Endocarditis (infectious). Endocarditis: its symptoms, diagnosis and treatment

At myocarditis of various etiologies In the intramural, subendocardial or subepicardial layers of the ventricular wall, parenchymal focal or diffuse inflammation develops with predominant damage to any area of ​​the heart. Uneven myocardial damage leads to changes in the resting and action transmembrane potential during the period of repolarization (S - T - T).

Inflammatory process may lead to damage to the conduction system. As a result, atrioventricular, sinoatrial, intraatrial and intraventricular blockades appear on the ECG with myocarditis, especially often with rheumatic one. With rheumatic heart disease in the first days acute period in most cases, a slowdown of atrioventricular conduction develops (Zuckermann R. 1962).

Other types violations Conduction in myocarditis is observed less frequently, but still quite often. Conduction disturbances often persist in myocardial cardiosclerosis. Taran Z. M. and Szilagyi N. (1958) note an increase in the duration of the Q-T interval in 90% of cases of rheumatic carditis.

At myocarditis. especially with the idiopathic Abramov-Fiedler type, various arrhythmias often develop. First of all, these are rhythm disturbances based on the re-entry mechanism: extrasystole, paroxysmal tachycardia, atrial fibrillation. This direction is probably due to the blockade process, which plays a significant role in the mechanism of the occurrence of a circular wave. However, other rhythm disturbances are also observed: ectopic rhythms, rhythm migration, atrioventricular dissociations.

Rarely on ECG changes in the QRS complex are determined, indicating large-focal necrotic (sclerotic) changes. Basically, their cause is not myocarditis, but concomitant diseases or complications (for example, coronary insufficiency, coronaryitis, coronary artery embolism due to endocarditis).

Often on ECG signs of overload (hypertrophy) of the heart parts are determined. Sometimes there is a decrease in the amplitude of ECG waves. ECG changes are especially pronounced in idiopathic and infectious-allergic myocarditis, in which rhythm disturbances often alternate and pathological symptoms gradually increase.

Patient Z., 23 years old. Clinical diagnosis: rheumatism, acute rheumatic carditis. Rheumatic heart disease: failure mitral valve. On the ECG: sinus rhythm, 67-75 per minute. Interval P - Q = 0.23 - 0.24 sec. P = 0.13 sec. QRS = 0.07 sec. Q - T = 0.36 sec. (norm 0.35 - 0.33 sec.). RI>SI. AQRS = +84°. The PI, II, III, aVF tooth is bifurcated. PV1-V2 two-phase (+ -) with an increased negative phase. Complex QRSV1 type rSr’. Complex QRSV2 type rS. Complex QRSI,V5,V6 type RS.

Complex QRSIII type qR. The QRS transition zone is slightly shifted to the left. Segment RS - TI, aVL, V3-V6 is slightly shifted downward from the isoelectric line. The TV2-V5 tooth is negative “coronary”. TV1,V6 negative shallow. TI,aVL two-phase (- +), low.

Slowing of atrioventricular conduction. intraatrial block and changes in the RS-T segment and T wave (“coronary” negative) are associated with rheumatic carditis. There are signs of either right ventricular hypertrophy or incomplete blockade of the right branch of the His bundle: shift of the transition zone to the left, rSr’V1 and RSI,V6 with RV4

Signs of severe left atrial hypertrophy and intraatrial block may be due to two reasons: moderate mitral valve insufficiency and dilatation of the left atrium, which developed as a result of myocarditis.

Conclusion. Deceleration of A - V conduction (incomplete A - V blockade of the 1st degree). Intraatrial block. Changes in the myocardium of the anteroseptal region and the anterolateral wall of the left ventricle associated with current myocarditis. The vertical position of the electrical axis of the heart, clockwise rotation of the heart, displacement of the transition zone to the left and incomplete blockade of the right branch of the His bundle, probably characterizing right ventricular hypertrophy. Left atrial hypertrophy.

Endocarditis

Endocarditis is an inflammatory infectious disease that affects the inner lining of the heart - the endocardium.

Endocarditis usually occurs when an infection - bacteria or fungi - enters the body. This infection can get to the inner lining of the heart most often from other sources of infection in the body. With endocarditis, the infection can also affect the heart valves and the inner lining of nearby vessels. The same infection can cause simultaneous disease of the kidneys, liver and spleen. If left untreated, endocarditis can damage the heart valves and lead to a defect (called acquired heart disease). These heart defects can have life-threatening consequences. Treatment for endocarditis includes antibiotics and, in severe cases, surgery.

Symptoms of endocarditis

Endocarditis can develop either slowly or quite quickly, depending on the cause and the presence of concomitant diseases in the patient.

Symptoms of endocarditis include:

  • Fever
  • Chills
  • The appearance of new or changes in previously existing heart murmurs
  • Fatigue
  • Pain in joints and muscles
  • Night sweats
  • Dyspnea
  • Pale skin
  • Constant cough
  • Swelling in the legs and abdomen
  • Unexplained weight loss
  • Hematuria (blood in urine)
  • Pain in the spleen area
  • Osler's nodes are red, painful nodules under the skin on the fingers.
  • Petechiae are reddish or purple dotted spots that represent hemorrhages in the skin and mucous membranes

When to see a doctor

If you experience the signs described above that may occur with endocarditis, especially if you are at high risk of this disease, for example, if you suffer from heart disease, or have previously had endocarditis, you should consult a doctor.

Causes of endocarditis

Endocarditis occurs when microbes enter the bloodstream and then attack the heart valves. Most often, the microorganisms that cause endocarditis can be bacteria, but there can also be fungi or others.

Sometimes endocarditis can be caused by bacteria that normally live in the mouth, throat, or other areas of the body. In other cases, bacteria that cause endocarditis can enter the bloodstream in the following ways:

  • Normal daily activity. This may include brushing your teeth or chewing food, especially if your teeth are damaged by caries.
  • Infections or other diseases. Bacteria can enter the bloodstream from other infected areas, such as skin lesions. Another possibility for bacteria to enter the bloodstream is gum damage, sexually transmitted diseases and intestinal pathology.
  • Catheters and needles. Bacteria can also enter the bloodstream through a catheter, a thin plastic tube through which various medications are injected into the bloodstream. Bacteria that can cause endocarditis can also enter the bloodstream through needles during a tattoo or piercing procedure.
  • Some dental procedures.

Typically, the immune system successfully fights microorganisms that enter the bloodstream. And even if bacteria get into the heart, they may never cause anything.

In most cases, endocarditis affects people who already had heart defects - an ideal environment for bacteria. In such patients, the inner lining of the heart - the endocardium - is damaged and allows bacteria to settle on it and multiply.

Risk factors

In a patient with a healthy heart, the risk of developing endocarditis is minimal. Even the most common heart diseases do not increase the risk of developing endocarditis.

The risk of developing endocarditis is highest in the following cases:

  • Artificial heart valves. Germs tend to settle on artificial heart valves than on normal ones. The risk of infection is highest in the first year of valve transplantation.
  • Congenital heart defects. The risk of endocarditis is higher in patients with congenital heart defects.
  • Previously suffered endocarditis. With endocarditis, damage to the heart tissue, especially the valves, remains, and this, in turn, increases the risk of developing endocarditis in the future.
  • Heart valve damage. Some diseases, such as rheumatic fever or other infectious diseases, can affect one or more heart valves, increasing the risk of them being affected by endocarditis.
  • Use of intravenous drugs. Drug addicts mostly use unsterile syringes and needles, or their sterilization leaves much to be desired. This greatly increases the risk of microbes entering the bloodstream, which can cause endocarditis.

If you have a heart defect or other heart disease, talk to your doctor about your risk of endocarditis. Even if you have had heart surgery and are no longer bothered by your existing heart defect, the risk of endocarditis still remains.

Complications of endocarditis

Endocarditis can lead to several complications, including:

  • Stroke or damage to internal organs. With endocarditis, the so-called endocarditis occurs on the inner lining of the heart - the endocardium. vegetation - proliferation of affected endocardial tissue with bacteria and cellular fragments. These vegetations can break away from their place of origin and be carried by the bloodstream to the brain, causing a stroke, or to internal organs, such as the kidneys, lungs, intestines, or to the limbs.
  • Infectious foci in other parts of the body. Endocarditis can cause pockets of infection in other tissues and organs, causing the formation of a collection of pus called an abscess. Such abscesses can occur in the lungs, kidneys, liver, and spleen. An abscess can also occur in the heart wall itself, causing heart rhythm disturbances. Severe cases of abscess may require surgery.
  • Heart failure. In the absence of adequate treatment for endocarditis, damage to the heart valves can occur, and a heart defect occurs (if there was none before) or a new defect is added to the existing one. As a result of heart disease, the normal functioning of the heart is disrupted, it is overloaded, and heart failure develops - weakening of the heart muscle, when the heart is no longer able to adequately pump blood. If not properly treated, the outcome can be fatal.

