Acute myocardial infarction (MI) indicates irreversible myocardial injury resulting in

necrosis of a significant portion of myocardium (generally >1 cm). The term "acute" denotes
infarction less than 3-5 days old, when the inflammatory infiltrate is primarily neutrophilic.
Acute MI may be either of the nonreperfusion type, in which case the obstruction to blood
flow is permanent, or of the reperfusion type, in which the obstruction or lack of blood flow
is long enough in duration (generally hours) but is reversed or restored after myocardial cell
death occurs.

Go to Myocardial Infarction and Right Ventricular Infarction for complete information on

these topics.

Pathophysiology
Acute myocardial infarction (MI) generally refers to segmental (regional) myocardial
necrosis, typically endocardium-based, secondary to occlusion of an epicardial artery. In
contrast, concentric subendocardial necrosis may result from global ischemia and reperfusion
in cases of prolonged cardiac arrest with resuscitation. Areas of myocardial infarction may be
subepicardial if there is occlusion of smaller vessels by thromboemboli originating from
coronary thrombi. In the majority of patients, there is obstructive coronary disease at
angiography.

The area of infarct occurs in the distribution of the occluded vessel. Left main coronary artery
occlusion generally results in a large anterolateral infarct, whereas occlusion of the left
anterior descending coronary artery causes necrosis limited to the anterior wall. There is often
extension to the anterior portion of the ventricular septum with proximal left coronary
occlusions.

In hearts with a right coronary dominance (with the right artery supplying the posterior
descending branch), a right coronary artery occlusion causes a posterior (inferior) infarct.
With a left coronary dominance (about 15% of the population), a proximal circumflex
occlusion will infarct the posterior wall; in the right dominant pattern, a proximal obtuse
marginal thrombus will cause a lateral wall infarct only, and the distal circumflex is a small
vessel.

The anatomic variation due to microscopic collateral circulation, which is not evident at
autopsy, plays a large factor in the size of necrosis and distribution. Unusual patterns of
supply to the posterior wall, such as wraparound left anterior descending or posterior
descending artery supplied by the obtuse marginal artery, may also result in unexpected areas
of infarct in relation to the occluded proximal segment.

A proximal occlusion at the level of an epicardial artery results in a typical distribution that
starts at the subendocardium and progresses towards the epicardium (the so-called wavefront
phenomenon).[1] Therefore, an area of necrosis or scarring is considered to have an "ischemic
pattern" if it is largest at the endocardium, with a wedge-shaped extension up to the epicardial
surface.

Ischemic injury, however, may be located in the mid myocardium or even the subepicardium
if the level of the coronary occlusion is distal within the myocardium. Therefore, in cases of
thromboemboli from epicardial thrombi (especially plaque erosions), there may be patchy
infarction, often associated with visible thrombi within the myocardial vessels, not centered
in the endocardium but occurring anywhere in the myocardium, including midepicardial and
subepicardial locations.

