Stress kardiomyopathy triggered by unusual situation.

Stress - “takotsubo” cardiomyopathy - is a reversible mimicking acute myocardial infarction. The trigger is extreme mental or physical stress. The main diagnostic examination is ventriculography with typical left ventricle apical ballooning wall motion abnormality. We present a case report of 63 years old woman, hospitalized at the Department of IV. internal Clinic Medical Faculty and University Hospital Bratislava due to angina. The main trigger was atypical stress situation - urgent need to urinate. On admission, the patients condition was dominated by the hypertension emergency, tachycardia and psychic tension. The ECG on admission revealed the sinus tachycardia and only marked ST elevation in leads I, II, V3-V6. The negative T wave in the leads I, II, V1-V6 was documented on latter ECG. Following the dynamics of troponin levels we assumed the non-STEMI, but due to psychic stress we also considered stress cardiomyopathy. Our patient underwent the coronary angiography and only marginal changes were present. The catecholamine cardiomyopathy with left ventricular apical wall motion abnormality, mild reduction of ejection fraction (48-50 %) and 1st degree of diastolic dysfunction was proved by ventriculography and echocardiography. After the 2 months follow-up, echocardiography confirmed the physiologic finding. This case report points out to the atypical urgent situation that provoked the stress cardiomyopathy.

Prognostic value of echocardiography and ECG in heart failure with preserved ejection fraction.

OBJECTIVE: The aim of this study was to evaluate characteristics of patients with heart failure (HF) with preserved ejection fraction (HFPEF) and to assess prognostic predictors in 2-year follow-up. METHODS: We included prospectively 109 patients admitted to the internal department for HF, grouped into HFPEF (EF>40 %, n = 63) and HF with reduced EF (HFREF) (EF≤40 %, n=46). Preserved right ventricular systolic function (PRV) was defined as the peak systolic tricuspid annular velocity (S') >10.8 cm/s. RESULTS: HFPEF and HFREF patients had non-significantly different 2-year all-cause and CV mortality (28.6 % vs 37.0 %, 17.5 % vs 21.7 %). Patients with HFPEF and PRV vs dysfunctional RV had a better survival (76.6  % vs 56.3 %, p=0.045). In HFPEF, the patients who survived had a trend to better S' (13.6±3.1 cm/s vs 11.9±3.4 cm/s, p=0.055), shorter QTc (427±42ms vs 454±42ms, p=0.058), and all-cause mortality was lowered only by anticoagulants (12.0 % vs 39.5 %, p=0.02). QTc interval and PRV emerged as predictors of all-cause mortality (HR 1.7 per 40 ms change, 95  % CI 1.1-2.6, p = 0.02, HR 0.38, 95 % CI 0.15-0.93, p=0.03). CONCLUSIONS: In HFPEF, we observed a trend to lower all-cause and CV mortality compared to HFREF and anticoagulants were the only therapy that significantly lowered mortality. PRV and QTc interval emerged as independent predictors of survival (Tab. 6, Fig. 2, Ref. 26).

[Changes in NT-proBNP levels in patients with atrial fibrillation related to heart failure]. / Zmeny hladín NT-proBNP u pacientov s fibriláciou predsiení v iávislosti od srdcového zlyhávania.

INTRODUCTION: NT-proBNP, a well-established diagnostic and prognostic marker in clinical practice, is significantly elevated in individuals with atrial fibrillation (AF), even in absence of heart failure or major structural heart disease. OBJECTIVES: The aim of this study was to determine the cut-off value of NT-proBNP for diagnosis of heart failure in individuals with atrial fibrillation. METHODS: We compared 44 patients (25 male/19 female) with AF and concomitant overt heart failure [age 76 (62-82) years; median (interquartile range - IQR)] versus 29 patients (16 male/13 female) with AF with no signs of heart failure [age 59 (50-67) years; median (IQR)]. We considered the underlying causes of heart failure and its severity, comorbidities, echocardiographic and selected laboratory parameters, the body mass index as well as the treatment at discharge. We determined the cut-off value for heart failure and major structural heart disease using ROC curve analysis. RESULTS: Median NT-proBNP in the group of patients with AF and concomitant heart failure was 3 218 ng/l (IQR 1 758-7 480 ng/l) vs 981 ng/l (IQR 431-1 685 ng/l) in the group of patients with AF with no signs of heart failure; this difference was statistically significant (p < 0.001). The level of NT-proBNP higher than 1 524 ng/l in patients with AF was diagnostic of major structural heart disease and pointed towards a possible heart failure (sensitivity 80%, specificity of 76%, accuracy 78%, positive predictive value 83%, negative predictive value 71%). The NT-proBNP levels significantly correlated with age (p < 0.001), left atrial diameter (p < 0.01) and furosemide dose at discharge (p < 0.05). The NT-proBNP levels significantly negatively correlated with left ventricular ejection fraction (p < 0.001) and body mass index (p < 0.05). CONCLUSION: We found out that NT-proBNP is significantly elevated in patients with AF with preserved left ventricular function and in absence of heart failure and significantly correlates with age, left ventricular ejection fraction, left atrial diameter, body mass index and the furosemide dose necessary to achieve cardiac compensation. Furthermore, we determined the NT-proBNP cut-offvalue predictive of a possible heart failure in patients with AF.