Diagnosis of endocarditis

The doctor may suspect the presence of endocarditis based on the history and physical data, for example, fever, heart murmurs, etc., namely the appearance of new murmurs or changes in previously existing ones.

In the initial stages, the infection can mimic other diseases. Therefore, different diagnostic methods are used to diagnose endocarditis:

Blood tests.

The most important research method in diagnosing endocarditis, which allows you to detect the presence of bacteria in the blood. A blood culture is usually performed to identify the bacterial culture. In addition, a blood test can reveal other signs of endocarditis - anemia, leukocytosis, etc.

  • Echocardiography.

    Echocardiography is an ultrasound method for examining the heart. It is absolutely safe and inexpensive, and at the same time provides a lot of necessary information to the doctor. When diagnosing endocarditis, the echocardiography method currently used is transesophageal echocardiography, that is, transesophageal. It is somewhat reminiscent of gastroscopy, which is used for diseases of the stomach, but the patient “swallows” not just a probe, but a probe with an ultrasound sensor. This method, unlike the traditional one, allows you to bring the sensor directly to the heart, and only a thin wall of the esophagus will separate them. This allows the doctor to get a clearer picture.

  • Electrocardiogram (ECG).

    Chest X-ray.

    A chest x-ray can show enlargement of the heart, which can be seen with endocarditis, as well as damage to the lungs (such as an abscess).

  • Computed tomography (CT) or magnetic resonance imaging (MRI).

    These methods allow you to obtain a layer-by-layer section of a particular area of ​​the body. They make it possible to identify various damage to organs and tissues, for example, abscesses that can occur with endocarditis.

  • Treatment of endocarditis

    Treatment for endocarditis usually begins with the use of antibiotics. In cases where there is already irreversible damage to the heart valves with the development of a defect, surgical intervention is required.

    Antibiotics

    Antibiotics are drugs that destroy germs. They can affect different types of microbes that cause endocarditis, including fungi. For endocarditis, antibiotics are usually administered only intravenously. Usually, before prescribing an antibiotic, a culture test is performed to determine the best antibiotic for a given microbe. I would like to note that today medicine has quite powerful antibiotics in its arsenal.

    Typically, the course of antibiotic therapy for endocarditis is from 4 to 6 weeks or more to completely destroy the microbes. If the fever and the most severe symptoms of endocarditis have passed, the patient can be discharged and receive a further course of antibiotics at home with regular monitoring of the condition by a doctor.

    You should tell your doctor about any symptoms that may indicate your condition is getting worse:

    • Fever
    • Chills
    • Headache
    • Joint pain
    • Dyspnea

    Diarrhea, skin rash, itching, or joint pain may indicate a reaction to an antibiotic, which is also a reason to call a doctor.

    If you experience shortness of breath or swelling of the legs, which may indicate heart failure, you should also consult your doctor.

    Surgical treatment

    In the case when endocarditis causes damage to the heart valves, even after complete destruction of the infection with antibiotic therapy, it is impossible to restore the previous state of the affected heart valves using conservative methods. Surgery is required. Sometimes surgery is required to treat a persistent infection in the patient's body or to replace damaged heart valves. In addition, surgery may be required to treat fungal endocarditis.

    Depending on your condition, your doctor may recommend either repairing the damaged heart valve or replacing it with an artificial one.

    Date: from 01/01/2015 to 31/12/2015

    Electrocardiography (ECG) is an informative, accessible and non-invasive method of graphically depicting the electrical activity of the heart, which is traditionally used to diagnose coronary insufficiency, rhythm and conduction disorders and some other conditions. In some cases, an ECG can serve as an additional criterion for assessing the severity and prognosis of infectious diseases as a marker of involvement of the cardiovascular system (CVS) in the pathological process. ECG changes in infectious diseases, as a rule, are insignificant and nonspecific, but in some cases they highly reliably indicate the development of serious complications, for example, myocardial abscesses in infective endocarditis.

    The causes of damage to the cardiovascular system and, accordingly, changes in the ECG can be classified into one of three categories: 1) direct (due to the damaging effect of an infectious agent or its toxins) or indirect (due to immunopathological processes) action of the pathogen; 2) disturbances of metabolism, electrolyte balance or function of the autonomic nervous system due to the characteristics of the infectious process; 3) adverse drug events (ADEs) of antimicrobial drugs.

    Viral infections

    HIV infection. Involvement of the cardiovascular system is observed mainly in the later stages of HIV infection. The most significant risk factor for the development of cardiac complications is a decrease in the number of CD4+ T-lymphocytes less than 100 cells/l. The most common ECG changes in HIV-infected patients are sinus tachycardia, decreased QRS voltage, nonspecific changes in the ST segment and T wave, and prolongation of the QT interval. The cause of these changes may be mitral valve prolapse, myocarditis with a decrease in the systolic function of the left ventricle, dilatation of the cavities of the heart, including its right parts, up to the clinical picture characteristic of dilated cardiomyopathy. Pericardial effusion may also occur, and much less commonly, infective endocarditis.

    Prolongation of the QT interval, even asymptomatic, in the absence of ventricular arrhythmias, is associated with an increased risk of death, and the incidence of this syndrome increases as immune disorders worsen.

    Rhythm disturbances in HIV-infected people, both children and adults, are relatively rare and are characterized by a benign clinical course. The most typical rhythm/conduction disorders are sinus tachycardia, first-degree atrioventricular (AV) block, supraventricular extrasystoles, which almost never progress to supraventricular or ventricular tachycardia, and high-degree AV block.

    Quite often, ECG signs of right ventricular hypertrophy are detected, reflecting pulmonary hypertension, which often develops with HIV infection.

    Rubella. An acute viral disease predominantly of childhood, the prevalence of which has a steady downward trend due to mass vaccination. The disease occurs with fever, lymphadenopathy and maculopapular rash with a clear phasing of the rashes from the face to the torso. Myocardial damage is extremely rare, but the appearance of changes on the ECG indicates a more severe course of rubella. Most often, changes in the ST segment and T wave are detected on the ECG. Deviation of the electrical axis to the left reflects transient or permanent damage to the left bundle branch and is often accompanied by hemodynamic disturbances.

    Spirochetoses

    Lyme disease. Systemic tick-borne borreliosis (Lyme disease, chronic migratory erythema) is an infectious natural focal disease. It is characterized by transmissible transmission (the causative agent is the spirochete Borrelia burgdorferi, carried by the tick Ixodes scapularis), polymorphism of clinical manifestations (damage to the skin, nervous and cardiovascular systems, joints), and a tendency to a protracted relapsing course. There are early and late periods of the disease. In the early period there are 2 stages. At the 1st stage, developing after a few days - 1 month. after a tick bite, the most permanent symptom is migratory ring-shaped erythema (erythema migrans) at the site of the tick bite; other symptoms of the acute period are variable and transient (Fig. 1). In approximately 20% of cases, skin lesions are the only manifestation of stage 1 Lyme disease. Changes in the ECG with isolated erythema migrans are observed rarely, mainly in the form of 1st degree AV block and an increase in the amplitude of the S wave.

    In the 2nd stage of the disease, along with general symptoms (weakness, headache, fever with chills, lymphadenopathy), signs of damage to the nervous system are observed (meningitis, encephalitis, neuritis of the cranial and peripheral nerves), and cardiac disorders occur in 4-10% of patients , most often in the form of myopericarditis with the development of left ventricular dysfunction and cardiomegaly. Rhythm disturbances occur in the form of sinus arrhythmia, bradycardia, and ventricular extrasystole. Changes in the terminal part of the ventricular complex may be recorded. The most common ECG symptom is conduction disturbances of the AV block type, up to complete transverse block, which, although rare, is a typical manifestation of systemic tick-borne borreliosis. It is difficult to record transient blockade due to its transient nature, but ECG recording is desirable in all patients with migratory erythema annulare, since complete transverse block is usually preceded by less severe rhythm disturbances. Conduction disturbances usually resolve on their own within 2-3 weeks, but complete AV block requires the intervention of cardiologists and cardiac surgeons. Stage 3 develops in 10% of patients 6 months to 2 years after the acute period. At this stage of the disease, the most studied are joint lesions (chronic Lyme arthritis), skin lesions (atrophic acrodermatitis), as well as chronic neurological syndromes, reminiscent in terms of development of the tertiary period of neurosyphilis. The appearance of any new specific ECG manifestations at this stage is not typical.

    On average, CVS damage in Lyme disease occurs in 8% of patients over the age of 18 years; the most typical ECG changes are conduction disturbances, which are characterized by a benign course and tend to resolve spontaneously; the need to install an artificial pacemaker is extremely rare. Rapid reverse development of AV blockade is observed against the background of parenteral administration of ceftriaxone (Fig. 2).