Patofisiologi
Infark miokard akut (MI) umumnya mengacu segmental (regional) nekrosis miokard, biasanya
berbasis endocardium, sekunder oklusi arteri epikardial. Sebaliknya, konsentris nekrosis
subendokard mungkin akibat dari iskemia global dan reperfusi dalam kasus-kasus serangan jantung
yang berkepanjangan dengan resusitasi. Area infark miokard mungkin subepicardial jika ada oklusi
pembuluh kecil dengan thromboemboli berasal dari trombus koroner. Pada sebagian besar pasien,
ada penyakit koroner obstruktif pada angiografi.
Luas infark terjadi dalam distribusi kapal tersumbat. Meninggalkan oklusi arteri koroner utama
umumnya menghasilkan infark anterolateral besar, sedangkan oklusi dari anterior kiri turun arteri
koroner menyebabkan nekrosis terbatas pada dinding anterior. Ada sering perluasan ke bagian
anterior septum ventrikel dengan proksimal sumbatan koroner kiri.
Dalam hati dengan dominasi koroner kanan (dengan arteri yang tepat memasok posterior turun
cabang), oklusi arteri koroner kanan menyebabkan posterior (inferior) infark. Dengan dominasi
koroner kiri (sekitar 15% dari populasi), oklusi sirkumfleksa proksimal akan infark dinding posterior;
dalam pola dominan yang tepat, trombus marjinal tumpul proksimal akan menyebabkan dinding
infark lateral yang hanya, dan sirkumfleksa distal adalah kapal kecil.
Variasi anatomi karena sirkulasi kolateral mikroskopis, yang tidak jelas pada otopsi, memainkan
faktor besar dalam ukuran nekrosis dan distribusi. Pola yang tidak biasa dari pasokan ke dinding
posterior, seperti sampul kiri turun anterior atau posterior turun arteri dipasok oleh arteri marjinal
tumpul, juga dapat mengakibatkan daerah yang tak terduga dari infark dalam kaitannya dengan
segmen proksimal tersumbat.
Sebuah oklusi proksimal pada tingkat dari hasil arteri epikardial dalam distribusi khas yang dimulai
pada subendokardium dan berkembang menuju epikardium (yang disebut fenomena muka
gelombang). [1] Oleh karena itu, daerah nekrosis atau jaringan parut dianggap memiliki "Pola
iskemik" jika terbesar di endocardium, dengan ekstensi berbentuk baji ke permukaan epicardial.
Cedera iskemik, bagaimanapun, mungkin terletak di pertengahan miokardium atau bahkan
subepicardium jika tingkat oklusi koroner distal dalam miokardium. Oleh karena itu, dalam kasus-
kasus thromboemboli dari trombus epikardial (erosi terutama plak), mungkin ada infark tambal
sulam, sering dikaitkan dengan trombus terlihat dalam pembuluh miokard, tidak berpusat di
endocardium tetapi terjadi di mana saja di miokardium, termasuk lokasi midepicardial dan
subepicardial.

Etiology
Acute myocardial infarction (MI) results from lack of oxygen supply to the working
myocardium. Regional infarcts are due to lack of blood flow that occurs when an epicardial
artery is blocked by atheroma or thrombus, or other obstructions. Global subendocardial
infarcts occur when there is lack of oxygenation despite circulation—for example, when there
is a respiratory arrest followed by prolonged hypoxemia.

Autopsies of hospital inpatients dying of acute regional MI reveal an acute thrombus

overlying atherosclerotic plaque in more than 95% of cases when the coronary arteries are
carefully inspected.[2] In the remaining hearts, there will be severe coronary diseases without
thrombus.
Rare causes of acute MI include no apparent cause (usually attributed to coronary spasm),
coronary embolism (varied causes, including valve vegetations and tumors), spontaneous
coronary artery dissections, congenital anomalies of the coronary origins, and thrombosis in
nonatherosclerotic normal coronary arteries (hypercoagulable states).

Risk factors

There is a known genetic predisposition to coronary artery disease that leads to acute MI. In
general, about 50-85% of the risk of coronary atherosclerosis is secondary to acquired
conditions. The remainder is secondary to genetic polymorphisms, which involve pathways
of inflammation, lipid metabolism, coagulation, the renin-angiotensin-aldosterone system,
and other components of atherogenesis.[3, 4]

Epidemiology
Acute myocardial infarctions (MIs) are common. In the United States, they result in the
hospitalization of approximately 4 men and 2 women per 1000 population each year.[5]

