The majority of premature deaths related to tobacco cigarettes (TCs) are attributable to cardiovascular disease, so it is fitting and timely to review the overall cardiovascular impact of electronic cigarettes (ECs), which have recently exploded onto the tobacco product market. Longitudinal studies of EC users are necessary, but not yet available, to answer the question whether cardiovascular disease is lower in chronic EC users compared to TC smokers, so we must rely on biomarker studies. Several biomarkers that portend increased cardiovascular risk, including markers of increased sympathetic nerve activity, oxidative stress and inflammation, vascular dysfunction, and thrombosis, have been reported to be abnormal after EC use, although often not to the degree found in TC smokers. We conclude that if all FDA-certified strategies for TC smoking cessation have been tried without success, then ECs may be a reasonable strategy for TC smoking cessation, but the message to non-TC smokers must be clear and unwavering: non TC-smokers should not use ECs - they are not harmless.

While tobacco cigarette (TC) smoking has continued to drop to all-time lows, the use of electronic cigarettes (ECs), introduced in the US in 2007, has been rising dramatically, especially among youth. In EC emissions, nicotine is the major biologically active element, while levels of carcinogens and harmful combustion products that typify TC smoke are very low or even undetectable. TCs cause cardiovascular harm by activation of inflammatory pathways and oxidative damage, leading to atherogenesis and thrombosis, as well as through sympathetic activation triggering ischemia and arrhythmia. While ECs are generally believed to be safer than TCs, there remain many uncertainties regarding the overall cardiovascular health effects of EC usage. In this review, we discuss the various components of EC smoke and review the potential mechanisms of cardiovascular injury caused by EC use. We also discuss the controversy regarding the increasing epidemic of youth EC use weighed against the use of ECs as a smoking-cessation aid.

Abnormal neurocirculatory control during exercise is one important mechanism leading to exercise intolerance in patients with both end-stage renal disease (ESRD) and earlier stages of chronic kidney disease (CKD). This review will provide an overview of mechanisms underlying abnormal neurocirculatory and hemodynamic responses to exercise in patients with kidney disease. Recent studies have shown that ESRD and CKD patients have an exaggerated increase in blood pressure (BP) during both isometric and rhythmic exercise. Subsequent studies examining the role of the exercise pressor reflex in the augmented pressor response revealed that muscle sympathetic nerve activity (MSNA) was not augmented during exercise in these patients, and metaboreflex-mediated increases in MSNA were blunted, while mechanoreflex-mediated increases were preserved under basal conditions. However, normalizing the augmented BP response during exercise via infusion of nitroprusside (NTP), and thereby equalizing baroreflex-mediated suppression of MSNA, an important modulator of the final hemodynamic response to exercise, revealed that CKD patients had an exaggerated increase in MSNA during isometric and rhythmic exercise. In addition, mechanoreflex-mediated control was augmented, and metaboreceptor blunting was no longer apparent in CKD patients with baroreflex normalization. Factors leading to mechanoreceptor sensitization, and other mechanisms underlying the exaggerated exercise pressor response, such as impaired functional sympatholysis, should be investigated in future studies.

Tobacco cigarette smoking is the most prevalent reversible risk factor for cardiovascular disease in the USA. Electronic cigarettes, invented as an alternative nicotine source for smokers unable or unwilling to stop smoking, have gained skyrocketing popularity, but their cardiovascular risk remains uncertain. Although data recently analysed in a Cochran report do support their superior effectiveness to other forms of nicotine replacement therapies for smoking cessation, electronic cigarettes are also frequently used by non-smokers-especially high school students. There are no long-term outcome studies on the cardiovascular risk of vaping electronic cigarettes, but the effects of electronic cigarettes on known risk factors for cardiovascular disease, including neurohumoural activation, oxidative stress and inflammation, endothelial function and thrombosis, have been studied. In this review, we summarise evidence in humans that supports the notion that while electronic cigarettes may be less harmful than traditional cigarettes, they are not harmless. Additionally, the increasing popularity of vaping marijuana with its unknown cardiovascular risks as well as the outbreak in 2019 of EVALI (electronic cigarette, or vaping, product use-associated lung injury) related to bootlegged vaping products raise further concerns. Before physicians can confidently advise their smoking patients about the role of electronic cigarettes as a means of smoking cessation to lower cardiovascular risk, improved regulation and quality control is necessary.

