Community-acquired pneumonia (CAP) is the most common infection leading to hospitalization in
intensive care units and the most common cause of death associated with infection disease.
Epidemiological studies have shown that respiratory tract infections are associated with an
increased risk for the development of acute cardiovascular and cerebrovascular events.
This link is further supported by studies indicating that influenza vaccination is associated
with a reduced risk of hospitalization for pneumonia as well as heart disease,
cerebrovascular disease and the risk of death from all causes during influenza seasons in
elderly.
Data connecting acute respiratory tract infections and cardiovascular events stemmed almost
exclusively from cross-sectional or retrospective studies and the pathophysiological
relationship between pneumonia and cardiovascular damage is still elusive.
The first aim of the study will be to analyze the prevalence of major adverse cardiac and
cerebrovascular events (MACCE) in patients hospitalized for CAP, followed up for two years
after hospitalization.
During hospitalization myocardial damage will be strictly monitored by measuring cardiac
troponins until discharge.
Cardiac troponins are established markers of myocardial damage. Cardiac troponin elevation is
seen not only in the setting of acute coronary syndromes but also in a variety of conditions
not directly related to flow-limiting coronary stenosis or occlusion of the coronary
arteries, such as pulmonary embolism, sepsis, heart failure and stroke. In these settings, it
is well documented that elevated circulating levels of troponins are associated with poor
prognosis, regardless of underlying disease.
Sparse information exists concerning the significance of troponin elevation during
respiratory tract infections. Most of the studies investigated the role of troponin elevation
in patients admitted in hospital for acutely exacerbated chronic obstructive pulmonary
disease (COPD); only a recent study investigates specifically CAP, showing a correlation
between troponin elevation and oxygenation impairment; however, the underlying mechanism was
not explored.
Inflammation plays a major role in the pathogenesis of coronary artery disease. The increased
concentrations of proinflammatory cytokines together with the activation of coagulation, the
down-regulation of anticoagulant mechanisms and the enhanced platelet aggregation may trigger
atheroma's instability, plaque rupture and thrombus formation.
Systemic coagulation abnormalities including clotting activation and inhibition of
anticoagulant factors have been observed in patients with severe sepsis; in patients with CAP
similar changes have been detected only in the lung compartment. Changes of clotting system
activation are of potential relevance as they could elicit myocardial damage with several
mechanisms including coronary ischemia and/or direct inflammation of cardiac cells.
Concerning this last point it is of interest that Protein C, an anticoagulant factor with
anti-inflammatory property, is reduced in severe sepsis where it correlates with disease
severity and mortality. Accordingly, infusion of recombinant human activated Protein C
improves survival of patients with severe sepsis due to pneumococcal pneumonia.
Until now no data exists about the behavior of Protein C in patients with CAP and its
interplay with myocardial damage.
Moreover no data on platelet reactivity and activation during pneumonia exist. Very limited
data is only available on common viral respiratory tract infections in which enhanced
platelet reactivity has been shown.
The investigators speculated that inhibition of Protein C as well as enhanced platelet
activity may be implicated in myocardial damage in patients with CAP. Therefore the
investigators will perform a prospective study to investigate whether this relationship
exist.
Data obtained could have important clinical consequences: new therapeutic strategies
targeting these systems could prevent myocardial damage and eventually MACCEs in these
patients.