Heart failure due to myocardial infarction

Robin Hermans Victor Lamin

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Content
Pathophysiology of myocardial infarction Risk Factors of myocardial infarction Evolution of myocardial infarction The treatment of myocardial infarction

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General introduction Myocardial Infarction

Myocardial infarction (MI) or acute myocardial infarction (AMI), is the interruption of blood supply and oxygen to part of the heart. This is commonly due to occlusion of a coronary artery, due to the rupture of a vulnerable atherosclerotic plaque. The resulting ischemia, can cause damage or death of the myocardium.

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The Pathophysiology of Myocardial Infarction

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Heart failure due to myocardial infraction (MI) is most frequently a manifestation of coronary artery disease. The rupture of an atherosclerotic plaque is the most common cause of myocardial infarction. -This rupture can lead to partly or total occlusion of the coronary artery ischemia irreversible damage of myocardium If impaired blood supply lasts too long - Due to Apoptosis - Later on there is necrosis collagen scar tissue

This collagen scar formation results in the loss of the contractile function of the affected part of the heart!

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Activated macrophages and T-lymphocytes localized at the site of plaque rupture, release MMPs and cytokines weakening the fibrous cap. Plaque rupture reveals subendothelial collagen, which serves as a site of platelet adhesion, activation and aggregation, resulting in:
-The release of Thromboxane A2 (TXA2) -Fibrinogen -5-hydroxytryptamine (5-HT) -ADP Activation of the clotting cascade leads to fibrin formation and stabilization of the occlusive thrombus

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Less severe and protracted ischemia can arise when

-Coronary occlusion is followed by spontaneous reperfusion. -The infarct-related artery is not completely occluded. -Occlusion is complete, but an existing collateral blood supply prevents complete ischemia. -The oxygen demand in the affected zone of myocardium is smaller.

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The pathophysiology of acute myocardial infarction is complex!

The loss of myocardium impairs the cardiac function, which lead to: -Reduction of cardiac output -Cardiac shock (if damage is severe) Systolic and diastolic dysfunction are associated with ischemic myocardium If left ventricular function is reduced significantly, pulmonary congestion and edema can occur. Reduced cardiac output and arterial pressure can elicit baroreceptor reflexes, that lead to the activation of neurohumoral compensatory mechanisms e.g. -Activation of sympathetic nerves -Activation of the renin-angiotensin-aldosterone system
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Ischemia can precipitate abnormal cardiac rhythms and conduction blocks, that can further impair the cardiac function. Conduction problems in the heart after myocardial infarction can occur -Injured myocardium conducts electric pulses more slowly than healthy myocardium. The difference in conduction velocity between injured and uninjured myocardium can trigger re-entry or a feedback loop that may cause lethal arrhythmias like: -Ventricular Fibrillation -Ventricular Tachycardia These arrhythmias may cause an inefficient pumping of the heart -Cardiac output reduced -Blood pressure falls This can lead to further extension of the infarct
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DEATH

Ventricular Fibrillation

Ventricular Tachycardia
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Summary

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Sign of a Myocardial Infarction

Acute myocardial infarction is often described as a sensation of tightness, pressure, or squeezing.

Regions of angina pectoris

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Other signs of a Myocardial Infarction

Shortness of breath Excessive sweating Weakness Nausea Vomiting Palpitations

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Risk Factors for Myocardial Infarction

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There are a multiple risk factors for developing Myocardial Infarction (MI). These risk factors can be genetic of non-genetic. Genetic Hypertension High LDL / Low HDL Diabetes I Family History of heart disease (onset <55) Non-Genetic Age Gender Smoking Hypertension High LDL / Low HDL Diabetes II High fat diet Lack of physical activity Severe stress Alcohol/drug abuse
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Evolution of Myocardial Infarction

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Ischaemia
 Immediate loss of contractility in the affected myocardium, a condition termed hypokinesis  In some areas the myocardium is stunned and will eventually recover if bloodflow is restored.  Contractility in the remaining viable myocardium increases, a process termed hyperkinesis

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Necrosis
 develop in the subendocardium, about 1530 min after coronary occlusion.  The necrotic region grows outward towards the epicardium over the next 36 h, eventually spanning the entire ventricular wall.  A progression of cellular, histological and gross changes develop within the infarct.

