GeneHealth - Your precision medicine

Acute Myocardial Infarction

Disease Details

Family Health Simplified

Buy Membership

Description: Acute myocardial infarction, commonly known as a heart attack, occurs when blood flow to a part of the heart is blocked for a long enough period that part of the heart muscle is damaged or dies.
Type: Acute myocardial infarction (AMI), commonly known as a heart attack, is primarily a multifactorial disease. It is influenced by a combination of genetic and environmental factors rather than following a simple pattern of genetic transmission such as autosomal dominant or recessive inheritance. Genetic predispositions can increase the risk, but lifestyle factors like diet, exercise, and smoking also play significant roles.
Signs And Symptoms: Chest pain that may or may not radiate to other parts of the body is the most typical and significant symptom of myocardial infarction. It might be accompanied by other symptoms such as sweating.
Prognosis: The prognosis after myocardial infarction varies greatly depending on the extent and location of the affected heart muscle, and the development and management of complications. Prognosis is worse with older age and social isolation. Anterior infarcts, persistent ventricular tachycardia or fibrillation, development of heart blocks, and left ventricular impairment are all associated with poorer prognosis. Without treatment, about a quarter of those affected by MI die within minutes and about forty percent within the first month. Morbidity and mortality from myocardial infarction has, however, improved over the years due to earlier and better treatment: in those who have a STEMI in the United States, between 5 and 6 percent die before leaving the hospital and 7 to 18 percent die within a year.It is unusual for babies to experience a myocardial infarction, but when they do, about half die. In the short-term, neonatal survivors seem to have a normal quality of life.
Onset: Acute myocardial infarction (AMI), commonly known as a heart attack, typically presents with a sudden onset of symptoms. The most common symptom is severe chest pain or discomfort that may radiate to the arms, neck, jaw, or back. This pain often persists for more than a few minutes or can go away and come back. Other symptoms may include shortness of breath, sweating, nausea, vomiting, lightheadedness, and a feeling of impending doom. Prompt medical attention is crucial to reduce damage to the heart muscle.
Prevalence: Prevalence of acute myocardial infarction (AMI) can vary based on geography, demographics, and data sources. Generally, it is a leading cause of morbidity and mortality worldwide. For instance, in the United States, it is estimated that about 805,000 Americans have a heart attack each year. Globally, the incidence and prevalence can be higher due to various factors, including lifestyle, healthcare access, and underlying health conditions.
Epidemiology: Myocardial infarction is a common presentation of coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease; with it being the leading cause of death in high- or middle-income countries and second only to lower respiratory infections in lower-income countries. Worldwide, more than 3 million people have STEMIs and 4 million have NSTEMIs a year. STEMIs occur about twice as often in men as women.Rates of death from ischemic heart disease (IHD) have slowed or declined in most high-income countries, although cardiovascular disease still accounted for one in three of all deaths in the US in 2008. For example, rates of death from cardiovascular disease have decreased almost a third between 2001 and 2011 in the United States.In contrast, IHD is becoming a more common cause of death in the developing world. For example, in India, IHD had become the leading cause of death by 2004, accounting for 1.46 million deaths (14% of total deaths) and deaths due to IHD were expected to double during 1985–2015. Globally, disability adjusted life years (DALYs) lost to ischemic heart disease are predicted to account for 5.5% of total DALYs in 2030, making it the second-most-important cause of disability (after unipolar depressive disorder), as well as the leading cause of death by this date.
Intractability: Acute myocardial infarction (AMI), commonly known as a heart attack, is not inherently intractable. With prompt medical treatment, such as reperfusion therapy (e.g., percutaneous coronary intervention or thrombolytic therapy), many patients can recover and manage their condition effectively. Long-term management typically includes lifestyle modifications, medications, and sometimes surgical interventions to prevent recurrence and improve heart function. However, the prognosis depends on various factors, including the extent of heart damage, the speed of treatment, and the patient's overall health condition.
Disease Severity: Acute myocardial infarction, commonly known as a heart attack, varies in severity from mild to life-threatening, depending on the extent of the heart muscle damage and the promptness of medical intervention. The severity can be influenced by factors such as the size and location of the affected artery, the patient’s overall health, and the speed at which treatment is administered.
Healthcare Professionals: Disease Ontology ID - DOID:9408
Pathophysiology: Acute myocardial infarction (AMI), commonly known as a heart attack, occurs when blood flow to a part of the heart muscle is abruptly reduced or stopped, causing tissue damage. This usually results from a blockage in one or more of the coronary arteries due to plaque rupture and subsequent thrombus (blood clot) formation. The lack of oxygenated blood leads to ischemia and, if not quickly resolved, to necrosis (death) of the heart muscle tissue.
Carrier Status: For acute myocardial infarction (heart attack), the concept of carrier status is not applicable. Acute myocardial infarction is not a genetic or infectious disease that involves carriers; it is a medical condition that results from the sudden blockage of blood flow to the heart muscle. This blockage is typically caused by the buildup of plaque in the coronary arteries. Key risk factors include high blood pressure, high cholesterol, smoking, diabetes, and a family history of heart disease.
Mechanism: Acute myocardial infarction (AMI), commonly known as a heart attack, occurs when blood flow to a part of the heart muscle is abruptly cut off, causing tissue damage. This usually happens due to a blockage in one or more coronary arteries.

