It is commonly believed and nearly completely accepted that cigarette smoking is a
major cardiovascular risk factor for the heart and blood vessels because of the effects
of some compounds, primarily nicotine and carbon monoxide, which are able to harm
the cardiovascular system [1–5]. As a result of this, even passive smoking was included
by the American Heart Association in their group of cardiovascular risk factors for
both adolescents and adults .
Ischemic heart disease and endothelial dysfunction are the main effects observed as
a result of both types of smoking – active and passive smoke exposure [6–9]. These
changes have been clearly documented by clinical, pathological and experimental findings
and, although they are of a different degree and extent in various reports, are reproducible
in the same standardized procedures [10–12]. Functional, but initially reversible,
and structural alterations [11,12], which become over the years firm lesions [13,14],
may often be seen as a consequence of nicotine and carbon monoxide activity.
Briefly, impaired endothelium-dependent vasodilation due to a decrease in nitric oxide
availability; reduced tolerance to exercise in both healthy individuals and individuals
suffering from ischemic heart disease; as well as enhanced heart rate and systolic
blood pressure due to sympathetic nervous system stimulation, carboxyhemoglobin and
increased catecholamine release, are the transient and functional responses observed
during acute exposure to smoking. On the other hand, chronic exposure to tobacco smoke
causes well-established pathological disorders, typically due to carbon monoxide,
consisting of myocardial lesions related to ischemic heart disease, and smoke cardiomyopathy
with intracellular and ultrastructural alterations, primarily identified in experimental
animals . These lead to heart failure of various degrees, which mainly depends
on the duration of the exposure. Moreover, vascular alterations of a degenerative
type, which develop into atherosclerosis and its complications, affect primarily coronary,
carotid and cerebral arteries. In addition, it is worth noting that microcirculation,
because of the structure of resistance arteries, shows arteriosclerosis with enhanced
vascular tone, which is the result of the anatomical lesions in the artery wall characterized
by elastic fiber fragmentation and collagen deposits . Increased arterial stiffness
has also been documented in heavy smokers .
Therefore, it is worth noting that six markers often may change as a consequence of
smoking exposure: endothelium with endothelial dysfunction; artery wall with lesions
of different degrees including up to atherosclerotic plaque formation; blood pressure,
which increases systolic values; heart rate, which closely follows blood pressure
characteristics; myocardial function impairment and structural alterations of myocardial
fibers leading up to necrosis.
Smoking compounds exert cardiovascular damage by direct and mediated mechanisms involving
sympathetic and adrenergic stimulation, increased blood carboxyhemoglobin concentrations
and cellular hypoxia .
By carefully analyzing these data, a fundamental concept emerges: cigarette smoking
always causes the same damage to the heart and blood vessels in all subjects exposed,
although the characteristics and type depend on various factors, primarily duration
of the exposure to smoking toxics. In addition, there is evidence that a strongly
adverse relationship, which is undoubtedly above a mere risk, exists between smoking
and the cardiovascular system.
A risk factor  is associated with the underlying disease with a statistical, but
probabilistic relation. The risk is expressed through a statistical estimate that,
as it becomes closer to 100% – which, however, never can be reached – as a higher
occurrence of the event related is demonstrated. Removing the risk factor can dramatically
reduce, but not completely abolish the rate of the underlying disease since other,
not always well-assessed conditions often contribute to its maintenance.
On the contrary, an etiologic factor  recognizes a link of cause–effect with the
underlying disease, taking into account, however, that the occurrence of the disease
is dependent on the power and potential charge of the pathogenic agent. When it reaches
levels able to determine a disease, this event will always be seen with the same,
even if of a different degree, type of alterations. So for example, when, in an infective
disease with known etiology the causative micro-organism reaches a bacterial charge
able to develop the disease, it always will occur.
It is worth noting, as aforementioned, that cigarette smoking should be considered
an etiologic rather than a major cardiovascular risk factor. Thus smoking leads, in
time, to the occurrence of the same cardiovascular disease, but with different degrees
of changes. These are dependent on several factors such as number of cigarettes smoked,
duration of exposure and health characteristics of the individual, among others. However,
in pathological findings [19–21], when the experimental procedures are the same and
well standardized, the cardiovascular damage from smoking is always reproducible in
Finally, it is worth noting that cigarette smoking itself is able to cause a toxic
disease whose etiologic factor should be considered the tobacco with its chemical
It is the author's personal opinion that a real link of cause–effect may certainly
be identified between cigarette smoking and cardiovascular lesions, primarily ischemic
heart disease and endothelial dysfunction, allowing tobacco smoke to be undoubtedly
considered an etiologic factor of cardiovascular disease.