Etiologi
Akut infark miokard (MI) hasil dari kurangnya pasokan oksigen ke miokardium kerja. Infark
regional karena kurangnya aliran darah yang terjadi ketika arteri epikardial diblokir oleh
ateroma atau trombus, atau penghalang lainnya. Infark subendokard global terjadi ketika ada
kekurangan oksigenasi meskipun contoh sirkulasi-untuk, ketika ada pernapasan diikuti oleh
hipoksemia berkepanjangan.
Otopsi pasien rawat inap rumah sakit sekarat MI daerah akut mengungkapkan trombus akut
atasnya plak aterosklerosis di lebih dari 95% dari kasus-kasus ketika arteri koroner secara
hati-hati diperiksa. [2] Dalam hati yang tersisa, akan ada penyakit koroner berat tanpa
trombus.
Penyebab yang jarang dari MI akut termasuk tidak ada penyebab yang jelas (biasanya
dikaitkan dengan kejang koroner), emboli koroner (penyebab bervariasi, termasuk vegetasi
katup dan tumor), pembedahan arteri koroner spontan, anomali kongenital dari asal-usul
koroner, dan trombosis di nonatherosclerotic arteri koroner normal ( negara hiperkoagulasi).
Faktor risiko
Ada kecenderungan genetik yang dikenal dengan penyakit arteri koroner yang mengarah ke
MI akut. Secara umum, sekitar 50-85% dari risiko aterosklerosis koroner adalah sekunder
untuk kondisi yang diperoleh. Sisanya adalah sekunder untuk polimorfisme genetik, yang
melibatkan jalur peradangan, metabolisme lipid, koagulasi, sistem renin-angiotensin-
aldosteron, dan komponen lain dari aterogenesis. [3, 4]
Epidemiologi
Infark miokard akut (MI) yang umum. Di Amerika Serikat, mereka menghasilkan rawat inap
sekitar 4 pria dan 2 wanita per 1000 penduduk setiap tahun. [5]

Clinical Features
The symptoms of acute myocardial infarction (MI) are chest pain, which may radiate to the
arm or jaw, sweating, nausea, and chest tightness or pressure. The diagnosis rests on
laboratory findings of myocardial necrosis, which causes leakage of myocardial enzymes,
such as troponin, into the circulating blood. Acute infarcts are divided by
electrocardiographic findings into ST-elevation myocardial infarction (STEMI) and non ST-
elevation infarction (non-STEMI).

STEMI is usually the result of blockage of a coronary artery with large elevations of cardiac
enzymes in the serum and eventually result in Q waves on the electrocardiogram. In contrast,
non-STEMI, which overlaps with the acute coronary syndrome unstable angina, causes
modest elevations of cardiac enzymes in the serum and pathologically shows small or patchy
areas of necrosis. Q waves do not develop in non-STEMI

Gambaran Klinis
Gejala-gejala infark miokard akut (MI) adalah nyeri dada, yang dapat menyebar ke lengan
atau rahang, berkeringat, mual, dan sesak dada atau tekanan. Diagnosis bersandar pada
temuan laboratorium nekrosis miokard, yang menyebabkan kebocoran enzim miokard,
seperti troponin, ke dalam sirkulasi darah. Infark akut dibagi dengan temuan
elektrokardiografi ke ST-elevasi infark miokard (STEMI) dan non ST-elevasi infark (non-
STEMI).
STEMI biasanya merupakan hasil dari penyumbatan arteri koroner dengan peningkatan besar
enzim jantung dalam serum dan akhirnya mengakibatkan gelombang Q pada
elektrokardiogram. Sebaliknya, non-STEMI, yang tumpang tindih dengan koroner sindrom
akut angina tidak stabil, menyebabkan peningkatan sederhana enzim jantung dalam serum
dan patologis menunjukkan daerah kecil atau tambal sulam nekrosis. Q gelombang tidak
berkembang di non-STEMI

Gross Findings
The earliest change that can be grossly discerned in the evolution of acute myocardial
infarction (MI) is pallor of the myocardium, which is visible 12 hours or later after the onset
of irreversible ischemia. The gross detection of infarction can be enhanced by the use of
tetrazolium salt solutions, which form a colored precipitate on gross section of fresh heart
tissue in the presence of dehydrogenase-mediated activity. Myocardial necrosis can be
detected as early as 2-3 hours in dogs and in humans by this method.

In nonreperfused MI, the infarcted area is well defined at 2-3 days, with a central area of
yellow discoloration surrounded by a thin rim of highly vascularized hyperemia (see the first
image below). In reperfused MI, the infarcted region appears red because of trapping of the
red cells and hemorrhage from ruptured necrotic capillaries (see the second image below).

