Myocardial Infarction

In 2006 425.425 people died from a heart attack, 1.255.000 new and recurrent coronary attacks took place, about 34% died, 17.600.000 victims of angina, heart attack and other forms of coronary heart disease are still living.

These numbers only account for the United States.

Pathofysiology

A heart attack or myocardial infarction (MI) is an acute presentation of a process that has been going on much longer. The process responsible is atherosclerosis. Atherosclerosis is a chronic disease of the arteries in which artery walls thicken by deposition of fatty materials such as cholesterol. The result over decades are plaques, which can narrow the lumen of the arteries significantly and progressively causing symptoms as angina pectoris. Plaques can also suddenly rupture, trigger a cascade which results in a thrombus and thereby cause myocardial infarction.

History

Classic presentation of a myocardial infarction is acute chest pain which lasts longer than a few minutes. The pain does not decrease at rest and is only temporarily relieved with nitroglycerin. Common accompanying symptoms are radiating pain to shoulder, arm, back and/or jaw. Shortness of breath can occur, as well as sweating, fainting, nausea and vomiting, so called vegetative symptoms. Some patients not really complain about chest pain but more about abdominal pain so as with angina pectoris the presentation can be very a specific.

It is important to complete the history with information about past history (prior history of ischemic events or vascular disease), risk factors for cardiovascular disease (o.a. smoking, hypertension, hyperlipidemia, obesity) and family history (direct family with myocardial infarction and/or sudden cardiac death).

Signs of heart failure such as orthopnea (not able to sleep without a pillow), progressive dyspnoea and oedematous ankles are indicative for the extent of the problem.

A suspected myocardial infarction should be rapidly evaluated to initiate appropriate therapy.

Physical Examination

On physical examination evidence of systemic hypoperfusion can be found such as hypotension, tachycardia, impaired cognition, pale and ashen skin. If during auscultation pulmonary crackles are heard and pitting oedema of the ankles is seen heart failure is complicating the myocardial infarction.

History and physical examination are helpful to determine myocardial infarction as diagnosis and to exclude other causes of chest pain, such as angina pectoris, aorta dissection, arrhythmias, pulmonary embolism, pneumonia, heartburn, hyperventilation or musculoskeletal problems.

Electrocardiogram

An electrocardiogram (ECG) should be made within 10 minutes of arrival in every patient with suspected myocardial infarction.

An ECG is important to differentiate between myocardial ischemia and infarction:

• ST elevation in myocardial infarction
• ST depression in myocardial ischemia

And to differentiate between STEMI and NSTEMI:

• STEMI stands for ST elevated (>20 min) Myocardial Infarction
• NSTEMI stand for Non ST elevated Myocardial Infarction

It can however take 90 minutes after the onset of the symptoms to see abnormalities on the ECG. Therefore it is important to make a serial ECG, certainly if a patient has ongoing symptoms.

An ECG is also helpful in localising the ischemia: Anterior wall ischemia - One or more of leads V1-V6 Anteroseptal ischemia - Leads V1 to V3 Apical or lateral ischemia - Leads aVL and I, and leads V4 to V6 Inferior wall ischemia - Leads II, III, and aVF

Cardiac Markers

Cardiac markers are essential for confirming the diagnosis of infarction. Elevated CK MB and Troponin I indicate damage of the myocardium. It can however take 4-8 hours, after the symptoms started, before the cardiac markers are elevated. The advise is to repeat the measurements after 4-6 hours. A pitfall concerning elevated Troponin I can be patients with renal failure or pulmonary embolism. Although cardiac markers are helpful for confirming the diagnosis reperfusion should not always wait till the cardiac markers are known.

ST elevated Myocardial Infarct

Initial treatment of STEMI is relief of ischemic pain, stabilize the hemodynamic status and reduce the ischemia as quickly as possible by fibrinolysis or primary percutaneous coronary intervention (PCI). Meanwhile other measures as continuous cardiac monitoring, oxygen and intravenous access are necessary to guarantee the safety of the patient.

Rapid revascularisation is essential to minimize the impact of the myocardial infarction and thereby reduce mortality. In the first hours after symptom onset the amount of salvageable myocardium by reperfusion is greatest. Revascularisation can be achieved by fibrinolysis or PCI.