X-ray of the heart: what does it show and how to prepare?

Sometimes during intrauterine development, while the fetus is still in the mother’s body, disturbances may occur during the formation of the heart, which leads to abnormal structure of the walls of the heart, abnormal arrangement of blood vessels and valves. As a result, a mixture of oxygenated and deoxygenated blood occurs, or its improper distribution throughout the circulation. As a result, the body does not receive enough oxygen, which leads to the appearance of characteristic symptoms.

What is cardiac radiography?

X-ray of the heart is a fairly old research method and is to a certain extent inferior to some modern diagnostic procedures. However, to this day, radiography is quite informative. It allows you to quickly and accurately find out the condition of the heart chambers and great vessels. You can also obtain data on the contractility of the organ. Heart disease can be detected without radiography; it is often prescribed as an adjunct. X-rays of the heart are possible in both public and private clinics. This diagnostic method is very common.

What to do with an enlarged heart?

The first thing that worries parents if an X-ray reveals an enlarged heart in a child is the measures that can be taken.

• First you need to pull yourself together and put aside panic. If the disease is detected by chance, and not by diagnosis based on specific complaints and symptoms, then the baby is clearly not suffering, the organ copes with its task normally.
• It is necessary to contact a cardiologist who will prescribe additional studies and diagnostics to confirm or refute the suspected diagnosis.
• Proceed with the intended treatment. The sooner this happens, the greater the chance of a favorable prognosis.

As for the treatment itself, it is prescribed individually, depending on the symptoms, the baby’s well-being, the severity and cause of the disease.

X-ray anatomy

If you need to take a picture, it is worth learning the x-ray anatomy of large vessels and the heart. The X-ray anatomy of this organ consists of its shadow, the pulmonary artery, the aorta, and the vena cava. 2/3 of the listed structures are located to the left of the midline of the chest, only 1/3 protrudes to the right side. Chest X-ray anatomy includes the lungs, bronchi and trachea.

There are several types of location of the heart shadow, depending on its angle and the patient’s constitution. Namely:

• vertical – the angle is more than 45 degrees;
• oblique – the angle is 45 degrees;
• horizontal – angle less than 45 degrees.

As X-rays of the heart show, the horizontal position is usually characteristic of women, and the vertical position is usually characteristic of tall people.

Based on our own experience and literature data, a description of the genetic nature of hypertrophic cardiomyopathy, its clinical picture, and the results of instrumental studies is given. Treatment is being discussed. Criteria for poor prognosis are given.

Hypertrophic cardiomyopathy in children

Based on our experience and the literature describes the genetic nature of hypertrophic cardiomyopathy, its clinical presentation, results of instrumental studies. It is discuss the treatment. Some criteria of poor prognosis were held.

Hypertrophic cardiomyopathy (HCM) is a structural and functional lesion of the myocardium with an increase in its thickness (mass) with a known or suspected genetic defect of the cardiomyocyte sarcomere protein, inherited autosomal dominantly with varying penetrance and expressivity in the absence of systemic hypertension, storage diseases, hypothyroidism, atherosclerotic coronary sclerosis, valve defects, congenital heart defects and other conditions that could explain the increase in myocardial mass. Modern possibilities for the treatment of HCM with long-term support of a sufficiently high quality of life have actualized the problems of early diagnosis and adequate choice of patient management tactics [1, 2].

Etiology.HCM is inherited according to Mendelian laws in an autosomal dominant manner. The form of the disease in probands and their closest relatives is the same in 60% of cases. The genes responsible for the disease are localized on chromosome 6 (15 genes) and on the long arm of chromosome 14 [3]. Gene changes are represented by more than 400 missense mutations responsible for the regulatory, structural or functional characteristics of thin or thick filaments of cardiac sarcomeres (β-myosin heavy chain, actin, titin, myosin-binding protein C, tropomyosin T, etc.). The number of mutations itself determines the clinical variability of HCM. More than half of all genetically identified cases of HCM are determined by mutations in 3 genes that determine defects in the β-myosin heavy chain, myosin-binding protein C, and cardiac troponin T. Another 13 genes are responsible for infrequent cases of defects in titin, α-tropomyosin, α-actin, and cordial troponin I, myosin light chain. But among people with clinically and instrumentally diagnosed HCM and subjected to molecular genetic testing, gene abnormalities were detected only in 50-80% of cases [4, 5]. This means that in 20-50% we are dealing with mutations that have not yet been identified. It is likely that different populations will have their own mutations. Thus, it is suggested that the Russian population may be characterized by a missense mutation in the β-MHC gene.