Temuan bruto
Perubahan awal yang dapat terlalu dilihat dalam evolusi infark miokard akut (MI) adalah pucat
miokardium, yang terlihat 12 jam atau lebih setelah onset iskemia irreversible. Deteksi kotor infark
dapat ditingkatkan dengan penggunaan tetrazolium larutan garam, yang membentuk endapan
berwarna pada bagian kotor jaringan jantung segar dengan adanya aktivitas dehidrogenase-
dimediasi. Nekrosis miokard dapat dideteksi sedini 2-3 jam pada anjing dan manusia dengan metode
ini.
Dalam nonreperfused MI, daerah infark didefinisikan dengan baik di 2-3 hari, dengan daerah pusat
perubahan warna kuning dikelilingi oleh rim tipis hiperemia sangat vascularized (lihat gambar
pertama di bawah ini). Dalam reperfusi MI, wilayah infark tampak merah karena perangkap dari sel
darah merah dan perdarahan dari pecah kapiler nekrotik (lihat gambar kedua di bawah).
days, there is a zone of Acute myocardial infarct. At 3 yellow necrosis surrounded by darker
hyperemic borders. The arrow points to a transmural infarct in the posterior wall of the left
ventricle, in this short axis slice through the left and right ventricular chambers.
hari, ada zona infark miokard akut. Pada 3 nekrosis kuning dikelilingi oleh perbatasan hyperemic
gelap. Panah menunjuk ke sebuah infark transmural di dinding posterior ventrikel kiri, dalam hal ini
sepotong sumbu pendek melalui ruang ventrikel kiri dan kanan

Acute myocardial infarction, reperfusion type. In this case, the infarct is diffusely
hemorrhagic. There is a rupture track through the center of this posterior left ventricular
transmural infarct. The mechanism of death was hemopericardium.

At 5-7 days, the regions are much more distinct, with a central soft area and a depressed
hyperemic border. At 1-2 weeks, the infarct begins to appear depressed, especially at the
margins where organization takes place, and the borders take on a white hue.

Healing may be complete as early as 4-6 weeks for small infarcts or may take as long as 2-3
months for large ones (see the images below). Areas of congestion and vasodilatation within
healed scars may appear hemorrhagic. In these cases, mottled myocardium that gives the
gross appearance of acute MI may, upon histologic examination, demonstrate only old
fibrosis.

Infark miokard akut, jenis reperfusi. Dalam hal ini, infark adalah difus hemoragik. Ada trek pecah
melalui pusat posterior ini ventrikel kiri infark transmural. Mekanisme kematian adalah
hemopericardium.
Pada 5-7 hari, daerah jauh lebih berbeda, dengan area yang lembut tengah dan perbatasan
hyperemic tertekan. Pada 1-2 minggu, infark mulai muncul depresi, terutama pada margin mana
organisasi berlangsung, dan perbatasan mengambil rona putih.
Penyembuhan mungkin lengkap sedini 4-6 minggu untuk infark kecil atau mungkin memakan waktu
selama 2-3 bulan untuk yang besar (lihat gambar di bawah). Area kemacetan dan vasodilatasi dalam
bekas luka sembuh mungkin muncul hemoragik. Dalam kasus ini, berbintik-bintik miokardium yang
memberikan penampilan kotor MI akut dapat, setelah pemeriksaan histologis, menunjukkan hanya
fibrosis tua.

Healing myocardial infarction, lateral left ventricle. In this heart, there is a variegated or
mottled appearance to the lateral left ventricle (left). This infarct began 19 days prior to
death.

Early healed myocardial

infarction, anterior septum. There is a glistening gelatinous appearance to this infarction, that
occurred 6 weeks prior to death, from embolization during valve surgery.

Healed infarcts are white from the scarring, and the ventricular wall may be thinned
(aneurysmal), especially in transmural infarction (see the image below). In general, infarcts
that occupy more than 50% of the ventricular wall, from the subendocardial to the epicardial
surface, are considered transmural and are associated with Q-wave changes on
electrocardiography.
 Healed myocardial infarction,
anterior left ventricle. There is diffuse scarring (white) with marked thinning of the ventricle
(aneurysm).

Microscopic Findings
Microscopically, the diagnosis of acute myocardial infarction (MI) rests on the presence of
necrotic myocardium, with an interface of acute inflammation separating it from viable
myocardium. Areas of inflammation with a scar or areas of mummified dead myocardium
bordered by granulation tissue do not indicate the presence of acute MI.