    ECG recording is a valuable screening method for suspected Lyme borreliosis: according to one study, 3 out of 10 children with suspected borreliosis had ECG changes.

    Leptospirosis. An acute infectious disease caused by various serotypes of Leptospira. Characterized by general intoxication, fever, damage to the kidneys, liver, nervous system and muscles. In severe forms, acute renal failure, jaundice and hemorrhagic syndrome are observed. Refers to zoonoses with natural focality. Human infection occurs through contaminated water bodies, less often through food or through contact with infected animals (pigs, etc.).

    With leptospirosis, the ECG often shows first-degree AV block, as well as ECG signs characteristic of acute pericarditis. Detection of ECG changes in leptospirosis highly likely indicates involvement of the cardiovascular system, most often in the form of myocarditis, and as a result, a worsening prognosis.

    Endemic (tick-borne) relapsing fever (synonyms: tick-borne borreliosis, tick-borne spirochetosis, tick-borne relapsing fever) is an infectious disease that occurs in the form of febrile attacks alternating with periods of normal temperature (apyrexia - a fever-free period). In the USSR by 1938 it was basically eliminated. Foci of infection remain in a number of countries in Asia, Africa and America. Caused by Borrelia B.hermsii and B.turicatae and is characterized by high relapsing fever with sudden onset. Febrile episodes last from 3 to 6 days and are accompanied by headache, arthralgia, myalgia, nausea and neck tension, and neuritis of the cranial nerves. Myocarditis develops rarely; a typical ECG manifestation of myocarditis is prolongation of the QT interval.

    Trichinosis. Develops as a result of eating meat contaminated with Trichinella larvae larvae. Clinical manifestations include fever, myalgia, headache, skin rash, nausea, vomiting, diarrhea, leg swelling, cough, subconjunctival and subungual hemorrhages. The frequency of detection of ECG changes, according to different authors, is different: for example, previously it was reported that ECG changes were detected in 21-75% of patients; according to later observations, this figure is 13%. Most often, transient nonspecific disturbances in the processes of ventricular repolarization are recorded on the ECG in the form of changes in the ST segment and T wave. Less often, ECG signs characteristic of pericarditis are detected.

    Bacterial infections

    Diphtheria. The causative agent is Corynebacterium diphtheriae, a gram-positive rod. Infection occurs by airborne droplets and through direct contact with respiratory tract secretions, infected objects and through third parties. The most significant risk factors for cardiovascular disease include older age, low socioeconomic status, and severe airway disease. In 2/3 of patients with diphtheria, signs of mild myocarditis are detected, in 10-25% - cardiac dysfunction. Diphtheria is characterized by two types of ECG changes: asymptomatic disorders in the form of prolongation of the PQ interval and changes in the T wave and deviations that have clinical manifestations of varying severity in the case of the development of high-degree AV blockades and intraventricular blocks. ECG changes in severe diphtheria last for several days after the disappearance of clinical symptoms. ECG abnormalities (changes in the ST segment and T wave) were observed in experimental animals after vaccination against diphtheria/tetanus/pertussis.

    Damage to the cardiovascular system is the leading cause of death in adult patients with diphtheria, accounting for approximately 1/3 of all causes of death in this infection. Diphtheria toxin causes severe acute myocarditis. Daily ECG monitoring upon admission of a patient to the hospital makes it possible to more reliably predict heart damage in diphtheria. The risk of CV involvement is higher in patients with fever, toxic and membranous forms of the disease. A worsening prognosis is indicated by ventricular arrhythmias, an increase in AST levels above 80 U/l, leukocytosis above 25.0∙109/l and the spread of fibrinous films to more than 2 anatomical areas.

    Tetanus is caused by the anaerobic gram-positive bacillus Clostridium tetani. There are 4 forms of tetanus: generalized, localized, neonatal and cephalgic. Involvement of the cardiovascular system is most often observed in the generalized form, the characteristic clinical manifestations of which are trismus, “sardonic smile” due to increased tone of the orbicularis oris muscle, and generalized convulsions. The ECG reveals sinus tachycardia, prolongation of the QT interval, nonspecific changes in the ST segment and T wave.

    Whooping cough. The causative agent of whooping cough is Bordetella pertussis - a small, non-motile, non-spore-forming, aerobic gram-negative coccobacilli. The disease is characterized by acute catarrh of the respiratory tract and attacks of spasmodic cough. The course of whooping cough can be complicated by the addition of secondary infections, damage to the central nervous and cardiovascular systems. The most typical ECG changes with the development of cardiac complications are sinoauricular and atrioventricular blockades. These changes develop due to activation of sodium channels of the cardiac conduction system by guanine nucleotide-binding protein of pertussis toxin.

    Streptococcal infections. Damage to the cardiovascular system occurs both as a result of the development of inflammatory processes, for example, in acute rheumatic fever (ARF) caused by β-hemolytic streptococci of group A, and due to the direct damaging effect of streptococcal toxins in other diseases of streptococcal etiology.

    The most characteristic ECG changes in ARF is first degree AV block, which is one of the minor diagnostic criteria for the disease. Other conduction abnormalities, in particular complete AV block and second-degree AV block type Mobitz I, are much less common in ARF. The most characteristic ECG changes in invasive streptococcal infections are changes in the ST segment - T wave. Other ECG abnormalities in ARF are less common: sinus tachycardia, P wave changes, T wave inversion, extrasystolic rhythm disturbances. Clinical manifestations of ARF include cardiomegaly, congestive heart failure, and the development of dysfunction of the mitral and/or aortic valves with a corresponding auscultation pattern.

    Myocarditis caused by group B streptococci is accompanied by a decrease in ECG voltage in the limb leads; pericardial involvement with the development of myopericarditis is also possible.

    Damage to the pericardium in the form of acute purulent pericarditis with ST segment elevation on the ECG has been described in diseases caused by group G streptococci.

    ECG changes in invasive streptococcal infections usually disappear with adequate antibiotic therapy.

    Typhoid fever is an acute, cyclical intestinal infection caused by Salmonella typhoid, Salmonella typhi, with a fecal-oral transmission mechanism, characterized by fever, symptoms of general intoxication with the development of typhoid status, roseola rashes on the skin, hepatosplenomegaly and damage to the lymphatic system of the small intestine. Every year, about 16 million cases of the disease are reported worldwide, of which about 600,000 are fatal.

    Complications in the form of intestinal obstruction, ulceration and perforation usually develop in the 4th week of the disease. Changes in the ECG are recorded both during the acute period of the disease, which lasts up to 4 weeks, and during the period of convalescence, which lasts up to 2 months. Damage to the cardiovascular system develops as a result of direct effects on the myocardium due to invasion of Salmonella typhi or under the influence of toxins (endotoxin, enterotoxin, cytotoxin) produced by salmonella. The level of cardiac-specific enzymes increases only in the acute period. The severity of myocarditis in typhoid fever depends on the patient’s previous health status; the greatest negative impact is exerted by anemia, cardiovascular pathology and nutritional deficiency.

    Typical ECG changes in typhoid fever include ECG signs of myocarditis: prolongation of the PQ interval, prolongation of the QT interval, ST segment depression and T wave inversion. In some cases, ECG changes in typhoid myocarditis resemble those in acute myocardial infarction of posterior inferior localization, especially in patients with concomitant Wolff-Parkinson-White syndrome.

    Although typhoid fever is characterized by relative bradycardia, that is, a heart rate that does not correspond to the height of the fever, sinus bradycardia as such is very rare in typhoid fever. There are only a few reports of sinus bradycardia caused by sick sinus syndrome developed against the background of typhoid fever. Sinus bradycardia in typhoid fever is refractory to atropine, but in most cases disappears on its own when the patient recovers.

    A brief description of ECG abnormalities in various infectious diseases is presented in Table. 1.

    Infectious heart diseases

    Changes in the ECG during myocarditis can be a consequence of myocarditis itself, caused by one or another infectious agent, or be secondary in nature, reflecting the influence of fever, hypokalemia, vitamin deficiency or adverse drug events when taking drugs for the treatment of myocarditis, primarily antimicrobial agents.

    Myocarditis can develop against the background of many infectious diseases, although the most common causative agents are viruses, especially enteroviruses (Coxsackie).

    Pathogens that cause acute myocarditis:

    1. Bacteria: Borrelia burgdorferi, Brucella spp. Campylobacter spp. Chlamydophila pneumoniae, Chlamydia psittaci, Clostridium perfringens, Corynebacterium diphtheriae, Coxiella burnetii, Ehrlichia spp. Legionella pneumophila, Listeria monocytogenes, Mycobacterium tuberculosis, Mycoplasma pneumoniae, Neisseria meningitidis, Rickettsia spp. Salmonella spp. Shigella spp. Staphylococcus aureus, Streptococcus pyogenes, Vibrio cholerae.

