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Atrial fibrillation is the most prevalent cardiac arrhythmia with a high risk of ischemic stroke. Thromboprophylaxis plays a key role in prevention of cardioembolic and non-cardioembolic events. Oral antithrombotic drugs are most often used to reduce hypercoagulable state. Patients may suffer from both under- and overtreatment compromising the outcomes. Medication peculiarities at large are well-known and widely debated. Non-adherence to antithrombotic drug regimen poses a significant risk of stroke. There is a pressing need for more detailed delineation of risk factors, namely by incorporation of the letter "N" (meaning "Non-adherence to drug therapy") into the well-known risk score alphanumeric display: CHA2DS2N-VASc. Better delineation of risk factors related to antithrombotic treatment as well as those related to treatment for congestive heart failure, hypertension, diabetes are desirable. Similarly, the bleeding risk score formula HAS-BLED might be improved by an additional risk factor, marked as the symbol "E", meaning "Excessive antithrombotic dosing" i.e. HAS-BLEDE. Improved formulas would help raise the predictive scores value and awareness for clinicians facing the problem of non-adherence to treatment regimen. If patients properly followed the prescribed drug therapy regimen it would potentially reveal that we already have ideal or near ideal antithrombotic drug(s). These drugs, herein non-specified, are widely used, but due to non-adherence they are not categorized as the best ones. That is why considerable efforts are focused on continued research and new developments. [ABSTRACT FROM AUTHOR]

The underlying pathophysiology of supraventricular and ventricular arrhythmias remains a matter of intense investigation. Though evolving, the contemporary explanations do not encompass all aspects of arrhythmogenicity. An improved understanding of arrhythmia substrate is needed to augment therapeutic capabilities. Our observation and literature sources demonstrate relatively high incidence of transitory arrhythmias which are non-intentionally generated by the endocardial lead/catheter manipulation. These findings are interesting and potentially may crystallize the reflex-dependent proarrhythmic cardiac activity. Herein we suggest the "reflexogenic arrhythmogenicity" concept extending an overall spectrum of known hypotheses. Cardiovascular reflex action can be categorized into three-tiered levels -intra-cellular, inter-cellular and inter-organic. The first two levels of the triplicate system reside within the cardiac anatomical landmarks (in fact intramurally, intra-organically), however the third one implicates central (cerebral) activity which boomerangs back via centripetal and centrifugal connections. These levels likely compose synoptic ternary reflex set system which may be validated in future studies. To hypothesize, coordinated mutual reciprocity of reflex activity results in stabilization of heart rhythm in robust heart. Any stressful cardiac event may lead to the shift of the rhythm toward unfavorable clinical entity probably via the loss of the influence of dominant reflex. Overall, an interaction and likely intrinsic inter-tiered competition along with possible interplay between physiological and pathological reflexes may be treated as contributing factors for the inception and maintaining of arrhythmias and cardiac performance as well. These assumptions await further documentation. If such a tenet were recognized, the changes in the clinical approach to arrhythmia management might be anticipated, preferably by selective reflex suppression or activation strategy. [ABSTRACT FROM AUTHOR]

Ischemia plays a key role in cardiac arrhythmogenesis, particularly in elderly patients. Healthy, non-ischemic and structurally normal myocardium is universally free from dysrhythmias. Thereby intact coronary blood flow prevents potential cardiac events. Hypothetically, ischemia-related electrophysiological differences are responsible for the supraventricular and/or ventricular rhythm irregularities. The goal of this review is to determine the role of systemic and coronary circulatory peculiarities and their association with heart rhythm abnormalities. The current analytical review extends and enriches previous knowledge about the influence of these peculiarities on the genesis of ischemia-dependent conflictogenic arrhythmias. Different intensity of coronary blood flow resulting from stenotic obstacles or vasospasm potentially leads to the non-uniform perfusion of myocites thus creating albeit subtle but vulnerable and powerful electrophysiologic substrate impending cardiac rhythm disturbances. Apparently, the behavior of both non-ischemic and iso-ischemic myocardium in respect to electric cardiac activity is very similar, at least theoretically. Some different clinical entities, e.g. arterial hypotension and/or anemia containing ischemic component, in most cases are free from arrhythmias. This postulation may be helpful in furthering arrhythmogenicity insights which have been generated previously. On the contrary, increased blood pressure often concurs with the supraventricular and/or ventricular arrhythmias; this pattern also favorably reflects our previous hypothetical assumptions associated with the mechanisms of arrhythmogenesis. Conclusively, both non-ischemic and iso-ischemic myocardium may be attributed to nonarrhythmogenic milieu. Nevertheless, the inventive analysis and more explorative data are required to support the suggested postulations. [ABSTRACT FROM AUTHOR]

