Showing papers on "Cardiac arrhythmia published in 1997"

Pathophysiological Mechanisms of Dominant and Recessive KvLQT1 K+ Channel Mutations Found in Inherited Cardiac Arrhythmias

Abstract: The inherited long QT syndrome (LQTS), characterized by a prolonged QT interval in the electrocardiogram and cardiac arrhythmia, is caused by mutations in at least four different genes, three of which have been identified and encode cardiac ion channels. The most common form of LQTS is due to mutations in the potassium channel gene KVLQT1, but their effects on associated currents are still unknown. Different mutations in KVLQT1 cause the dominant Romano-Ward (RW) syndrome and the recessive Jervell and Lange-Nielsen (JLN) syndrome, which, in addition to cardiac abnormalities, includes congenital deafness. Co-expression of KvLQT1 with the IsK protein elicits slowly activating potassium currents resembling the cardiac Iks current. We now show that IsK not only changes the kinetics of KvLQT1 currents, but also its ion selectivity. Several mutations found in RW, including a novel mutation (D222N) in the putative channel pore, abolish channel activity and reduce the activity of wild-type KvLQT1 by a dominant-negative mechanism. By contrast, a JLN mutation truncating the carboxyterminus of the KvLQT1 channel protein abolishes channel function without having a dominant-negative effect. This fully explains the different patterns of inheritance. Further, we identified a novel splice variant of the KVLQT1 gene, but could not achieve functional expression of this nor of a previously described heart-specific isoform.

Increased expression of the cardiac L-type calcium channel in estrogen receptor-deficient mice

Abstract: Steroid hormones control the expression of many cellular regulators, and a role for estrogen in cardiovascular function and disease has been well documented. To address whether the activity of the L-type Ca2+ channel, a critical element in cardiac excitability and contractility, is altered by estrogen and its nuclear receptor, we examined cardiac myocytes from male mice in which the estrogen receptor gene had been disrupted (ERKO mice). Binding of dihydropyridine Ca2+ channel antagonist isradipine (PN200-110) was increased 45.6% in cardiac membranes from the ERKO mice compared to controls, suggesting that a lack of estrogen receptors in the heart increased the number of Ca2+ channels. Whole-cell patch clamp of acutely dissociated adult cardiac ventricular myocytes indicated that Ca2+ channel current was increased by 49% and action potential duration was increased by 75%. Examination of electrocardiogram parameters in ERKO mice showed a 70% increase in the QT interval without significant changes in PQ or QRS intervals. These results show that the membrane density of the cardiac L-type Ca2+ channel is regulated by the estrogen receptor and suggest that decreased estrogen may lead to an increase in the number of cardiac L-type Ca2+ channels, abnormalities in cardiac excitability, and increased risk of arrhythmia and cardiovascular disease.

Dynamic control of cardiac alternans

Abstract: A dynamic control technique was used to suppress a cardiac arrhythmia called an alternans rhythm ina piece of dissected rabbit heart. Our control algorithm adapted to drifting system parameters, makingit well suited for the control of physiological rhythms. Control of cardiac alternans rhythms may haveimportant clinical implications since they often precede serious cardiac arrhythmias and are a harbingerof sudden cardiac death. [S0031-9007(97)03337-1]

Compensated cardiac hypertrophy: arrhythmogenicity and the new myocardial phenotype. I. Fibrosis

Abstract: The high incidence of arrhythmias in compensated cardiac hypertrophy is related to two independently regulated components-fibrosis and the adaptational phenotypic changes in membrane proteins linked to cardiac hypertrophy, and fibrosis. During the regression of hypertensive cardiopathy in middle-aged spontaneously hypertensive rats, the roles of cardiac hypertrophy and fibrosis can be analysed separately, revealing that both correlate independently with arrhythmias. In an experimental model of myocardial infarction it is possible to prevent arrhythmias with propranolol at the same time as cardiac hypertrophy, despite ventricular fibrosis. Fibrosis would appear to create arrhythmias both by anatomical uncoupling and by a re-entry mechanism generated by the zig-zag propagation of the transverse waveform. Triggered activity and automaticity depend on the membrane phenotype of the cardiocyte. They also play an important role, which is aggravated by myocardial heterogeneity.

Electroencephalography in syncope.

