PREMATURE VENTRICULAR CONTRACTION (lat. extra out of, outside + Greek systole reduction, compression) — the disturbance of a heart rhythm which is characterized by emergence of single or pair premature reductions of heart (extrasystoles) caused by the excitement of a myocardium proceeding, as a rule, not from a physiological source of a cordial rhythm (a sinus and atrial node), i.e. being geterotopny. AA. is among so-called active geterotopny automatic equipment (see. Arrhythmias of heart ). Rub and one by one extrasystoles usually consider more following as a paroxysm of tachycardia (see. Bouveret's disease ).
Depending on the location of the center of ectopic activity of an extrasystole divide on atrial, atrioventricular (atrioventricular, nodal) and ventricular. In extremely exceptional cases it is observed sinus E., at a cut premature excitement arises in a physiological pacemaker of heart — a sinus and atrial node.
AA. treats the most frequent disturbances of a cordial rhythm. According to Katts and Peak (L. N. Katz, A. Pick, 1956), at registration about 100 thousand ECGs at 50 thousand patients having various diseases (not only heart troubles), atrial E. it was revealed in 2836 cases, atrioventricular — in 555 and ventricular — in 3745 cases. However with the advent of long monitoring (see. Monitor observation ) it became clear that true frequency E. much higher and in random samples of persons 50 years are more senior it is approximately equal to 90% (the indicator fluctuates depending on duration of monitoring).
The conditions contributing to emergence E., can arise at all heart troubles (myocarditis, heart diseases, coronary heart disease, a cardiomyopathy, etc.), and also at many diseases exerting adverse impact on a cardiac muscle (intoxication at inf. diseases, poisonings, neoplastic processes, a hyperthyroidism, allergic reactions, increase in load of heart at hypertensia in a big or small circle of blood circulation, etc.) and leading to her dystrophy (see. Myocardial dystrophy ). It is established that E. it can be caused by strengthening of catecholamines in blood, e.g. at patients with hromaffinomy in the period of katekholaminovy crisis, at ischemia of a myocardium even at slight increase of concentration of catecholamines in blood. At the same time at experimental animals with initially intact myocardium E. it is possible to cause influence only very high (injuring a cardiac muscle) concentration of catecholamines. Many researchers believe that E. can be manifestation of viscerovisceral reflexes (at cholecystitis, stomach diseases, phrenic hernias); however it is unknown whether these reflexes in an intact myocardium can be implemented. The same treats the so-called neurogenic extrasystoles which are quite often arising at almost healthy faces under the influence of strong emotions. In considerable number of cases the reason E. in clinical conditions it is not possible to reveal, despite use of a complex of the most perfect methods of a research.
There are two main theories of an origin E. It agrees one of them, at the heart of E. the mechanism of a repeated entrance of excitement in system of fibers of Purkinye lies. This theory assumes that among Purkinye's fibers there are branchings, branches to-rykh connect the shunting bridges (fig. 1). If in one of branches carrying out excitement is broken anterograde, i.e. in the usual direction, but kept retrograde, then an impulse of excitement, passing through normally functioning branch, and then through the bridge between branches, gets to a branch with the broken anterograde conduction since its distal end, and with lateness when the specific carrying-out fabric of the proximal site of this branch can already come out a condition of the refrakternost caused by the first passing of an impulse of excitement on it therefore he will repeat the movement on the specific carrying-out tissue of a myocardium and will cause its premature reduction. In favor of the theory of a repeated entrance a number of reasoned arguments, in particular that fact that time between normal cordial reduction and the extrasystole following it if it proceeds from the same ectopic center, in all cardial cycles remains very constant testifies, varying within 0,02 — 0,03 sec. This time is called an interval of coupling («coupling» between normal cordial reduction and an extrasystole means). The second fact testifying in favor of this theory — existence of so-called frequency-dependent forms E., differing in the fact that extrasystoles arise only at a certain heart rate (e.g., only at 70 — 72 in 1 min.), therefore, at strictly certain duration of the refractory period.