The polymorphism of the clinical picture is explained by the insufficiently studied interaction of various genes (mutation MYH7 - pronounced hypertrophy, early onset and severe course; mutation TNNT2 - moderate hypertrophy; mutation MYBPC3 - incomplete penetrance and relatively late onset), gender, and external factors.

Pathophysiology . The gene defect leads to discoordination of the activity of myofibrils and subsequent fibrosis and hypertrophy of the myocardium. Chaotic cellular structure already occurs in areas without signs of hypertrophy and which are an arrhythmogenic substrate of ventricular tachycardia and fibrillation. At the same time, the intima of the intramural coronary arteries thickens, oxygen transport into the thickened myocardium is disrupted, ischemia, cell death, and sclerosis occur. The walls of the ventricles thicken, but the internal size remains unchanged or even decreases. Systolic function does not change for a long time, myocardial rigidity increases sharply, end-diastolic pressure increases, and blood return is inhibited. Hypertrophied myocardium can narrow the LV outflow tract. The degree of obstruction varies depending on the thickness of the interventricular septum, the location of the mitral annulus, anterior systolic movement of the mitral valve leaflets, and the intensity of myocardial contraction (therefore, digitalis preparations are contraindicated). The degree of obstruction does not correlate with the risk of sudden death. Progression of the disease leads to ventricular dilatation.

An experiment on animals with a positive HCM genotype but a negative phenotype showed that the administration of calcium channel blockers before the development of hypertrophy can prevent the disease [6]. Such experimental therapy is also carried out in people who are presymptomatic carriers of the HCM genotype.

The prevalence of HCM in children is 3-5: 1 million, median age is 7 years, 1/3 of all cases are diagnosed before the age of 1 year. In 25-58% of 1st degree relatives, echographic signs of HCM are detected. The incidence of HCM is approximately the same in different populations, although atypical variants of HCM are more common in Asia. Among children, there are gender differences in the incidence of HCM, but in adulthood, the disease is more often detected in men. The differences are explained by hormonal factors, environmental influences, more severe symptoms or a greater degree of LV outflow tract obstruction in men. All this determines more frequent studies leading to the diagnosis of HCM.

Clinical picture. There may be no complaints, and in these cases the diagnosis of HCM is the result of random echocardiographic studies. According to the results of our own studies (84 patients), indications of fainting, shortness of breath, a feeling of interruptions in the heart, etc. are more common. According to the results of 24-hour blood pressure monitoring, a tendency to bradycardia is recorded, apparently due to a decrease in LV ejection.

Shortness of breath is one of the earliest symptoms and occurs in 90% of patients. Dyspnea is caused by high rigidity of the thickened myocardium, increased end-diastolic pressure and transfer of pressure to the pulmonary circulation.

Syncope and presyncope are common in HCM, especially in children and adolescents with small LV diameter and ventricular tachycardia or sick sinus syndrome or sinus node dysfunction on 24-hour monitoring. In our group of patients they occurred in 27%, more often in the obstructive form of HCM. The presence of fainting is an indicator of a high probability of sudden death. Presyncope, which occurs during a sudden transition to a vertical position, can be caused by transient atrial or ventricular tachyarrhythmia and is considered a predictor of sudden death.

Dizziness is common in children with HCM with a high gradient in the left ventricular outflow tract and is aggravated by physical activity or hypovolemia (profuse sweating in the heat), rapid transition to an upright position, or a Valsalva reaction during bowel movements. Dizziness can occur with rhythm disturbances with decreased cerebral perfusion. Short-term episodes of arrhythmia are manifested by presyncope and dizziness, while persistent arrhythmias lead to fainting and sudden death.

