Ludzkie koronawirusy - autor: Krzysztof Pyrć z Zakładu Mikrobiologii, Wydział Biochemii, Biofizyki i Biotechnologii, Uniwersytet Jagielloński, Kraków

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© Borgis - Postępy Nauk Medycznych 8/2015, s. 603-606
*Wojciech Brzozowski, Andrzej Wysokiński
Tachykardiomiopatie
Tachycardiomyopathy
Chair and Department of Cardiology, Medical University, Lublin
Head of Department: prof. Andrzej Wysokiński, MD, PhD
Streszczenie
Tachykardiomiopatię (TCM) określaną również jako kardiomiopatią indukowaną tachykardią można zdefiniować jako wtórną formę kardiomiopatii rozstrzeniowej indukowaną nadmierną tachykardią towarzyszącą różnym postaciom tachyarytmii nadkomorowych i komorowych.
Pojawia się w każdym wieku i prowadzić może do dysfunkcji czynnościowej jak również zmian morfologicznych mięśnia sercowego.
Tachykardiomiopatia cechuje się istotnym upośledzeniem czynności lewej komory, częściowo lub nawet całkowicie odwracalnym po przywróceniu podstawowego rytmu zatokowego lub uzyskaniu kontrolowanej względnie prawidłowej częstości akcji serca.
Pojęcie tachykardiomiopatii nie obejmuje swoim zakresem stanów wynikających z choroby nadciśnieniowej serca, uszkodzenia zastawek serca i choroby wieńcowej.
Chorzy z tachykardiomiopatią prezentują szeroki zakres różnorodnych objawów, najczęściej jednak objawy te wynikają z postępującej wraz z czasem trwania tachyarytmii niewydolności serca.
Leczona, tachykardiomiopatia jest w większości przypadków w pełni odwracalna. Nieleczona prowadzić może do ciężkiej niewydolności serca i zgonu chorego. Rozpoznanie tachykardiomiopatii jest utrudnione z uwagi na fakt, że poszerzenie jam serca może być zarówno przyczyną tachyarytmii jak i jej skutkiem.Brak jest ponadto specyficznych dla tej jednostki markerów diagnostycznych, co sprawia, że szczegółowa analiza obrazu klinicznego pozostaje jak na razie jedyną drogą rozpoznania w codziennej praktyce.
Summary
Tachycardiomyopathy (TCM) or tachycardia-induced cardiomyopathy, caused by improper tachycardia in the course of supraventricular or ventricular arrhythmias is a form of secondary dilated cardiomyopathy.
This disease may occur at any age and leads to both dysfunction and changes in heart muscle structure.
Tachycardiomyopathy is characterized by a significant reduced left ventricular function. This dysfunction is partially or completely reversible with normalization of basic sinus rhythms and heart rate.
The concept of tachycardiomyopathy does not include disorders resulting from hypertensive disease, heart valve damage and coronary heart disease.
Tachycardiomyopathy is characterized by a wide range of symptoms, most commonly corresponding to heart failure in course of cardiomyopathy. If treated casually, tachycardiomyopathy is fully reversible. In the extreme, not treated cases, this condition leads to severe heart failure and death. The diagnosis of tachycardiomyopathy is not easy because dilation of the ventricles may cause or be a result of tachyarrhythmias. Moreover, there are no specific markers available to precise diagnose and clinical features remain the most useful tool in everyday practice.
Long-term persistence of tachyarrhythmia for many years has been identified as one of the possible causes of heart failure and cardiomyopathy in the wake of the mostly dilated nature (1). In the cases of heart failure, it was noted that there is a close relationship between inhibition deterioration progress of heart muscle function and elimination of the arrhythmia or at least release frequency of arrhythmia. This involved a substantial improvement of the prognosis if arrhythmia were reduced. The actual incidence of tachycardiomyopathy is not known, it is difficult to conclusively determine whether tachyarrhythmia is the leading cause of heart failure in the patient, or is only a secondary process to an existing, significant muscle damage.
Tachycardiomyopathy may develop on any form of supraventricular arrhythmias (2). However, it should be specified as the main atrial fibrillation, atrial flutter, and various forms of atrial paroxysmal tachycardia. Also arrhythmias such as ventricular tachycardia and ventricular premature beats may lead to tachycardiomyopathy.
Common causes of tachycardiomyopathy is described in table 1.
Table 1. Types of arrhythmia-inducing tachycardiomyopathy.
Supraventricular arrhythmiasVentricular arrhythmias
– Atrial fibrillation
– Atrial flutter
– Atrial tachycardia
– AVRT
– AVNRT
– Junctional tachycardia
– Sinus tachycardia (pathological)
 