Atrial fibrillation (AF) as a severe arrhythmia is now spreading worldwide at overwhelmingly high rates, particularly in elderly patients. Despite new insights, the mechanisms underlying AF are not conclusively determined yet. Taking into account the ischemic origin of arrhythmia induction (according to the so-called conflictogenic atrial fibrillation, declared recently) restoration of regional electrophysiological parameters is essential in tackling AF. We hypothesized that some atrial electrophysiological parameters, preferably the effective refractory period, might need to be controlled to prevent AF. All the remaining parameters - conduction velocity, conduction time, recovery time, vulnerability, excitability, repolarization etc. being as if secondary and less important could be ignored. Homogenization of the milieu producing AF might be implemented, at least theoretically, through restoration of blood supply in ischemic areas and/or via attenuation of electrophysiological differences between conflicting regions by delivery of atrial sub-threshold non-captured pulse-trains. Adjunctive therapy by drugs containing vasodilatory features and affecting the effective refractory period appears to be fundamental. Thus, stabilization of disorganized atrial cellular activities likely may lead to the recovery of atrial excitable characteristics. Despite the lack of compelling evidence, the application of the concept may be helpful in order to search for more precise and more effective methods to favorably change the refractory period. Further studies are necessary to determine whether restoration or improvement of blood circulation of atrial wall is feasible. Based on such considerations a novel preventive AF strategies are to be designed. [ABSTRACT FROM AUTHOR]

Underlying mechanisms of atrial fibrillation occurrence and its self-extinguishing remain not completely investigated yet. The role of autonomic tone and sinoatrial node in the interplay between atrial fibrillation and sinus rhythm is also not fully understood. The influence of inflammation as a possible source of arrhythmia and likelihood of its pharmacologic treatment deserves special attention. These complex issues are important for better understanding of arrhythmogenesis and rhythm control. Conceptual reconsiderations through the new insights primarily on the hypothetic basis may delineate new therapeutic and preventive strategies. The aim of this analytical review was to reinforce the clinical and laboratory studies regarding the role of: 1) autonomic tone and sinoatrial node in restitution of sinus rhythm, 2) new concept of "vibrantly quiescent stroboscopic tuning" as a matured status of atrial fibrillation being prepared for its abruption by slight impulse, 3) inflammation in the interplay between atrial fibrillation and sinus rhythm, 4) anti-inflammation and anti-allergic therapy to prevent and to treat the arrhythmia. [ABSTRACT FROM AUTHOR]

To improve electrode construction the following main problems have been considered: (1) reliable initial fixing in the endocardium, and (2) reducing the area of contact surface and improving threshold values. In this article we have described three original electrodes: 1) an endocardial electrode with a multi-edged tip (contact area 28 mm2, which gives high electric field strength and low thresholds; 2) a spreading tip electrode, which was created on the basis of morphological data. The tissues grow into the spread spaces of this tip and ensure better stability (contact area 17.8 mm2): and 3) a double-screw-in electrode which differs from the other corkscrew types. The contact end (surface area-10.4 mm2) consists of two sickle-shaped hooks. The sickle handle is 0.7 mm in length which prevents further hook penetration in the wall of the heart. It was found that a multi-edged electrode and electrodes supplied with a fixation device are, in terms of energy consumption, more effective compared to electrodes with spherical or cylindrical tips of the same area of contact surface. The double-screw-in endocardial electrode has useful features: reliable fixation and a small contact surface area and, therefore, a low threshold value. Thirty-five double-screw-in electrodes were inserted into an atrial position and 28 into a ventricular position. We have not observed any displacement of such electrodes during the past two years. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor commenting on an article related to implanted cardioverter defibrillator.