Anginal pain is typical for children with HCM. There is no atherosclerotic coronary sclerosis. The symptoms of myocardial ischemia are explained by the increased need of the thickened myocardium for oxygen, which, if diastole is disturbed, leads to subendocardial hypoxia, especially during physical exertion. The feeling of interruptions in the heart is explained by premature atrial or ventricular contractions, intermittent atrioventricular block, supraventricular or ventricular tachycardia. Undiagnosed ventricular tachycardia is an indicator of a high risk of sudden death.

Orthopnea and paroxysmal nocturnal dyspnea are signs of heart failure in severe types of HCM with venous congestion in the lungs. Congestive heart failure in children occurs in only 10% of cases (much less often than in adults) and mainly before the age of 1 year. It is characteristic of patients with the most pronounced thickening of the myocardium. Congestive heart failure is the result of two damaging factors: high myocardial stiffness and subendocardial ischemia.

The apical impulse is diffuse, elevating, shifted to the left. A double impulse is typical, the upper part of which is formed by increased contraction of the left atrium. The most typical for HCM is the triple apical impulse, the last part of which is caused by isometric contraction of the ventricle. But this option is extremely rare.

Venous jugular pulse - a pronounced wave “a” on the venogram: a sharp increase in end-diastolic pressure in the left ventricle with an increase in pressure in the pulmonary circulation and thickening of the interventricular septum with a decrease in the cavity of the right ventricle, ultimately with inhibition of inflow to it.

The carotid pulse is high, fast and short, which is explained by the high speed of blood flow through the narrowed LV outflow tract. In some cases, the carotid pulse appears as a successive double pulsation of the carotid artery: 1st peak - as described earlier, 2nd - a low rise of the artery in late systole after the fall of the gradient.

Auscultation of the first tone is not changed, the second is usually split, and with a very high gradient it is paradoxical. A gallop rhythm or a third sound is often heard, but in HCM it does not have the same prognostic value as in valvular aortic stenosis. The IV tone is often determined due to forced atrial systole, overcoming resistance to blood flow into the LV. The diamond-shaped systolic ejection murmur (crescendo-decrescendo) is best heard at the point between the apex and the left edge of the sternum, radiates suprasternally, but is not transmitted to the carotid arteries. The intensity of the noise is determined by the subaortic gradient in the LV outflow tract. Since the degree of pressure gradient varies depending on the obstruction and the volume of inflowing blood, the intensity of the noise is not constant. The noise decreases with increasing preload: Valsalva maneuver, Müller maneuver (after forced exhalation, the inhalation movement is performed with the mouth and nose closed (subatmospheric pressure occurs in the chest and lungs = inverted Valsalva maneuver), squatting position. The gradient increases and the noise becomes louder as it decreases preload (nitrates, diuretics, standing) or decrease after exercise (vasodilators). A holosystolic murmur occurs with anterior systolic movement of the mitral valve and a very high gradient in the LV outflow tract. In 10% of children with HCM, a diastolic murmur is heard decrescendo regurgitation at the aortic valve, but with Doppler ultrasound, minimal and moderate aortic regurgitation is detected in 33%.

Additional research. Electrocardiography most often reveals signs of LV hypertrophy, deviation of the electrical axis of the heart, conduction disturbances, sinus bradycardia (33%) with ectopic atrial rhythm and atrial enlargement. With adenosine monophosphate mutation activated PRKAG2, HCM is combined with congenital Wolf-Parkinson-White syndrome and conduction disorders.

Deep Q waves in the precordial leads (40%), atrial fibrillation (a poor prognostic sign) and P wave abnormalities are relatively common. The size of the Q wave directly correlates with the thickness of the myocardium of the posterior wall of the LV (Fig. 1).

Figure 1. Electrocardiogram of patient N., 5 years old, with obstructive form of HCM. There is a pathologically deep Q wave in leads I, AVL, V5-V6. The voltage of the R wave in leads II, III, AVF, V6 is reduced. The thickness of the interventricular septum according to echocardiography is 1.5 cm, the posterior wall of the left ventricle is 0.7 cm.

