Ministry of Higher Education and

Scientific Research

College of Medicine, University of Baghdad

Myocardial infarction

Presented by

Supervised by
Assist. Teacher. Ammar Adel Jassim

Ramadan 7, 1445 March 17, 2024

Contents:
1. Definition of Myocardial infarction…………………….2

2. Pathophysiology of Myocardial Infarction…………….3

3. Signs and Symptoms of Myocardial infarction…….4-6

4. Diagnosis of Myocardial Infarction……………7-8

5. Treatment Options for Myocardial Infarction…...9-10

6. Complications of Myocardial Infarction

7. Long-term Survival Rate Following Myocardial

Infarction and the Effect of Discharge Medications on the
Survival Rate…………………………………...12-13

8. Early intervention and prevention of myocardial

infarction…………………………………………14

9.refernces…………………………………………15-18

1
 Definition of Myocardial infarction

Myocardial infarction (MI), colloquially known as “heart attack,” is caused

by decreased or complete cessation of blood flow to a portion of the myocardium.
Myocardial infarction may be “silent” and go undetected, or it could be a
catastrophic event leading to hemodynamic deterioration and sudden death. Most
myocardial infarctions are due to underlying coronary artery disease. With
coronary artery occlusion, the myocardium is deprived of oxygen. Prolonged
deprivation of oxygen supply to the myocardium can lead to myocardial cell death
and necrosis. Patients can present with chest discomfort or pressure that can
radiate to the neck, jaw, shoulder, or arm. In addition to the history and physical
exam, myocardial ischemia may be associated with ECG changes and elevated
biochemical markers such as cardiac troponins.[1]

Figure 1: illustration of blockage in coronary arteries caused by thrombus

2
Pathophysiology of Myocardial Infarction

The culprit behind most MIs is coronary artery disease (CAD). CAD
involves the buildup of fatty deposits (atheromas) within the walls of the
coronary arteries, the vessels supplying blood to the heart muscle. Over time,
these atheromas can rupture, triggering the formation of blood clots (thrombi).
A large enough thrombus can completely block the artery, stopping blood flow
to a specific heart region. [2]

The lack of oxygen due to the blockage sets off a cascade of events
within the affected heart tissue:

1-Ischemia: Reduced oxygen supply triggers a state of oxygen deprivation

(ischemia) in the heart muscle. This disrupts the normal metabolic processes of
heart cells, leading to a buildup of waste products and a decline in cellular
energy production.[2]
2-Cell Death: Prolonged ischemia ultimately leads to cell death through two
main pathways: necrosis (violent cell death) and apoptosis (programmed cell
death). The extent of cell death determines the size and severity of the
myocardial infarction.[2]
3-Inflammatory Response: The damaged heart tissue triggers an inflammatory
response, aimed at clearing dead cells and initiating repair processes. However,
excessive inflammation can further damage healthy tissue.
4-Scar Formation: As healing progresses, the infarcted area is replaced by scar
tissue. While scar tissue helps maintain the structural integrity of the heart, it
lacks the contractile function of healthy muscle, potentially leading to heart
failure. [2]

3
Signs and Symptoms of Myocardial infarction

Symptoms of myocardial infarction vary among patients and some are

Typical which happen to most of patients while some are Atypical and happen
due to other diseases and may cause false diagnosis of MI, most common and
typical symptom is:

Chest Pain: This is the most frequent and characteristic symptom, affecting
around 90% of patients experiencing a heart attack. The pain is often described
as a squeezing, pressure, or tightness in the chest, located behind the breastbone
(sternal). It can be persistent or come and go, sometimes lasting for more than
20 minutes. This pain may also radiate to other areas like the shoulders, jaw,
arm, or back.[18]

Chest Pain Characteristics: While chest pain is the most common

symptom, its nature can vary from:
Quality: The pain is often described as a squeezing, pressure, or
tightness, rather than a sharp or stabbing pain [19].

Location: The pain is typically felt behind the breastbone (sternal) but
can radiate to other areas like the shoulders, jaw, arm, or back [19].
Duration: The pain may be persistent or come and go in waves,
sometimes lasting for more than 20 minutes [19]. This persistent nature
is a key differentiating factor from other causes of chest discomfort like
heartburn or muscle strain.[19]
Discomfort with Exertion: The chest pain may worsen with physical
activity or exertion and often improves with rest [19].

4
 Figure 2: myocardial infarction chest pain radiation areas

Associated Symptoms: While chest pain is the most prominent

symptoms, other signs and symptoms can occur alongside it, sometimes even in
the absence of chest pain. These include:
1-Shortness of Breath (Dyspnea): This symptom arises due to compromised
heart function, making it difficult to breathe adequately [2]. It can occur at rest
or with exertion.
2-Nausea and Vomiting: Activation of the autonomic nervous system during a
heart attack can trigger these symptoms [2].
3-Sweating (Diaphoresis): Cold, clammy sweating can be a response to the
stress and pain associated with a heart attack [2].
4-Fatigue and Lightheadedness: A general feeling of weakness, fatigue, and
dizziness can also occur during a heart attack [2].