Atrial fibrillation is the most prevalent cardiac arrhythmia with a high risk of ischemic stroke. Thromboprophylaxis plays a key role in prevention of cardioembolic and non-cardioembolic events. Oral antithrombotic drugs are most often used to reduce hypercoagulable state. Patients may suffer from both under- and overtreatment compromising the outcomes. Medication peculiarities at large are well-known and widely debated. Non-adherence to antithrombotic drug regimen poses a significant risk of stroke. There is a pressing need for more detailed delineation of risk factors, namely by incorporation of the letter "N" (meaning "Non-adherence to drug therapy") into the well-known risk score alphanumeric display: CHA 2 DS 2 N-VASc. Better delineation of risk factors related to antithrombotic treatment as well as those related to treatment for congestive heart failure, hypertension, diabetes are desirable. Similarly, the bleeding risk score formula HAS-BLED might be improved by an additional risk factor, marked as the symbol "E", meaning "Excessive antithrombotic dosing" i.e. HAS-BLEDE. Improved formulas would help raise the predictive scores value and awareness for clinicians facing the problem of non-adherence to treatment regimen. If patients properly followed the prescribed drug therapy regimen it would potentially reveal that we already have ideal or near ideal antithrombotic drug(s). These drugs, herein non-specified, are widely used, but due to non-adherence they are not categorized as the best ones. That is why considerable efforts are focused on continued research and new developments.

The underlying pathophysiology of supraventricular and ventricular arrhythmias remains a matter of intense investigation. Though evolving, the contemporary explanations do not encompass all aspects of arrhythmogenicity. An improved understanding of arrhythmia substrate is needed to augment therapeutic capabilities. Our observation and literature sources demonstrate relatively high incidence of transitory arrhythmias which are non-intentionally generated by the endocardial lead/catheter manipulation. These findings are interesting and potentially may crystallize the reflex-dependent proarrhythmic cardiac activity. Herein we suggest the "reflexogenic arrhythmogenicity" concept extending an overall spectrum of known hypotheses. Cardiovascular reflex action can be categorized into three-tiered levels - intra-cellular, inter-cellular and inter-organic. The first two levels of the triplicate system reside within the cardiac anatomical landmarks (in fact intramurally, intra-organically), however the third one implicates central (cerebral) activity which boomerangs back via centripetal and centrifugal connections. These levels likely compose synoptic ternary reflex set system which may be validated in future studies. To hypothesize, coordinated mutual reciprocity of reflex activity results in stabilization of heart rhythm in robust heart. Any stressful cardiac event may lead to the shift of the rhythm toward unfavorable clinical entity probably via the loss of the influence of dominant reflex. Overall, an interaction and likely intrinsic inter-tiered competition along with possible interplay between physiological and pathological reflexes may be treated as contributing factors for the inception and maintaining of arrhythmias and cardiac performance as well. These assumptions await further documentation. If such a tenet were recognized, the changes in the clinical approach to arrhythmia management might be anticipated, preferably by selective reflex suppression or activation strategy.

In patients with atrial fibrillation antithrombotic prophylaxis for stroke is associated with an increased risk of bleeding. Cerebrovascular risk-benefit ratio for oral anticoagulation therapies continues to be debated. Macro and/or microhematomas as well as visible or cryptic ones may appear unexpectedly in any anatomic region. The diagnostic and prognostic value of subcutaneous hematomas (petechia, ecchymosis, bruise) potentially predisposing intracerebral micro- or macrobleeding might be reconsidered. Hypothetically, subcutaneous hemorrhagic events are "transparent" signs and reflect the coexistence of remote vulnerable sites that are potential bleeding sources. Obviously vigilance is needed for early signs of drug-related petechiae evaluation to determine whether it is a local/superficial subtlety or a systemic problem. Any bleeding complication, regardless of its scale and anatomical location, might be treated as a worrisome clinical symptom requiring subtle correction of antithrombotic regimen. The focus of this article is to review the current knowledge of drug-related hemorrhage with special emphasis on underlying mechanisms and links between the visible bleeding (predominantly subcutaneous) and remote (such as cerebral) hemorrhagic sources. To mitigate inappropriate therapy, we should consider new conceptual insights and more individualized approaches to achieve an optimal balance of efficacy and safety. We hypothesize that bleeding complications occur as a result of two factors - impact of antithrombotic drugs and related detrimental effect on microvascular network. Most likely the microvasculature undergoes pro-hemorrhagic medication stress leading to unfavorable vascular wall "fenestration" with ensuing consequences. If so, it suggests the presence of dual substrate responsible for hemorrhagic events.

