Acute Coronary Syndrome Clinical Trial
Official title:
Platelets Count Alterations in Patients With Acute Coronary Syndrome: Epidemiology and Prognostic Role
Platelet count alterations (thrombocytopenia and thrombocytosis) are a common condition in
patients hospitalised for acute coronary syndrome (ACS), both at disease onset and in the
following recovery phase.1-3 Different factors can explain this phenomenon. Thrombocytopenia
could be either due to neurohormonal activation and the inflammatory process following
myocardial necrosis leading to increased macrophage activation with increased clearance of
platelets, or to an immuno-modulated mechanism caused by the administration of
antiaggregant/anticoagulant drugs (heparin, glycoprotein IIb/IIIa inhibitors, P2Y12
inhibitors).
Even the invasive treatment of coronaropathy during hospitalization, with angioplasty and
stent implantation procedures and/or the eventual implantation of temporary mechanical blood
circulation assistant devices [aortic counterpulsation, Impella, ECMO (Extracorporeal
Membrane Oxygenation)], could further favour the phenomenon.4 Vice versa, thrombocytosis
occurring during ACS has a reactive origin, caused by increased IL-6 production which, in
turn, leads to an increase in thrombopoietin formation in the liver, causing a consequent
stimulatory activity on megakaryocytes.2 Different studies have demonstrated a significant
correlation between platelets count disorders and patient outcome (survival during
hospitalization and in the immediate follow-up).5-11 This association has, however, often
been considered an epiphenomenon of the underlying pathology. Platelets count alterations
are, indeed, usually consensual to other hemogram alterations (anaemia and neutropenia), an
indication of a coexisting medullar insufficiency (thrombocytopenia) or other heterogenous
diseases such as cancer, iron deficiency or immuno-modulated diseases, usually associated
with an increase in comorbidity indexes.12 Those alterations, moreover, can usually influence
changes to the therapeutic approach (reduction/suspension of recommended standard therapies)
and further condition the prognosis.13 Since a few years, the investigators have been
established a cardiac-haematological collaboration aiming at finding early alterations in
platelets count or, more generally, in cell blood count (CBC), collegially evaluating those
alterations with a cardiologist and a haematologist (even in mild cases) and scheduling, on
the basis of the aforementioned evaluations, a more precise and tailored therapeutic approach
toward the specific patient needs in order to minimize the downgrading of potentially
life-saving therapies.14 Until now, however, no precise evaluation of the impact that this
strategy had in influencing the therapeutic approach and in improving patient outcome in our
population has been performed.
A retrospective evaluation of consecutive ACS patients, their clinical, biohumoral and
procedural characteristics and the adopted pharmacological treatments is, therefore, an
important epidemiologic tool for the characterization of this phenomenon and for identifying
potential associations which could suggest possible future therapeutic developments.
Even the invasive treatment of coronaropathy during hospitalization, with angioplasty and
stent implantation procedures and/or the eventual implantation of temporary mechanical blood
circulation assistant devices [aortic counterpulsation, Impella, ECMO (Extracorporeal
Membrane Oxygenation)], could further favour the phenomenon. Vice versa, thrombocytosis
occurring during ACS has a reactive origin, caused by increased IL-6 production which, in
turn, leads to an increase in thrombopoietin formation in the liver, causing a consequent
stimulatory activity on megakaryocytes. Different studies have demonstrated a significant
correlation between platelets count disorders and patient outcome (survival during
hospitalization and in the immediate follow-up). This association has, however, often been
considered an epiphenomenon of the underlying pathology. Platelets count alterations are,
indeed, usually consensual to other hemogram alterations (anaemia and neutropenia), an
indication of a coexisting medullar insufficiency (thrombocytopenia) or other heterogenous
diseases such as cancer, iron deficiency or immuno-modulated diseases, usually associated
with an increase in comorbidity indexes. Those alterations, moreover, can usually influence
changes to the therapeutic approach (reduction/suspension of recommended standard therapies)
and further condition the prognosis. Since a few years,the investigators have been
established a cardiac-haematological collaboration aiming at finding early alterations in
platelets count or, more generally, in cell blood count (CBC), collegially evaluating those
alterations with a cardiologist and a haematologist (even in mild cases) and scheduling, on
the basis of the aforementioned evaluations, a more precise and tailored therapeutic approach
toward the specific patient needs in order to minimize the downgrading of potentially
life-saving therapies. Until now, however, no precise evaluation of the impact that this
strategy had in influencing the therapeutic approach and in improving patient outcome in our
population has been performed.
A retrospective evaluation of consecutive ACS patients, their clinical, biohumoral and
procedural characteristics and the adopted pharmacological treatments is, therefore, an
important epidemiologic tool for the characterization of this phenomenon and for identifying
potential associations which could suggest possible future therapeutic developments.
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