According to the second theory E. results from periodic activation of the «dozing» center of geterotopny automatism. The theory of spontaneous automatism is applicable to a parasystole (see. Arrhythmias of heart ), differing in lack of a constant interval of coupling in the presence of identical or multiple to some period of intervals between ectopic complexes. The parasystole can be caused various patol. processes in a myocardium. Due to the development of methods of cardiostimulation appeared also herds even more often to come to light a special form of a parasystole — the so-called artificial parasystole which is characterized by simultaneous existence of two heart rhythms having different frequency; own (sinus, atrioventricular) and imposed by a stimulator. Existence artificial parasystoles demonstrates that parasystoles in general are connected with the mechanism patol. automatism of a myocardium. Nek-ry researchers nevertheless believe, as usual E. it can be caused by the ectopic automatism connected with so-called late potentials, or the post-potentials arising owing to tranzitorny changes of transmembrane potential of action (see. Heart , physiology) upon termination of the period of repolarization. The extrasystole, according to representations of these researchers, appears if the size of late potential surpasses threshold level. Existence of late potentials is shown in experiments with impact on a myocardium of alkaloids — veratrine and aconitine, but it is not revealed in an intact myocardium, and also at modelled in an experiment patol. states (ischemia, overload).
If the extrasystolic center is in one of ventricles of heart, the excitement caused by it, moving on the carrying-out system of heart in the retrograde direction, usually reaches atrioventricular connection that is followed by development of its refrakternost. The last in most cases makes impossible passing of the next impulse from a sinus and atrial node in ventricles in this connection the next reduction of ventricles drops out and there is a diastolic pause extended in comparison with the main rhythm, to-ruyu call post-extrasystolic or (conditionally) compensatory. At the extrasystoles arising in ventricles of heart the interval between pre-and post-extrasystolic reductions of heart is usually equal to time of two normal cardial cycles; such compensatory pause call full (fig. 2; in fig. 2 and the subsequent on the right below the vertical piece designated the scale of amplitude of teeth of an ECG in millivolts; a horizontal piece — time scale in seconds). Sometimes the refrakternost of the carrying-out fabric of atrioventricular (atrioventricular) connection caused by an extrasystole manages to disappear by the time of its achievement by the impulse of excitement which arose in a sinus and atrial node, and the next normal reduction of ventricles happens timely. Such extrasystoles carry the name interpolated, or inserted. The extrasystoles arising in auricles or in a zone of atrioventricular connection unlike ventricular extrasystoles extend retrogradno on auricles and «discharge» a sinus and atrial node, i.e. induce its premature excitement which is not followed by distribution on the auricles which are in a condition of a refrakternost. The following normal impulse is generated in a sinus and atrial node through time equal to intervals between atrial teeth of the main rhythm. Thereof the compensatory pause after atrial and atrioventricular (atrioventricular) extrasystoles is shorter, than after ventricular (an incomplete compensatory pause).
Extrasystoles, even frequent, as a rule, do not influence or influence a hemodynamics a little if there are no expressed diffusion or macrofocal damages of a myocardium. It is connected with effect of a so-called post-extrasystolic potentsiation — increase in force of the reduction following an extrasystole, a cut, according to Lendrum (V. Lendrum with sotr., 1960), it is not connected with increase in enddiastolic volume of ventricles of heart. Mechanisms of a post-extrasystolic potentsiation are not opened yet, but is established that it is characterized by a number of features: 1) the interval of coupling, the more force of the reduction following an extrasystole is less; 2) the potentsiation after pair extrasystoles is more, than after single; 3) can potentsiirovatsya several following behind an extrasystole of complexes of the main heart rhythm (sinus, a ciliary arrhythmia, etc.); 4) at a bigeminal pulse (regular alternation of reductions of the main rhythm with extrasystoles) the potentsiation progressively accrues to the known limit. It is less expressed at a trigeminy (regular alternation of two reductions of the main rhythm and one extrasystole), a quadrigeminia (emergence of an extrasystole after each three normal reductions) and other forms of allorhythmias, i.e. regular emergence of an extrasystole through a certain number of normal reductions of heart. In addition to a potentsiation in increase in force of the reduction following an extrasystole the compensatory pause (if it is full) providing increase in enddiastolic volume of ventricles of heart can play a role. The listed mechanisms of compensation are insolvent at heavy pathology of a myocardium; in this case E. can be the cause of decrease in cordial emission or promote development of congestive heart failure (see).
