Transmural infarction

Author Ольга Кияница


Among all forms of heart attack, the most severe is transmural myocardial infarction. Its rapid development threatens a high risk of death. With the timely provision of medical care, the patient's condition can be improved, but there is a possibility of serious complications.

Transmural myocardial infarction (TIM) is necrosis of the heart muscle, which covers the entire thickness or almost the entire wall of the ventricle (from the endocardium to the epicardium). Usually, the anterior and posterior walls of the right ventricle are affected (in 15-30% of cases). Isolated TIM of the right ventricle and right atrium are rare.

Most often, TIM develops because of coronary artery occlusion by more than 75%. In addition, the association of TIM with epicarditis is determined.

To determine the cause of the development of transmural myocardial infarction, various instrumental and laboratory studies are carried out. Much depends on the completeness of the medical history that the attending physician collects during the initial examination of the patient. Also, the presence of characteristic symptoms of the disease allows you to make an accurate diagnosis and conduct effective treatment.

Video Myocardial infarction


The most significant risk factors for myocardial infarction are:

  • elderly age;
  • smoking;
  • high blood pressure;
  • diabetes;
  • increased total cholesterol and high-density lipoprotein

Additional factors that predispose to the disease include male gender, low level of physical activity, a burdened family history, obesity and alcohol use [1 - Britton, the editors Nicki R. Colledge, Brian R. Walker, Stuart H. Ralston; illustated by Robert (2010). Davidson's principles and practice of medicine (21st ed.). Edinburgh: Churchill Livingstone / Elsevier.pp. 588-599]

At any age, men are more at risk of developing a heart attack than women. A high level of cholesterol in the blood creates favorable conditions for the development of coronary disease, especially important role is played by low-density lipoprotein, very low-density lipoprotein and triglycerides.

Many of the risk factors for myocardial infarction can be changed, most often smoking (including passive smoking).Smoking, apparently, contributes to the development of coronary artery disease in 36% of cases, and obesity - in 20%.The lack of physical activity is associated with 7-12% of cases.

Less common causes are associated with stress arising at work, which is the basis of the disease in 3% of cases. Also chronic stress can contribute to the development of pathology.


There are various evidences of the particular importance of saturated fats in the development of myocardial infarction.The use of polyunsaturated fats instead of saturated fats, as shown in the studies, helps reduce the risk of heart attack.At that time, in other studies there is little evidence that reducing fat intake or increasing the intake of polyunsaturated fats affects the risk of a heart attack.

Dietary cholesterol does not seem to have a significant effect on blood cholesterol levels, so recommendations for its consumption are not significant. Trans fats, apparently, increase the likelihood of MI. The intake of a large number of alcoholic beverages (3-4 or more) increases the risk of a heart attack.

Genetic predisposition

The family history of coronary heart disease or MI, especially if someone has a first-line relative (father, brother) who had a myocardial infarction before age 55, or a first-line relative (mother, sister) aged less than 65 years increases the risk appearance of MI.

In studies of genomic associations, 27 genetic variants have been identified that are associated with an increased risk of myocardial infarction [2 - O'Donnell CJ, Nabel EG (December 2011). "Genomics of cardiovascular disease". The New England Journal of Medicine. 365 (22): 2098-109]. The strongest association of MI was found with chromosome 9 on short arm p at locus 21, which contains the CDKN2A and 2B genes, although the included single nucleotide polymorphisms are in the non-coding region. Most of these variants are in areas that were not previously involved in coronary artery disease. The following genes are directly related to MI: PCSK9, SORT1, MIA3, WDR12, MRAS, PHACTR1, LPA, TCF21, MTHFDSL, ZC3HC1, CDKN2A, 2B, ABO, PDGF0, APOA5, MNF1ASM283, COL4A1, HHIPC1, SMAD3, ADAMTS7, RAS1, SMG6, SNF8, LDLR, SLC5A3, MRPS6, KCNE2.


  • The risk of myocardial infarction increases with age, low physical activity and low socioeconomic status. Heart attacks are more common in the morning, especially between 6 am and noon. Studies show that MI is at least three times more common in the morning than in the late evening. [3 - Shaw E, Tofler GH (July 2009). "Circadian rhythm and cardiovascular disease". Current Atherosclerosis Reports. 11 (4): 289-95] Working with a floating schedule is also associated with a higher risk of myocardial infarction.
  • Women who use combined oral contraceptives have a moderately increased risk of myocardial infarction, especially if there are other risk factors. The use of non-steroidal anti-inflammatory drugs (NSAIDs), even for a short period a week, contributes to the development of an attack.
  • Endometriosis in women under the age of 40 years is a certain risk factor.
  • The short-term exposure of polluted air to a substance such as carbon monoxide, nitrogen dioxide and sulfur dioxide (but not ozone) is associated with MI.
  • A number of acute and chronic infections, including respiratory chlamydia, influenza, Helicobacter pylori and periodontitis among others are associated with atherosclerosis and myocardial infarction.
  • Calcium deposition in the coronary arteries can be detected during CT scanning. Calcium, observed in the coronary arteries, can provide prognostic information, different from the classical risk factors.
  • High levels of homocysteine in amino acids are associated with the premature development of atherosclerosis, which in turn provokes a heart attack.
  • In people without obvious coronary artery disease, possible reasons for myocardial infarction are coronary spasm or coronary dissection.