Abstract: Electroencephalographic (EEG) findings in syncope are reviewed. There are four major categories of syncope: neurally mediated (neurocardiogenic), neurologic, decreased cardiac output, and orthostatic hypotension. However, regardless of cause, whether the syncope is due to a vasovagal effect, a cardiac arrhythmia, an epileptic seizure, or hypotension, EEG findings are similar and reflect cerebral hypoperfusion. Initially there may be a slowing of background rhythms. This is followed by high amplitude delta activity, maximal anteriorly. If the hypoperfusion persists there is subsequent flattening of the EEG. The EEG returns to normal in the reverse sequence. In cases with severe and prolonged ischemia, convulsive syncope may occur at the time of the EEG flattening. Although not an epileptic phenomena, clinically this is often mistaken for epilepsy. Conversely, epileptic disorders, such as the ictal bradycardia syndrome, may occasionally mimic syncope. Therefore, in patients in whom EEGs are performed for the evaluation of an episode of loss of consciousness, simultaneous ECG should be used.

Methods of treating or preventing cardiac arrhythmia

Abstract: A method of treating or preventing supraventricular tachyarrhythmias is disclosed which comprises the use of a compound which selectively blocks the ultra-rapidly-activating delayed rectifier K+ current (IKur) of the human atrium.

Is impaired baroreflex sensitivity a predictor or cause of sudden death in insulin-dependent diabetes mellitus?

Abstract: Sudden death at night is known to occur in young patients with insulin-dependent (Type 1) diabetes mellitus (IDDM) but the aetiology is uncertain. A cardiac arrhythmia has been postulated, but there has been little evidence to support this. We present the case of a 31-year-old man with IDDM of 17 years duration, who died suddenly while asleep. Over preceding months, he had had strict glycaemic control (HbA1 8.9 %), normal 24 h blood pressure (mean 131 ± 2.1/76 ± 2.2 mmHg), no evidence of microangiopathy or endothelial dysfunction and normal standard clinical tests of autonomic function. An electrocardiogram was similarly unremarkable, with a QTc interval of 0.414 s, and an echocardiogram had demonstrated normal left ventricular mass index (96.4 g m−2). However, there was no nocturnal dip in heart rate (daytime 74 ± 2.7, and nocturnal 68 ± 1.6 beats min−1), and he had grossly impaired baroreflex sensitivity during Phase 4 of the Valsalva manoeuvre (0.5 ms mmHg−1), with power spectral analysis studies suggesting an abnormality of parasympathetic function. The coroner’s autopsy demonstrated no structural abnormalities. We hypothesize that abnormal baroreflex sensitivity could either predict a risk of or account for some of the unexplained deaths in IDDM, in that relative overactivity of the sympathetic nervous system could cause ventricular arrhythmias. © 1997 by John Wiley & Sons, Ltd.

Using the right drug. A treatment algorithm for atrial fibrillation.

Abstract: Atrial fibrillation is the commonest sustained cardiac arrhythmia. Its incidence increases with age and in association with organic heart disease, in particular valvular heart disease, left ventricular dysfunction and in association with thyrotoxicosis and alcohol excess. Atrial fibrillation may present as paroxysms of self-terminating arrhythmia or as a sustained arrhythmia. In the former instance, management is directed towards suppression of paroxysms and will commonly involve class 1C, class 2 or class 3 agents. If atrial fibrillation is sustained, a decision as to the desirability of cardioversion must be made. If this can be acheived successfully, particularly if the episode was of brief duration and associated with a reversible cause, sinus rhythm may be preserved without further antiarrhythmic therapy. Otherwise prophylactic therapy as used for paroxysmal atrial fibrillation is appropriate. In patients who fail to respond to cardioversion, or in those with advanced organic heart disease, long-standing atrial fibrillation or marked dilatation of the left atrium in which case cardioversion is unlikely to be successful, the principal therapeutic strategy is to control ventricular rate. Classically, digoxin is used for this purpose. Additional agents which will slow the ventricular rates, such as beta-blockers, amiodarone or calcium channel antagonists (verapamil or diltiazem), may be necessary if the ventricular rate remains uncontrolled and continues to produce severe symptoms. In the event of failure of medical therapy to control ventricular rate, atrioventricular nodal modification or ablation may be appropriate.