    2. Fungi: Aspergillus spp. Blastomyces spp. Candida spp. Coccidioides immitis, Cryptococcus spp. Histoplasma capsulatum.

    4. Viruses: Coxsackie viruses A and B, cytomegalovirus, echovirus, Epstein-Barr virus, hepatitis B and C virus, human immunodeficiency virus, paramyxovirus.

    Since the pathological focus of a viral infection is localized in ischemic areas, such lesions are usually located in the subendocardial layer of the myocardium. Manifestations of viral myocarditis depend on the virulence of the infectious agent and on the hormonal and immunological status of the macroorganism. Infection of the fetus with rubella virus, paramyxovirus and coxsackievirus can cause congenital malformations. Myocarditis is accompanied by various changes on the ECG, most often by AV blocks of varying degrees, other conduction disturbances, changes in the ST segment and T wave, sometimes simulating acute coronary syndrome, and ventricular arrhythmias (Fig. 3).

    Pericarditis- an inflammatory disease of the pericardium, caused by many infectious agents, and in some cases simultaneous damage to the peri- and myocardium is possible.

    Typical causative agents of acute pericarditis:

    1. Bacteria: Haemophilus influenzae, Mycobacterium spp. Neisseria gonorrhoeae, Neisseria meningitidis, Salmonella spp. Staphylococcus aureus, Streptococcus pneumoniae.

    2. Fungi: Aspergillus spp. Blastomyces spp. Candida spp. Coccidioides immitis, Cryptococcus neoformans, Histoplasma capsulatum.

    3. Viruses: Coxsackie viruses A and B, echovirus, Epstein-Barr virus, HIV, influenza virus, paramyxovirus, parvovirus B19.

    In the early stage of pericarditis, the ECG shows depression of the PQ segment, followed by ST segment elevation, ST segment normalization, T wave inversion and ECG normalization (Fig. 4; Table 2). In pericarditis, the ECG may resemble the ECG in acute coronary syndrome. Differential diagnosis of ECG changes due to myopericarditis, acute coronary syndrome and premature ventricular repolarization syndrome is presented in Table. 3. The evolution of ECG changes can last from several days to several weeks. With the formation of effusion in the pericardium, a decrease in the voltage of the ECG waves is observed (Fig. 5).

    Endocarditis. With endocarditis, ECG changes often develop, the appearance of which indicates an invasive form of infection, a high risk of complications and fatal outcome. Impaired conductivity indicates the spread of the infectious process to the perivalvular area. ECG changes are very often recorded in patients with artificial valves. Unfortunately, there have been no prospective studies of ECG changes in infective endocarditis. Autopsy studies confirm that the most common change on the ECG is sinus tachycardia, recorded in 53% of patients with verified infective endocarditis. Less frequently, other changes were detected on the ECG: decreased voltage of the QRS complex (44%), AV block of varying degrees (9%), ST segment elevation, atrial fibrillation, ventricular tachycardia and supraventricular tachycardia (Fig. 6).

    In patients with infective endocarditis, in whom, despite adequate antimicrobial therapy, fever persists for a long time and chest pain and shortness of breath appear, the detection of AV blockades on the ECG indicates the development of a perivalvular abscess and requires surgical treatment (Fig. 7).

    Mycoplasmosis. Mycoplasma pneumoniae causes diseases of the upper and lower respiratory tract in approximately 70% of those infected; 20% are asymptomatic. Epidemiological outbreaks are observed in closed communities (army, prisons). Involvement of the cardiovascular system is rare and in the vast majority of cases - in individuals with clinically manifest forms of mycoplasma infection. The most common ECG abnormalities are changes in the terminal part of the ventricular complex in the form of T wave inversion. Bradycardia, prolongation of the PQ interval and a narrow QRS complex can also be recorded. In the absence of symptoms of cardiovascular disease, ECG changes are rare and nonspecific. Previous cardiac pathology does not affect the risk of development and severity of ECG abnormalities.

    An increase in intracranial pressure of infectious origin due to meningitis (as, indeed, in non-infectious diseases, for example, subarachnoid hemorrhage, brain tumors) can also cause abnormalities on the ECG. The mechanism of development of ECG changes in patients with increased intracranial pressure depends on the etiology of the disease and is realized through an increase in the tone of the sympathetic and parasympathetic nervous system during the acute period of subarachnoid hemorrhage; release of large amounts of norepinephrine and epinephrine from brain tumors; electrolyte disturbances in meningitis and arrhythmogenic effect in tumor damage to the limbic structures of the brain. Hypokalemia, which develops with brain tumors, hemorrhages and with increased activity of the autonomic nervous system, also contributes to the development of ECG abnormalities. Characteristic changes on the ECG with increased intracranial pressure include a tall P wave, a tall U wave, an inverted U wave, changes in the ST segment and T wave, notched T waves, and sinus tachycardia (Fig. 8).

    Antimicrobials

    Antimicrobials can block sodium channels, leading to prolongation of repolarization and prolongation of the QT interval. Fluoroquinolones have a similar proarrhythmic effect, prolonging the QT interval and increasing the risk of developing torsades de pointes (Fig. 9). The proarrhythmic effect of fluoroquinolones increases significantly in the presence of electrolyte disturbances (hypomagnesemia, hypokalemia, hypocalcemia), alcoholism, and concomitant use of class I antiarrhythmic drugs, especially quinidine, and class III. The arrhythmogenic effect disappears after stopping fluoroquinolones. Most often, prolongation of the QT interval occurs during the use of sparfloxacin (14.5 cases per 1 million prescriptions); ciprofloxacin causes prolongation of the QT interval much less frequently (1 case per 1 million prescriptions). Antifungal drugs of the azole class also have the property of prolonging the QT interval. The proarrhythmic effect of azoles is especially often realized when combined with antihistamines (loratadine, terfenadine, ebastine). Antimicrobial drugs of the macrolide class have the same effect. Erythromycin has the most powerful proarrhythmic effect among macrolides, followed by clarithromycin, roxithromycin and azithromycin. For example, clarithromycin causes QT prolongation in 3 cases per 1 million prescriptions.

    Conclusion

    The main provisions regarding the role of ECG in infectious diseases are presented in table. 4. ECG changes in various infectious diseases develop for various reasons: under the influence of the infectious process itself, as well as due to metabolic disorders or dysfunction of the autonomic nervous system caused by this process. In some cases, identifying changes in the ECG facilitates the differential diagnosis of the underlying disease, for example, Lyme borreliosis or ARF. However, much more often, the assessment of changes in the ECG, without providing additional diagnostic value, provides important information for assessing the severity of the infectious disease, its prognosis, as well as the effectiveness and safety of treatment. Many antimicrobial drugs have a proarrhythmic effect, and timely identification of ECG signs of a high risk of developing rhythm disturbances can significantly reduce the incidence of severe NDEs.

    Inflammation of the inner lining of the heart. The heart muscle itself consists of many layers, walls, vessels, and each of these elements performs vital functions. Damage to the endocardium leads to disruptions in the smoothness and elasticity of the internal chambers of the heart.

    Even microscopic defects in the functioning of the heart often lead to death, but here we are talking about damage to an entire layer of connective tissue, without which the effective functioning of the heart muscle is impossible.

    Endocarditis rarely manifests itself - more often it is a consequence of another, even more significant disease. Only bacterial endocarditis, which is caused by streptococcus, forms on its own.

    Causes of endocarditis

    Causes of bacterial endocarditis

    The causes of endocarditis are divided into two broad categories depending on many factors:

    1. Primary endocarditis.
    2. Secondary endocarditis.

    Diseases first group caused by microbiological flora. The pinnacle of popularity is streptococcus - a very underrated and dangerous enemy of human health. The causes of the disease are also gonococci, which can also cause diseases such as syphilis, meningococci, and E. coli.

    Next, vegetations and dangerous inflammatory processes in the connective tissue form. A process occurs in the heart valves, dangerously approaching the main muscle of a person. A dangerous feature of endocarditis is the possibility of vegetation moving to any organs of the body through the bloodstream.

    The cause may also be surgical intervention in an organ affected by infection. When teeth are removed, the chance of a bacterial infection occurring is 18-85%. When removing tonsils, the chance of streptococcal infection is 100%.

    There are numerous types of endocarditis, which seriously complicates diagnosis.

    Classification of endocarditis

    Infectious (also known as septic or bacterial) endocarditis - develops under the influence of pathogenic microflora.

    Acute septic endocarditis

    Acute bacterial endocarditis is a complication of general sepsis. This version of the disease differs little from the subacute form, except that it occurs under the influence of an acute septic condition, or surgery on the vessels and cavities of the heart, or severe injuries.

    The more acute course of this type of endocarditis makes it dangerous. Most often, the patient is immediately sent to the outpatient clinic and undergoes a cycle of examinations within a week.

