Friday, December 13, 2013

ECG Phenomena of the Early repolarization

ECG phenomena of early repolarization clinical interest in the ECG phenomenon of early repolarization (RJR) has recently flared up, mainly due to the establishment of its clinical connection with fatal cardiac arrhythmias, particularly in patients without (or with minimal) organic changes of the heart .

For a long time ECG phenomena RJR misdiagnosed or misinterpreted because of the widespread opinion of their benign nature.


Thus, violations of repolarization in Brugada syndrome for over three decades been regarded as safe, and early repolarization syndrome (CPP) considered are normal, benign early repolarization until 2000.


In 2008, an article Ha? Ssaguerre et al., Dedicated to the increasing prevalence of CPP in patients with idiopathic ventricular fibrillation episodes. However, the clinical significance of the phenomenon of RJR as a marker for sudden cardiac death (SCD) and its role in risk stratification is not yet fully defined.


Ventricular repolarization begins after the end of ventricular depolarization. In a normal cardiac cycle transition from one process to another is relatively fast and the amount of overlap between the late and early repolarization depolarization does not exceed 10 ms.


The length of the overlap is largely determined by physiological and pathological cardiac and extracardiac conditions that cause or spread of excitation wavelength on the wall of the ventricle, or the return of the drive, or both processes simultaneously.


Among the cardiac factors play a central role CPP configuration early phase of action potentials (AP) in different layers of the ventricular wall, as well as the dispersion of repolarization of the ventricular wall and transmural voltage gradient.


The transition of ventricular depolarization repolarization corresponds to a point on the ECG J (moment of transition of the QRS complex in the segment ST).


For ECG phenomenon characterized by RJR:


? elevation contour line above the point J (J-deviation);


? smooth transition of the QRS complex in the ST segment or a notch, ie offset contour line on the J point on the downward bend of the R wave or an upward knee prong S;


? Prong J (increase in amplitude and duration of J-deflection taking the form of the dome or hump) with elevation (or without) the segment ST.


J-point elevation of the contour line is a characteristic feature of the CPP, and may also occur in acute myocardial ischemia, hyperkalemia, and intraventricular conduction disorders. It should be emphasized that the standard ECG is not always possible to find clear differences between the slowing intraventricular conduction and RJR. In this division the two phenomena is an important task, because in most cases RJR has a significantly higher risk of arrhythmias, particularly in patients without organic heart disease.


Tooth J


At various times, tooth J wore a variety of names: camel hump, prong K, tooth H, late delta tooth, tooth points of J, hypothermic prong hypothermic hump prong Osborne.


At the moment, there is the following classification of the teeth J:


? hypothermic


? negipotermichesky


? idiopathic


Hypothermic tooth J


Several studies have noted the emergence of J-wave on the electrocardiogram in patients with hypothermia, reflecting a violation of repolarization. Clinical and experimental evidence linking the hypothermic prong J with cardiac arrhythmias, are contradictory. Episodes of ventricular tachyarrhythmias in patients with hypothermic tooth J according to different studies ranged from 0 to nearly 100%.


Sodium channel blockers, such as lidocaine, procainamide, and are ineffective for the prevention and treatment of malignant ventricular tachyarrhythmias in patients with hypothermia.


Negipotermichesky tooth J


ECG changes similar to those of hypothermia have been observed in different clinical and experimental conditions in patients with normal body temperature. They include such conditions as acute myocardial ischemia, acute pulmonary thromboembolism, myocardial RV, electrolyte and metabolic disorders, pulmonary diseases, inflammatory diseases of the central or peripheral nervous system toxicity heterocyclic antidepressants and cocaine, and many other conditions. Among them the most arrhythmogenic potential was detected in teeth J acute myocardial ischemia and hyperkalemia.


Idiopathic tooth J


In the absence of organic heart disease and noncardiac diseases RJR considered primary or idiopathic.


Describes several forms of idiopathic J wave with concomitant segment elevation ST (or not). Among them, the most studied is the Brugada syndrome. Idiopathic prong J, followed by ST-segment elevation with T-wave inversion in the right precordial ECG is a marker of a typical Brugada syndrome.


In many cases, symptomatic Brugada syndrome (combination ECG characteristics with atrial and / or ventricular tachyarrhythmias or VSS) ST-T changes, and / or localization of ECG may differ from those of typical Brugada syndrome. In such cases, use the term atypical tooth or J-like Brugada syndrome.


CPP


The term early repolarization syndrome was introduced almost 50 years ago, and the RAF was traditionally considered as idiopathic and benign ECG phenomenon of RJR. In 2000, on the basis of pre-clinical experimental data Dr. Charles Antzelevitch, scientists have concluded that the CPP should not be regarded as normal or benign a priori, and in certain conditions (a predisposition to segment elevation ST) patients with SSR may be at high risk of fatal ventricular arrhythmias.


CPP is detected on an electrocardiogram as elevation contour line on the J-point, followed by a horizontal ST-segment elevation in leads V2-V4 (5). CPP is often associated with a shorter duration of the interval QT. When it (15%) may also slightly increase QRS (up to 110 ms).


True CPP is defined as a combination of ECG markers CPP with arrhythmogenic complications, and / or familial cases of SCD in healthy individuals. CPP is seen in 1-2% of the general population and is more common in men (77%), at a young age (27.5%), those with a predisposition to vagotonia, athletes, smokers, those with obstructive hypertrophic cardiomyopathy and defects and / or hypertrophy of the interventricular septum. Cases of the RAF family.


In many clinical situations is difficult to differentiate between changes in the USSR from those of Brugada syndrome, as well as various disorders of intraventricular conduction syndrome and short QT. Many clinical signs similar to those in the RAF and Brugada syndrome, including the prevalence in young healthy men, family history, transient normalization of ECG changes, and a similar response to an increase in heart rate and use of certain medications. So, slow heart rate increases the severity of the tooth and J-segment elevation ST, and the increase in heart rate during exercise or isoproterenol administration reduces or even eliminates these ECG changes.


Sodium channel blockers (known ability to initiate the Brugada syndrome) increase of ST segment elevation in the RAF and the hypothermia tooth J. Sympathetic stimulation and?-Agonists normalize the ST segment in these syndromes, while?-Blockers increase the segment elevation ST, and propranolol may even induce a classic version of the RAF.


The possible cellular and ionic mechanisms

ECG: "T" and "U" Waves








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