E-cigarettes may significantly increase plasma nicotine, CO concentration, and heart rate within the first five minutes of administration. Vansickel AR, Cobb CO, Weaver MF, Eissenberg TE. A clinical laboratory model for evaluating the acute effects of electronic "cigarettes": nicotine delivery profile and cardiovascular and subjective effects. Cancer Epidemiol Biomarkers Prev. 2010 Aug;19(8):1945-53.
In a study where MI was induced in rats, those that were exposed to CO at levels corresponding to tobacco smoke had worse ventricular remodeling and increased infarct size, leading to worse heart failure. Mirza A, Eder V, Rochefort GY, Hyvelin JM, Machet MC, Fauchier L, Bonnet P. CO inhalation at dose corresponding to tobacco smoke worsens cardiac remodeling after experimental myocardial infarction in rats. Toxicol Sci. 2005 Jun;85(2):976-82
The number of circulating endothelial progenitor cells (EPCs) was reduced in chronic smokers. Smoking cessation led to a rapid restoration of EPC levels. Kondo T, Hayashi M, Takeshita K, Numaguchi Y, Kobayashi K, Iino S, Inden Y, Murohara T. Smoking cessation rapidly increases circulating progenitor cells in peripheral blood in chronic smokers. Arterioscler Thromb Vasc Biol. 2004 Aug;24(8):1442-7.
The transdermal nicotine system significantly increased heart rate compared with the control group without nicotine substitution. Puura A. Transdermal nicotine increases heart rate after endotracheal intubation. Methods Find Exp Clin Pharmacol. 2003 Jun;25(5):383-5.
Heart rate of smokers and the neuroendocrine responses of smokers was significantly higher than nonsmokers after tracheal intubation. Paventi S, Santevecchi A, Ranieri R. Control of haemodynamic response to tracheal intubation in cigarette smokers compared with non-smokers. Eur Rev Med Pharmacol Sci. 2001 May-Jun;5(3):119-22.
Current smoking is a significant independent risk factor for morbidity (recurrent heart failure and MI) and mortality in patients with left ventricular dysfunction. Abstinence has a substantial effect on decreasing morbidity and mortality in patients with left ventricular dysfunction. Suskin N, Sheth T, Negassa A, Yusuf S. Relationship of current and past smoking to mortality and morbidity in patients with left ventricular dysfunction. J Am Coll Cardiol. 2001 May;37(6):1677-82.
Patients who continued to smoke after CABG had a greater risk of death and underwent repeat revascularization procedures more frequently than patients who stopped smoking. van Domburg RT, Meeter K, van Berkel DF, Veldkamp RF, van Herwerden LA, Bogers AJ: Smoking cessation reduces mortality after coronary artery bypass surgery: A 20-year follow-up study. J Am Col Cardiol 2000; 36:878–83
Smokers had significantly greater increases in heart rate, systolic and diastolic blood pressure after administration of desflurane, when compared to nonsmokers. Fitz-Henry J, Curran J, Griffiths D. Smokers and haemodynamic responses to desflurane. Anaesthesia 1999; 54: 800–803.
Patients under age 65 without symptoms of ischemic heart disease who smoked shortly before surgery had more episodes of ST segment depression than nonsmokers. Woehlck HJ, Connolly LA, Cinquegrani MP, Dunning MB III, Hoffmann. Acute smoking increases ST depression in humans during general anesthesia. Anesth Analg 1999; 89:856–60
Cigarette smoking alone increased blood pressure and decreased muscle sympathetic nerve activity. Narkiewicz K, van de Borne PJ, Hausberg M, Cooley RL, Winniford MD, Davison DE, Somers VK. Cigarette smoking increases sympathetic outflow in humans. Circulation. 1998 Aug 11;98(6):528-34.
Nicotine patches, when used to promote smoking cessation, significantly reduce the extent of exercise-induced myocardial ischemia. Mahmarian JJ, Moye LA, Nasser GA, Nagueh SF, Bloom MF, Benowitz NL, Verani MS, Byrd WG, Pratt CM: Nicotine patch therapy in smoking cessation reduces the extent of exercise-induced myocardial ischemia. J Am Coll Cardiol 1997; 30:125–30
Nicotine contributes to acute cardiovascular events but does not appear to enhance thrombosis among humans on its own. Benowitz NL. The role of nicotine in smoking-related cardiovascular disease. Prev Med. 1997 Jul-Aug;26(4):412-7.
Compared with patients who stopped smoking since surgery, smokers at 1 year after surgery had more than twice the risk for myocardial infarction and reoperation. Patients who were still smoking at 5 years after surgery had these same risks plus significantly increased risk for angina pectoris compared with patients who stopped smoking since surgery and patients who never smoked. Voors AA, van Brussel BL, Plokker HW, Ernst SM, Ernst NM, Koomen EM, Tijssen JG, Vermeulen FE: Smoking and cardiac events after venous coronary bypass surgery: A 15-year follow-up study. Circulation 1996; 93:42–7
Nicotine reduces DNA synthesis and collagenase activity in cardiac fibroblasts. Tomek RJ, Rimar S, Eghbali-Webb M. Nicotine regulates collagen gene expression, collagenase activity, and DNA synthesis in cultured cardiac fibroblasts. Mol Cell Biochem. 1994 Jul 27;136(2):97-103.
Elements of environmental tobacco smoke (ETS) have significant adverse effects on the cardiovascular system. This increase in risk translates into about 10 times as many deaths from ETS-induced heart disease as lung cancer. Glantz SA, Parmley WW. Passive smoking and heart disease. Epidemiology, physiology, and biochemistry. Circulation. 1991 Jan;83(1):1-12.
Cardiovascular benefit from smoking cessation begins within 12-24 hours of abstinence, likely due to carbon monoxide and nicotine elimination. Pearce AC, Jones RM. Smoking and anesthesia: preoperative abstinence and perioperative morbidity. Anesthesiology. 1984 Nov;61(5):576-84.