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 [in-fark´ shun]
2. formation of an infarct.
cardiac infarction myocardial infarction.
cerebral infarction an ischemic condition of the brain, causing a persistent focal neurologic deficit in the area affected.
myocardial infarction see myocardial infarction.
pulmonary infarction localized necrosis of lung tissue caused by obstruction of the arterial blood supply, most often due to pulmonary embolism. Clinical manifestations range from the subclinical to pleuritic chest pain, dyspnea, hemoptysis, and tachycardia.


1. An area of tissue necrosis caused by impairment of arterial or venous blood supply due to mechanical factors (for example, emboli, thrombi) or to blood pressure alterations.
2. Synonym(s): infarct


1. The formation or development of an infarct.
2. An infarct.


Medtalk Dying of tissue, necrosis


1. Sudden insufficiency of arterial or venous blood supply due to emboli, thrombi, vascular torsion, or pressure that produces a macroscopic area of necrosis; the heart, brain, spleen, kidney, intestine, lung, and testes are likely to be affected, as are tumors, especially of the ovary or uterus.
2. Synonym(s): infarct.


(in-fark'shon) [ infarct]
Death of tissue from deprivation of its blood supply.

aborted myocardial infarction

Reperfusion of an occluded coronary artery before damage is done to the muscle that receives blood from that artery.

cardiac infarction

Myocardial infarction.

cerebral infarction

See: cerebral infarct

exercise-related myocardial infarction

A myocardial infarction whose symptoms begin within an hour of vigorous physical exercise.

lacunar infarction

A small stroke deep within the brain (as in the internal capsule, basal ganglia, thalamus, or pons) caused by damage to or a blockage of a tiny penetrating artery. Lacunar infarctions are associated with a kind of vascular damage caused by chronic high blood pressure called lipohyalinosis. They may be asymptomatic, showing up only on brain imaging, or may produce pure motor, pure sensory, ataxic, or mixed motor and sensory symptoms. Synonym: lacunar stroke

malignant cerebral artery infarction

A massive stroke involving the middle cerebral artery, in which swelling of the brain leads either to herniation and death or to additional strokes in other arteries.
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MYOCARDIAL INFARCTION: Myocardial infarction as seen on an electrocardiogram
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myocardial infarction

Abbreviation: MI
The loss of living heart muscle as a result of coronary artery occlusion. MI or its related syndromes (acute coronary syndrome or unstable angina) usually occurs when an atheromatous plaque in a coronary artery ruptures, and the resulting clot obstructs the injured blood vessel. Perfusion of the muscular tissue that lies downstream from the blocked artery is lost. If blood flow is not restored within a few hours, the heart muscle dies. Synonym: cardiac infarction

Acute MI affects 1.1 million people each year, and approx. 350,000 of them die. The probability of dying from MI is related to the patient's underlying health, whether arrhythmias such as ventricular fibrillation or ventricular tachycardia occur, and how rapidly the patient seeks medical attention and receives appropriate therapies (such as thrombolytic drugs, angioplasty, antiplatelet drugs, beta blockers, and intensive electrocardiographic monitoring). See: illustration; advanced cardiac life support; atherosclerosis; cardiac arrest; sudden death


Proven risk factors for MI are tobacco use, diabetes mellitus, abnormally high cholesterol levels, high blood pressure, gender, advanced age, obesity, physical inactivity, chronic kidney disease, a family history of MI at an early age, and loss of albumin in the urine. Some research suggests that high C reactive protein levels, and other conditions may also lead to increased risk.


Classic symptoms of MI in men are a gradual onset of pain or pressure, felt most intensely in the center of the chest, radiating into the neck, jaw, shoulders, or arms, and lasting more than a half hour. Pain typically is dull or heavy rather than sharp or stabbing, and often is associated with difficult breathing, nausea, vomiting, and profuse sweating. Clinical presentations, however, vary considerably, and distinct presentations are seen in woman and the elderly, in whom, e.g., unexplained breathlessness is often the primary symptom. Many patients may mistake their symptoms for indigestion, intestinal gas, or muscular aches. About a third of all MIs are clinically silent, and almost half present with atypical symptoms. Often patients suffering MI have had angina pectoris for several weeks before and simply did not recognize it.


A compatible history associated either with segment elevation (on a 12-lead electrocardiogram) or with elevated blood levels of cardiac muscle enzymes such as troponins or creatine kinase can establish the diagnosis. An ST-segment elevation of more than 1 mm above baseline in at least two contiguous precordial leads or two adjacent limb leads suggests myocardial injury. Myocardial infarctions with this presentation are known as ST-segment elevation MI (STEMI). This finding usually indicates significant muscle damage in the infarct area, a poorer prognosis, and a higher incidence of complications (arrhythmias, cardiogenic shock) than in a non-ST-segment elevation MI (NSTEMI). The differential diagnosis of chest pain must always be carefully considered because other serious illnesses, such as pulmonary embolism, pericarditis, aortic dissection, esophageal rupture, acute cholecystitis, esophagitis, or splenic rupture may mimic MI.