The earliest morphologic characteristic of MI occurs between 12 and 24 hours after the onset
of chest pain. Hypereosinophilia of the cytoplasm as assessed by hematoxylin-eosin staining
is characteristic of myocardial ischemia (see the first image below). Neutrophil infiltration is
present by 24 hours at the border areas (see the second image below).

Temuan mikroskopis
Mikroskopis, diagnosis infark miokard akut (MI) bertumpu pada keberadaan miokardium nekrotik,
dengan antarmuka peradangan akut memisahkannya dari miokardium yang layak. Area peradangan
dengan bekas luka atau daerah dari mumi miokardium mati berbatasan dengan jaringan granulasi
tidak menunjukkan adanya MI akut.
Karakteristik morfologi awal MI terjadi antara 12 dan 24 jam setelah onset nyeri dada.
Hipereosinofilia dari sitoplasma yang dinilai oleh hematoxylin-eosin pewarnaan adalah karakteristik
dari iskemia miokard (lihat gambar pertama di bawah ini). Infiltrasi neutrofil hadir dengan 24 jam di
daerah perbatasan (lihat gambar kedua di bawah).
 Acute myocardial infarct. The
earliest change is hypereosinophilia (above) with an intense pink cytoplasm. There is no
inflammation at border between the necrotic myocardium and the viable myocardium (left
and below), indicating that the necrosis is about 12-24 hours in age.

Acute myocardial infarct. After

24 hours, there is a neutrophilic infiltrate at the border of the infarct. Viable myocardium is at
the left, and neutrophils with apoptosis (karyorrhexis) are seen infiltrating the necrotic
muscle. This patient experienced abdominal pain 35 hours prior to death.

As the infarct progresses between 24 and 48 hours, coagulation necrosis is established, with
various degrees of nuclear pyknosis, early karyorrhexis, and karyolysis. The myocyte
striations are preserved and the sarcomeres elongate. The border areas show prominent
neutrophil infiltration by 48 hours.

At 3-5 days, the central portion of the infarct shows loss of myocyte nuclei and striations; in
smaller infarcts, neutrophils invade the infarct and fragment, resulting in more severe
karyorrhexis (nuclear dust). By 5-7 days, macrophages and fibroblasts begin to appear in the
border areas. By 1 week, neutrophils decline and granulation tissue is established (see the
image below), with neocapillary invasion and lymphocytic and plasma cell infiltration.
24 jam, ada menyusup neutrophilic di perbatasan infark. Miokardium layak adalah di sebelah kiri,
dan neutrofil dengan apoptosis (karyorrhexis) terlihat infiltrasi otot nekrotik. Pasien ini mengalami
sakit perut 35 jam sebelum kematian.
Sebagai infark berlangsung antara 24 dan 48 jam, koagulasi nekrosis didirikan, dengan berbagai
tingkat pyknosis nuklir, karyorrhexis awal, dan karyolysis. Striations miosit yang diawetkan dan
sarkomer memanjang. Daerah perbatasan menunjukkan menonjol neutrofil infiltrasi oleh 48 jam.
Pada 3-5 hari, bagian tengah infark menunjukkan hilangnya inti miosit dan striations; di infark yang
lebih kecil, neutrofil menyerang infark dan fragmen, menghasilkan karyorrhexis lebih parah (debu
nuklir). 5-7 hari, makrofag dan fibroblas mulai muncul di daerah perbatasan. Dengan 1 minggu,
neutrofil menurun dan jaringan granulasi didirikan (lihat gambar di bawah), dengan invasi
neocapillary dan limfositik dan infiltrasi sel plasma.

Healing myocardial infarct. This patient died 8 days after experiencing sudden chest pain at
rest. There is a large area of necrosis with hypereosinophilia of myocytes, with a rim of
viable myocardium at the very bottom. At the border, there is chronic inflammation with
early granulation tissue, with ingrowth of endothelial cells.