    The complexity of treatment is relatively low, but early diagnosis of the disease is too important.

    Subacute bacterial endocarditis

    Subacute is a systematic process belonging to the category of infectious-inflammatory. Immunity is impaired and the heart valves are affected.

    Most often, both valves are affected, but there are flows only in the oral or only in the mitral valves. The disease develops slowly. The absence of a purulent focus impairs the ability to diagnose and detect the disease at an early stage.

    The most popular pathogen is viridans streptococcus, which accounts for 80% of disease cases. Less commonly, the cause of the disease is Escherichia coli or Proteus.

    Non-infectious thromboendocarditis

    The reasons for the development of this type of endocarditis can be poisoning and general weakening of the body.

    Rheumatic endocarditis

    Rheumatism can cause endocarditis, which subsequently leads to the development of heart defects. The inflammatory process spreads to the connective tissue of the valves, chordae tendineae, and parietal endocardium.

    Rheumatic endocarditis is divided into four separate types of disease:

    • Acute warty- such endocarditis is characterized by damage to endothelial tissue in the deep layers. The name “warty” comes from the characteristic gray-brown formations (tubercles-warts). If left untreated, the growths grow and unite into clusters - acute polypous endocarditis.
    • Recurrent verrucous- the same as acute warty endocarditis, only formations occur on valves already affected by sclerosis.
    • Simple (diffuse)- only tissue swelling occurs without deep damage to the endothelium (Talalaev’s valvulitis). Treatment must be started as soon as possible, since at the onset of the disease there is a high probability of restoration of the normal structure of the endocardium. In advanced cases, it turns into a fibroplastic type of endocarditis.
    • Fibroplastic- is a consequence of any of the above forms of endocarditis. If the disease develops into this form, the patient faces serious complications and persistent pathological changes in the endocardium.

    Leffer's endocarditis

    The disease causes the chambers of the heart to thicken or narrow. Very often the myocardium is also affected by the inflammatory process, which leads to heart failure.

    Stages of the disease:

    1. Acute (necrotic)- inflammation spreads to the ventricle and upper part of the heart muscle. Whole pockets of dead cells are formed, which even appear in the vessels of internal organs and skin. This stage lasts about 1-1.5 months.
    2. Thrombotic- the endocardium of the left ventricle is affected, some of the muscle fibers hypertrophy, the rest, on the contrary, atrophy. Sclerosis develops.
    3. Fibrosis- narrowing of the chambers and scarring of the chordae tendineae contribute to the development of heart disease. Pathological changes affect not only the endocardium, but also nearby vessels.

    Endocarditis in children

    Rarely seen. In 85% of cases it is infective endocarditis. Symptoms include acute toxicosis, severe endocardial damage, and vascular blockage.

    The inflammatory process affects the entire inner lining of the heart. In general, the picture is similar to the symptoms of adults, but due to the fact that the children’s body is not yet formed, everything happens more chaotically.

    Symptoms

    Symptoms of endocarditis are always based on the cause of the disease. The first warning sign of endocarditis is fever. It can be confusing and chaotic - the temperature either rises or falls, you do not see the external reasons for the temperature change and you do not know whether to fight to lower or increase it.

    With syphilis and tuberculosis, the appearance of endocarditis is not manifested by fever, and the temperature is unlikely to cause concern - it usually rises only to 37.5 degrees.

    A striking symptom is a change in skin color to a “café au lait” shade, but less commonly the shade can be pale or sallow. Such changes scare people enough to see a doctor.

    Most likely, symptoms appear only a week or two after infection, but powerful strains of infection can cause a more rapid development of the disease and its severe course. The first signs may resemble regular flu or ARVI - high fever, weakness, chills.

    Symptoms of endocarditis may be similar to signs of blood poisoning. If pathogens accumulate on the heart valves, inflammation occurs. The cause of the infection can be purulent otitis, sinusitis, cystitis, salpingoophoritis.

    Possible symptoms of endocarditis:

    • fever;
    • sweating, especially at night;
    • weight loss;
    • muscle or joint pain;
    • severe coughing attacks;
    • dyspnea;
    • hemorrhages under the nails and skin (spots - petechiae), on the mucous membranes, fundus of the eye;
    • painful thickening of the fingertips (Osler's nodes);
    • skin rashes.

    In addition to signs of sepsis, the disease is characterized by severe intoxication with headaches, enlargement of the spleen and liver. Blood tests reveal leukocytosis, anemia, and elevated ESR. Bacterial emboli of various organs with the formation of purulent metastases may be observed.

    Heart sounds are muffled, new heart murmurs are added, and it begins. If the infection is not eliminated in time, endocarditis takes on the characteristics of acute heart failure.

    Note that high fever, nausea, aches and pains in the muscles and some other symptoms may be absent. However, diagnosing the disease is not difficult - a blood test is used, since infectious agents are found in arterial blood.

    Diagnostics

    Diagnosis of endocarditis is made difficult by the fact that the disease can begin in various ways. The main criteria are: fever with chills, results of bacteriological examination confirming infection and valve defects detected on echocardiography (ultrasound of the heart).

    An electrocardiogram (ECG) can reveal signs of ventricular enlargement and conduction disturbances, which can occur already in the early stages of endocarditis.

    Blood tests can differentiate different types of endocarditis from each other.

    Treatment

    Treatment of endocarditis has two directions - medication and surgery.. Surgery is quite dangerous, but in cases where drug treatment does not produce results, heart failure may develop and surgery is the only way to save the patient’s life.

    During treatment, the level of microorganisms in the blood and the condition of the heart are constantly monitored using ECG and echocardiography.

    At subacute endocarditis Prescribe benzylpenicillin sodium salts in high doses or cephalosporins in combination with gentamicin. Antibiotics are administered primarily intravenously. As a last resort, replacement of a damaged heart valve is used.

    Antibacterial treatment

    When treating endocarditis, attention is primarily paid to the treatment of the underlying pathology - rheumatism, sepsis, systemic lupus erythematosus. The method of using antibacterial drugs has proven itself to be excellent. In most cases they are used. Antibiotics are selected according to the results of blood cultures for microflora in order to deliver an accurate blow to the infection, while minimizing the toxic effect on the body.

    As a rule, the patient is hospitalized in order to monitor his condition and administer antibiotics through an intravenous drip. Blood samples are constantly taken from the patient; the results of the analysis will clearly show progress in treatment. Then you can return home and take the antibacterial drugs prescribed by your doctor on your own. Penicillin and gentamicin are commonly used. Talk to your doctor in advance if you are allergic to these medications. Vancomycin is used as an analogue.

    A significant effect is achieved through a combination of drugs, which complicates the selection procedure. The classic options are ampicillin and sulbactam, as well as vancomycin and ciprofloxacin.

    70% of the success in the antibacterial treatment of endocarditis comes from drugs that stimulate the immune system.

    Surgical treatment

    Endocarditis can cause serious damage to the heart. Surgical treatment of endocarditis is based on excision and removal of the affected area. About 20% of patients with endocarditis may require surgical treatment. Operations are recommended in cases:

    • Symptoms and/or test results indicate the occurrence of heart failure (a serious condition in which the heart is unable to meet the body's needs).
    • For a long time, despite treatment with antibacterial and antifungal drugs, high temperature and fever persist.
    • The patient has an artificial heart valve.

    The three main surgical procedures for treating endocarditis are:

    • repair of a damaged heart valve;
    • replacement of damaged heart valves with prostheses;
    • removing any abscesses that may form in the heart muscle.

    Surgery is offered only to patients with severe disease. Unfortunately, even in the case of a successful operation, every tenth patient dies during or some time after the operation. If possible, your own valves are preserved through plastic surgery. In cases where the valve is deformed too much, it must be replaced with an artificial one.

    A successful operation transfers the person to outpatient monitoring with constant collection of tests and examinations. For the next 6 months, the person undergoes monthly examinations - this is a very dangerous zone for recurrent infections. Further inspection must be carried out twice a year.

    Thus, it is very important not to skip treatment for endocarditis. With timely and adequate treatment, complications can be completely avoided.

    Treatment of endocarditis is based on the main goal - the need to completely restore or remove tissue that has undergone inflammatory processes.

    Complications

    Endocarditis can lead to damage to the heart valves, conduction problems, and heart failure.

    Neoplasms that occur with endocarditis can break off and move with the bloodstream throughout the body. This can lead to blockage of blood vessels and organ death.

    Forecast

    The prognosis of endocarditis is often serious. Complete healing is achieved only with the earliest possible recognition of the disease and precisely selected effective treatment. Broad-spectrum antibiotics greatly improve the chances of rapid healing.

    No doctor can guarantee to prevent a possible relapse of the disease, which can develop within four weeks after stopping therapy.

