Myocardial Infarction: Difference between revisions

An acute coronary syndrome (ACS) is most commonly caused by rupture or erosion of an atherosclerotic plaque with superimposed thrombus formation. The underlying process is atherosclerosis, a chronic disease in which artery walls thicken by deposition of fatty materials such as cholesterol and inflammatory cells. The accumulation of this material results in the formation of an atherosclerotic plaque, encapsulated by connective tissue, which can narrow the lumen of the arteries significantly and progressively causing symptoms as angina pectoris or lead to an ACS. Depending on the presence of myocardial damage and typical ECG characteristics, ACS can be divided into ST-segment elevation myocardial infarction (STEMI), and non-ST-segment ACS including non-ST-segment elevation MI (NSTEMI) and unstable angina. In the case of STEMI and NSTEMI, there is biochemical evidence of myocardial damage (infarction).  PMID: 11084798

The most typical characteristic of an ACS is acute prolonged chest pain. PMID 16304077 The pain does not decrease at rest and is only temporarily relieved with nitroglycerin. Frequent accompanying symptoms include a radiating pain to shoulder, arm, back and/or jaw. PMID 10099685 Shortness of breath can occur, as well as sweating, fainting, nausea and vomiting, so called vegetative symptoms. Some patient groups like elderly and diabetics might present with aspecific symptoms. PMID 10866870, PMID 10751787

It is important to complete the history with information about the medical history (prior history of ischemic events or vascular disease), risk factors for cardiovascular disease (a.o. diabetes mellitus, current smoking, hypertension, hyperlipidemia) and family history (first degree relatives with myocardial infarction before the age 55 of (males) or 65 (females) and/or sudden cardiac death). PMID15138242

Symptoms of heart failure such as orthopnea (dyspnoea when lying flat), progressive dyspnoea and peripheral oedema are indicative for the extent of the problem. PMID 15289388

The focus of the physical examination should be to recognize signs of systemic hypoperfusion such as hypotension, tachycardia, impaired cognition, pale and ashen skin. PMID 15289388

In more stable ACS patients, history and physical examination are helpful to exclude other causes of chest pain, such as angina pectoris, aorta dissection, arrhythmias, pulmonary embolism, pneumonia, heartburn, hyperventilation or musculoskeletal problems. PMID 15289388

An electrocardiogram (ECG) should be made within 10 minutes of arrival in every patient with suspected ACS. PMID 15289388

It can however take 90 minutes after the onset of the symptoms to see abnormalities on the ECG. Furthermore, the ECG does not reflect the dynamic pathophysiology of the ACS. Therefore it is important to make serial ECGs, certainly if a patient has ongoing symptoms. PMID 15289388

Cardiac markers are essential in order to confirm the diagnosis of MI, indicated by elevated Creatine Kinase isoenzyme MB (CK MB) and/or (high-sensitive) troponins. Troponins are more specific and sensitive than CK MB. The cardiac troponin concentration begins to rise around 4 hours after the onset of myocardial cell damage. PMID 16556688

It can take 4-6 hours before the CK MB concentration is elevated. Serial measurements are advised in order to estimate infarct size and increase the sensitivity of the (older) assays. PMID 7702648

A pitfall concerning mildly elevated cardiac markers can be patients with renal failure or pulmonary embolism. PMID: 17951284 Although cardiac markers are helpful for confirming the diagnosis, reperfusion should not always wait till the cardiac markers are known if the ECG or symptoms are evident.  

As the formation of an intracoronary thrombus is the most common cause of the ACS and (recurrent) subsequent outcomes, the cornerstone in the treatment of ACS is antithrombotic treatment. All patients diagnosed with ACS should start with aspirin and a P2Y12 receptor blocker (clopidogrel, prasugrel or ticagrelor). PMID 21873419 Aspirin and the P2Y12 receptor blocker are both platelet aggregation inhibitors. The treatment of ACS also focuses on medication to keep the workload of the heart as low as possible. β blockers lower heart rate and blood pressure, to decrease the oxygen demand of the heart. PMID 16735367 Nitrates dilatate the coronary arteries so the heart receives more oxygenated blood. PMID 3925741

Initial treatment of STEMI is relief of ischemic pain, stabilize the hemodynamic status and restoration of coronary flow and myocardial tissue perfusion. Reperfusion therapy should be initiated as quickly as possible within 12 hours after symptom onset by preferably primary percutaneous coronary intervention (PCI) or otherwise fibrinolysis. Meanwhile other measures as continuous cardiac monitoring, oxygen and intravenous access are necessary to guarantee the safety of the patient. PMID 15289388

Rapid revascularisation is essential to minimize the size of the myocardial infarction and thereby reduce mortality. In the first hours after symptom onset the amount of salvageable myocardium by reperfusion is greatest. PMID 8712096, PMID16311237 There is no consensus whether reperfusion after 12 hours from the onset of symptoms is still beneficial.  

*  Patients with contraindications for fibrinolysis, such as:  active bleedings, recent dental surgery, past history of intracranial bleeding. PMID 14532318

* Patients with cardiogenic shock, severe heart failure and/or pulmonary oedema complicating the myocardial infarction. PMID 16186438, PMID 12472924

Available data support the pre-hospital initiation of fibrinolytics if this reperfusion strategy is indicated. Fibrinolytics like streptokinase stimulate the conversion of plasminogen to plasmin. Plasmin demolishes fibrin which is an important constituent of the thrombus. Fibrinolytics are most effective the first hours after the onset of symptoms, and a benefit is observed in terms of reducing mortality within the first twelve hours. PMID 16311237 The hazards of thrombolysis are the increased bleeding risk, including strokes. Because re occlusion after fibrinolysis is possible patients should be transferred to a PCI qualified hospital once fibrinolysis is done. PMID 15769784  

There are circumstances in which CABG could be indicated, such as failed fibrinolysis and/or PCI, when the patient develops cardiogenic shock, life threatening ventricular arrhythmias, has three vessel disease, or mechanical complications of the MI. PMID:18191746

stay, and improves prognosis. However, NSTE-ACS patients represent a heterogenous population, and indication and timing of revascularization depend on many factors, including the baseline risk of the patient. According to current guidelines, depending on early risk stratification a choice has to be made between a routine invasive or a selective invasive (or “conservative strategy”) PMID 15289388

Early risk stratification is helpful to identify patients at high risk who might benefit the most from a more aggressive therapeutic approach in order to prevent further ischemic events. PMID 10938172