### Mechanism
1. **Plaque Rupture or Erosion**: Atherosclerotic plaques within the coronary arteries can rupture or erode, exposing the underlying lipid core to the blood.
2. **Thrombus Formation**: The exposure leads to the activation of platelets and the coagulation cascade, resulting in the formation of a thrombus (blood clot).
3. **Occlusion**: The thrombus can partially or completely occlude the coronary artery, significantly reducing or stopping blood flow to the heart muscle.
4. **Ischemia and Necrosis**: The lack of oxygenated blood (ischemia) leads to the death (necrosis) of heart muscle cells in the affected area.

### Molecular Mechanisms
1. **Inflammatory Response**: Plaque rupture triggers an inflammatory response. Macrophages and other immune cells release cytokines and enzymes that degrade the fibrous cap of the plaque.
2. **Platelet Activation**: Exposed collagen and tissue factor promote platelet adhesion, activation, and aggregation at the site of injury.
- **Glycoprotein IIb/IIIa Pathway**: Activated platelets express glycoprotein IIb/IIIa receptors, which bind fibrinogen and facilitate platelet aggregation.
3. **Coagulation Cascade**: Tissue factor exposure initiates the extrinsic pathway of the coagulation cascade, leading to thrombin generation.
- **Thrombin**: Thrombin converts fibrinogen to fibrin, forming a stable clot.
4. **Occlusion and Hypoxia**: The developing clot obstructs blood flow, causing hypoxia.
5. **Cell Death Pathways**:
- **Apoptosis and Necrosis**: Hypoxia and nutrient deprivation lead to cellular energy crisis, oxidative stress, and activation of cell death pathways.
- **Mitochondrial Dysfunction**: Disrupted ATP production and release of pro-apoptotic factors from mitochondria exacerbate cell death.
6. **Reperfusion Injury**: Restoration of blood flow (e.g., via medical intervention) can sometimes cause additional injury through oxidative stress and inflammation.

Understanding these mechanisms helps in the development of targeted therapies to prevent and treat AMI, such as antiplatelet drugs, thrombolytics, and interventions to stabilize atherosclerotic plaques.
Treatment: Treatment for acute myocardial infarction (AMI) typically involves the following:

1. **Medications:**
- **Antiplatelets** (e.g., aspirin, clopidogrel) to prevent further clotting.
- **Anticoagulants** (e.g., heparin) to prevent new clots from forming.
- **Thrombolytics** (e.g., alteplase) to dissolve existing clots.
- **Beta-blockers** to reduce heart workload and decrease oxygen demand.
- **ACE inhibitors** to lower blood pressure and reduce heart strain.
- **Pain relief** (e.g., morphine) to manage chest pain.