    In the long term, the chances of endocarditis returning are high, so you need to constantly undergo medical examinations and identify the disease at the earliest stage.

    Prevention

    Prevention of endocarditis involves monitoring your health. It is very important to promptly treat all infectious diseases and prevent their chronic course.

    Never hesitate to point out to a healthcare professional if you notice that instruments are not being handled carefully. You should be interested in the sterility of the instruments used, especially when visiting the dentist.

    People with artificial heart valves and diseases of the heart muscle should be regularly monitored by a doctor, since this category of patients is at risk.

    « Healthy Heart» / Published: 09/11/2015

    Today, carditis is increasingly coming to the fore among diseases of the cardiovascular system - the main cause of death in the adult population.

    They are especially dangerous due to the development of life-threatening complications for the patient, therefore their diagnosis and treatment are one of the main areas of fundamental medical science in the field of cardiology.

    One of these types of heart problems is endocarditis - what kind of disease is this? The pathology is an infectious-inflammatory disease of the heart of an acute or chronic nature, in which the main target of pathogenic microorganisms is the inner lining (endocardium) of the atria and ventricles, as well as the valve apparatus.

    Statistics

    The disease is common in all countries of the world and in different climate zones. The incidence ranges from 3.1 to 11.6 per 100,000 inhabitants. Men suffer from endocarditis 2–3 times more often than women.

    Recently, in developed countries there has been a clear “aging” of this pathology. If previously the average age of patients with endocarditis was 35 years, now it is 50. The risk of developing the disease in early childhood is also higher, especially in the presence of congenital heart defects.

    The mortality rate for this disease varies from 15 to 45%.

    Species

    The division into types of disease is made on the basis of the reasons that caused it. Conditionally divided into two large groups: aseptic and bacterial inflammation.

    The first group includes rheumatic, Libman-Sachs and Leffler. The second is diagnosed much more often; it includes a bacterial or septic and infectious process.

    Etiology: causes and risk factors


    Among the predisposing factors for the development of endocarditis are:

    • hidden foci of dormant infection of various locations: tonsillitis, carious teeth;
    • congenital and acquired heart defects, hereditary anomalies of its development;
    • primary and secondary immunodeficiency;
    • stress, sluggish chronic diseases that weaken the body’s defenses;
    • addiction;
    • old age.

    An increase in the number of episodes of inflammation of the inner lining of the heart in older people is associated with a history of diseases that predispose to endocardial damage: calcification, involutive processes in the immune system, deterioration of rheological blood parameters, an increase in the frequency of operations and therapeutic and diagnostic procedures.

    Learn more about this disease from the video:

    Classification

    According to the nature of the flow

    Here they highlight:

    • primary: occurs on healthy heart valves;
    • secondary: develops on pathologically altered structures of the heart and blood vessels during rheumatism, congenital and acquired defects, syphilis, after surgery for valve replacement, etc.

    According to the clinical course there are:

    • spicy: lasts up to 2 months. The reason is staphylococcal origin, trauma and therapeutic and diagnostic manipulations in the field of the cardiovascular system.

      With this form of inflammation, infectious and toxic manifestations rapidly increase, as well as valve vegetation and thrombus formation, and purulent metastases to various organs are not uncommon;

    • subacute: lasts more than 2 months. Develops with inadequate treatment of acute endocarditis;
    • chronic relapsing: more than 6 months. Formed with deep damage to the myocardium or dysfunction of the valve apparatus. It is more common in newborns and infants with hereditary heart defects, drug addicts and people who have undergone surgical interventions.

    Check out the ECG signs of left atrial hypertrophy - detailed information is waiting for you.

    Stages

    There are three stages of the pathogenesis of endocarditis: infectious-toxic, immunoinflammatory and dystrophic.

    By localization

    According to the localization of endocarditis, they are distinguished:

    • left-sided inflammation of the native (natural) valve;
    • left-sided endocarditis of the prosthetic valve, which is divided into early (less than a year after installation) and late (more than a year has passed since the operation);
    • right-sided endocarditis;
    • associated with devices such as a pacemaker.

    In addition, valvular, parietal and chordal pathologies are distinguished.

    When a disease develops on the valve apparatus, only the leaflets may be involved in the process (valvulitis), which is more common in the rheumatic process. Whereas it covers all parts of the valve: leaflets, valve ring, chords and papillary muscles.

    The main signs of right atrial hypertrophy are described in detail in. Find out all the details!

    Treatment

    Conservative

    Antibiotic therapy is prescribed in a hospital setting after accurate identification of the microorganism strain.Preference in the treatment of endocarditis is given to broad-spectrum antibiotics. For fungal infections, Amphotericin B and Flucytosine are prescribed for a long time.

    To maintain the functioning of the heart muscle and eliminate symptoms such as shortness of breath, high blood pressure and tachycardia, edema, ACE inhibitors, beta-blockers, aldosterone receptor antagonists, diuretics, and cardiotonics are used.

    Hemolytics that thin the blood are also in demand, especially in the postoperative period to prevent thrombosis. Plasmapheresis, ultraviolet irradiation of autologous blood, and intravenous laser irradiation of blood are prescribed as detoxification measures and for immunomodulation.

    Surgical

    The need for surgical treatment arises in case of complications Surgical intervention involves mechanical excision of the altered valve with implantation of an artificial one in its place with additional sanitation of the inflammation site with broad-spectrum antibiotics.

    Pathological areas can also be treated with low-frequency ultrasound.

    Special symptoms in children

    In childhood, this pathology is very rare. Most often in children it develops acutely and is characterized by the following symptoms:

    • acute intoxication of the body, manifested by weakness, headache, joint pain;
    • inflammatory process in the endocardium;
    • Blood clots appear on the affected endocardium, which contribute to the development of thromboembolism.

    The course of childhood endocarditis does not differ from the development process in adults, but the symptoms increase rapidly, in addition, the treatment of the pathology also does not differ much. The destructive process affects all internal organs, especially the urinary system. Any infectious disease is a risk factor that needs to be treated immediately.

    Course of the disease in HIV-infected people

    Nonbacterial thrombotic endocarditis most often develops in HIV-infected patients(marantic). It occurs in 3-5% of virus carriers and in almost all AIDS patients. Typically, this form of pathology develops asymptomatically and less commonly causes thromboembolism. Anticoagulants are used for treatment to prevent the formation of blood clots. Therapy is carried out aimed at eliminating damage to the valve apparatus.

    Infectious endocarditis (IE, bacterial endocarditis) is a severe inflammatory disease of the heart valves with an unfavorable prognosis and the formation of persistent complications affecting…

    Infectious endocarditis is a disease that occurs when the inner lining of the heart (endocardium) is damaged by an infectious process. In the absence of timely diagnosis and adequate treatment, this pathology will quickly lead to a decrease in the patient’s quality of life, and may cause his death.

    Causes and mechanisms of development

    The infection leading to the development of the disease can be caused by staphylococci, streptococci, enterococci, Escherichia coli, Proteus, Klebsiella and other microorganisms. Microbes enter the surface of the endocardium from chronic foci of infection (dental caries, chronic tonsillitis, pyelonephritis, and so on) or when intravenous injection techniques are not followed, including drug addiction. The appearance of bacteria in the blood (bacteremia) can be short-term (after tooth extraction, during tooth brushing, urethral catheterization and many other conditions and medical procedures). The infection can affect healthy heart valves or those damaged by heart defects.

    A healthy endocardium is resistant to microbial influence. But under the influence of various harmful factors, microtraumatization occurs. Platelets and fibrin are deposited on the surface of microcracks, forming “patches.” Pathogenic microorganisms settle on them.
    The formation of such foci on the surface of the endocardium triggers the main pathogenetic mechanisms of the disease:

    • microbes constantly enter the bloodstream, leading to the development of intoxication, fever, loss of body weight, causing the development of anemia;
    • vegetations (growths) occur on the valves themselves, leading to disruption of their function; vegetation contributes to damage to the surrounding tissues of the heart;
    • fragments of microbial vegetation spread throughout the vessels of the whole body, causing blockage of the vessels of internal organs and the formation of purulent foci in them;
    • formation in the blood of circulating immune complexes consisting of microbial antigens and protective antibodies; these complexes are responsible for the appearance of glomerulonephritis and arthritis.


    Clinical picture

    Signs of the disease in the initial stage

    The initial manifestations of the disease are varied and nonspecific; they largely depend on the variant of the disease, the type of pathogen, and the age of the patient.
    A highly virulent infection can cause disease in intact heart valves with the development of primary endocarditis. The onset of the disease is sudden, accompanied by high fever and intoxication. The general condition of the patient quickly deteriorates to the point of serious condition.
    Secondary infective endocarditis (when already damaged valves are affected) can develop gradually. General health worsens, fatigue and weakness appear, and performance decreases. Body temperature rises to 37 - 38˚С.
    In some cases, the disease manifests itself in cerebral vessels with the development of a stroke. These phenomena may be mistakenly regarded as a complication of atrial fibrillation in patients with rheumatic heart valve disease.
    Sometimes, at the onset of the disease, persistent
    Temperature response may vary. In some patients, the body temperature does not increase; in others, a short episode of fever up to 40˚C is observed, followed by prolonged low-grade fever. More rarely, a wave-like variant is observed, in which there are relapses of high fever.
    In about a third of patients, an increase in body temperature is accompanied by tremendous chills, and a decrease is accompanied by profuse sweating.