The Q wave in leads II, III, aVF was recorded mainly in patients with moderate isolated myocardial hypertrophy. In severe progressive HCM, in addition to leads II, III, aVF, the Q wave was recorded in leads V4-V6; in cases of combined hypertrophy of the LV and right ventricular myocardium - in leads I, II, aVL, V4-V6. It can be assumed that the pathological Q wave is not only an isolated sign of hypertrophy of the interventricular septum, but also an indirect sign of the characteristics of LV hypertrophy. Changes in the repolarization process are typical: a decrease in the amplitude of the T wave (21% of those examined), its pronounced inversion (61%) up to giant negative T waves in leads V1-V6. Patients with the obstructive form of HCM are characterized by atrioventricular blockades.

With Holter monitoring, rhythm and conduction disturbances are recorded much more often than with simultaneous ECG recording.

There are major and minor ECG criteria for HCM. Major criteria include: 1) Q wave change (>40 ms or 1/3R) in at least 2 leads and 2) T wave inversion (≥3 mm) in at least 2 leads. Minor: 1) left atrium enlargement (Pv1), 2) PR<120 ms, 3) His bundle block or hemiblock (or interventricular conduction disorder: QRS≥120 ms), 4) deep wave Sv2, 5) reoplarization disorders. ECG criteria are nonspecific and must be combined with ultrasound data. For adults, echographic criteria are stable due to the completeness of the body’s development. For a child, the concept of normal is more blurred. Therefore, in children it is advisable to use the ratio of the thickness of the interventricular septum and the posterior wall of the LV. The latter is normally always thicker than the interventricular septum.

2D echocardiography is a leading diagnostic technique. The interventricular septum is thickened relative to the posterior wall of the LV. The internal diameter of the ventricle is at the lower limit of normal or reduced (Fig. 2).

Figure 2. Echogram along the long axis of the LV with asymmetric hypertrophy of the interventricular septum. The interventricular septum is sharply thickened and overlaps the LV outflow tract by almost half. 1 and 2 – aortic wall, 3 – interventricular septum, 4 – posterior wall of the LV.

The smaller the LV diameter, the higher the likelihood of fainting. With mitral regurgitation and/or low LV compliance, the left atrium cavity expands. A typical sign of HCM is anterior systolic motion of the mitral valve. It is explained by the displacement of the mitral ring into the outflow tract of the LV due to thickening of the interventricular septum and the shift of the valve leaflets to the septum (the pressure behind the closed leaflets of the mitral valve is high, and in front of them in the outflow tract, according to Bernoulli’s law, the pressure in the fast fluid flow is low) during systole (echographic Venturi phenomenon). Doppler ultrasonography is used to determine the rate of blood ejection in the LV outflow tract or the rate of blood flow in diastole through the left atrioventricular orifice. In the latter case, the velocity in the rapid filling phase (VEF) is reduced, the peak velocity in the systole phase of the left atrium (VA) relative to VEF is increased. This pathological relationship is also found in genotypically positive but asymptomatic patients.

The X-ray picture varies from unchanged to enlarged cardiac shadow. The left atrial arch bulges with high LV stiffness and mitral regurgitation.

Magnetic resonance imaging makes it possible to clarify the degree of obstruction and the anatomy of cardiac structures and reveals myocardial fibrosis, the prevalence of which directly correlates with the risk of sudden death.

Cardiac catheterization is performed to determine the degree of obstruction, the state of diastolic function, the interventricular septum and the coronary arteries.

Laboratory tests are nonspecific and are required only when secondary forms of myocardial thickening are excluded. Genetic testing most often (80% of HCM cases) reveals mutations in 9 sarcomeric genes MYH7, MYBPC3, TNNT2, TNNI3, TNNC1, TPM1, ACTC, MYL2, andMYL3 and in the CAV3 regulator gene.