Myocardial infarction is a medical emergency; diagnosis and treatment should not be delayed. People who experience symptoms suggestive of MI should be taught to call 911 immediately and chew and swallow aspirin. Oxygen is administered at 4 L/min as soon as it is available. History is gathered throughout the first few minutes after admission even as a 12-lead ECG is being done and blood taken for biomarkers. Cardiac troponins may not become elevated until 4 or more hr after symptoms begin. If the patient is hypotensive or in cardiogenic shock, right-sided ECG leads are assessed for a right ventricular (RV) infarct. An intravenous access is established along with continuous cardiac monitoring, and medications (which may include chewed aspirin [162 to 325 mg], heparins, or other medications to inhibit platelet aggregation, nitroglycerin [given SL, sprayed or IV], IV morphine, and beta-blockers) are administered as prescribed. Pain is assessed on a 1 to 10 intensity scale, and morphine 2 to 10 mg administered IV, with incremental doses of 2 to 8 mg every 5 to 15 min until relief is obtained. Beta-blockers (such as metoprolol or atenolol) decrease myocardial oxygen demand, helping to limit the amount of heart muscle damaged. An IV beta-blocker should be given if the patient is hypertensive or has a tachyarrhythmia as long as no contraindications exist. Patients with STEMI who arrive at the hospital within 6 hr of the onset of symptoms are treated with fibrinolytic therapy or percutaneous coronary intervention (PCI). The goal for administration of fibrinolytic therapy is 30 min postsymptom onset (door-to-needle); for PCI 90 min (door-to-balloon inflation). Absolute contraindications of fibrinolytic therapy include previous intracranial hemorrhage or ischemic stroke within 3 months ( intracranial malignancy), active bleeding, or bleeding disorders (except menses), significant closed head or facial trauma within 3 months (known structural cerebral vascular lesions), and suspected aortic dissection. Reperfusion is the immediate goal, usually best accomplished with balloon angioplasty and endovascular stent placement, although emergency coronary bypass surgery may be needed in cases when PCI fails. An angiotensin-converting enzyme (ACE) inhibitor is administered within 24 hr of a STEMI to suppress the renin-angiotensin-aldosterone system and prevent excess fluid retention. ACE inhibitors also prevent conversion of angiotensin I to angiotensin II (a potent vasoconstrictor), thus reducing afterload to help prevent heart failure.

In MI complicated by pulmonary edema, diuretics are administered, and dobutamine infusions may be necessary to increase cardiac output. Strict glucose control (maintaining blood sugars below 150 mg/dl, and preferably in the normal range) reduces mortality in acute MI. Hypotension and circulatory collapse frequently occur in patients with significant RV infarctions, and fluid challenge is administered to optimize RV preload. If this is unsuccessful, the patient with an RV infarct will require inotropic support, correction of bradycardia, and measures to achieve atrioventricular synchrony (cardioversion for atrial fibrillation, etc). In patients with ventricular arrhythmias, defibrillation, or cardioversion, lidocaine, vasopressin, or amiodarone infusions, or other drugs, may be necessary. Anemic patients (hematocrit less than 30 or those actively bleeding) benefit from blood (packed red cell) transfusions.

With contemporary care, about 95% of patients with acute MI who arrive at the hospital in time will survive. These patients are referred to nutrition therapists to learn how to use low-fat, low-cholesterol diets, and to cardiac rehabilitation programs for exercise training, tobacco cessation, and psychosocial support.

Patient care

Acute Care: On admission, all diagnostic and treatment procedures are explained briefly to reduce stress and anxiety. Continuous electrocardiographic monitoring is used to identify changes in heart rhythm, rate, and conduction. Location, radiation, quality, severity, and frequency of chest pain are documented and relieved with IV morphine. Bleeding is the most common complication of antiplatelet, anticoagulant, and fibrinolytic therapies. The complete blood count, prothrombin time, and activated partial thromboplastin time are monitored at daily intervals. IV sites are assessed for evidence of bleeding. Fluid balance and pulmonary status are closely monitored for signs of fluid retention and overload. Breath sounds are auscultated for crackles (which may resolve by having the patient cough when caused by atelectasis, or which may indicate pulmonary edema when they do not). Heart sounds are auscultated for S3 or S4 gallops or new heart murmurs. Patient care and other activities should be organized to allow for periods on uninterrupted rest. Stool softeners are prescribed to prevent straining during defecation, which can cause vagal stimulation and slow the heart rate. Antiembolism stockings help to prevent venostasis and deep vein thrombosis. Emotional support is provided to decrease stress and anxiety. Adjustment disorders and depression are often experienced by MI patients, and the patient and family are assisted to deal with these feelings. Stress tests, coronary angiography, cardiac imaging procedures, reperfusion techniques, and other interventions are explained. The patient receives assistance in coping with changes in health status and self-concept.