 
– Ventricular tachycardia originated from right ventricular outflow tract
– Ventricular tachycardia bi-static beam
– A number of premature ventricular beats
– Idiopathic ventricular tachycardia from the left ventricle
Other (less common) causes
Stimulation of the atria with a high frequencyStimulation of the ventricles with a high frequency
Other causes of tachycardiomyopathy
– Myocarditis accompanied by tachycardias and tachyarrhythmias
– Thyreotoxicosis
– Glucagonoma
Pathophysiology
Macroscopic changes: prolonged maintenance of arrhythmia running with high incidence of heart rate leads primarily to the progressive impairment of systolic function in both the left and right ventricle (3-5). Ventricular filling is due to the inscreased pressure, the cardiac output is reduced and elevated systemic vascular resistance is observed. The lack of increase in left ventricular muscle mass is a characteristic for this disease. Contractility of the myocardium is reduced, while reducing its contractile reserve. The lack of left ventricular muscle hypertrophy causes enlargement and the advent of usually at least moderate mitral regurgitation. These changes are observed due to dilatation of the mitral ring, changes in left ventricular geometry and lack of the mitral leaflets coaptation. As a result of the deterioration of the function of the left atrium, the increase of existing most supraventricular arrhythmias is observed. Increase rigidity and impairment of left ventricular torsion affects both systolic and diastolic function. These changes are substrate in damage to skeletal proteins, extracellular matrix proteoglycan.
Microscopic changes: changes in the course of tachycardiomyopathy include primarily the loss of myocyte contraction, significant increase in myocyte length, the disruption of connections between the basement membrane and sarcolemma. This reduces the possibility of adequate transmission of stress in the wall of the heart muscle. In addition, the reduction in the number of T-tubules type L calcium channels and beta-adrenergic receptors takes place. This affects negatively the duration of action potential of myocardial cells, leading to the development of the incorrect activation and reduces the systolic dysfunction. After heart rate normalization some of microscopic changes recede much slower than macroscopic. This mainly applies to the focal fibrosis of the heart muscle. These areas become the arrhythmia substrate and relapse.
Prolonged tachycardia affects not only the systolic impairment but also interferes with the relaxation of the heart muscle (6). The heart muscle is in so-called partial relaxation. This is due to the sustained, disproportionately elevated calcium ions contained in the tanks of sarcolemma during diastole. It can be illustrated as the functionally spasmolytic contracture of the heart muscle. This phenomenon also affects indirectly reducing flows in the sub endocardial layers of the heart muscle due to lingering high end-diastolic pressure in the left ventricle. Ischemia and hypoxia can also be the result of an increased distance between capillary and myocytes. Ischemia probably corresponds to the myocardial hibernation phenomenon. After the suppression of the arrhythmia rapid improvement is observed.
Acceleration of the rhythm also causes depletion of myocardium in high-energy compounds adequately to the higher incidence of rhythm and duration of tachyarrhythmia. Oxidative stress can also be a significant factor responsible for the diminished systolic function during atrial fibrillation. Patients with the DD genotype of angiotensin converting enzyme are characterised by elevated level of this enzyme which is responsible for the accelerated changes in the length of cardio myocytes and increase volume of cardiac cavities and the end-diastolic pressure.
Taking into account morphological changes discussed above, the irregularity of neurohormonal are very close to the classic heart failure of the other substrate (7, 8). Typically activation of the renin-angiotensin-aldosterone system occur. Increased levels of angiotensin II and endothelin are observed. An elevated level of atrial natriuretic peptide is observed due to increased pressure in atria and reduced sodium expulsion. Its concentration decreases, with the progression of heart failure. The concentration of cerebral natriuretic factor is also higher. Aldosterone – the final component of the renin-angiotensin-aldosterone system – affects the progressive fibrosis and enhances the arrhythmias and conduction in the damaged heart muscle. Expression of beta-adrenoreceptors on the surface of the cells of the myocardium is significantly reduced.
It should be noted that right ventricle reacts a little differently on the load generated by prolonged arrhythmias. Both the mass and the possibility of contraction by myocytes are increased.
Diagnosis
Currently there is no strictly defined, clear criteria for diagnosis of tachycardiomyopathy. Arrhythmias present in the patient with newly diagnosed heart failure running with a fast rhythm of the ventricles, not controlled in an appropriate manner, with a frequency of over 100/min should induce to consider this entity as the underlying disease. Coronary heart disease should be ruled out. The diagnosis of tachyarrhythmias can be considered in a situation:
– no other causes of non-ischemic events (such as: hypertension, alcohol intoxycation, drugs intoxycation, stress),

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Piśmiennictwo
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7. Morris Robinson PD, Channer KS: Reversible heart failure: toxins, tachycardiomyopathy and mitochondrial abnormalities. Postgrad Level Med J 2012 Dec; 88(1046): 706-712.
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otrzymano: 2015-06-08
zaakceptowano do druku: 2015-07-09

Adres do korespondencji:
*Wojciech Brzozowski
Chair and Department of Cardiology, Medical University
ul. Jaczewskiego 8, 20-954 Lublin
tel. +48 (81) 724-41-51
brzozo@wp.pl

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