[Late recurrences of atrial fibrillation in patients after direct-current cardioversion]. / Neskoré recidívy fibrilácie predsiení u patientov po elektrickej kardioverzii.

AIM: To analyze factors after successful direct-current cardioversion in patients with atrial fibrillation and to explore late recurrences of the arrhythmia. METHODS: Forty-three patients with atrial fibrillation without associated valvular heart disease, who underwent non-emergent cardioversion within the years 2002-2006, were included. We retrospectively analyzed clinical data from the medical records. Late reccurence of the arrhythmia was defined as arrhythmia in patients discharged with sinus rhythm. RESULTS: Median follow-up of the patients was 33 (17, 48) months. We found 20 late recurrences of atrial fibrillation in the total group of 43 patients after successful direct-current cardioversion (46.5%). In a 6-month period after direct-current cardioversion the recurrence of arrhythmia was found in two patients, in a one-year period in 6 patients and in a period longer than one year in 12 patients. Median time to recurrence was 15 (6, 33) months. Females relapsed more frequently than males (p < 0.02), what could be explained by higher age, incidence of hypertension and thyreopathy in females. Patients with a history of thyropathy had more frequent occurrence of arrhythmia, despite normal values of TSH, as compared to patients without a history of thyropathy (p < 0.04). Patients with recurrence of the atrial fibrillation had higher systolic pressure (130 vs 120 mm Hg, p < 0.05) and pulse arterial pressure (50 vs 40 mm Hg, p < 0.01) after cardioversion. No significant difference between the two groups in age, left atrium diameter, left ventricle ejection fraction and cardiovascular, or non-cardiovascular risk factors was found. CONCLUSION: Despite successful direct-current cardioversion, the risk of late recurrence of the atrial fibrillation in a following period is at least 46.5%. Females, patients with a history of thyropathy and those with higher systolic and pulse arterial pressures are at higher risk of late recurrences.

[Effectiveness and safety of adenosine in the therapy and diagnosis of arrhythmias]. / Ucinnost' a bezpecnost' adenozínu v terapii a diagnostike arytmií.

Adenosine is a drug with unique clinical and electrophysiological properties. Despite this, its use in Slovakia is rare. The decisive reason, besides its price, is the physicians fear of potential adverse effects and their limited knowledge regarding its clinical use. This study was aimed at analysis of the contribution of adenosine to the treatment and diagnostics of arrhythmias and evaluation of its safety. We studied the effect of adenosine in 62 patients. Adenosine terminated paroxysmal supraventricular tachycardia (PSVT) in 16 of 44 patients (36.4%) and in another 21 patients (47.7%) we revealed the type of unclear PSVT. We observed contribution to the diagnostics of wide QRS complex tachycardia in 3 of 6 patients (50.0%). Latent ventricular preexcitation was induced in 2 of 12 patients (16.7%). Subjective complaints after adenosine were frequent (at least 1 symptom in 80.6% patients), but all of them were of short duration and clinically not significant. We did not observe any relevant complication of adenosine. The average maximal RR interval after adenosine was 1.75 sec. We consider adenosine in adequately indicated patients with respect for its contraindications as highly effective drug in the treatment and diagnostics of specific arrhythmias.