Quite often at patients with subjectively not felt and not influencing the general state E. frequent registration of an ECG, fixing of attention of the doctor on identification of subjective or objective signs E. become the reason of iatrogenic phobic neurosis (see. Iatrogenic diseases ).
Clinical displays of premature ventricular contraction vary at different patients and at its various forms. Many patients do not show any complaints and do not know about existence at them E., until they are informed on it by the doctor. Quite often after that the patient begins to perceive the extrasystoles which are available for it. The most often sick with E. complain of feeling of interruptions in cardiac performance, the dying down in heart reminding feeling at bystry decrease in the airplane or a start of motion down of the high-speed elevator; feeling short-term (1 — 1,5 sec.) cardiac standstills with aftersensation of strong blow of heart in a chest wall (a post-extrasystolic potentsiation). Sometimes the described feelings are followed short-term (1 — 2 sec.) by an acute pain in the field of a top of heart. At patients with the expressed damages of a myocardium frequent extrasystoles are followed by feeling of shortage of air, weakness, dizziness that is connected with deterioration in blood supply of a brain. Sometimes at the time of emergence of an extrasystole tolchkoobrazny swelling of cervical veins is noted; after an extrasystole it is quite often possible to see or palpate the single strengthened cardiac impulse (the investigation of a post-extrasystolic potentsiation). Come to light the loss of pulse blows corresponding to hemodynamically inefficient early extrasystoles, or the premature weakened pulse blows (at rather hemodynamically effective late extrasystoles) which are followed by the extended (compensatory) pause after a cut the blow which is a little strengthened pulse follows. The bigeminal pulse is usually shown by a bradysphygmia (see. Pulse ), since the palpated artery is reached, as a rule, by only pulse blows caused by normal reductions of heart. Auskultativno an extrasystole is perceived as loud tone or as two tones close remote from each other, intensity of the first of to-rykh is increased, and the second is sharply weakened. This rutting arises in a diastole prematurely and is followed by a compensatory pause. The noise listened the back by heart at an extrasystole sometimes disappear (owing to a short shot of ventricles blood); in some cases, on the contrary, pumas it is listened only during estrasystolic reduction that demonstrates emergence of a turbulent flow of blood in an aorta at the time of an extrasystole. Inserted extrasystoles are auskultativno distinguished as the premature reductions which are not followed by a compensatory pause. At frequent polytopic ekstrasnstola the physical research not always allows to make the diagnosis E., as in this case she on a wedge, can remind manifestations a ciliary arrhythmia.
Current E. individually. At acute diseases, such, as myocarditis (see), myocardial infarction (see), it can stop with recovery or at stabilization of a state (e.g., posl. full scarring of a zone of a heart attack). Quite often E. remains during all life of the patient, it is sometimes spontaneous or under the influence of treatment disappearing for more or less long time. Such current E. connect with formation after acute diseases cardiosclerosis (see), myocardial dystrophies (see). At the chronic progressing heart troubles, such as recurrent infectious and allergic myocarditis, cardiomyopathy (see), coronary heart disease (see), weight E. over time accrues; ventricular E. can lead to development of fibrillation of ventricles of heart (see). B. Loen (1976) suggested to distinguish ventricular extrasystoles on degrees depending on «zlokachestvennost» (ability to cause fibrillation of ventricles): The I degree — rare (no more than 30 in an hour) monotopny (coming from one center) extrasystoles; The II degree — frequent (more than 30 in an hour) monotopny extrasystoles; The III degree — allorhythmias (a bigeminal pulse, a trigeminy, a quadrigeminia, etc.) and polytopic coming from the different ectopic centers in ventricles) extrasystoles;
The IV degree — group extrasystoles (steam rooms, three extrasystoles in a row and more); The V degree — extrasystoles like «R on T», or early. The last type of extrasystoles differs in a short interval of coupling, i.e. early emergence after the main reduction; at the same time on the electrocardiogram a tooth I extrasystoles am the share of a tooth of T of the previous complex, top to-rogo, on Uiggersa (C.J. Wiggers, 1937), corresponds to a so-called vulnerable phase of a cardial cycle when even weak electric irritation (such irritation in patol. conditions there can be also an early extrasystole) can cause fibrillation of ventricles (fig. 2).
