Acute effects of using an electronic nicotine-delivery device (electronic cigarette) on myocardial function: Comparison with the effects of regular cigarettes

BMC Cardiovascular Disorders (Impact Factor: 1.88). 06/2014; 14(1):78. DOI: 10.1186/1471-2261-14-78
Source: PubMed

ABSTRACT Electronic cigarettes have been developed and marketed in recent years as smoking substitutes. However, no studies have evaluated their effects on the cardiovascular system. The purpose of this study was to examine the immediate effects of electronic cigarette use on left ventricular (LV) function, compared to the well-documented acute adverse effects of smoking.

Download full-text


Available from: Konstantinos E Farsalinos, Jul 15, 2014
130 Reads
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Smoking is a major risk factor for a variety of diseases. Electronic cigarettes are battery-operated devices that deliver nicotine to the lungs by evaporation of a liquid. Chronic idiopathic neutrophilia is a condition characterized by elevated white blood cell and neutrophil counts without any underlying disease; smoking has been implicated as a potential cause. A male Caucasian patient, born in 1977, presented in September 2005 with asymptomatic elevation of white blood cell and neutrophil count, and mildly-elevated C-reactive protein levels. He was a smoker since 1996 and was treated with 20 mg/day of simvastatin since 2003 due to hyperlipidemia. Clinical examination, and laboratory and imaging investigations ruled out any infectious, haematological, rheumatological, or endocrine conditions. He was followed-up regularly and was advised to stop smoking. He had 2 unsuccessful attempts to quit smoking; one was unassisted and the second was performed with the use of both varenicline and nicotine replacement therapy (patches). During the subsequent 6.5 years, his leukocyte and C-reactive protein levels were repeatedly elevated; the condition was consistent with chronic idiopathic neutrophilia. In February 2012, he started using electronic cigarettes and he managed to quit smoking within 10 days. After 6 months, laboratory examination showed normalized leukocyte count and C-reactive protein levels, confirmed immediately by a second laboratory and by repeated tests after 1 and 2 months. Smoking cessation with the use of electronic cigarette led to reversal of chronic idiopathic neutrophilia. The daily use of electronic cigarette may help preserve the beneficial effects of smoking cessation.
    Clinical Medicine Insights: Case Reports 01/2013; 6:15-21. DOI:10.4137/CCRep.S11175
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The stretch of cardiac muscle increases developed force in two phases. The first phase, which occurs rapidly, constitutes the well-known Frank-Starling mechanism and it is generally attributed to enhanced myofilament responsiveness to Ca2+. The second phase or slow force response (SFR) occurs gradually and is due to an increase in the calcium transient amplitude as a result of a stretch-triggered autocrine/paracrine mechanism. We previously showed that Ca2+ entry through reverse Na+/Ca2+ exchange underlies the SFR, as the final step of an autocrine/paracrine cascade involving release of angiotensin II/endothelin, and a Na+/H+ exchanger (NHE-1) activation-mediated rise in Na+. In the present review we mainly focus on our three latest contributions to the understanding of this signalling pathway triggered by myocardial stretch: 1) The finding that an increased production of reactive oxygen species (ROS) from mitochondrial origin is critical in the activation of the NHE-1 and therefore in the genesis of the SFR; 2) the demonstration of a key role played by the transactivation of the epidermal growth factor receptor; and 3) the involvement of mineralocorticoid receptors (MR) activation in the stretch-triggered cascade leading to the SFR. Among these novel contributions, the critical role played by the MR is perhaps the most important one. This finding may conceivably provide a mechanistic explanation to the recently discovered strikingly beneficial effects of MR antagonism in humans with cardiac hypertrophy and failure.
    Current Cardiology Reviews 08/2013; 9(3). DOI:10.2174/1573403X113099990034
  • [Show abstract] [Hide abstract]
    ABSTRACT: Atrial fibrillation (AF), the most common cardiac arrhythmia, is an electrocardiographic description of a condition with multiple and complex underlying mechanisms. Oxidative stress is an important driver of structural remodeling that creates a substrate for AF. Oxidant radicals may promote increase of atrial oxidative damage, electrical and structural remodeling, and atrial inflammation. AF and other cardiovascular morbidities activate angiotensin (Ang-II)-dependent and independent cascades. A key component of the renin-angiotensin-aldosterone system (RAAS) is the mineralocorticoid aldosterone. Recent studies provide evidence of myocardial aldosterone synthesis. Aldosterone promotes cardiac oxidative stress, inflammation and structural/electrical remodeling via multiple mechanisms. In HF patients, aldosterone production is enhanced. In patients and in experimental HF and AF models, aldosterone receptor antagonists have favorable influences on cardiac remodeling and oxidative stress. Therapeutic approaches that seek to reduce AF burden by modulating the aldosterone system are likely beneficial but underutilized.
    International journal of cardiology 08/2013; 168(6). DOI:10.1016/j.ijcard.2013.08.022 · 4.04 Impact Factor
Show more