[Early diagnosis and reasons for not administering thrombolytic therapy in acute myocardial infarct]. / Vcasná diagnóza a príciny nerealizácie trombolytickej liecby u chorých s akútnym infarktom myokardu.

In Slovakia we are lacking data on early (before examination of serum markers of myocardial necrosis) pertaining to thrombolytic treatment (TLL) which is inevitable in case of acute myocardial infarction (AIM) as well as data on the reasons why TLL is not implemented. This why the authors analyze the results of completed comprehensive project Audit concerned with diagnostic and therapeutic procedures in patients with acute coronary syndromes during the pre-hospital and hospital stage (AUDIT). The investigation was a perspective multi-centre study. Data were collected from 3123 patients with AIM in 66 departments (in 64 health institutions) during Sept. 16 1997 till Sept. 15 1998. The group included patients admitted within 96 hours after the development of complaints with the diagnosis or suspicion of AIM and discharged with the diagnosis of a first/repeated AIM. Early diagnosis of AIM was made in 1736 (55.6%) patients. In the AUDIT study TLL was assessed in 1074 (34.6%) patients. A marked difference between the number of candidates for TLL and the number of patients with TLL where TLL was implemented requires that in analyses of TLL in patients with AIM attention should be paid also to reasons why it was not implemented. The most frequent cause why TLL was nor implemented was late admission of the patient to hospital (in patients who attended hospital < 6 hours, TLL was not implemented in 48.5%, after admission between 6 and 12 hours in 70% and in patients admitted > 12 hours in as many as 90.8% patients), equivocal indication of TLL (in 29.9% patients) and contraindications (in 16.1% patients). The presented results are priority data on the early diagnosis of AIM and reasons why TLL was not implemented. It is part of data essential needed for elaboration of a (national) programme of better care (management) of patients with AIM taking into account also economic factors.

Thrombolytic therapy for patients with acute myocardial infarction. Causes increasing the probability of not receiving thrombolytic therapy.

Intravenous thrombolysis is the most accessible and the most common form of reperfusion therapy. The aim of this study was to identify demographic, clinical and electrocardiographic factors, which based on published data and in patients included in the project Audit of diagnostic and therapeutic procedures in patients with acute myocardial infarction (AUDIT), increased the probability of not receiving thrombolytic therapy. In order to maximize the impact of thrombolytic therapy to reduce the case fatality rate associated with an acute myocardial infarction, we review, which a number of studies provide evidence on the usage of thrombolytic therapy in elder, women, patients with diabetes mellitus, bundle-branch block and after stroke. (Fig. 10, Ref. 52.).

Special character of atrial paroxysmal fibrillation in coincidence with WPW syndrome.

The paper summarizes the knowledge on paroxysmal atrial fibrillation in WPW syndrome. The peculiarities, ECG features, risk markers of sudden cardiac death, pharmacologic and non farmacologic therapy and prevention of this arrhythmia are presented. Potentially dangerous effects of drugs such as digoxin, verapamil, adenosine and betablockers are emphasized.

Electrophysiologic characteristics and radiofrequency ablation of concealed nodofascicular and left anterograde atriofascicular pathways.

INTRODUCTION: True nodoventricular or nodofascicular pathways and left-sided anterograde decremental accessory pathways (APs) are considered rare findings. METHODS AND RESULTS: Two unusual patients with paroxysmal supraventricular tachycardia were referred for radiofrequency (RF) ablation. Both patients had evidence of dual AV nodal conduction. In case 1, programmed atrial and ventricular stimulation induced regular tachycardia with a narrow QRS complex or episodes of right and left bundle branch block not altering the tachycardia cycle length and long concentric ventriculoatrial (VA) conduction. Ventricular extrastimuli elicited during His-bundle refractoriness resulted in tachycardia termination. During the tachycardia, both the ventricles and the distal right bundle were not part of the reentrant circuit. These findings were consistent with a concealed nodofascicular pathway. RF ablation in the right atrial mid-septal region with the earliest atrial activation preceded by a possible AP potential resulted in tachycardia termination and elimination of VA conduction. In case 2, antidromic reciprocating tachycardia of a right bundle branch block pattern was considered to involve an anterograde left posteroseptal atriofascicular pathway. For this pathway, decremental conduction properties as typically observed for right atriofascicular pathways could be demonstrated. During atrial stimulation and tachycardia, a discrete AP potential was recorded at the atrial and ventricular insertion sites and along the AP. Mechanical conduction block of the AP was reproducibly induced at the annular level and at the distal insertion site. Successful RF ablation was performed at the mitral annulus. CONCLUSION: This report describes two unusual cases consistent with concealed nodofascicular and left anterograde atriofascicular pathways, which were ablated successfully without impairing normal AV conduction system.