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 Cell damage is progressive, becomingly increasingly irreversible over about 12 h.  coagulation necrosis :cell swelling, organelle breakdown and protein denaturation.  After about 18 h, neutrophils enter the infarct  After 3 4 days, granulation tissue appears at the edges of the infarct zone

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Infarct expansion
- This is the stretching and thinning of the infarcted wall within the first day or so after a MI. - progressive dilatation, not only of the infarct zone, but also of healthy myocardium. - ventricular remodelling is caused by an increase in enddiastolic wall stress. - Infarct expansion puts patients at a sub-stantial risk for the development of congestive heart failure, ventricular arrhythmias, and free wall rupture.
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Treatment/ Therapeutic intervention

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1. Anti-platelet Agents
 Aspirin (ASA)  - at least 160mg immediately  - Interferes with function of cyclooxygenase and inhibits the formation of thromboxane  - ASA alone has one of the greatest impact on the reduction of MI mortality
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2. Supplemental Oxygen
 Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and other tissues may be diminished

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3. Nitrates
 IV nitrates to all patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI  vasodilator effect  Metabolized to nitric oxide in the vascular endothelium, relaxes endothelium  Vasodilatation reduces myocardial oxygen demand and preload and afterload.
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4. Beta-blockers
 Recommended within 12 hours of MI symptoms and continued indefinitely  Reduces Myocardial mortality by decreasing arrythmogenic death.  Decrease the rate and force of myocardial contraction and decreases overall oxygen demand

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5. Unfractionated heparin
 Forms a chemical complex with antithrombin III inactivates both free thrombin and factor Xa  Recommended in patients with MI who undergo PTCA or fibrinolytic therapy with alteplase

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6. Low-molecular weight heparin

 Direct activity against factors Xa and Iia  Proven to be effective in treating ACS that are characterized by unstable angina or non STelevation MI

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7. Thrombolytics
 MI and ST segment elevation greater than 0.1mV  The plasminogen activators have been shown to restore coronary blood flow in 50-80% of patients.  Contraindication active intracranial bleeding

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8. Glycoprotein IIb/IIIa Antagonists

 Potent inhibitors of platelet aggregation  Use during PCI and in patients with high risk features ACS.

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9. Percutanous Coronary Intervention

 PCI can successfully restore coronary blood flow in 90 to 95% of MI patients  PCI definitive survival advantage over fibrinolytics for MI patients who are in cardiogenic shock

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10. Lipid Management

 All post MI patients should be on AMA step II diet ( < 7% of calories from saturated fats)  Post MI patients with LDL > 100 mg/dl are recommended to be on drug therapy to try to lower levels to <100 mg/dl  Recent data indicate that all MI patients should be on statin therapy, regardless of lipid levels or diet

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11. Long term Medications

 Most oral medications instituted in the hospital at the time of MI are continued long term  Aspirin, beta blockers and statin are continued indefinitely  ACEI indefinitely in patients with CHF, ejection fraction <.40, hypertension, or diabetes

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References
http://www.spiritus-temporis.com/myocardialinfarction/pathophysiology.html http://www.cvpharmacology.com/clinical%20topics/myocardial %20infarction.htm http://emedicine.medscape.com/article/759321-overview http://en.wikipedia.org/wiki/Myocardial_infarction http://www.blackwellpublishing.com/content/BPL_Images/Con tent_store/Sample_chapter/1405113278/Sample%20of%20Aar onson.pdf http://www.medicinenet.com/heart_attack/article.htm http://imaginis.org/heart-disease/heartattack.asp http://www.healthsystem.virginia.edu/uvahealth/adult_cardiac/ attack.cfm

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