Atrial fibrillation (AF) as the most common supraventricular arrhythmia is scarcely amenable to contemporary treatment. Due to the diverse origin and variable clinical course of AF there is a broad spectrum of therapy options. However, optimal AF management has not become a gold standard yet. In general, the recurrence rate of AF is most often clinically unacceptable despite drug, surgical and/or ablation therapy. Substrate-based approach and ongoing ablation of atrial wall in its selected areas including the vicinity of pulmonary veins can be harmful. Applied physical factors do produce total disintegration of cardiomyocites - both intra- and inter-cellular damage which, in turn, leads to functional hypo-/inactivation of atria irrespective of whether the sinus rhythm is restored or not. In fact, iatrogenic phenomenon of ablation-induced atrial incompetence did emerge. Heterogeneity in clinical results reflects the uncertainty regarding the efficacy, risks and benefits of invasive AF therapy. In this regard the overall burden of AF may increase when using current therapy methods. Applicability of destructive techniques is yet to be fully elucidated and discussed. We hypothesize that currently used ablation and/or surgical techniques are potentially harmful since the success rates are likely achieved through violation of atrial myocardium. That is why a new and well-designed therapeutic strategy is needed. Invention of highly selective curative methods producing fibrillatory/electric blockage with concomitant saving of atrial transport function is to be encouraged.

Ischemia plays a key role in cardiac arrhythmogenesis, particularly in elderly patients. Healthy, non-ischemic and structurally normal myocardium is universally free from dysrhythmias. Thereby intact coronary blood flow prevents potential cardiac events. Hypothetically, ischemia-related electrophysiological differences are responsible for the supraventricular and/or ventricular rhythm irregularities. The goal of this review is to determine the role of systemic and coronary circulatory peculiarities and their association with heart rhythm abnormalities. The current analytical review extends and enriches previous knowledge about the influence of these peculiarities on the genesis of ischemia-dependent conflictogenic arrhythmias. Different intensity of coronary blood flow resulting from stenotic obstacles or vasospasm potentially leads to the non-uniform perfusion of myocites thus creating albeit subtle but vulnerable and powerful electrophysiologic substrate impending cardiac rhythm disturbances. Apparently, the behavior of both non-ischemic and iso-ischemic myocardium in respect to electric cardiac activity is very similar, at least theoretically. Some different clinical entities, e.g. arterial hypotension and/or anemia containing ischemic component, in most cases are free from arrhythmias. This postulation may be helpful in furthering arrhythmogenicity insights which have been generated previously. On the contrary, increased blood pressure often concurs with the supraventricular and/or ventricular arrhythmias; this pattern also favorably reflects our previous hypothetical assumptions associated with the mechanisms of arrhythmogenesis. Conclusively, both non-ischemic and iso-ischemic myocardium may be attributed to nonarrhythmogenic milieu. Nevertheless, the inventive analysis and more explorative data are required to support the suggested postulations.

Atrial fibrillation (AF) as a severe arrhythmia is now spreading worldwide at overwhelmingly high rates, particularly in elderly patients. Despite new insights, the mechanisms underlying AF are not conclusively determined yet. Taking into account the ischemic origin of arrhythmia induction (according to the so-called conflictogenic atrial fibrillation, declared recently) restoration of regional electrophysiological parameters is essential in tackling AF. We hypothesized that some atrial electrophysiological parameters, preferably the effective refractory period, might need to be controlled to prevent AF. All the remaining parameters - conduction velocity, conduction time, recovery time, vulnerability, excitability, repolarization etc. being as if secondary and less important could be ignored. Homogenization of the milieu producing AF might be implemented, at least theoretically, through restoration of blood supply in ischemic areas and/or via attenuation of electrophysiological differences between conflicting regions by delivery of atrial sub-threshold non-captured pulse-trains. Adjunctive therapy by drugs containing vasodilatory features and affecting the effective refractory period appears to be fundamental. Thus, stabilization of disorganized atrial cellular activities likely may lead to the recovery of atrial excitable characteristics. Despite the lack of compelling evidence, the application of the concept may be helpful in order to search for more precise and more effective methods to favorably change the refractory period. Further studies are necessary to determine whether restoration or improvement of blood circulation of atrial wall is feasible. Based on such considerations a novel preventive AF strategies are to be designed.