5-Anxiety: The experience of a heart attack can be frightening, leading to

feelings of anxiety and a sense of impending doom [2].

5
 Importance of Recognizing Atypical Presentations:
It's vital to remember that not everyone experiences a classic heart attack
presentation. Some individuals, particularly women and diabetics, may exhibit
atypical symptoms [20]. These can be more subtle or even misleading, making
early diagnosis more challenging. Atypical presentations might include:
Atypical chest pain: Burning, aching, or discomfort in the upper abdomen or back
instead of the classic squeezing chest pain [20].
Isolated symptoms: Some individuals may only experience shortness of breath,
nausea, fatigue, or jaw pain without classic chest pain [20].
Silent ischemia: In some cases, particularly in diabetics, a heart attack might
occur without any noticeable symptoms [20].
Early Recognition and Intervention is Key
Regardless of the specific presentation, early recognition and intervention are
crucial for minimizing heart damage and improving outcomes after a heart attack.
If you or someone you know experiences any of these symptoms, especially chest
pain, it's essential to seek immediate medical attention. Delaying medical care
can worsen the heart attack's severity and increase the risk of complications.

6
Diagnosis of Myocardial Infarction

When evaluating the results of diagnostic tests for STEMI, the temporal
phase of the infarction must be considered. The laboratory tests of value in
confirming the diagnosis may be divided into three groups: (1) ECG, (2) serum
cardiac biomarkers, (3) cardiac imaging,[21]

1- Electrocardiogram (ECG): An ECG is a crucial diagnostic test for myocardial

infarction. It measures the electrical activity of the heart and can detect
abnormalities such as ST elevations, ST depressions, T-wave inversions, and
pathological Q-waves that may indicate myocardial ischemia and infarction.[21]

2- Serum Cardiac Biomarkers: The elevation of cardiac biomarkers in the blood

is key to diagnosing myocardial infarction. Troponin is the most commonly
used cardiac enzyme for this purpose. When heart muscle cells are damaged,
they release troponin into the bloodstream, which can then be detected by blood
tests.[21]

3- Cardiac Imaging: Cardiac imaging plays a significant role in the diagnosis of

myocardial infarction. Techniques such as cardiac magnetic resonance imaging
(MRI) can provide detailed images of the heart and help identify areas of
damage. In addition, coronary angiography can be used to visualize the
coronary arteries and detect any blockages.[21]

7
Figure 3: show relation of biomarkers level in Figure 4: Coronary angiography-lateral
blood and duration after chest pain occurring. angiographic view shows both RCA and
LCA originating from same ostium (arrow).

Figure 5: presents two patients

with acute STEMI and there are
evident reciprocal ST depressions
in both cases.

8
Treatment Options for Myocardial Infarction

1. Medications:
• Thrombolytics: Drugs like alteplase, reteplase, or tenecteplase are used to
dissolve blood clots in the coronary arteries. [3]
• Antiplatelet drugs: Aspirin, clopidogrel, and ticagrelor are commonly used to
prevent further clot formation. [4]
• Beta-blockers: Drugs like metoprolol or carvedilol reduce heart rate, blood
pressure, and myocardial oxygen demand. [5]
• ACE inhibitors or ARBs: Medications like lisinopril or losartan improve heart
function and reduce mortality post-MI. [6]
2. Medical Procedures:
• Percutaneous Coronary Intervention (PCI): This involves balloon angioplasty
and stent placement to open blocked coronary arteries. [8]
• Coronary Artery Bypass Grafting (CABG): Surgery may be necessary for
patients with complex coronary artery disease. [9]
3. Lifestyle Changes:
• Dietary modifications: A heart-healthy diet rich in fruits, vegetables, whole
grains, and lean proteins is recommended. [10]
• Regular physical activity: Exercise helps improve cardiovascular health and
reduces the risk of recurrent myocardial infarction. [11]
• Smoking cessation: Quitting smoking significantly reduces the risk of further
cardiac events. [12]
• Weight management: Maintaining a healthy weight reduces strain on the heart
and lowers cardiovascular risk. [13]
4. Cardiac Rehabilitation:
• Structured exercise programs: Supervised exercise regimens improve
cardiovascular fitness and overall health. [14]

9
• Patient education: Programs provide information on medication adherence,
symptom recognition, and lifestyle modification. [15]
5. Monitoring and Follow-up:
• Regular medical check-ups: Follow-up appointments with a cardiologist are
essential to monitor heart function and adjust treatment as needed. [16]
• Diagnostic tests: Electrocardiograms, echocardiograms, and stress tests help
assess cardiac health and detect any complications. [17]