B. Laun's classifications adhere not all researchers. Fibrillation of ventricles at coronary heart disease can arise without communication with E. and, on the contrary, many patients with coronary heart disease within 5 years and more suffer from E. high degrees, keeping not only life, but in some cases and working capacity.
The diagnosis is established on the basis of complaints of the patient, data of the anamnesis (the instruction on myocarditis, acute and persistent infections, especially tonsillitis, a hyperthyroidism, rheumatism, stenocardia, a myocardial infarction) and results of a physical research. Make for specification of the diagnosis electrocardiography (see). If the usual electrocardiography does not reveal extrasystoles, at an opportunity resort to long a monitorirovapiya of an ECG.
Atrial premature ventricular contraction is characterized by the following electrocardiographic signs (fig. 3, a): premature emergence and deformation of an atrial tooth of P; duration of an interval is P — Q more than 0,12 sec.; a ventricular complex of an extrasystole, on a configuration and duration not different from ventricular complexes of the main rhythm if it proceeds from a sinus and atrial node or a myocardium of auricles; incomplete compensatory pause. Sometimes the extrasystolic QRST complex owing to aberrant carrying out on ventricles (if by the time of emergence of an extrasystole intra ventricular conductivity was not recovered completely) is deformed and reminds a ventricular extrasystole (fig. 3, b). In similar cases the extrasystolic tooth P quite often accumulates on a tooth of T of the previous normal complex (T + P), causing its deformation. If the extrasystole arises during the period corresponding to a refrakternost of atrioventricular connection after the previous reduction, the excitement which arose in an auricle does not extend to ventricles. Such atrial extrasystoles call blocked; they are reflected in an ECG prematurely appearing teeth P which are not followed by ventricular complexes; after a tooth of P blocked extrasystoles the incomplete compensatory pause is defined (fig. 3, c). The extrasystoles arising in a sinus and atrial node also belong to atrial. They meet extremely, seldom and are reflected in an ECG the expressed prematurity of the PQRST complex which is not differing in a form from complexes of the main rhythm.
Atrioventricular nodal) premature ventricular contraction of an elektrokardiograficheska on changes of QRS corresponds atrial (therefore they are combined under the name supraventricular, or supraventricular, ekstrasistoliya), but differs from the last in changes of a tooth P which is always inverted and holds in relation to a ventricular complex various position depending on from what part (upper, average or lower extrasystoles proceed. The tooth of P is inverted because excitement from the ectopic center extends on auricles retrogradno. At a verkhneuzlovy extrasystole (fig. 4, a) the inverted tooth P precedes QRS, at the same time an interval of P — Q less than 0,12 sec. At a sredneuzlovy extrasystole (fig. 4, 6) the tooth P can accumulate on its ventricular complex, deforming the last a little. Nizhneuzlovy extrasystole (fig. 4. c) it is characterized by the fact that the inverted tooth P is registered right after an extrasystolic ventricular complex. Atrioventricular extrasystoles with an aberrant ventricular complex on an ECG can be not otlichima in a form from ventricular extrasystoles. If at the same time a tooth P extrasystoles accumulate on its ventricular complex, differential diagnosis of atrioventricular and ventricular extrasystoles is quite often possible only on the basis of results vuutripolostnogo an electrophysiologic research of heart (see. Heart , methods of a research); in the analysis of data of the usual ECG the correct diagnosis is promoted by existence after aberrant atrioventricular extrasystoles of an incomplete compensatory pause.