Atrial fibrillation continues to be a challenging arrhythmia. There are some conventional, time-tested explanations of atrial fibrillation genesis, however some uncertainty of its complete understanding still exists. We focused on atrial ischemia which, hypothetically, could be responsible for manifestation of the arrhythmia, irrespective of the underlying heart disease. Evidences abounds that atrial fibrillation has an extremely strong association with nutritional/oxidative status of myocardium. This arrhythmia seemingly may stem from the electrophysiological differences taking place in the boundary areas. To validate such assumptions we have surveyed widely accepted theories based on clinical and experimental evidence. There was an attempt to integrate some well-known theoretical explanations (focal, multifocal, ectopic, reentrant activity, atrial remodeling, etc.) into a new conceptually systematized arrhythmogenesis. Confronting ischemic and non-ischemic atrial zones electrophysiologically on their borderlines presumably creates a substrate vulnerable to the development of atrial fibrillation. The behavior of these interrelated areas is likely ischemia-dependent; the separating borderline(s) may be treated as conflictogenic, releasing triggers/drivers to commence and to perpetuate the arrhythmia. Ischemically damaged and non-damaged myocardial areas likely participate in the relay-race carousel of arrhythmogenicity due to their mutual interactions, accompanied by the "fireworks" at the separating borderlines. It could be concluded that myocardial ischemia as a nonspecific proarrhythmic factor presumably plays a key role in the genesis and sustenance of atrial fibrillation. Theoretically the most important step in eradication of arrhythmogenic substrate might be an overall abolition of ischemia regardless of the characteristics of underlying heart disease. Innovative intellectual and explorative research is needed to render innocuous the ischemia that might help us win the century's cardioarrhythmological battle.

Underlying mechanisms of atrial fibrillation occurrence and its self-extinguishing remain not completely investigated yet. The role of autonomic tone and sinoatrial node in the interplay between atrial fibrillation and sinus rhythm is also not fully understood. The influence of inflammation as a possible source of arrhythmia and likelihood of its pharmacologic treatment deserves special attention. These complex issues are important for better understanding of arrhythmogenesis and rhythm control. Conceptual reconsiderations through the new insights primarily on the hypothetic basis may delineate new therapeutic and preventive strategies. The aim of this analytical review was to reinforce the clinical and laboratory studies regarding the role of: 1) autonomic tone and sinoatrial node in restitution of sinus rhythm, 2) new concept of ?vibrantly quiescent stroboscopic tuning? as a matured status of atrial fibrillation being prepared for its abruption by slight impulse, 3) inflammation in the interplay between atrial fibrillation and sinus rhythm, 4) anti-inflammation and anti-allergic therapy to prevent and to treat the arrhythmia.

Cardiac resynchronization therapy appears to be useful for patients with severe chronic congestive heart failure. However, many questions still arise concerning the effectiveness of this kind of therapy since hemodynamic improvement is not observed in all patients. Heterogeneity of conclusions reported by several multicenter clinical trials and prominent experts demonstrates that many uncertainties related to cardiac resynchronization therapy still exist. We tried to reveal some inadequacies in clinical results by focusing on cardiac venous blood return which is likely complicated by the presence of lead inside the coronary sinus and its branches. Downstream traversing lead may occlude (partially or completely) the ostia of minor tributaries and target vein of lead final positioning. Thrombosis may also be incited within the coronary sinus itself. Remaining lumen predetermined by the lead body and subsequent thrombosis may be insufficient to provide adequate blood flow. Resulting detrimental venous return presumably may slightly depress myocardial contractility which may be significant in very sensitive group of patients assigned to the New York Heart Association class III or IV. Cardiac venous blood pumping conditions (or venous drainage) are likely also complicated by abnormal activation of left ventricle. The contributory role of these two subtle causes unfavorably influencing venous drainage is still unknown. It may be treated as a hypothetical attempt to find the clue and needs future studies for verification.

Survey of pacemaking activities of the three Lithuanian centers (located in Kaunas, Vilnius and Klaipeda) is presented. Results of the last eight years are analyzed and compared with the activities of the rest European countries. According to the index of number of primary implantations per 1 million of population/per year Lithuania has ranked in 19th position. Annual number of implantations of cardioverter-defibrillators is approximately 5-10. These results demonstrate that Lithuania lags behind the majority of European countries. There is a need to increase the activities both in implantation of pacemakers and cardioverter-defibrillators as well.