Histologically, the myocardium is hypertrophied, myocardiocytes and myofibrils are arranged randomly, and fields of fibrosis are visible. In 80% of patients, the walls of the intramural branches of the coronary arteries are thickened, and the lumen is unevenly narrowed. These changes are most often recorded in the interventricular septum and are accompanied by fields of fibrosis. Along with the listed changes, even in supposedly unchanged areas of the myocardium, defects in calcium transport, disturbances in glycogen metabolism and other transformations are found that adversely affect the prognosis of the disease. This point of view can be confirmed by the fact that in 60% of those who died from HCM, according to light microscopy, 10-15% of the myocardial mass was changed, while for a fatal outcome in myocardial infarction or post-infarction cardiosclerosis, damage to at least 50% of the myocardial mass is required [7 , 8].

Doctor's tactics. After identifying myocardial thickening, it is necessary to carry out differential diagnosis with secondary causes of cardiac muscle hypertrophy:

• "the heart of an athlete" Long-term exercise can lead to myocardial hypertrophy, but with an appropriate history, concentric myocardial hypertrophy with expansion of the LV cavity is detected, which is not typical for HCM;
• aortic stenosis, aortic, subvalvular, coarctation of the aorta;
• restrictive cardiomyopathy;
• storage diseases (glycogenosis, mucopolysaccharidosis, amyloidosis, etc.);
• arterial hypertension (including neonatal);
• congenital hypothyroidism, newborn from a mother with diabetes mellitus;
• neuromuscular diseases;
• ventricular fibrillation.

General recommendations, monitoring physical activity and dynamics of disease symptoms. There is no special diet. Parents and patients should be warned about limiting physical activity, abolishing anaerobic exercise, and avoiding sports (especially in cases of arrhythmias and familial cases of sudden death). Avoid dehydration, control body weight. In dynamics, the thickness of the myocardium (myocardial mass), indicators of LV diastolic function, the diameter of its outflow tract, the pressure gradient, the presence of anterior systolic movement of the mitral valve, and arrhythmias are assessed. In the absence of emergency indications, an ECG is performed every 6 months, an ultrasound examination of the heart - annually, during puberty - every 6 months. If symptoms of HCM or signs of obstruction occur, it is advisable to initiate therapy with calcium channel blockers or β-blockers. In case of severe obstruction, together with surgeons, determine the indications for myectomy (or alcohol ablation) and pacemaker implantation. Prevention of bacterial endocarditis with antibiotics is not indicated. Diuretics, inotropic drugs, nitrates and sympathomimetics are contraindicated. Rule out digitalis unless there is uncontrolled atrial fibrillation.

Controlling risk factors for sudden death is the goal of any therapy for HCM. There are no uniform recommendations. Prognostic factors include familial cases of sudden death, familial variants of HCM, anamnestic indications of periods of asystole, unexplained fainting, pressure gradient (disputed), arrhythmias, thickness of the interventricular septum.

Drug therapy. The drugs of choice are β-blockers and calcium channel blockers. For heart rhythm disturbances, amiodarone and other antiarrhythmic drugs are prescribed. β-blockers reduce the pressure gradient in the LV outflow tract and optimize LV compliance. The effect of treatment was recorded in ½ patients. There is no evidence that β-blockers reduce the risk of sudden death. An alternative to β-blockers are calcium channel blockers. They improve diastolic function and reduce the pressure gradient by reducing LV contractility.

Propranolol (Inderal) is a non-selective β-blocker, the dose is adjusted according to the clinical effect. Atenolol (tenormin) is a selective β1 receptor blocker with minimal effect on β2 receptors. Efficiency is higher than that of propranolol.

Verapamil (isoptin) blocks slow calcium channels in vascular smooth muscle cells and myocardiocytes. The dose is selected individually, maximum effectiveness has been recorded during physical activity.

Amiodarone (cordarone), an effective antiarrhythmic drug, has several points of application. If long QT syndrome is excluded, it is the drug of choice in the treatment of life-threatening ventricular arrhythmias refractory to β-blockers.

Implantation of a pacemaker [7] leads to an improvement in the course of HCM and a reduction in pharmacological load.

LV myectomy with a gradient of 50 mm. rt. Art. regardless of whether it was recorded at rest or during provocative tests. In most cases, the positive dynamics of symptoms persists for 5 years. There is no complete correlation between the success of myectomy and the likelihood of sudden death. Catheter transvenous alcohol ablation of the interventricular septum is more dangerous than open surgery. It is fraught with irreversible atrioventricular block, myocardial infarction, necrosis of the interventricular septum with its iatrogenic defect [9].