Radiofrequency ablation of a concealed nodoventricular Mahaim fiber guided by a discrete potential.

INTRODUCTION: We present the case of a 17-year-old woman who underwent an electrophysiological study and radiofrequency (RF) ablation of supraventricular tachycardia refractory to medical treatment. Two right-sided, concealed, nondecremental atrioventricular accessory pathways (AV-APs) involved in orthodromic circus movement tachycardias were identified. After RF ablation of both AV-APs, evidence of bidirectional dual AV nodal conduction was demonstrated and regular narrow complex tachycardia was induced. METHODS AND RESULTS: During the tachycardia, retrograde slow and fast AV nodal pathway conduction with second-degree ventriculoatrial (VA) block and VA dissociation were observed. During the tachycardia with second-degree VA block, ventricular extrastimuli elicited during His-bundle refractoriness advanced the next His potential or terminated the tachycardia. Mapping the right atrial mid-septal region, a distinct high-frequency activation P potential was recorded in a discrete area, two thirds of the way from the His bundle toward the os of the coronary sinus. Detailed electrophysiologic testing with the recordable P potential demonstrated that the tachycardia utilized a concealed nodoventricular AP arising from the proximal slow AV nodal pathway. CONCLUSION: The tachycardia with slow 1:1 VA conduction could be reset by ventricular extrastimuli elicited during His-bundle refractoriness advancing the subsequent activation P potential and atrial activation. RF ablation guided by recording of the activation P potential resulted in elimination of both the slow AV nodal pathway and the nodoventricular connection with preservation of the normal AV conduction system.

[Pharmacotherapeutic profile of patients with acute myocardial infarct in the early hospitalization period]. / Farmakoterapeutický profil chorých s akútnym infarktom myokardu vo vcasnom období hospitalizácie.

BACKGROUND: The early treatment efficacy of patients with acute myocardial infarction (AMI) with thrombolysis, antiplatelet drugs, betablockers and ACE inhibitors has been well documented in randomized mega trials. However, little is known about the fact to what extend the results of these mega trials have influenced the treatment practices. Moreover, in the view of a complete lack of data on management of patients with AMI in Slovak Republic a project of the Ministry of Health "Audit of diagnostic and therapeutic management in patients with acute coronary syndromes" (AUDIT) has been conducted. OBJECTIVES: To obtain preliminary information on the present state of pharmacotherapy of patients with AMI in Slovak Republic during the early hospitalization phase (EHP) from the Pilot Study (PS) of the project AUDIT. METHODS: Pharmacotherapy of AMI during EHP was analysed in 336 patients (232 males and 104 females, mean age 65 12 years, age range 30-93 years). Patients admitted with diagnosis of the first or repeated AMI or with suspect AMI were included. PS was done in prospective multicentric study between November 1, 1996 and December 31, 1996. 23 hospitals from various parts of Slovakia participated in this study. Data were compiled by means of questionaires and were processed by ACCES 97 and EXCEL 97. RESULTS: Antiplatelet therapy with acetylosalicylic acid (almost exclusively Anopyrin) received as much as 87.8% of patients with AMI during EHP. Thrombolytic therapy (TLT), almost exclusively with streptokinase, was performed in 105, i.e. in 31.8% of patients with AMI. TLT was performed in a statistically significantly smaller proportion of patients older than 65 years compared to patients 65 years of age and younger (20.9% vs 41.2%, p < or = 0.01). Females were treated with TLT statistically significantly less frequently than males (24.5% vs 35.1%, p < or = 0.05). The major cause for not performing the TLT was late arrival to hospital (in 32.1% patients). Betablockers were administered to a total of 42.9% of patients during EHP. Betablockers received only 3.6% of patients intravenously (!) and only 39.3% of patients orally. Treatment with oral betablockers was performed in a statistically significantly smaller proportion of patients older than 65 years compared to patients 65 years of age and younger (27.4% vs 49.7%, p < or = 0.01). