Coronary thrombosis is formation of a blood clot inside a blood vessel of heart. Thrombosis in the heart can pave to a myocardial infarction. Coronary Thrombosis is general in high blood pressure patient, diabetic, and victims of atherosclerosis. The treatment is decreasing pain, improving blood flow to the heart muscle, and preventing irreversible damage to the heart muscle. Coronary Thrombosis in the heart can pave to a myocardial infarction. Coronary thrombosis and myocardial infarction are sometimes availed as synonyms, although this is technically much inaccurate as the thrombosis refers to the blocking of blood vessels, while the infarction refers to the tissue death due to the consequent loss of blood flow to the heart tissue. The heart comprises many connecting blood vessels, and depending upon the location of the thrombosis, the infarction may cause no symptoms [1, 2] (Fig: 1 &2). Fig: 1. Coronary Thrombosis Fig: 2. Heart with blood clot Facts of Coronary Thrombosis Studies in Thrombosis and Hemostasis, Thrombosis and Haemostasis, Arteriosclerosis, Thrombosis, and Vascular Biology, Clinical and Applied Thrombosis/Hemostasis were a key investigation topics and research are carried out to encounter problems in these fields

1. Coronary Thrombosis: Clinical
Manifestation & Case Study
BY
Dr. S.SREEREMYA
FACULTY OF BIOLOGY

3. • INTRODUCTION
• Coronary thrombosis is formation of a blood clot inside a blood vessel of heart. Thrombosis in the
heart can pave to a myocardial infarction. Coronary Thrombosis is general in high blood pressure
patient, diabetic, and victims of atherosclerosis. The treatment is decreasing pain, improving blood
flow to the heart muscle, and preventing irreversible damage to the heart muscle.
• Coronary Thrombosis in the heart can pave to a myocardial infarction. Coronary thrombosis and
myocardial infarction are sometimes availed as synonyms, although this is technically much
inaccurate as the thrombosis refers to the blocking of blood vessels, while the infarction refers to
the tissue death due to the consequent loss of blood flow to the heart tissue. The heart comprises
many connecting blood vessels, and depending upon the location of the thrombosis, the infarction
may cause no symptoms [1, 2] (Fig: 1 &2).
• Fig: 1. Coronary Thrombosis
• Fig: 2. Heart with blood clot
• Facts of Coronary Thrombosis
• Studies in Thrombosis and Hemostasis, Thrombosis and Haemostasis, Arteriosclerosis, Thrombosis,
and Vascular Biology, Clinical and Applied Thrombosis/Hemostasis were a key investigation topics
and research are carried out to encounter problems in these fields

4. • Health surveys reported of a case of intracoronary thrombosis causing significant
myocardial ischemia during elective coronary angiography, treated promptly with
the local brinolytic therapy, in a patient with severe vasovagal reaction during
femoral artery puncture [3].
• CORONARY ARTERY DISEASES
• Understanding of the pathophysiology of coronary artery disease (CAD) has
undergone quiet a remarkable evolution. Researchers review how these advances
have altered our concepts of and clinical approaches to both the chronic and acute
phases of CAD. Previously considered that a cholesterol storage disease, recently it
was assessed that atherosclerosis as an inflammatory disorder [4]. The
appreciation of arterial remodelling (compensatory enlargement) has typically
expanded attention beyond stenosis evident by angiography to encompass the
biology of nonstenotic plaques. Revascularization effectively relieves ischemia, but
we now recognize the need to attend to non-obstructive lesions as well.
Aggressive management of modifiable risk factors to reduces cardiovascular events
and should accompany appropriate revascularization. Researchers now recognize
that disruption of plaques that may not produce critical stenosis causes many
acute coronary syndromes (ACS). The disrupted plaque represents a “solid-state”
stimulus to the thrombosis.

5. • Alterations in circulating prothrombotic or antifibrinolytic
mediators in “fluid phase” of the blood can also predispose
toward the ACS. Recent results have quietly established the
multiplicity of “high-risk” plaques and the widespread
nature of inflammation in patients prone to develop ACS.
These findings challenge our traditional view of coronary
atherosclerosis as a segmental or localized disease. Thus,
the treatment of ACS should involve 2 overlapping phases:
first, addressing the culprit lesion, and second, aiming at
rapid “stabilization” of the other plaques that may produce
recurrent events. The concept of the “interventional
cardiology” must typically expand beyond mechanical
revascularization to embrace preventive interventions that
forestall future events [5]

6. • Clinical and morphologic findings are delineated in a 22 year old man with
prolonged thrombocytosis, and coronary and splenic arterial thrombi
causing myocardial and splenic infarcts. The absence of the pre-existent
extensive coronary atherosclerosis, the presence of thrombus in more
than one epicardial artery and in several intramural coronary arteries, the
presence of arterial thrombosis in a noncoronary artery (splenic) and the
absence of another apparent cause of arterial thrombisis are evidences
that the intra-arterial clotting in this patient was related to the severe
thrombocytosis. A review of the reported cases of vascular occlusion allied
with thrombocytosis indicates that thrombi have infrequently been
confirmed as the mechanism of the vascular occlusion. Although the
frequency of vascular thrombisis in patients with thrombocytosis has not
yet been established, it is clear that vascular thrombosis can be a
consequence of thrombocytosis and, as it is mainly demonstrated by the
present patient, that the coronary artery may be the site of the vascular
occlusion, a here to fore unconfirmed event [6

7. • Research & Review: Management of
Cardiovascular and Orthopedic Complications,
Coronary Thrombosis: Clinical Manifestation &
Case Study S.Sreeremya, 2018.Vol1(1):1-5.