Forecast. Sudden death may be the first and fatal manifestation of HCM in previously asymptomatic patients. In children and adolescents, sudden death is provoked by physical activity and sports activities. The maximum mortality rate was recorded in children with HCM diagnosed before the age of 1 year. In the group of children over 1 year of age, mortality is 1-1.4% per year [10, 11]. In 80-85% of cases, sudden death is the result of atrial flutter. Ventricular flutter develops after atrial flutter or fibrillation, ventricular tachycardia, supraventricular tachycardia in combination with Wolff-Parkinson-White syndrome, or catastrophically low cardiac output with hemodynamic collapse. The most important condition for preventing sudden death is early diagnosis of HCM, which allows changing lifestyle, physical activity, prescribing medication, determining indications for surgical treatment or implantation of a cardioverter defibrillator. Taking into account the autosomal dominant type of inheritance, in order to prevent familial cases of sudden death, examination of relatives is required.

Other complications of HCM include infective endocarditis, heart failure, arrhythmias, and atrial fibrillation with intramural thrombosis.

The criteria for poor prognosis and progressive course of HCM in children are:

• family history of sudden death;
• formation of a QS type complex and increasing conduction disturbance along the left bundle branch;
• high grade ventricular arrhythmia;
• atrial fibrillation;
• sick sinus syndrome;
• distal atrioventricular block 1-2 degrees;
• initially low rates of heart rate variability or their decrease by 30% during observation;
• decreased heart rate variability while taking β-blockers.

Conclusion

Hypertrophic cardiomyopathy is a genetically determined disease that rarely manifests itself in childhood and is more often detected in adults. Myocardial hypertrophy is often asymmetrical. Although any sector of the LV can be affected, the interventricular septum often becomes thickened with obstruction of the LV outflow tract. Systolic functions remain intact for a long time, but compliance suffers early. HCM is a chronic disease with a variable clinical picture from the complete absence of clinical symptoms to significant limitation of vital activity with sudden death. HCM is the leading cause of sudden death during exercise in adolescents. The pediatrician is required to organize interdisciplinary and interprofessional support for patients with the choice of therapeutic or surgical tactics, determine the degree of risk of sudden death and its prevention, and screening examinations of relatives.

V.M. Delyagin, E.A. Tikhomirova, A. Urazbagambetov

Federal Scientific and Clinical Center for Pediatric Hematology, Oncology and Immunology, Moscow

Delyagin Vasily Mikhailovich - Doctor of Medical Sciences, Chief Researcher of the Department of Rare Diseases, Head of the Department of Functional Diagnostics

Literature:

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2. Maron B., McKenna W., Danielsen W. et. al. American College of Cardiology // Eur. Heart J. - 2003. - Vol. 24. - P. 1665-1691.

3. Jarcho J., McKenna W., Pare J. et. al. Mapping a gene for familial hypertrophic cardiomyopathy to chromosome 14q1 // New Engl. J. Med. - 1989. - Vol. 321. – P. 1372-1378.

4. Bos J., Towbin J., Ackerman M. Diagnostic, prognostic, and therapeutic implications of genetic testing for hypertrophic cardiomyopathy // J. Am. Coll. Cardiology. - 2009. - Vol. 54. - P. 201-211.

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6. Semsarian C., Ahmad I., Giewat M. et. al. The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model // J. Clin. Invest. - 2002. - Vol. 109. - P. 1013-1020.

7. Epstein A., DiMarco J., Ellenbogen K., Estes N. et. al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology // J. Am. Col. Cardiol. - 2008. - Vol. 51. - P. 62.

8. Siegenthaler W. Differential diagnosis innerer Krankheiten // Neubearbeitete Auflage. - Stuttgart: Georg Thieme Verlag, 1993.

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What can an x-ray reveal?

An X-ray of the heart will provide a large amount of information regarding the position, size and condition of the organ and its structures. Based on these data, the doctor will be able to draw a conclusion about the presence of pathologies and identify the cause of the patient’s deterioration in well-being.

