Cardiovascular Journal of Africa: Vol 26 No 3 (May/June 2015)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 26, No 3, May/June 2015 118 AFRICA
occurrence of cardiac arrhythmias in MP users with a high blood
nicotine level may also be high. Furthermore, it is well known
that myocardial ischaemia, systemic inflammation, oxidative
stress and increased sympathetic activity play an important role
in the pathogenesis of atrial fibrillation (AF). In addition, a case
report was found that indicated that the use of MP may lead to
the occurrence of paroxysmal AF.30
Atrial electromechanical delay can be measured by invasive
or non-invasive methods. Recent studies have assessed atrial
electromechanical delay with TDI echocardiography, which is an
alternative, non-invasive method to invasive electrophysiological
studies.31,32 In previous studies, it was found that atrial conduction
time measured by TDI was an independent predictor of
new-onset or recurrence of AF.13,31
LA mechanical function consists of reservoir, and passive and
active emptying functions at different stages of the cardiac cycle.
The reservoir function takes effect during ventricular systole,
the passive emptying function in early diastole and the active
emptying function during ventricular diastole in the presence
of sinus rhythm. When LV dysfunction develops, the LA may
possibly preserve adequate cardiac output by regulation of the
reservoir and booster pump function.
We demonstrated that LA mechanical function was impaired
in MP users and smokers, but there was no significant difference
between the MP users and cigarette smokers. LAPEF was
significantly decreased and LAAEV was significantly increased
in the MP group but not in the control group. LAAEF was
significantly increased in the cigarette smoking group but not
in the control group. LAPEF is related to elevated end-diastolic
LV pressure, and the increase in LAAEV is associated with a
compensatory mechanism in LA contraction. These findings
may be an indirect indication that nicotine has greater effects on
the atrial tissue over time.
Additionally, Eroglu et al. demonstrated that chronic
cigarette smoking caused changes in long-axis systolic and
diastolic function of the right and left ventricles in healthy
young subjects.33 Our study population consisted of relatively
young subjects. LA electromechanical and mechanical functions
were impaired in our smokers and MP users without overt
cardiovascular disease, probably due to the negative effects
of nicotine. This may be an early sign of atrial dysfunction
preceding AF in these subjects.
Study limitations
The major limitation of our study was its cross-sectional design
and lack of follow up of the patients. The subjects could not
be followed up for episodes of arrhythmia, therefore, we do not
know whether parameters of prolonged atrial electromechanical
delay and impaired LA mechanical function can be used for the
prediction of arrhythmias and heart failure in MP users and
smokers. For these reasons, long-term follow up and large-scale
prospective studies are needed to determine the predictive value
of prolonged atrial electromechanical delay parameters and LA
mechanical function in this population.
The absence of detailed parameters of diastolic function
and measurement of blood nicotine levels were also potential
limitations of our study. Furthermore, factors such as the
subjects’ diet and exercise habits, which may affect diastolic
function, could not be evaluated in our study.
Conclusion
On the basis of our findings, we suggest that atrial
electromechanical coupling intervals were prolonged and left
atrial mechanical function was impaired in MP users and
cigarette smokers, but there was no significant difference between
MP users and cigarette smokers. Furthermore, the amount
of MP use and cigarette smoking (pack years) was correlated
with LAAEV and LAAEF. These findings may be markers of
subclinical cardiac involvement and a risk for AF.
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