  • Pain

The most common symptom of acute myocardial infarction, including transmural, is chest pain. It is often described as a feeling of squeezing or squeezing. Pain most often spreads to the left arm, but can also irradiate to the lower jaw, neck, right arm, back and upper abdomen.

The pain that most suggests the acute myocardial infarction is pain transmitted to the right arm and shoulder. Pain associated with MI is usually blurred, does not change with position and lasts more than 20 minutes.

Levin's sign, in which a person indicates pain in the chest, clenching one or both fists in the sternum, was previously considered a classic diagnostic feature, although a prospective observational study showed that it has insufficient diagnostic value.

Pain that responds to nitroglycerin is not a reliable indication of the presence or absence of myocardial infarction.

  • Other symptoms

Pain in the chest can be accompanied by sweating, nausea or vomiting and fainting. These symptoms can also occur without any pain.

In women, the most common symptoms of myocardial infarction are shortness of breath, weakness and fatigue.Shortness of breath is common, and sometimes the only symptom that occurs when heart damage is limited to the left ventricle. There is shortness of breath, either because of a low level of oxygen in the blood, or because of the pulmonary edema. Other less common symptoms include weakness, palpitations and changes in heart rate or blood pressure lowering. These symptoms are probably caused by a massive outbreak of catecholamines produced by the sympathetic nervous system that arises in response to pain and, if available, low blood pressure.

Loss of consciousness develops because of insufficient blood flow to the brain, cardiogenic shock or sudden death. A common cause of syncope is ventricular fibrillation. Cardiac arrest and atypical symptoms, such as heart palpitations, are more common in women, the elderly, patients with diabetes and with a previous operation.

"Silent" myocardial infarction can occur without any symptoms. These cases can be detected later on electrocardiograms, using tests on blood enzymes or at autopsy after the death of a person. Such silent myocardial infarctions account for 22 to 64% of all myocardial infarctions and are more common in the elderly, in patients with diabetes mellitus and after heart transplantation.

People with diabetes, as possible explanations for the absence of symptoms, indicated differences in the pain threshold, as well as the presence of autonomic neuropathy and psychological factors. In heart transplantation, the donor organ is not completely innervated by the recipient's nervous system.

Video Symptoms of an Infarction


To clarify the diagnosis of transmural myocardial infarction, various instrumental and laboratory methods of investigation are used.


  • The height of the ST segment (specificity - 91%, sensitivity - 46%). The higher the rise of the segment, the greater the heart attack and the risk of death.
  • Inversion of the T-wave
  • Wide and deep Q waves appear

Cardiac markers in serum

Intracellular macromolecules that enter the blood with myocardial infarction;

most often determined in laboratory tests.

  • Creatine kinase. There are three isoenzymes of creatine kinase:
    • MM - cardiac and skeletal muscles
    • CF - exclusively the heart muscle
    • BB - the brain, intestines and bladder
  • Troponins
  • Myoglobin

Creatine kinase

  • The first detection occurs 3-4 hours after the onset of an attack, the peak concentration is 8-24 hours, determined over 3-4 days.
  • It is not a strictly specific indicator, since it is found in skeletal and smooth muscles, so it is often detected in muscle trauma, severe CNS trauma.

Creatine kinase MB is a more specific indicator of heart muscle damage than total creatine kinase. At the same time, it rises and falls slightly earlier than the total number of QCs.


These are protein compounds present in the cardiac and skeletal muscles. Cardiac troponin (cTnT and cTnI) usually does not enter the total blood flow. It is considered a very sensitive and specific marker of myocardial infarction.

  • In the blood serum, they are mostly presented in the form of CK-MB and are determined early enough, 2-4 hours after the onset of the attack, with it being in the blood for a long time (up to 10-14 days).
  • Are good markers in cases when patients enter the examination due to MI much later.
  • Can be mildly elevated with unstable angina

Lactate dehydrogenase

  • Nonspecific indicator, which can come from the liver, lungs, kidneys, muscles, erythrocytes
  • The increase in isoenzyme LDG1 is considered a more specific indicator
  • The ratio of LDH1 to LDH2 is 1 and is useful in the conduct of diagnosis
  • The amount of LDH changes after 24 hours and remains at this level for 4-5 days
  • If necessary, this indicator is replaced by troponin T


  • The first marker, which is detected 1-4 hours after the onset of the attack and reaches a maximum after 6 hours. The duration of its high concentration is 24 hours
  • Nonspecific indicator, since myoglobin is also present in skeletal muscles
  • Not often used in diagnosis, but may be useful for early detection of MI

Video Myocardial infarction - how and why occurs

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