Heart sizes

An X-ray of the heart must be taken to find out whether the size of the organ is normal. They are very important in determining pathologies. The size is determined not by the width and length that are visible on an x-ray, but by the cardiothoracic index. To do this, you need to measure the width of the chest at the level of the fourth rib, and also find out the width of the heart in the same area. If the cell is twice as wide as the organ, the index will be 50%. If it is higher, then the heart muscle is enlarged. Myocardial hypertrophy may indicate ischemia or hypertension. Dilation of the chambers may be associated with cardiomyopathy or heart failure.

Condition of the great vessels

When thinking about what an X-ray of the heart shows, it is worth knowing that the condition of the great vessels will become known. The doctor will be able to find out if there are plaques, calcium deposits, or any lumps in the aorta. It will also be possible to identify a disease that is characterized by the accumulation of fluid in the pericardial sac. It is otherwise called “pericarditis”. If the fluid accumulates slowly, the organ becomes like a bag, but if it accumulates quickly, it becomes like a ball. If the condition is aggravated by calcium salt deposits, the doctor will diagnose constrictive pericarditis.

What symptoms should not be ignored

The following symptoms may indicate an enlarged heart in a child:

• increased heart rate;
• pallor or bluishness of the skin;
• rapid breathing;
• blueness of the nasolabial triangle;
• weak appetite.

Since the heart rate in children is always higher than in adults, it is impossible to say for sure whether your baby’s heart beats often or not. Only a doctor can determine this. But if the pulse is more than 160 beats per minute, then this is clearly not a good signal.

Breathing with cardiomegaly is not just rapid, but also shallow, uneven in inhalation and exhalation.

Pale skin occurs as a result of poor circulation due to poor functioning of the heart muscle and the organ itself.

Features of the procedure in children

Sometimes heart x-rays may be performed in children. This type of study is very rarely prescribed to children, since the procedure is contraindicated under 15 years of age. However, it may be required to identify heart defects, as well as when planning surgical interventions or to evaluate the effectiveness of the chosen treatment method. X-rays may also be needed to identify tumor processes.

If we are talking about a very young child, an X-ray of the heart will be taken using a special device. It is a stand on which the child is placed and his torso, head and limbs are secured with belts. This will ensure that the patient remains completely still while the doctor takes the image. The procedure will take no more than a couple of seconds, and discomfort is possible only from the belts with which the fixation is carried out. If we are talking about older children, they can undergo the procedure even without adults.

Causes

The causes of an enlarged heart in a child depend on the type of cardiomegaly. It can be primary or secondary. The secondary course of the disease occurs due to:

• severe toxic injuries;
• past infectious diseases that provoked various heart complications;
• respiratory failure of the lungs;
• acute viral infections.

If we are talking about the primary type of enlarged heart in a child, then the reasons for its occurrence are still not fully understood.

Preparation and carrying out diagnostics

You will only need to prepare if you need to undergo a cardiac X-ray with contrast. It involves taking tests to determine if you have an allergy to contrast, as well as visiting the office on an empty stomach, which will help avoid nausea.

To begin the procedure, you need to remove all jewelry or metal accessories that may affect the quality of the photo. The procedure is performed in 4 different projections:

• front;
• lateral left;
• oblique left (at an angle of 45 degrees);
• right.

Thanks to this, the description and conclusion of the heart x-ray will be as accurate as possible. The doctor will examine all planes of the organ and note the presence of pathological processes.

Contraindications

Such a study cannot be called completely safe. In this regard, there are a number of situations in which such diagnostics are not performed, but a more gentle method is selected. Often, an ultrasound

or MRI, as well as other studies.

Pregnant women

Before finding out what a heart x-ray is and what this procedure shows, a woman should be absolutely sure that there is no pregnancy. This situation is an absolute contraindication to the procedure, since there is a risk that X-ray radiation will have an adverse effect on the body of both the expectant mother and the baby. It is also not recommended for breastfeeding mothers to undergo diagnostics. However, in some situations, a doctor may prescribe such a procedure if its benefits are significantly higher than the likely risks. Therefore, it is best to trust the doctor.