Table 1: mnemonic way to

memorize treatment options

10
Figure 6: myocardial infarction prevention
Complications of Myocardial Infarction

1. Arrhythmias: MI can disrupt the heart’s electrical system, leading to

arrhythmias such as ventricular fibrillation, ventricular tachycardia, or
atrioventricular block. These can be fatal if not promptly managed. [24]
2. Heart Failure: A significant MI can weaken the heart muscle, reducing its
ability to pump blood effectively, leading to heart failure. This can result in
symptoms such as shortness of breath, fatigue, and fluid retention. [25]
3. Cardiogenic Shock: In severe cases, a large MI can cause cardiogenic
shock, where the heart is unable to pump enough blood to meet the body’s
needs. This is a life-threatening complication requiring immediate intervention.
[26]
4. Pericarditis: Inflammation of the pericardium, the sac surrounding the heart,
can occur post-MI, leading to chest pain and other symptoms. [27]
5. Ventricular Septal Defect (VSD): A rupture in the wall separating the
heart’s chambers can occur, leading to a VSD. This can result in hemodynamic
instability and requires surgical repair. [28]
6. Papillary Muscle Rupture: Rupture of the papillary muscles, which anchor
the heart valves, can lead to acute mitral regurgitation and heart failure.
Emergency surgery is often required. [29]
7. Thromboembolism: Blood clots may form in the heart’s chambers or
arteries, leading to thromboembolic events such as stroke or pulmonary
embolism. [30]
8. Post-Infarction Angina: Recurrent chest pain may occur due to ongoing
ischemia or unstable angina post-MI, indicating ongoing coronary artery
disease. [31]

11
Long-term Survival Rate Following Myocardial Infarction and
the Effect of Discharge Medications on the Survival Rate
The evaluation of the risk factors associated with the long-term survival
rate of patients with myocardial infarction (MI) and the effects of discharge
medications can significantly help select the most effective strategies for
improving treatment. [23]

Study Design: A retrospective cohort study.

Methods: The participants of this retrospective cohort study were 21,181

patients who suffered from MI and were hospitalized in the cardiac care unit
(CCU) of different public, private, and military hospitals in Iran from 20 March
2013 to 20 March 2014. Participants were followed up until February 2020 for
any cardiovascular disease (CVD) mortality. To evaluate survival rate, the
differences between groups, and the factors related to MI death, Kaplan-Meier,
log-rank test, and Cox proportional-hazards model were used, respectively. [23]

Results: One, three, five, and seven-year survival rates of patients were 88%,
81%, 78%, and 74%, respectively. Regarding the interaction effect of prescribed
medical drugs, the highest 7-year survival rate of 86% (95% CI: 72%, 93%) was
related to people who consumed anticoagulants, aspirin, clopidogrel, beta
blockers, angiotensin-converting enzymes (ACEs), and angiotensin II receptor
antagonist simultaneously. Considering the effect of other variables, the
consumption of anticoagulants was associated with a decrease in survival rate
(HR=1.13 CI: 1.06, 1.19). [23]

Conclusion: As evidenced by the results of this study, different combinations of

prescribed medication drugs had protective effects on long-term mortality
compared to the group without any drug. Nonetheless, according to the drugs in

12
each combination therapy, this protective effect ranged from HR=0.27 to
HR=0.89. It is recommended that further studies compare the long-term effects
of different drug combinations and also consider adherence to treatment in
evaluating the effects of these combinations.[23]
Table 2: survival rate by gender groups.

Table 3: Survival rate for different medication group.

13
 Early intervention and prevention of myocardial infarction
Although there has been a decline in the incidence of ischaemic heart
disease in Western Europe, North America and Australia/New Zealand, it
remains a major cause of morbidity and mortality worldwide due to rapidly
increasing incidences in developing countries. Prevention is key to reducing the
burden of this disease. The INTERHEART study performed in 52 countries
around the world has shown that the major risk factors are tobacco smoking,
elevated apolipoprotein A, hypertension, diabetes mellitus, abdominal obesity,
psychosocial factors, low fruit and vegetable intake, physical inactivity and
alcohol consumption. Strategies for prevention by reducing risk factors are
applicable universally. Individual healthcare providers can implement primary
and secondary preventive measures to individual patients. Primary prevention
involves the avoidance of disease in high-risk subjects free of disease, whereas
the purpose of secondary prevention is to avoid recurrence of myocardial
infarction. The general principle is to encourage improved and proven lifestyle
measures and to prescribe evidence-based effective medications. Primary
prevention requires greater investment and planning to identify people at high
risk, plus the implementation of life-style intervention and pharmacological
prevention. In both situations, strategies will have to be tailored to suit
individual countries and economies. Life-style measures (i.e. sensible diet,
physical exercise and smoking cessation) are effective and need to be promoted.
Compliance with preventive measures is achievable. Primordial prevention,
which involves reducing the prevalence of risk factors, rests mainly on public
education, media, legislation and government policy, and is very dependent on
individual governments' commitment and determination. It requires promoting a
healthier life-style in the population as a whole by encouraging people to seek
alternatives and making them available.[24]

14
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15
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16
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17
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