Premature Myocardial Infarction: An
updated Overview
Wael Ibrahim Alkhiary
M.B.B.ch- MSc.
Assistant Lecturer of Clinincal Pathology Department, Hemostasis & Thrombosis
Unit, Faculty of Medicine– Mansoura University, Egypt
Dr.Solafa Abd Al-Raoof Al-Sharawy
Professor of Hematology-Clinical Pathology Dept. Hemostasis & Thrombosis
Unit, Faculty of Medicine– Mansoura University, Egypt
Dr. Hanan Ahmed Galal Azzam
Assistant Professor of Clinical Pathology Hemostasis & Thrombosis Unit,
Faculty of Medicine– Mansoura University, Egypt
Dr. Mahmoud Mohammed Abdou Yousuf
Professor of Internal Medicine-Faculty of Medicine – Mansoura University, Egypt
Abstract:
Although myocardial infarction (AMI) is usually the disease of older people
over 45 years of age, an increasing number of younger patients is being recorded.
Additionally, AMI in very young patients aged 35 years and younger has been
poorly described. Besides atherosclerotic coronary artery disease, nonatherosclerotic coronary artery diseases or hypercoagulability should be
considered for young cases of myocardial infarction. The predominance of
angiographic
single-vessel
disease
and
myocardial
infarction with normal coronary arteries in these patients primarily suggest that
premature myocardial infarction probably result from a rapid progressive event,
such as thrombosis or plaque rupture, rather than a gradually evolving process,
such as atherosclerosis. In the future, atherosclerotic burden, hemostatic function,
characterization of stressors and inflammation will be important targets for
research in this group of patients.
Advancing age is a well-acknowledged risk factor for AMI in both men and
women. Although myocardial infarction (MI) is usually the disease of older
people over 45 years of age, an increasing number of younger patients is being
recorded presenting with premature myocardial infarction (1). It is estimated that
about less than 10% of individuals presenting with documented CAD are <45
years of age (2). However, this estimate could vary considerably depending on the
population at study. The increased prevalence in young adults can be partly
attributed to the increased prevalence of risk factors for atherosclerosis among the
population under the age of 40 (3). Besides atherosclerotic coronary artery
disease, non-atherosclerotic coronary artery diseases or hypercoagulability should
be considered for young cases of myocardial infarction (4,5).
Although CHD is an uncommon entity in young patients, it constitutes an
important problem for both the patient and the physician because of the
devastating effect of this disease. More importantly, these patients have different
risk factor profiles, clinical presentations, and prognoses than older patients.
Myocardial infarction presenting at a young age shows a different clinical,
angiographic findings and pathophysiological profile compared to older (2, 6-11).
Additionally, MI in very young patients (aged 35 years and younger) has been
poorly described (12).
Traditional risk factors of CAD seen in the elderly age group do not apply to
younger age group (13-15). Young patients tend to have less extensive
atheromatous lesions and the contribution of prothrombotic and inflammatory
indices may be particularly implicated in the initiation and development of such
atherosclerotic lesions (8,9). It is also known that the long-term prognosis and
functional status of young patients who have acute myocardial infarction (MI) is
not benign (2,6,16).
Myocardial
Infarction with Normal Coronary
Arteries (MINCA)
is
an
important subgroup of myocardial infarction in young patients with a frequency of
at least 3-4% of all myocardial infarctions. The proposed mechanisms for MINCA
include coronary vasospasm, coronary thrombosis in situ or embolization from a
distal source with spontaneous lysis, cocaine abuse, viral myocarditis, aortic
dissection, hypercoagulable states, autoimmune vasculitis and carbon monoxide
poisoning (17).
Moreover, the predominance of angiographic single-vessel disease in these
young patients primarily suggest that premature myocardial infarction probably
result from a rapid progressive event, such as thrombosis or plaque rupture, rather
than a gradually evolving process, such as atherosclerosis, and thus substantiate
the need for an intense and aggressive approach directed towards primary and
secondary preventions of premature cardiovascular disease (11).
It is unknown whether the incidence of MI at an early age incorporates a grave
prognosis or warrants an approach that is different from that used in older patients
(12). Nevertheless, it is unclear whether AMI at the younger age can be
considered an autonomous representation of the infarct process or a more
premature and accelerated expression of the same atherosclerotic process
witnessed in older population. Attempts to study this aspect have been stalled by
the relative infrequency of AMI in the young, as well as the inconsistencies
regarding the definition of youth (10).
Intravascular thrombogenesis is influenced by a complex interplay of
procoagulant, anticoagulant, fibrinolytic, endothelial damage/dysfunction and
inflammatory factors. Abnormalities of these biological systems would contribute
to coronary artery disease presenting at a young age (9). Clinical features
suggesting underlying arterial thrombophilia in Premature CAD include:1)
Previous arterial thrombosis and age ≤ 50 (male) or ≤ 55 (female); 2) Age ≤
55(male) or ≤ 60 (female) with no other traditional risk factors present; 3) No
significant coronary stenosis on angiography; and 4) Age ≤ 55 (male) or ≤ 60
(female) with strong family history (defined as at least one first-degree relative
affected at age 50 years if male or 55 years if female) (4,18). In the future,
atherosclerotic burden, hemostatic function, characterization of stressors and
inflammation will be important targets for research in this group of patients (17).
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