Pulmonary Embolism From Diagnosis to Treatment


Pulmonary embolism (PE) is the third
greatest cause of mortality from cardiovascular
disease, after myocardial
infarction and cerebrovascular stroke.
From hospital epidemiological data it has
been calculated that the incidence of PE in
the USA is 1 per 1,000 annually.1 The real
number is likely to be larger, since the condition
goes unrecognised in many patients.
Mortality due to PE has been estimated to
exceed 15% in the first three months after
PE is a dramatic and life-threatening
complication of deep venous thrombosis
(DVT). For this reason, the prevention, diagnosis
and treatment of DVT is of special
importance, since symptomatic PE occurs
in 30% of those affected. If asymptomatic
episodes are also included, it is estimated
that 50-60% of DVT patients develop PE.2
DVT and PE are manifestations of the
same entity, namely thromboembolic disease.
If we extrapolate the epidemiological
data from the USA to Greece, which has a
population of about ten million, 20,000 new
cases of thromboembolic disease may be expected
annually. Of these patients, PE will
occur in 10,000, of which 6,000 will have
symptoms and 900 will die during the first
Pathophysiology of pulmonary embolism
The pathophysiology and clinical manifestations
of PE depend upon four main factors:
a) the extent of occlusion of the vascular
tree and the size of the emboli; b) the
patient’s pre-existing cardiopulmonary condition;
c) chemical vasoconstriction due to
the release of serotonin and thromboxane
from platelets that adhere to the embolus,
as well as to fibropeptide B, which is a product
of fibrinogen breakdown; and d) the reflex
vasoconstriction that is likely to occur
as a consequence of pulmonary artery dilatation.