2. **Reperfusion Therapy:**
- **Percutaneous Coronary Intervention (PCI):** Often involves angioplasty and stent placement to open blocked arteries.
- **Coronary Artery Bypass Grafting (CABG):** Surgical option if PCI is not suitable.

3. **Supportive Care:**
- **Oxygen therapy** if oxygen levels are low.
- **Monitoring and managing complications** like heart failure or arrhythmias.

Follow-up typically includes lifestyle modifications, cardiac rehabilitation, and continued medical management to prevent recurrence.
Compassionate Use Treatment: For acute myocardial infarction (AMI), compassionate use treatment, off-label, or experimental therapies include several promising approaches:

1. **Stem Cell Therapy**: This experimental treatment involves the use of stem cells to repair and regenerate damaged heart tissue. Clinical trials are ongoing to evaluate its efficacy and safety.

2. **Gene Therapy**: Gene therapy aims to enhance the heart's ability to repair itself by introducing genes that promote tissue regeneration. This is still largely in the experimental stage.

3. **Monoclonal Antibodies**: Some monoclonal antibodies, initially developed for other conditions, are being explored for their potential to reduce inflammation and myocardial damage during an AMI.

4. **New Antithrombotic Agents**: These agents are designed to optimize blood clot prevention without increasing bleeding risk. While some are approved for other indications, they are being investigated for off-label use in AMI.

5. **Therapeutic Hypothermia**: Cooling the body to reduce metabolic demands and limit ischemic damage is being studied as an emergency intervention for AMI.

6. **Selective Androgen Receptor Modulators (SARMs)**: SARMs, which target androgen receptors with fewer side effects, are being explored for their potential to improve cardiac function post-AMI.

7. **Metabolic Modulators**: Drugs that optimize myocardial metabolism during ischemia, such as trimetazidine, are being investigated for off-label use in AMI patients.

These treatments are primarily restricted to clinical trials and specific compassionate use cases, reflecting their experimental nature and the need for further research to confirm their safety and efficacy.
Lifestyle Recommendations: For acute myocardial infarction (heart attack), lifestyle recommendations include:

1. **Healthy Diet**: Focus on a balanced diet rich in fruits, vegetables, whole grains, lean proteins, and healthy fats. Limit intake of saturated fats, trans fats, cholesterol, sodium, and added sugars.

2. **Regular Exercise**: Engage in moderate aerobic exercise for at least 150 minutes per week, or vigorous exercise for 75 minutes per week, as advised by a healthcare provider.

3. **Weight Management**: Maintain a healthy weight to reduce the strain on your heart.

4. **Smoking Cessation**: Quit smoking and avoid secondhand smoke to improve cardiovascular health.

5. **Stress Management**: Practice stress-reducing techniques such as meditation, yoga, or deep breathing exercises.

6. **Limit Alcohol**: If you drink alcohol, do so in moderation. For men, this typically means up to two drinks per day, and for women, one drink per day.

7. **Medication Adherence**: Take all prescribed medications as directed by your healthcare provider to manage risk factors such as high blood pressure, high cholesterol, and diabetes.