Ventricular premature ventricular contraction of an elektrokardiograficheska is characterized by the following signs (fig. 2): lack of the atrial tooth preceding an extrasystole P; sharp distinction of a form of a ventricular complex of an extrasystole and ventricular complexes of the main rhythm; lengthening of duration of a ventricular complex (over 0,12 sec.); existence of a full compensatory pause. The extrasystolic QRST complex usually reminds in a form the QRST complex at blockade of one of legs of an atrioventricular band. Considered earlier that if the extrasystolic complex reminds in a form the QRST complex at blockade of the right leg of a bunch (see. Heart block ), the extrasystole proceeds from a left ventricle if the QRST form same as at blockade of the left leg, the extrasystole proceeds from a right ventricle. It is established that the specified pattern is traced not always. Ventricular extrasystoles can be monotonous (excitement arises in one ectopic center); in this case all extrasystolic complexes are identical in a form and all intervals of coupling have equal size. Occasionally at a constant interval of coupling the form of extrasystolic complexes changes because the impulse, coming from one center, extends on ventricles in the different ways. Inconstancy of both an interval of coupling, and a form of an extrasystolic complex demonstrates that extrasystoles proceed from the different ectopic centers (polytopic premature ventricular contraction).
Treatment of premature ventricular contraction is defined by its etiology, a form and expressiveness a wedge. manifestations. Atrial and atrioventricular premature ventricular contraction, and also ventricular premature ventricular contraction of I and II degrees (on B. Laun's classification), the impacts on the general condition of the patient which are not shown subjective symptomatology and not exerting and his working capacity, treatments or purposes of the sparing mode do not demand. If these forms E. are followed by unpleasant feelings, especially in certain situations, napr, at nervousness, upon transition to lying situation or in a prone position on the left side (that prevents backfilling and promotes neurotization), use of tranquilizers in individually picked up doses at nervousness is shown or in anticipation of an alarming situation, and also before withdrawal to a dream. At patients with the increased uneasiness tranquilizers are appointed long courses and in the afternoon. Sometimes under the influence of psychotropic drugs E. disappears; in some cases the patient ceases se to feel. At inefficiency of tranquilizers and when E. reduces tolerance of the patient to loadings, and also carry out by the patient with ventricular premature ventricular contraction of the III—V degree (on B. Laun's classification) at an opportunity treatment of a basic disease. So, at a hyperthyroidism (see. Craw diffusion toxic ) can be effective concerning E. thyreostatic drugs or thyroidectomy. Cases of permanent disappearance ventricular E are described. after aneurysmectomy at the patients who had a myocardial infarction. Atrial E. at patients with mitral heart diseases can stop after corrective operations on the mitral valve (a commissurotomy, prosthetics). If E. serves as manifestation of an overload of a myocardium or heart failure, purpose of cardiac glycosides is shown. When treatment of a basic disease does not lead to elimination E., appoint antiarrhythmic means (see), using one of two empirical ways of selection of pharmaceuticals. Most often appoint any antiarrhythmic drug in an average daily dose and at its inefficiency replace in 2 — 3 days with another, repeating this procedure until the effective and well transferred by the patient drug is found. The second way — conducting acute pharmacological tests with single introduction of the sating dose of antiarrhytmic means, e.g. 0,4 — 0,6 g of quinidine inside, 10 ml of 10% of solution of a novokainamid intravenously slowly or 1 g in, 10 mg of verapamil (Isoptinum) intravenously or 80 mg inside, 150 mg of an Ethmosinum intravenously or to 300 mg inside, 100 mg of Disopyramidum (Rythmodanum, Rhytmilenum) intravenously or 300 mg orally, 25 mg of Ajmalinum intravenously, 5 mg of propranolol (anaprilin, Obsidanum) intravenously or 40 mg orally. During test make repeated registration of an ECG with extended (to 1 min.) records for determination of frequency of extrasystoles or carry out visual monitoring of an ECG, and at an opportunity long monitoring with the magnetic record (see. Monitor observation ). The special place among the pharmaceuticals applied to suppression E., occupies Amiodaronum (kordaron). Toxicity of Amiodaronum is less, than other antiarrhytmic means, and efficiency is very high and approaches 80%. However because of features of pharmacokinetics of Amiodaronum (slow accumulation and long, equal to about a month, an elimination half-life) definition of its suitability for treatment of each patient takes up to 2 weeks. Usually within the first week appoint Amiodaronum in a daily dose of 0,6 g (the number of receptions within a day does not matter), within the second week — but 0,4 g then pass a pas a maintenance dose (on 0,2 g 5 — 7 weekly). The maintenance dose can be insufficient that is found in several weeks. In these cases for 3 — 4 days drug give 0,6 g (subsaturation) in a daily dose again, and then pass on a little big, than initial, a maintenance dose (0,25 — 0,3 g a day). Amiodaronum is means of the choice at treatment of a parasystole.
