Acute and chronic sympathomimetic effects of e-cigarette and tobacco cigarette smoking: role of nicotine and non-nicotine constituents

Abstract

Electronic cigarettes (ECs) and tobacco cigarettes (TCs) both release nicotine, a sympathomimetic drug. We hypothesized that baseline heart rate variability (HRV) and hemodynamics would be similar in chronic EC and TC smokers and that after acute EC use, changes in HRV and hemodynamics would be attributable to nicotine, not non-nicotine, constituents in EC aerosol. In 100 smokers, including 58 chronic EC users and 42 TC smokers, baseline HRV and hemodynamics [blood pressure (BP) and heart rate (HR)] were compared. To isolate the acute effects of nicotine vs. non-nicotine constituents in EC aerosol, we compared changes in HRV, BP, and HR in EC users after using an EC with nicotine (ECN), EC without nicotine (EC0), nicotine inhaler (NI), or sham vaping (control). Outcomes were also compared with TC smokers after smoking one TC. Baseline HRV and hemodynamics were not different in chronic EC users and TC smokers. In EC users, BP and HR, but not HRV outcomes, increased only after using the ECN, consistent with a nicotine effect on BP and HR. Similarly, in TC smokers, BP and HR but not HRV outcomes increased after smoking one TC. Despite a similar increase in nicotine, the hemodynamic increases were significantly greater after TC smokers smoked one TC compared with the increases after EC users used the ECN. In conclusion, chronic EC and TC smokers exhibit a similar pattern of baseline HRV. Acute increases in BP and HR in EC users are attributable to nicotine, not non-nicotine, constituents in EC aerosol. The greater acute pressor effects after TC compared with ECN may be attributable to non-nicotine, combusted constituents in TC smoke.NEW & NOTEWORTHY Chronic electronic cigarette (EC) users and tobacco cigarette (TC) smokers exhibit a similar level of sympathetic nerve activity as estimated by heart rate variability. Acute increases in blood pressure (BP) and heart rate in EC users are attribute to nicotine, not non-nicotine, constituents in EC aerosol. Acute TC smoking increased BP significantly more than acute EC use, despite similar increases in plasma nicotine, suggestive of additional adverse vascular effects attributable to combusted, non-nicotine constituents in TC smoke.

Keywords: blood pressure; electronic cigarettes; heart rate variability; nicotine; tobacco cigarettes.

Fig. 1.

Baseline heart rate variability components. HRV components, including HF (vagal activity), LF (predominantly sympathetic activity), and LF-to-HF ratio (sympathetic:vagal balance), were not different in chronic EC users (n = 58) and TC smokers (n = 42) during ad libitum breathing (A) or controlled breathing (B). Means were compared between groups using t tests and are displayed as mean (25–75%) with whiskers to minimum to maximum of the data. EC, electronic cigarette; HF, high frequency; HRV, heart rate variability; LF, low frequency; TC, tobacco cigarette; nu, normalized units.

Fig. 2.

Baseline hemodynamics. Systolic blood pressure (A), diastolic blood pressure (B), mean blood pressure (C), and heart rate (D) were not different in chronic EC users (n = 58) and TC smokers (n = 42). Means were compared between groups using t tests and are displayed as mean (25–75%) with whiskers to minimum to maximum of the data. BP, blood pressure; EC, electronic cigarette; MBP, mean blood pressure; TC, tobacco cigarette; bpm, beats/min.

Fig. 3.

Change in heart rate variability components after acute EC exposures. HRV components, including HF (A), LF (B), or LF-to-HF ratio (C), did not change significantly after using an EC with nicotine (n = 36), EC without nicotine (n = 34), or nicotine inhaler (n = 20), compared with sham control (n = 44). Means were compared using a repeated measure (mixed) model adjusting for visit and controlling for nonindependence via random subject effects. Values are mean (25–75%) with whiskers to minimum to maximum of the data. EC, electronic cigarette; ECN, EC with nicotine; EC0, EC without nicotine; HF, high frequency; HRV, heart rate variability; LF, low frequency; NI, nicotine inhaler; nu, normalized units.

Fig. 4.

Change in hemodynamics after acute EC exposures. Blood pressure, including SBP (A), DBP (B), and MBP (C), and heart rate (D) significantly increased after using the EC with nicotine (n = 35) but not after EC without nicotine (n = 33) or nicotine inhaler (n = 19), compared with sham control (n = 44). Means were compared using a repeated measure (mixed) model adjusting for visit and controlling for nonindependence via random subject effects. Values are mean (25–75%) with whiskers to minimum to maximum of the data. BP, blood pressure; EC, electronic cigarette; ECN, EC with nicotine; EC0, EC without nicotine; MBP, mean blood pressure; SBP, systolic blood pressure; DBP, diastolic blood pressure; NI, nicotine inhaler; bpm, beats/min.

Fig. 5.

Change in heart rate variability components after acute TC smoking. HRV components, including HF (A), LF (B), or LF-to-HF ratio (C), did not change significantly after smoking 1 TC (n = 30) compared with sham control (n = 31). Means were compared using a repeated measure (mixed) model adjusting for visit and controlling for nonindependence via random subject effects. Values are mean (25–75%) with whiskers to minimum to maximum of the data. HF, high frequency; HRV, heart rate variability; LF, low frequency; TC, tobacco cigarette; nu, normalized units.

Fig. 6.

Change in hemodynamics after acute TC smoking. Blood pressure, including SBP (A), DBP (B), and MBP (C), and HR (D) significantly increased after smoking the TC (n = 30) compared with sham control (n = 31). Means were compared using a repeated measure (mixed) model adjusting for visit and controlling for nonindependence via random subject effects. Values are mean (25–75%) with whiskers to minimum to maximum of the data. BP, blood pressure; MBP, mean blood pressure; SBP, systolic blood pressure; DBP, diastolic blood pressure; TC, tobacco cigarette; bpm, beats/min.

Fig. 7.

Comparison of changes in hemodynamics after acute TC vs. EC smoking. Changes in SBP (A), DBP (B), and MBP (C) but not HR (D) were significantly greater after smoking 1 TC (n = 30) compared with a comparable exposure to the EC with nicotine (n = 35), as indicated by similar increases in plasma nicotine levels. Means were compared using a repeated measure (mixed) model adjusting for visit and controlling for nonindependence via random subject effects. Values are mean (25–75%) with whiskers to minimum to maximum of the data. BP, blood pressure; ECN, electronic cigarette with nicotine; MBP, mean blood pressure; SBP, systolic blood pressure; DBP, diastolic blood pressure; TC, tobacco cigarette; bpm, beats/min.