Ambulatory Care: Cardiac rehabilitation begins as soon as the patient is physiologically stable. The goal of cardiac rehabilitation is to have the patient establish a healthy lifestyle that minimizes the risk of another MI. Ambulation is slowly increased, and a low-level treadmill test may be ordered before discharge to determine exercise tolerance and the risk of future heart attacks. Patients are taught not only to measure their pulse but also to assess their response to exercise in terms of fatigue, ease of breathing, and perceived workload. Following discharge, exercise is slowly increased, first while being monitored closely by supervised cardiac rehabilitation, and then more independently. The patient also receives information about a low saturated fat, low cholesterol, low calorie diet, such as the DASH eating plan (Dietary Approaches to Stop Hypertension), resumption of sexual activity, work, and other activities. The patient is taught about desired and adverse affects of all medications: aspirin therapy is usually prescribed as ongoing antiplatelet therapy (with or without clopidogrel), but patients should be warned about the risk of bleeding and be advised to avoid products containing ibuprofen, which blocks aspirin’s antiplatelet effects. Smoking cessation is an important preventive for future MIs. High blood pressure, obesity, adverse cholesterol levels, and diabetes mellitus also should be carefully managed to help prevent future MIs. Alcohol intake should be limited to 1 drink daily (women), 2 drinks daily (men). Opportunities are created for patients and families to share feelings and receive realistic reassurance about common fears.


placental infarction

A localized necrotic area caused by abruption.
See: abruptio placentae

pulmonary infarction

An infarction in the lung usually resulting from pulmonary embolism that may appear on x-rays as a wedge-shaped infiltrate near the pleura. Immediate therapy includes control of pain, oxygen administered continuously by mask, intravenous heparin (unless the patient has a known blood clotting defect), and treatment of shock or dysrhythmias, if present.

silent myocardial infarction

Unrecognized myocardial infarction. The patient may experience difficulty breathing, heartburn, nausea, arm pain, or other atypical symptoms.


The deprivation of a part of a tissue or organ of its blood supply so that a wedge-shaped area of dead tissue (an infarct) forms. Infarction of part of the heart muscle is the process underlying a heart attack.


Death of tissue due to inadequate blood supply.


Area of tissue necrosis caused by impaired arterial or venous blood supply due to mechanical factors (e.g., emboli, thrombi) or to blood pressure alterations.
Synonym(s): infarct.
References in periodicals archive ?
Ischemic changes in the myocardium have a rapid course, so the key condition for the effective treatment of myocardial infarction is the diagnosis and immediate initiation of treatment aimed at rapid restoration of coronary perfusion.
It was found that 125 of 223 patients had acute MCA infarction, 91 of whom were intubated before admission to the NICU or during the follow-up in NICU.
Thus, it was observed that arrhythmias were more common in patients of acute myocardial infarction presenting with bundle branch block than in patients of acute myocardial infarction without bundle branch block and was statistically significant (p= 0.05).
Every third patient in group 1 had history of myocardial infarction; 12.8% of patients older than working age had stroke history.
At the same time, the age of patients with myocardial infarction ranged from 43 to 87 years.
The second co-primary outcome of cardiovascular death, myocardial infarction, or ischaemia-driven revascularisation occurred in 179 patients (8.9%) in the complete revascularisation group compared to 399 (16.7%) in the culprit-lesion only group (HR 0.51; 95% CI 0.430.61; p
Exclusive criteria included having severe heart, liver, lung, kidney dysfunction and advanced malignant tumors, having other intracranial lesions or cerebral hemorrhage, platelet count < 100x109/L in patients with abnormal coagulation function or undergoing anticoagulation therapy, undergoing major surgery or having a history of cerebrovascular accident in the past six months, and being suspected having posterior circulation infarction because of the existence of severe consciousness disorder or with NIHSS score higher than 25 points.
Although the clinical significance of delayed images of I-123-BMIPP remains to be elucidated, the relation between washout rates of I-123-BMIPP and improvement of ventricular function was observed in patients with successfully reperfused ST-segment elevation myocardial infarction. (17)
ESC guidelines on management of acute myocardial infarction in patients presenting with persistent ST-segment elevation.
During the follow-up period, after the adjustment for several confounding factors, such as sex, age, hypertension, heart failure, dyslipidemia, hemodialysis, and statin usage, the adjusted hazard ratios (HRs) for the risk of subsequent MACEs during hospitalization for IE in treatment cohort did not attain statistical significance; 1.18 (95% confidence interval [CI], 0.53-2.66) for myocardial infarction and 1.29 (95% CI, 0.87-1.91) for ischemic stroke [Table 2].
Two patients with venous infarction had minor psychiatric symptoms that were difficult to distinguish from the side effects of drug withdrawal.
hypothesized that patients with such pattern have a very extensive transmural ischemic area of infarction that generates only little current which is not sufficient to travel toward the precordial leads but can go toward the aVR lead [16].