At appointment to the patient with E. antiarrhythmic means it is important to take into account to feature of the basic (most often sinus) a heart rhythm. At the expressed bradycardia, e.g., blockers of beta and adrenergic receptors, Amiodaronum, verapamil are contraindicated. Data that various antiarrhythmic means are unequally effective at atrial, atrioventricular and ventricular E., not all researchers confirm.
After means, the most effective for this patient is found and not causing in it essential side reactions, by practical consideration establish an efficient daily dose of drug. Treatment chronically proceeding E. shall be constant (many months or years) since after cancellation of the accepted means E., as a rule, renews.
Almost all antiarrhythmic means negatively affect conductivity of a myocardium, especially in atrioventricular connection (under the influence of a novokainamid also intra ventricular conductivity can be broken). Therefore at patients with E. against the background of disturbances of conductivity it is reasonable to experience effect of the carbamazepine (Tegretolum, Finlepsinum) which is not oppressing conductivity. It is appointed in the increasing doses: in the first day of treatment 2 times on 0,1 g, next day — 3 times on 0,1 g, on the third — 2 times on 0,2 g and so before emergence of antiarrhythmic action or the expressed by-effects (drowsiness, an oglushennost). If the last are insignificant, and antiarrhythmic action is reached, recommend is long to accept drug in the picked-up dose. Drowsiness and an oglushennost disappear in 1 — 2 week of treatment at preservation of antiarrhythmic effect. In a combination with other antiarrhythmic means carbamazepine at E., the conductivity which is combined with disturbances, it is possible to appoint only on condition of careful and systematic electrocardiographic control. In similar cases effective doses of each of the means entering a combination shall be lower, than at their separate use.
Treatment E. at patients with an acute myocardial infarction it is characterized by a number of features (see. Myocardial infarction ). At iskusstven ache parasystoles urgently the issue of removal or reimplantation of a pacemaker is resolved.
The forecast concerning recovery at E. in most cases doubtful. Sometimes E. spontaneously stops for several months and even years, but further recurs. At the same time patients usually keep working capacity if only E. it is not connected with crushing and widespread damages of a myocardium (a heart attack, myocarditis, a cardiomyopathy, a cardiosclerosis).
Frequent atrial extrasystoles, especially at patients with tendency to bradycardia, and also at defects of the mitral valve serve as a harbinger of a ciliary arrhythmia (see). Ventricular E. high (III—V) degrees (on B. Laun's classification) it is connected with danger of development of fibrillation of ventricles; it concerns first of all to patients with coronary heart disease, to patients with severe damages of a myocardium of other etiology, but is sometimes observed also at almost intact myocardium. Constant preventive use of blockers of beta and adrenergic receptors, first of all propranolol (anaprilin, Obsidanum), considerably reduces this danger even if whether it is not possible to eliminate completely E. Obladayut with similar action other antiarrhythmic means, it is not established yet.
Prevention comes down to measures of the prevention of diseases and patol. the states most of which often are the cornerstone E. (coronary heart disease, infectious and allergic recurrent myocarditis, myocardial dystrophies of various origin), and also to the prevention of their aggravations.
Bibliography: Kushakovsky M. S. and Zhuravlev N. B. Arrhythmias and heart blocks: (Atlas of electrocardiograms), L., 1981; The Guide to cardiology, under the editorship of B. I. Chazov, t. 1, M., 1982; Chazov E. I. and Bogolyubov V. M. Disturbances of a heart rhythm, M., 1972; Cardiac electrophysiology today, ed. by A. Masoni a. P. Alboni, L. a. o., 1982; Diagnosis and treatment of cardiac arrhythmias, ed. by A. Bayes a. J. Cosin, Oxford a. o., 1980.
V. A. Bogoslovsky.