    Appearance changes

    In many cases, pale skin appears due to gradually developing anemia. With concomitant hepatitis or hemolysis of red blood cells as a result of autoimmune processes, yellowness of the skin and mucous membranes occurs. The previously described characteristic café au lait skin color is now rare.
    The appearance of the hands gradually changes: the fingers take the shape of drumsticks, and the nails - watch glasses.
    Many patients develop a petechial rash on the skin and mucous membranes. It looks like small red spots that fade when pressed. The rash is most often located on the front surface of the body, painless, and not accompanied by itching.
    In some patients, you can see the so-called Lukin-Libman symptom - petechial formations with a white center located on the conjunctiva of the lower eyelid. This symptom is now rare.
    Sometimes so-called Osler's nodes appear: painful round-shaped formations located on the palms and soles.
    In a small number of patients, joints change. They swell and their mobility decreases. These phenomena are caused by the development of arthritis.


    Heart damage

    Heart damage is the main clinical picture of infective endocarditis. It forms within 2–3 months from the onset of the disease. All layers of the organ are affected: endocardium, myocardium, and, less commonly, pericardium.
    Damage to the endocardium primarily causes pathology of the heart valves. There is a change in the auscultatory picture: noises and pathological tones appear. Signs of valve insufficiency gradually appear. When the aortic and mitral valves are damaged, insufficiency occurs. It is associated with stagnation of blood in the lungs and is manifested by shortness of breath with minimal exertion and at rest, including in the supine position, hemoptysis and other symptoms. Damage to the valves of the right half of the heart (tricuspid, pulmonary valve) leads to the development of signs of stagnation in the systemic circulation: enlarged liver, edema, ascites, and so on.
    Myocarditis is manifested by increasing shortness of breath, the appearance of severe circulatory failure, which is difficult to treat with medication. Severe arrhythmias such as atrial fibrillation and flutter, paroxysmal ventricular tachycardia, high-degree atrioventricular block and others are noted.
    It occurs more rarely with infective endocarditis. It is associated with blockage of a coronary vessel by a detached fragment of vegetation. Myocardial infarction often has a typical clinical picture, but in some cases it has a protracted or asymptomatic course.
    in infective endocarditis, it most often has a toxic-allergic nature, is dry in nature, manifests itself as intense pain in the heart area, and is accompanied by typical changes in the auscultatory pattern and electrocardiogram.

    Lesions of other organs

    Infectious endocarditis is characterized by polysyndromic nature.
    When small vessels are damaged, capillaritis occurs, accompanied by the appearance of a petechial rash. Arteritis and phlebitis may occur with the corresponding clinic. Blockage of a vessel (thrombosis) leads to infarction of internal organs.
    Splenic infarction is manifested by severe pain in the left hypochondrium and lumbar region, with irradiation to the left shoulder. Thromboembolism of the renal vessels is accompanied by intense pain in the lower back, radiating to the groin area. Urinary disorders occur, and blood appears in the urine (gross hematuria).
    Pulmonary embolism is accompanied by severe chest pain, shortness of breath, and hemoptysis. Thromboembolism of small branches may manifest as episodes of increasing shortness of breath or intermittent but recurring chest pain. Sometimes lung abscesses occur with the corresponding clinic.
    Thromboembolism of cerebral vessels is accompanied by either transient disturbances of cerebral circulation or severe strokes with the development of paresis and paralysis. Brain abscess may form, leading to death.
    Mycotic aneurysms are formed in the arteries, associated with inflammation of the vessel walls and their expansion. Mycotic aortic aneurysm is manifested by pain, impaired blood flow in the extremities, and abdominal syndrome. Aneurysms of mesenteric vessels are accompanied by abdominal pain, intestinal bleeding, and necrosis of the intestinal wall. Aneurysms of cerebral vessels are characterized by the development of neurological symptoms.

    Kidney damage manifests itself as infarction or nephritis. Nephritis is accompanied by changes in urine analysis. Nephrotic syndrome may develop with edema, proteinuria and hypertension. Renal failure often occurs, which often determines the prognosis of the disease.
    Damage to the spleen may be accompanied by its infarction with the appearance of acute abdominal pain, as well as hypersplenism with the development of anemia, bleeding, and decreased immunity due to leukopenia.
    Liver lesions often manifest as long-term hepatitis without significant impairment of organ function. Characterized by heaviness in the right hypochondrium and enlarged liver.
    Damages to the stomach, intestines, and pancreas are rare. They manifest themselves mainly as dyspepsia (pain and indigestion). With the development of intestinal infarction or acute pancreatitis, abdominal syndrome occurs, requiring immediate consultation with a surgeon.
    Sometimes damage to the nervous system occurs in the form of encephalitis, meningitis, and brain abscess. In milder cases, patients complain of headaches, sleep disturbances, and decreased mood.

    Diagnostics

    A general and biochemical blood test and repeated bacteriological examination are prescribed to determine the type of pathogen and its sensitivity to antibiotics.
    Ultrasound examination of the heart is very helpful in diagnosing the disease. It determines the affected valve, clarifies the severity and extent of the process, and describes the function of myocardial contractility.

    Treatment

    The earlier treatment is started, the greater the chance of success. It is carried out in a hospital setting and lasts for a long time.
    The basis of treatment for infective endocarditis is antibiotic therapy. Antibacterial antibiotics are used; they are administered parenterally for at least 4–6 weeks until a lasting effect is obtained. The following main groups are used: inhibitor-protected penicillins, cephalosporins, thienamicides, aminoglycosides, fluoroquinolones, quinolones and some others. A combination of antibiotics from different groups is often used. These drugs are prescribed taking into account the sensitivity of the isolated pathogen. For fungal and viral endocarditis, appropriate antifungal and antiviral agents are used.
    If antibiotic therapy is ineffective, indications for surgical treatment are considered. Such indications include:

    • persistence of fever and continued isolation of the pathogen from the blood (positive blood culture) for 2 weeks of adequate antibiotic therapy;
    • progressive circulatory failure with rational antibiotic therapy;
    • dysfunction of the prosthesis in patients with prosthetic valve endocarditis;
    • peripheral vascular embolism.

    With the development of immune disorders (myocarditis, nephritis, vasculitis), it is necessary to prescribe glucocorticosteroids
    .
    Direct anticoagulants are used in all cases except fungal endocarditis.
    When circulatory failure develops, its treatment is carried out according to accepted regimens, including peripheral vasodilators, angiotensin-converting enzyme inhibitors. For rhythm disturbances, it is prescribed.

    Prevention

    Primary prevention involves the sanitation of foci of chronic infections, general strengthening and health measures. Special preventive measures are carried out in patients with an increased risk of developing infective endocarditis. These include patients:

    • with prosthetic heart valves;
    • with congenital and acquired heart defects;
    • previously had infective endocarditis;
    • with idiopathic hypertrophic subaortic stenosis;
    • those on chronic hemodialysis;
    • with an implanted pacemaker;
    • after coronary artery bypass surgery;
    • drug addicts.

    Persons at risk require special medication preparation when carrying out the following manipulations:

    • dental;
    • tonsillectomy;
    • any interventions on the mucous membrane of the upper respiratory tract;
    • bronchoscopy;
    • opening of any purulent foci;
    • any therapeutic and diagnostic interventions on the organs of the gastrointestinal tract and genitourinary system;
    • uncomplicated childbirth, termination of pregnancy, caesarean section.

    For prophylaxis, regimens using penicillins, cephalosporins, and macrolides are used.

    Channel One, the program “Live Healthy” with Elena Malysheva on the topic “Endocarditis. Why is it so important to treat teeth on time?

    Infectious (bacterial) endocarditis. Video presentation.

    Endocarditis is an inflammatory process that occurs in the inner lining of the heart (endocardium). The main reason for its development is infection, but other pathologies should not be ruled out. The disease can equally affect both male and female populations. Very often, the disease overtakes the body of people taking various drugs. Young patients also have a tendency to develop a pathological process, so it is important to know the causes and symptoms of the pathology in order to prevent the development of severe complications.

    Reasons for development

    A variety of factors can provoke infective endocarditis. Recognizing them guarantees a positive effect from treatment. The most basic causes of the inflammatory process in the endocardium are:

    • connective tissue disease of a diffuse nature;
    • injuries;
    • poisoning by chemical elements;
    • infections.