8. **Regular Check-ups**: Attend follow-up appointments with your healthcare provider to monitor your condition and make any necessary adjustments to your treatment plan.
Medication: Following a heart attack, nitrates, when taken for two days, and ACE-inhibitors decrease the risk of death. Other medications include:
Aspirin is continued indefinitely, as well as another antiplatelet agent such as clopidogrel or ticagrelor ("dual antiplatelet therapy" or DAPT) for up to twelve months. If someone has another medical condition that requires anticoagulation (e.g. with warfarin) this may need to be adjusted based on risk of further cardiac events as well as bleeding risk. In those who have had a stent, more than 12 months of clopidogrel plus aspirin does not affect the risk of death.Beta blocker therapy such as metoprolol or carvedilol is recommended to be started within 24 hours, provided there is no acute heart failure or heart block. The dose should be increased to the highest tolerated. Contrary to most guidelines, the use of beta blockers does not appear to affect the risk of death, possibly because other treatments for MI have improved. When beta blocker medication is given within the first 24–72 hours of a STEMI no lives are saved. However, 1 in 200 people were prevented from a repeat heart attack, and another 1 in 200 from having an abnormal heart rhythm. Additionally, for 1 in 91 the medication causes a temporary decrease in the heart's ability to pump blood.ACE inhibitor therapy should be started within 24 hours and continued indefinitely at the highest tolerated dose. This is provided there is no evidence of worsening kidney failure, high potassium, low blood pressure, or known narrowing of the renal arteries. Those who cannot tolerate ACE inhibitors may be treated with an angiotensin II receptor antagonist.Statin therapy has been shown to reduce mortality and subsequent cardiac events and should be commenced to lower LDL cholesterol. Other medications, such as ezetimibe, may also be added with this goal in mind.Aldosterone antagonists (spironolactone or eplerenone) may be used if there is evidence of left ventricular dysfunction after an MI, ideally after beginning treatment with an ACE inhibitor.Statins, drugs that act to lower blood cholesterol, decrease the incidence and mortality rates of myocardial infarctions. They are often recommended in those at an elevated risk of cardiovascular diseases.Aspirin has been studied extensively in people considered at increased risk of myocardial infarction. Based on numerous studies in different groups (e.g. people with or without diabetes), there does not appear to be a benefit strong enough to outweigh the risk of excessive bleeding. Nevertheless, many clinical practice guidelines continue to recommend aspirin for primary prevention, and some researchers feel that those with very high cardiovascular risk but low risk of bleeding should continue to receive aspirin.
Repurposable Drugs: For acute myocardial infarction (AMI), certain drugs traditionally used for other conditions can be repurposed:

1. **Metformin**: Typically used for type 2 diabetes, it has been shown to have cardioprotective effects.
2. **Colchicine**: Used for gout and pericarditis, it may reduce inflammation and improve outcomes in AMI.
3. **SGLT2 inhibitors**: Originally for diabetes, they offer benefits in heart failure post-AMI.

Further clinical studies are essential to confirm these potentials.
Metabolites: In the context of acute myocardial infarction (AMI), several metabolites can be significant. Key metabolites include:

1. **Troponins (cTnI and cTnT)**: Cardiac-specific proteins released into the blood following heart muscle damage.
2. **Creatine Kinase-MB (CK-MB)**: An enzyme found in the heart muscle; elevated levels indicate cardiac damage.
3. **Myoglobin**: An early marker of muscle injury, including cardiac muscle.
4. **B-type Natriuretic Peptide (BNP)**: Levels can rise due to heart muscle stress and can be indicative of heart failure often associated with AMI.
5. **Lactate Dehydrogenase (LDH)**: An enzyme released during tissue breakdown, including from cardiac muscle damage.
Nutraceuticals: Nutraceuticals are foods or food products that provide health and medical benefits, including the prevention and treatment of disease. For acute myocardial infarction (AMI), certain nutraceuticals may be beneficial, such as omega-3 fatty acids, antioxidants (like vitamins C and E), Coenzyme Q10, and polyphenols found in foods like berries and green tea. They may help improve heart health by reducing inflammation, improving blood lipid profiles, and enhancing endothelial function. However, these should supplement, not replace, standard medical treatment. Always consult a healthcare professional before starting any new supplement regimen.
Peptides: Acute myocardial infarction (AMI), commonly known as a heart attack, involves peptides like natriuretic peptides (e.g., B-type natriuretic peptide, BNP) and troponins (cardiac-specific troponin I and T) that are important biomarkers for diagnosing and assessing the severity of the condition.

Regarding nanotechnology (nan), it has emerging applications in AMI for improved diagnosis and treatment. Nanoparticles can be used for targeted drug delivery to damaged heart tissue, enhancing the efficacy of therapeutic agents while minimizing side effects. Additionally, nanosensors are being developed for the rapid and sensitive detection of biomarkers associated with AMI, potentially allowing for quicker diagnosis and intervention.