Role of the Atrioventricular Node in Atrial Fibrillation

Abstract: Atrial fibrillation (AF) is probably the most cornmon cardiac arrhythmia in humans, particularly in the elderly (1-3). The irregularity and inequality of the he art beat first described by Hering in 1903 were, and continue to be, the landmark of the clinical diagnosis of AF (4,5). Sir Thomas Lewis (6) observed the gross irregularity ofthe arrhythmia and stated "the pauses betwixt the heart beats bear no relationship to one another." Thanks to work of Lewis (7), Mackenzie (8), Wenckebach (9), and others, the clinical syndrome of AF became well established, and gradually the pathophysiologic mechanisms involved were also recognized (10). In 1915 Einthoven and Korteweg (11) studied the effect of heart cycle duration on the size of the carotid pulse and concluded that the strength of the heart beat was related to the duration of the preceding cycle. Later we repeated those observations by studying in a quantitative fashion the effects of randomly varying RR intervals on the contractions of isolated Langendorff perfused rat hearts (12). Recently Hardmann confirmed the complicated relationship between the randomly irregular rhythm and left ventricular function in patients with AF, confirming the involvement of postextrasystolic potentiation and restitution (13). Animals mayalso develop AF (14,15). lndeed, Lewis (7) observed the arrhythmia in an open-chest horse and used this observation to establish that the irregular pulse noticed in humans was due to fibrillation ofthe atria. Until the 1950s, observations on AF were limited to its etiologic, clinical, and surface EeG manifestations. The beginning of the computer era enabled several groups of investigators to analyze the ventricular rhythm during AF in a more quantitative fashion (16-18). The results of these studies were fascinating and allowed for the development of theories on the behavior of the atrioventricular (AV) node during AF. Sophisticated computer techniques allowed Moe and Abildskov (19,20) to simulate atrial electrical activity during AF, and they formulated the so-called multiple wavelet theory, which was in 1985 supported by experimental evidence (21). Parallel to the growing insight into the electrical behavior of the atria during AF and into the corresponding ventricular rhythm, sophisticated experimental methods were designed to study AV nodal electrophysiology in a variety of circumstances, including induced AF (22,23). This chapter reexamines some of the established concepts of AV no dal function (24) because comparative physiology of the AV node and some specific electrocardiographic observations in patients with AF have demonstrated inexplicable flaws in the current theories of AV no dal function. Alternate mechanisms, which till now have hardly been considered as a basis for explaining AV nodal function during AF, will be discussed. In the first edition ofthis book (25) we postulated that the AV node, rather than acting as an intrinsic part of the cardiac conduction system, is primarily a pacemaker subject to e1ectrotonic influences from other areas in the heart. However, as will be made clear in this chapter, the pacemaker theory cannot explain all clinical phenomena inherent to AF. So a new model based on recently discovered cellular electrophysiologic principles (26,27) has been developed and will be presented.

Pharmacological Management of Arrhythmias in the Elderly

Abstract: The incidence of cardiac arrhythmia increases with advancing age, as does the prevalence of structural heart disease. Serious arrhythmias, such as sustained ventricular tachycardias, are uncommon in elderly patients, but nonsustained ventricular tachycardias and atrial fibrillation are relatively frequent.

Behçet's disease and cardiac arrhythmia

Abstract: Only few cases of cardiac conduction disturbances and arrhythmias have been reported in Behcet's disease. We recently observed the case of a 16-year-old woman with Behcet's disease in whom cardiac arrhythmia became the main clinical symptom. This observation and a review of the literature led us to the conclusion that arrhythmia could represent the clinical manifestation of an underlying myocarditis due to Behcet's disease and can be regarded as a feature of cardiac involvement of the disease.

Feedback control of pathological rhythms in two models of cardiac activity

Abstract: This report is a brief survey of some results using feedback to control two diverse models of cardiac electrical activity. A chaotic quadratic map has been used as a model of ventricular fibrillation. Here we describe simulations to control this map using a self-tuning feedback controller. We also demonstrate control of a one-dimensional circle map which has been used as a model of the cardiac arrhythmia known as modulated ventricular parasystole. We show that feedback control offers a straightforward and viable alternative for stabilization of these model systems in comparison to OGY or other control methods.

Telemetry system of daily life motion and arrhythmia

Abstract: An ambulatory electrocardiogram (ECG) recording system have been used to record cardiac arrhythmia in daily life. The system can continuously record the ECG waveform so that physicians could diagnose the cardiac disease, together with event recordings which can also provide the recording of activity of daily life (ADL), such as standing, walking, or eating. Patients, however, often forget to record the events. Our first approach to record ADL was AC-100 (GMS Co. Ltd.), which can record the zero-crossing count of three dimensional accelerometer outputs and RR intervals. We have been revised the instrument to make AC-4X, which can transmit an ECG signal, and acceleration wave signals. The signal received by the analyzing host computer is processed with finite impulse response (FIR) filters, and some other real-time filters. Also, the state transition charts and tables are used to recognize the output of filters. ECG signal is recognized by algorithm to indicate some types of arrhythmia, and acceleration signals are recognized to indicate some motion of daily life. The effort is on going to cover as many subjects as possible.

