A Controlled Trial of Sustained-Release Bupropion, a Nicotine Patch, or Both for Smoking Cessation

Jorenby, Douglas E.; Leischow, Scott J.; Nides, Mitchell; Rennard, Stephen I.; Johnston, J. Andrew; Hughes, Arlene R.; Smith, Stevens S.; Murãmoto, Myra L.; Daughton, David M.; Doan, Kimberli; Fiore, Michael C.; Baker, Timothy B.

doi:10.1056/nejm199903043400903

Cited by 1,422 publications

(997 citation statements)

References 15 publications

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“…For patients who cannot tolerate SSRI-induced sexual dysfunction or for patients who are planning to stop smoking, 58,72 bupropion is an effective alternative. 73 For bupropion, the initial dose is 100 mg twice a day, the usual effective dose is 100 mg 3 times a day, and the maximum dose is 150 mg 3 times a day.…”

Section: Pharmacotherapymentioning

confidence: 99%

Depression and Cardiovascular Disease

Whooley¹

2006

JAMA

218

163

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Major depressive disorder is a risk factor for the development of incident coronary heart disease events in healthy patients and for adverse cardiovascular outcomes in patients with established heart disease. Depression is present in 1 of 5 outpatients with coronary heart disease and in 1 of 3 outpatients with congestive heart failure, yet the majority of cases are not recognized or appropriately treated. It is not known whether treating depression improves cardiovascular outcomes, but antidepressant treatment with selective serotonin reuptake inhibitors is generally safe, alleviates depression, and improves quality of life. This article evaluates the importance of major depression in patients with cardiovascular disease, and provides practical guidance for identifying and treating this disorder. CASE PRESENTATIONA 58-year-old man with a history of coronary heart disease (CHD), type 2 diabetes mellitus, hypertension, smoking, and alcohol dependence presented for routine medical care. He had initially sought medical attention for exertional angina 5 years previously, at which time he underwent exercise treadmill testing with thallium that was positive for reversible perfusion defects in the anterior, septal, and inferior walls. Subsequent coronary angiography revealed diffuse heavy calcifications in the left anterior descending artery with a moderate lesion prior to the first diagonal. Several major septal perforators had significant lesions at their origins. In the dominant right coronary artery, there were diffuse calcifications but no significant lesions. The left circumflex and large ramus intermedius were free of discrete lesions. Left ventricular function was normal.The patient underwent single-vessel (left internal mammary artery to left anterior descending artery) coronary artery bypass grafting (CABG) surgery. He was prescribed atenolol 100 mg/ d, lisinopril 40 mg/d, lovastatin 80 mg/d, aspirin 325 mg/d, metformin 850 mg 3 times a day, and glipizide 10 mg 2 times a day. Despite being nonadherent to his prescribed medications, he remained stable for 5 years, but then one day, while doing household chores, he suddenly developed chest pressure, shortness of breath, and diaphoresis that lasted 12 hours. On admission to the hospital his troponin I was elevated and peaked at 0.7 ng/mL (normal, <0.05 ng/mL), consistent with a myocardial infarction (MI). His electrocardiogram had not changed.

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Section: Pharmacotherapymentioning

confidence: 99%

Depression and Cardiovascular Disease

Whooley¹

2006

JAMA

218

163

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“…While most smokers endorse a desire to quit (Fiore et al, 2000), very few will actually quit smoking without treatment, and only about 14-49% will achieve abstinence after 6 months or more of effective treatment (Holmes et al, 2004;Hughes et al, 1999;Hurt et al, 1997;Jorenby et al, 1999;Killen et al, 1999Killen et al, , 2000. Because cigarette smoking carries both considerable health risks (Bartal, 2001;Mokdad et al, 2004) and high societal costs (Leistikow et al, 2000a,b), there is an urgent need for improved treatments for this condition.…”

Section: Introductionmentioning

confidence: 99%

Functional brain imaging of tobacco use and dependence

Brody

2006

Journal of Psychiatric Research

176

136

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While most cigarette smokers endorse a desire to quit smoking, only about 14% to 49% will achieve abstinence after 6 months or more of treatment. A greater understanding of the effects of smoking on brain function may (in conjunction with other lines of research) result in improved pharmacological (and behavioral) interventions. Many research groups have examined the effects of acute and chronic nicotine/cigarette exposure on brain activity using functional imaging; the purpose of this paper is to synthesize findings from such studies and present a coherent model of brain function in smokers. Responses to acute administration of nicotine/smoking include: a reduction in global brain activity; activation of the prefrontal cortex, thalamus, and visual system; activation of the thalamus and visual cortex during visual cognitive tasks; and increased dopamine (DA) concentration in the ventral striatum/nucleus accumbens. Responses to chronic nicotine/cigarette exposure include decreased monoamine oxidase (MAO) A and B activity in the basal ganglia and a reduction in α 4 β 2 nicotinic acetylcholine receptor (nAChR) availability in the thalamus and putamen. Taken together, these findings indicate that smoking enhances neurotransmission through cortico-basal ganglia-thalamic circuits either by direct stimulation of nAChRs, indirect stimulation via DA release or MAO inhibition, or a combination of these factors. Activation of this circuitry may be responsible for the effects of smoking seen in tobacco dependent subjects, such as improvements in attentional performance, mood, anxiety, and irritability.

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“…6 In general, these drugs increase the risk of quitting by 1.5-2-fold; 7 however, there is large interindividual variability in response and few maintain long-term abstinence. 8,9 Thus, there is a need to better understand the biological determinants of nicotine dependence (ND) and cessation.…”

Section: Introductionmentioning

confidence: 99%

Overview of the pharmacogenomics of cigarette smoking

Tyndale

2007

Pharmacogenomics J

102

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Cigarette smoking increases the risk of numerous health problems, including cancer, cardiovascular and pulmonary disorders, making smoking the leading cause of preventable death in the world. Nicotine is primarily responsible for the highly addictive properties of cigarettes. Although the majority of smokers express a desire to quit, few are successful in doing so. Twin and family studies have indicated substantial genetic contributions to smoking behaviors. One major research focus has been to elucidate the specific genes involved; this has been accomplished primarily through genome-wide linkage analyses and candidate gene association studies. Much attention has focused on genes involved in the neurotransmitter pathways for the brain reward system and genes altering nicotine metabolism. This paper reviews the current state of knowledge for genetic factors implicated in smoking behaviors, and examines how genetic variations may affect therapeutic outcomes for drugs used to assist smoking cessation.

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A Controlled Trial of Sustained-Release Bupropion, a Nicotine Patch, or Both for Smoking Cessation

Cited by 1,422 publications

References 15 publications

Depression and Cardiovascular Disease

Depression and Cardiovascular Disease

Functional brain imaging of tobacco use and dependence

Overview of the pharmacogenomics of cigarette smoking

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