    Manifestations of endocarditis

    Symptoms of endocarditis appear the same in all patients at different stages of the disease. Based on them, it is not possible to recognize the cause of the disease, but they arise against the background of a lack of oxygen in the tissues. To make a diagnosis, patient complaints alone are not enough, since the symptoms are very similar to other pathological conditions. But they are very important for the victims themselves. Symptoms of infective endocarditis indicate a malfunction of our “engine”, so it is necessary to urgently consult a therapist.

    Infectious endocarditis has the following manifestations:

    • increased body temperature;
    • shiver;
    • increased sweating;
    • skin diseases;
    • ocular manifestations;
    • pain in the muscles and head.

    Fever

    This symptom is found in almost all people affected by infective endocarditis. At first, the temperature readings are moderate - 37–37.5 degrees. A few days later they reach a dangerous level of 39–40 degrees. This condition is due to the characteristics of the pathogen.

    Very often, fever is a consequence of the influence of specific components. During the inflammatory process in the inner shell of the human “motor”, the role of these substances is played by the waste products of the pathogen. After penetrating into the plasma, they affect the center responsible for thermoregulation and cause a rise in temperature.

    When there is no fever or a slight increase in temperature, this is typical for the following category of people:

    • elderly people;
    • after ;
    • with pronounced ;
    • with increased levels of uric acid in plasma.

    The diagnosis is complicated by the fact that a slight increase in temperature is not accompanied by heart symptoms. The fever lasts for 3–4 weeks.

    This condition involves involuntary contraction of muscle tissue, manifested in the form of tremors or convulsions. Chills are a characteristic manifestation of sepsis, as a result of which the movement of bacteria in the plasma and damage to internal organs is observed. Infectious endocarditis manifests itself in the form of chills when the body temperature rises.

    Excessive sweating

    The root cause of a person starting to sweat a lot is a fever. Sweating contributes to a drop in the victim's temperature. With sepsis, which causes infective endocarditis, this symptom bothers the victim, usually at night.

    Skin diseases

    Since harmful agents of an infectious nature affect the heart with a rush of blood, in most people suffering from endocarditis, damage to the vascular walls can be detected. Manifestations of this condition include the formation of a small rash and redness on the skin.

    Visual impairment

    The mechanism of formation of eye symptoms is similar to skin symptoms. They include a number of symptoms that form pinpoint bleeding in the eye area. The patient can detect such a sign in himself. The pathological process manifests itself as red pigmentation on the small conjunctiva. You can detect them yourself if you move the lower eyelid down.

    While being examined by an ophthalmologist, Roth spots may be noticed. They are areas of hemorrhage that affect the fiber of the eyes. They can only be identified during fundus diagnostics.

    Painful sensations in the head and muscles

    Symptoms of this kind occur in people who have infective endocarditis. If a person is affected by another form of the disease, then he does not have headaches or muscle pain. The reasons for such formations are intoxication of the body caused by the proliferation of microbes. They often coincide with the first stage of temperature rise.

    Rheumatoid form of the disease

    This condition is characterized by symptoms of damage to the heart valves. In the first stages of development, rheumatoid endocarditis does not cause any serious manifestations. It is possible to establish an accurate diagnosis only during a thorough cardiac examination and based on the results of laboratory tests. The formation of the disease at a late stage leads to the formation of symptoms of insufficient heart function. Rheumatic endocarditis and its symptoms begin to affect other organs and systems.

    The disease is often limited only to manifestations of the heart. Therefore, patients do not experience any serious symptoms characteristic of endocarditis.

    Septic form of the disease

    Septic endocarditis is a special form, the characteristic feature of which is damage to the heart valves. Bacterial endocarditis is classified according to the nature of the course or the presence of an accompanying disease.

    Taking into account the nature of the development of the inflammatory process, acute, subacute and protracted septic endocarditis is distinguished. The acute form lasts about 14 days, the subacute form lasts 3 months, the protracted form bothers people for months and even years. Today doctors note that the acute forms have gone away, so they diagnose subacute and protracted forms. Bacterial endocarditis, taking into account the background pathology, can be primary and secondary.

    Septic endocarditis manifests itself in the following form:

    • hemorrhage (leakage of blood from vessels) into the conjunctiva of the eyes;
    • thickenings in the form of nodules form on the palms;
    • wasting of fingers;
    • hemorrhage in the skin.

    Illness in young patients

    Infectious endocarditis in children is represented by inflammatory lesions of cardiac endocarditis. This pathological process is infectious.

    Often the disease serves as a complication of congenital or chronic heart disease, and especially after surgery. Various types of viruses and fungi contribute to the formation of defects. Often the cause of the disease lies in defects in the immune system, a source of chronic infection. Infectious endocarditis in young patients has a very high mortality rate.

    There are congenital and acquired forms of the disease. The main symptoms of childhood infective endocarditis include:

    • rapid weight loss;
    • weakness;
    • increased sweating;
    • increase in temperature in the evening;
    • pain in joints and muscles.

    The disease can begin acutely and be accompanied by rapid development of symptoms. However, most often the first stage of the pathology proceeds slowly and unnoticed. The duration of the process is sometimes prolonged and difficult to treat.

    Over time, infective endocarditis becomes generalized. As a result, damage is caused to other organs. Infectious endocarditis in young patients can cause complications such as blood clots, resulting in blockage of blood vessels in the internal organs and brain. Against the background of insufficient heart function, difficulty breathing, pallor and cyanosis of the skin, and swelling occur. The symptoms of the disease are so varied that it can be very difficult to immediately identify the disease.

    Diagnostic tests

    To make a diagnosis, the patient must undergo certain examination. Only after this will the doctor be able to accurately diagnose infective endocarditis and prescribe effective therapy. Diagnostics includes:

    • listening to the heart, during which rough murmurs can be detected;
    • electrocardiography;
    • X-ray;
    • bacterial cultures of plasma.

    When the patient has the results of a complete examination in hand, you can go directly to your doctor. Try to get all the tests done as quickly as possible, since the time spent may later affect your health and the effectiveness of subsequent treatment.

    Therapeutic measures

    Treatment of infective endocarditis includes a set of measures to eliminate the inflammatory process in the inner lining of the human “motor”. Most often, antibacterial therapy and surgical intervention are involved in the process. If formation occurs, then treatment should be aimed at correcting it. If infective endocarditis is suspected, the patient should be urgently hospitalized.

    Drug therapy

    When treating endocarditis with antibiotics, you should discuss this issue with your doctor. Their appointment takes into account the degree of sensitivity. The course of treatment should be at least 4–6 weeks. As a rule, a specialist prescribes a complex of medications to the patient in order to achieve maximum effect. It could be:

    • Ampicillin-Sulbactam with Gentamicin;
    • Vancomycin and Ciprofloxacin.

    In addition to antibiotic medications, treatment of infective endocarditis involves medications that affect the immune system.

    If the disease is not of a bacterial nature, then to treat endocarditis it is necessary to take into account the specifics of the underlying disease. When endocrine pathology is diagnosed, the patient is required to undergo hormone tests and undergo treatment under the supervision of an endocrinologist. Endocarditis, which is the result of intoxication, can be cured by stopping the use of a certain type of toxin.

    Operation

    Elimination of the inflammatory process by surgery involves removal of the affected area of ​​the heart valve with further prosthetics. If this is possible, the patient undergoes plastic surgery to preserve his own valves. After the rehabilitation period, the patient must be under the supervision of doctors. For six months, you need to go for examinations every month in order to detect a possible return of the infection and monitor your general well-being. Further examinations should be carried out 2 times a year.

    Consequences

    Complications from this disease occur due to growths on the heart valves. They can detach and, with the blood flow, affect other organs and systems. If they get stuck in a small vessel, this will cause an acute lack of blood supply, resulting in tissue death. The kidneys can also be damaged. This complication manifests itself in the form of an abscess and infarction of the organ. The nervous system gives complications in the form of stroke, meningitis. The most dangerous complication is the formation of blood clots in the pulmonary artery. This condition leads to death.

    Prevention

    If you do not want your body to pick up such a pathology, then you should know the basic measures that can protect you from endocarditis. Prevention involves the following series of actions:

    1. If you use drugs, you need to give them up urgently, since these people are at greater risk of getting sick.
    2. Those who have artificial valves or chronic heart disease should always be under the supervision of a specialist.
    3. Constantly monitor the quality of processing of medical equipment and ask your doctor about the quality of sterilization.

    Every person, both adults and children, can get endocarditis. The reason for this pathology lies in damage to the body by an infectious agent. The disease manifests itself with chills, fever and headaches. This condition can be cured, but only with an integrated approach. If you delay treatment, you can get a number of unpleasant and dangerous complications, which will later be very difficult to treat.