Management of Cardiac/ECG Complications of Stroke

Abstract: This chapter reviews the management of cardiac/electrocardiography (ECG) complication of stroke. Ischemic heart and cerebrovascular diseases frequently coexist in the same patient and they share similar risk factors. Most studies that investigated the precise frequency of cardiac complications after stroke failed to take this into account by not controlling for coexisting coronary artery disease. Forty-four percent of ischemic stroke patients showed either a recent onset ischemia pattern ECG or a cardiac arrhythmia. If stroke-induced electrocardiographic effects lead to an increase in the incidence of cardiac arrhythmias, then the prognosis should be adversely affected by their presence. Those patients who develop new or evolving ECG changes after stroke or have classical repolarization abnormalities including neurogenic T waves and prolongation of the QT interval may also pose a special risk. Such patients should be referred for continuous cardiac monitoring and followed closely in an intensive care setting for at least 3 days. Treatment of frequent runs of malignant ventricular tachyarrhythmia may even require the placement of an implantable defibrillator. Each patient causing cardiac concern should be evaluated by a cardiologist prior to the institution of therapy.

Arrhythmia curve interpretation using a dynamic system model of the myocardial pacemaker.

Abstract: A problem of identifying the phase response curve of the myocardial pacemaker was investigated using a simple dynamic system model of cardiac arrhythmia. A hybrid optimization method of a genetic algorithm and a local optimization technique was employed to obtain a solution of the model fitting. The method was applied to two categories of arrhythmias, ventricular parasystole and high-degree AV block. The present study offered a new insight into the mechanism of cardiac arrhythmias.

Measures for decreasing the early mortality after valvular replacement cardiovascular surgery

Abstract: To probe the effective measure for decreasing the early mortality after artificial valvular replacement. We analyzed the cause of death among 1215 patients receiving artificial valvular replacement who were admitted in our intensive care unit during 1990-1995. All 44 deaths were serious-illed patients with preoperative cardiac functions of 3-4 degree. The factors affecting surgical survival rate include: enhancement of patient's cardiac function before operation and prevention of cardiac arrhythmia; a clear operational view and myocardial protection, especially for reoperative patients; application of membrane oxygenator; treatment of LCOS without delay, including intraveously administered agents and IABP used promptly when necessary; prevention and treatment of postoperative cardiac arrhythmia; strict, intensive care and synthesized treatment.

Comparative study of mitral annular calcification (MAC) with cardiac arrhythmias in dialysis patients.

Abstract: Cardiac arrhythmias and myocardial malfunction are very frequent in uremic patients. The pathogenesis and etiology of arrhythmias are very complex and still unknown. The sedimentation of calcium salt in myocardial structures is one of the reasons for emergence of cardiac arrhythmias (AV conduction defects, ectopic arrhythmias). The appearance of mitral annular calcification (MAC), as the expression of the speed up process of atherosclerosis, was noted in younger uremic patients especially during hemodialysis. The aim of our research was to compare the incidence of MAC and cardiac arrhythmias in patients on hemodialysis. Our study included 40 patients, 24 male and 16 female, in the age between 20 and 60. Patients were mostly from Zagreb and the Counties of Zagreb (35%), Karlovac (10%), Slavonski Brod (7.5%), Varazdin (5%) and Pozega (5%). All 40 patients received 24 hours of Holter monitoring and 2-D echocardiography of M-mode. The patients were divided in two groups: I MAC+ (N = 23) and II MAC- (N = 17). Frequency of cardiac arrhythmias in group I was: atrial fibrillation N = 0; conduction defects N = 2 (1%); ventricularectopy Lown grade 3-5 N = 15 (65%); supraventricular ectopy N = 8 (34%), while the frequency of cardiac arrhythmias in group II was: atrial fibrillation N = 0; conduction defects N = 0; ventricular ectopy Lown grade 3-5 N = 6 (35%), supraventricular ectopy N = 6 (35%). During statistical processing the significant connection of MAC+ and frequency of cardiac arrhythmias was noticed. For both groups we have not noticed statistical significance in cardiac arrhythmia compared to electrolytes, risk factors PTH, and age. The time of hemodialysis treatment is one of possible factors for incidence of cardiac arrhythmias influenced by MAC. We noticed statistically significant (p < 0.05) difference of rhythm disorders between group I and group II especially for the ventricular ectopic activity, the frequency of which was higher in group I than in group II. MAC has probably significant role in dialysis patients for the development of cardiac arrhythmias within the framework of series of complicated multifactorial patogenetic mechanisms.

Ward, O.C.

Abstract: Romano-Ward syndrome manifests as episodic cardiac arrhythmia, which leads to syncope or sudden death. The electrocardiogram shows a characteristic prolonged Q-T interval.

Use of pyridazinone or phosphine oxide compounds to treat or prevent cardiac arrhythmia

Abstract: A method of treating or preventing supraventricular tachyarrhythmias is disclosed which comprises the use of a compound which selectively blocks the ultra-rapidly-activating delayed rectifier K+ current (IKur) of the human atrium.