce tissue remodeling, and pro-thrombotic processes which alongside the activation of inflammatory signals leading to atherogenic vessel wall changes (Messner & Bernhard, 2014).

Cardiovascular disease causes heart related problems that include coronary death, myocardial infraction, coronary insufficiency, and angina. It also includes the cerebrovascular conditions such as ischemic stroke, hemorrhagic stroke and transiet ischemic attack. The peripheral arterial disease includes intermittent claudication and heart failure (Clair et al., 2013). The American Heart Association provides the measure of measuring cardiovascular events. A myocardial infarctions are said to occur when two of the following symptoms are recorded: cardiac pain for at least twenty minutes, diagnosis of ECG code, increased levels of the cardiac enzymes levels (Price et al.)

Mechanisms

Cigarette smoking is known to produce acute myocardial ischemia thereby affecting the balance of the demand for the myocardial oxygen and nutrients with the levels of blood supply (CDC, 2010). Nicotine stimulation on the sympathetic nervous system and the heart causes an increase in demand for oxygen.  Smoking regularly increases the rate of the heartbeat in the short term and throughout the day. Nicotine has also been noted to hike the heart rate, blood pressure, and myocardial contractility. 

Controlling the Condition

Smoking Cessation

The risks caused by smoking can be reduced when one stops smoking. It was found that a comparison between smokers and those who quit smoking showed rapidly decreased levels of risks. However the risk does not completely reduce to the level of non-smokers. The reduction in the risk is noted within the first year and continues to be felt with continued adherence to the cessation program. Stopping smoking has been noted to reduce morbidity and mortality especially in patients with left ventricular dysfunction (CDC, 2010).

Nicotine Replacement Therapy

One way of helping a smoker is by recommending the nicotine replacement therapy.  It helps smokers to stop smoking and reduce nicotine withdrawal symptoms. It is initiated a few hours after quitting smoking and can go on to four weeks. Sudden cessation of smoking is known to cause typical withdrawal symptoms through features such as agitation, anxiety, depressed mood, and difficulty in concentration among other things. These withdrawal symptoms are causes of many relapses within the first week when the withdrawal symptoms are strongest. Some of the replacement methods of nicotine include the use of nicotine patches, nasal spray, and nicotine gum. The efficiency and effectiveness of these methods depend on the correct application of the techniques. Studies have indicated that through the use of nicotine replacement therapies there are no noted increment in cardiovascular risk (CDC, 2010).

Bupropion

This is an aminoketone approved by FDA for treating depression and smoking cessation. This system is considered to function by inhibiting the uptake of norepinephrine and dopamine by the neuronal. It has been found to be an effective and safe way for dealing with smokers with a stable cardiovascular disease. The use of bupropion has been declared safe for treating individuals either with as a stable or an acute disease.

Summary

As it has been discussed, cigarette smoking increases the risk to heart disease. Exposure to cigarette smoke makes one either as an active or passive smoker. It has been found that cigarette smoking is one of the major causes of atherosclerosis. Vascular dysfunction is another effect related to heart problem that arises from cigarette smoking. Continued smoking increases the risk of cardiovascular morbidity and mortality. The components of the tobacco smoke are known to cause degradation of the cardio protective high-density lipoprotein. Nicotine does not help the situation with the heart condition as it deregulates cardiac autonomic functions and increases the heart rate at rest (Papathanasiu at al., 2012). The best management for the arising condition would be smoking cessation and dealing with the withdrawal symptoms.

References

CDC. (2016). Current Cigarette Smoking Among U.S Adut Aged 18 Years and Older.

Centers for Disease Control and Prevention (CDC). (2010). How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease.

Clair, C., & Rogotti, N. P. (2013). Association of Smoking Cessation and Weight Change with Cardiovascular Disease Among Adults with and Without Doabetes. American Medical Association, Vol 309, No 10.

Hu, N. &. (2013). Nicotine, Cigarette Smoking and Cardiac Function: An Update. Toxicology Research, 7-10.

Messner, B., & Bernhard, D. (2014). Smoking and Cardiovascular Disease. AHA Journal, 509-515.

Papathanasiu, G., & Mamali, A. P. (2012). Effects of Smoking on Cardiovascular Function: the Role of Nicotine and Carbon Monoxide. Health Science Journal.