Although lymphocytes may be seen as early as 2-3 days, they are not prominent in any stage
of infarct evolution. Eosinophils may be seen within the inflammatory infiltrate but are
present in only 24% of infarcts. There is phagocytic removal of the necrotic myocytes by
macrophages, and pigment is seen within macrophages.[6]

By the second week, fibroblasts are prominent, but they may appear as early as 1 week at the
periphery of the infarct (see the image below). There is continued removal of the necrotic
myocytes as the fibroblasts are actively producing collagen, and angiogenesis occurs in the
area of healing.

Penyembuhan infark miokard. Pasien ini meninggal 8 hari setelah mengalami nyeri dada yang tiba-
tiba saat istirahat. Ada area besar nekrosis dengan hipereosinofilia miosit, dengan tepi miokardium
yang layak di bagian paling bawah. Di perbatasan, ada peradangan kronis dengan awal jaringan
granulasi, dengan ingrowth sel endotel.
Meskipun limfosit dapat dilihat sedini 2-3 hari, mereka tidak menonjol dalam setiap tahap infark
evolusi. Eosinofil dapat dilihat dalam infiltrasi inflamasi tetapi yang hadir hanya 24% dari infark. Ada
penghapusan fagosit dari miosit nekrotik oleh makrofag, dan pigmen terlihat dalam makrofag. [6]
Pada minggu kedua, fibroblas yang menonjol, tetapi mereka mungkin muncul pada awal 1 minggu di
pinggiran infark (lihat gambar di bawah). Ada penghapusan lanjutan dari miosit nekrotik sebagai
fibroblast secara aktif memproduksi kolagen, dan angiogenesis terjadi di daerah penyembuhan.

Healing myocardial infarct. At 10

days to 2 weeks, there is chronic inflammation, hemosiderin-laden macrophages, and early
fibroblasts without significant collagen deposition.

Healing continues and, depending on the extent of necrosis, may be complete as early as 4
weeks or may require 8 weeks or longer to complete (see the image below). The central area
of large infarction may remain unhealed and show mummified myocytes for extended
periods, even though the infarct borders are completely healed.

Healed myocardial infarct. At 3 months, there is dense scar, which is blue on this Masson
trichrome stain. This infarct was subendocardial, in the posterior left ventricle near the
ventricular septum.

The histologic dating of MI may be important from a medicolegal point of view. There is no
way of determining infarct age exactly, however, both because the histologic features that
define the stages of repair overlap and because infarcts may enlarge, resulting in
heterogeneity from one area to another. The border zone between necrotic myocardium and
viable myocardium is the focus of dating, which depends on the reaction of viable
myocardium to the area of infarct.

At 24 hours of occlusion followed by reperfusion after 6 hours in a canine model, myocytes

are thin, hypereosinophilic, and devoid of nuclei or showing karyorrhexis, with ill-defined
borders and interspersed areas of interstitial hemorrhage. There is a diffuse but mild
neutrophil infiltration. Within 2-3 days, macrophage infiltration is obvious and there is
phagocytosis of necrotic myocytes and early stages of granulation tissue.

Infarct healing is more rapid in dogs than in humans, most likely because of nondiseased
adjoining coronary arteries (collaterals) and a lack of underlying myocardial disease. In
humans with acute MI, there is often chronic ischemia secondary to extensive atherosclerotic
disease.

In humans, if reperfusion occurs within 4-6 hours after the onset of chest pain or
electrocardiographic (ECG) changes, there is myocardial salvage, and the infarct is likely to
be subendocardial without transmural extension. There will be a nearly confluent area of
hemorrhage within the infarcted myocardium, with extensive contraction band necrosis.
Within a few hours of reperfusion, sparse neutrophils are evident within the area of necrosis,
but they are usually sparse.

Macrophages begin to appear by day 2-3; by day 3-5, fibroblasts appear, with an accelerated
rate of healing as compared with that of nonreperfused infarcts. Subendocardial infarcts may
be fully healed as early as 2-3 weeks. Larger infarcts and those reperfused after 6 hours take
longer to heal. Infarcts reperfused after 6 hours show larger areas of hemorrhage than do
occlusions with more immediate reperfusion.

Immunohistochemistry
Immunohistochemistry is of limited use in the diagnosis of acute myocardial infarction (MI).
Immunolocalization of complement or fibrin may be helpful in identifying areas of myocyte
necrosis, where there is leakage of extracellular proteins into the myocytes. In addition,
markers of ischemia include hypoxia-inducible factor-1, complement leaking into myocytes,
and cyclooxygenase-2, which can be demonstrated immunohistochemically.

Infark miokard sembuh. Pada 3 bulan, ada bekas luka padat, yang biru di trichrome ini noda
Masson. Infark ini subendokard, di posterior kiri ventrikel dekat septum ventrikel.
Penanggalan histologis MI mungkin penting dari sudut pandang medikolegal pandang. Tidak
ada cara untuk menentukan umur infark persis, namun, baik karena fitur histologis yang
menentukan tahap perbaikan tumpang tindih dan karena infark dapat memperbesar,
menghasilkan heterogenitas dari satu daerah ke daerah lain. Zona perbatasan antara
miokardium nekrotik dan miokardium layak merupakan fokus dari kencan, yang tergantung
pada reaksi miokardium layak untuk daerah infark.
Pada 24 jam oklusi diikuti reperfusi setelah 6 jam dalam model anjing, miosit yang
hypereosinophilic, tipis, dan tanpa inti atau menampilkan karyorrhexis, dengan batas tidak
jelas dan daerah perdarahan interstitial diselingi. Ada difus tetapi ringan infiltrasi neutrofil.
Dalam waktu 2-3 hari, infiltrasi makrofag jelas dan ada fagositosis miosit nekrotik dan tahap
awal jaringan granulasi.
Penyembuhan infark lebih cepat pada anjing dari pada manusia, kemungkinan besar karena
arteri koroner nondiseased sebelah (agunan) dan kurangnya penyakit miokard yang
mendasari. Pada manusia dengan MI akut, sering ada iskemia kronis sekunder untuk penyakit
aterosklerosis yang luas.
Pada manusia, jika reperfusi terjadi dalam 4-6 jam setelah onset nyeri dada atau
elektrokardiografi (EKG) perubahan, ada penyelamatan miokard, dan infark yang mungkin
subendokard tanpa ekstensi transmural. Akan ada daerah hampir konfluen perdarahan dalam
miokardium infark, nekrosis dengan kontraksi Band yang luas. Dalam beberapa jam
reperfusi, neutrofil jarang yang jelas dalam area nekrosis, tetapi mereka biasanya jarang.
Makrofag mulai muncul hari 2-3; hari 3-5, fibroblast muncul, dengan tingkat percepatan
penyembuhan dibandingkan dengan yang dari infark nonreperfused. Infark subendokard
dapat sepenuhnya sembuh sedini 2-3 minggu. Infark yang lebih besar dan orang-orang
reperfusi setelah 6 jam lebih lama untuk menyembuhkan. Infark reperfusi setelah 6 jam
menunjukkan daerah yang lebih besar dari perdarahan dibandingkan oklusi dengan reperfusi
lebih cepat.
Imunohistokimia
Imunohistokimia adalah penggunaan terbatas dalam diagnosis infark miokard akut (MI).
Immunolocalization komplemen atau fibrin dapat membantu dalam mengidentifikasi bidang
miosit nekrosis, di mana ada kebocoran protein ekstraseluler ke dalam miosit. Selain itu,
penanda iskemia meliputi hipoksia-diinduksi faktor 1, melengkapi bocor ke miosit, dan
siklooksigenase-2, yang dapat ditunjukkan imunohistokimia

Prognosis and Predictive Factors

The morbidity and mortality of myocardial infarction (MI) result from arrhythmias, cardiac
rupture, heart failure, valve insufficiency, and embolization.

Arrhythmias include ventricular tachyarrhythmias, which are the most common cause of
sudden death, especially early after infarction, and various degrees of heart block.

Cardiac rupture occurs in approximately 5% of patients, has a high mortality, and is increased
in frequency in patients experiencing their first infarct, hypertensive patients, and women.[7]

The risk of heart failure is proportional to the size of the infarct and the presence of papillary
muscle necrosis. The size of infarct may be significantly decreased with prompt reperfusion
after the first symptoms, either by thrombolytic treatment or by percutaneous intervention.
Stem cell treatment is an investigative approach to minimizing myocardial infarct size.