Purpose

Electronic cigarettes (ECs) are the fastest growing tobacco product in the USA, and ECs, like tobacco cigarettes (TCs), have effects on the cardiovascular autonomic nervous system, with clinical implications. The purpose of this review was to collect and synthesize available studies that have investigated the autonomic cardiovascular effects of EC use in humans. Special attention is paid to the acute and chronic effects of ECs, the relative contributions of the nicotine versus non-nicotine constituents in EC emissions and the relative effects of ECs compared to TCs.

Methods

Using the methodology described in the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement, we conducted a literature search of the Ovid PubMed and Embase databases on 6 December 2019 using keywords in titles and abstracts of published literature. Acute (minutes to hours) and chronic (days or longer) changes in heart rate variability (HRV), heart rate (HR) and blood pressure (BP) were used as estimates of cardiovascular autonomic effects.

Results

Nineteen studies were included in this systematic review, all of which used earlier generation EC devices. Acute EC vaping increased HR and BP less than acute TC smoking. Nicotine but not non-nicotine constituents in EC aerosol were responsible for the sympathoexcitatory effects. The results of chronic EC vaping studies were consistent with a chronic sympathoexcitatory effect as estimated by HRV, but this did not translate into chronic increases in HR or BP.

Conclusions

Electronic cigarettes are sympathoexcitatory. Cardiac sympathoexcitatory effects are less when vaping using the earlier generation ECs than when smoking TCs. Additional studies of the latest pod-like EC devices, which deliver nicotine similarly to a TC, are necessary.

Purpose

Electronic cigarettes (ECs) are the fastest growing tobacco product in the USA, and ECs, like tobacco cigarettes (TCs), have effects on the cardiovascular autonomic nervous system, with clinical implications. The purpose of this review was to collect and synthesize available studies that have investigated the autonomic cardiovascular effects of EC use in humans. Special attention is paid to the acute and chronic effects of ECs, the relative contributions of the nicotine versus non-nicotine constituents in EC emissions and the relative effects of ECs compared to TCs.

Methods

Using the methodology described in the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement, we conducted a literature search of the Ovid PubMed and Embase databases on 6 December 2019 using keywords in titles and abstracts of published literature. Acute (minutes to hours) and chronic (days or longer) changes in heart rate variability (HRV), heart rate (HR) and blood pressure (BP) were used as estimates of cardiovascular autonomic effects.

Results

Nineteen studies were included in this systematic review, all of which used earlier generation EC devices. Acute EC vaping increased HR and BP less than acute TC smoking. Nicotine but not non-nicotine constituents in EC aerosol were responsible for the sympathoexcitatory effects. The results of chronic EC vaping studies were consistent with a chronic sympathoexcitatory effect as estimated by HRV, but this did not translate into chronic increases in HR or BP.

Conclusions

Electronic cigarettes are sympathoexcitatory. Cardiac sympathoexcitatory effects are less when vaping using the earlier generation ECs than when smoking TCs. Additional studies of the latest pod-like EC devices, which deliver nicotine similarly to a TC, are necessary.

Common drugs of misuse, including cannabis, opioids, stimulants, alcohol, and anabolic steroids, have strikingly disparate acute and chronic vascular effects, leading to a wide range of clinical cardiovascular presentations. Acute cannabis smoking has been associated with increased risk for myocardial infarction and ischemic stroke in otherwise healthy young people. However, it remains uncertain if people who exclusively smoke cannabis have increased risk for accelerated atherosclerosis similar to that found in people who exclusively smoke tobacco cigarettes. Cocaine and methamphetamines, both stimulants, increase risk for stroke, myocardial infarction, aortic dissection, and accelerated atherosclerosis, but only methamphetamine use is strongly linked to pulmonary hypertension. Chronic alcohol use is strongly associated with chronic hypertension and hemorrhagic stroke, but perhaps confers a lower risk for myocardial infarction. Finally, anabolic steroid use, presumably through adverse effects on circulating lipids and the hematopoietic system, is associated with increased risk for accelerated atherosclerosis and myocardial infarction. Physicians, especially cardiologists, emergency medicine, and internal medicine physicians, should be familiar with the short- and long-term vascular consequences of use of these substances, thereby ensuring appropriate, specific, and informed counselling and treatment.