Infarction or rupture of the posteromedial papillary muscle causes acute mitral insufficiency,
which greatly worsens cardiac output and which may be treated surgically. The improvement
in prognosis that has occurred in the last decade is due to early treatment with thrombolytic
agents and reperfusion.[8]

Mural thrombosis over the area of infarction may result in embolization and concomitant
stroke but is decreased in incidence with anticoagulation therapy.[9]

Prognosis dan Faktor prediktif

Morbiditas dan mortalitas miokard infark (MI) hasil dari aritmia, ruptur jantung, gagal
jantung, insufisiensi katup, dan embolisasi.
Aritmia ventrikel termasuk takiaritmia, yang merupakan penyebab paling umum kematian
mendadak, terutama di awal setelah infark, dan berbagai tingkat blok jantung.
Ruptur jantung terjadi pada sekitar 5% pasien, memiliki angka kematian yang tinggi, dan
meningkat pada frekuensi pada pasien yang mengalami infark pertama mereka, pasien
hipertensi, dan wanita. [7]
Risiko gagal jantung sebanding dengan ukuran infark dan kehadiran nekrosis otot papilaris.
Ukuran infark dapat menurun secara signifikan dengan reperfusi cepat setelah gejala pertama,
baik oleh pengobatan trombolitik atau intervensi perkutan. Pengobatan sel induk adalah
sebuah pendekatan investigasi untuk meminimalkan ukuran infark miokard.
Infark atau pecahnya otot papiler posteromedial menyebabkan insufisiensi mitral akut, yang
sangat memperburuk cardiac output dan yang dapat diobati dengan pembedahan.
Membaiknya prognosis yang terjadi dalam dekade terakhir ini disebabkan pengobatan dini
dengan agen trombolitik dan reperfusi. [8]
Trombosis mural di atas area infark dapat mengakibatkan embolisasi dan bersamaan stroke,

References

1. Burke AP, Virmani R. Pathophysiology of acute myocardial infarction. Med Clin

North Am. 2007 Jul. 91(4):553-72; ix. [Medline].
2. Arbustini E, Dal Bello B, Morbini P, Burke AP, Bocciarelli M, Specchia G, et al.
Plaque erosion is a major substrate for coronary thrombosis in acute myocardial
infarction. Heart. 1999 Sep. 82(3):269-72. [Medline]. [Full Text].
3. Shiffman D, Rowland CM, Sninsky JJ, Devlin JJ. Polymorphisms associated with
coronary heart disease: better by the score. Curr Opin Mol Ther. 2006 Dec. 8(6):493-
9. [Medline].
4. Tousoulis D, Briasoulis A, Papageorgiou N, Antoniades C, Stefanadis C. Candidate
gene polymorphisms and the 9p21 locus in acute coronary syndromes. Trends Mol
Med. 2008 Oct. 14(10):441-9. [Medline].
5. Rosamond WD, Chambless LE, Folsom AR, Cooper LS, Conwill DE, Clegg L, et al.
Trends in the incidence of myocardial infarction and in mortality due to coronary
heart disease, 1987 to 1994. N Engl J Med. 1998 Sep 24. 339(13):861-7. [Medline].
6. Fishbein MC, Maclean D, Maroko PR. The histopathologic evolution of myocardial
infarction. Chest. 1978 Jun. 73(6):843-9. [Medline].
7. Batts KP, Ackermann DM, Edwards WD. Postinfarction rupture of the left ventricular
free wall: clinicopathologic correlates in 100 consecutive autopsy cases. Hum Pathol.
1990 May. 21(5):530-5. [Medline].
8. Hayashi T, Miyataka M, Kimura A, Taniguchi M, Kurooka A, Yabushita H, et al.
Recent decline in hospital mortality among patients with acute myocardial infarction.
Circ J. 2005 Apr. 69(4):420-6. [Medline].
9. Keeley EC, Hillis LD. Left ventricular mural thrombus after acute myocardial
infarction. Clin Cardiol. 1996 Feb. 19(2):83-6. [Medline].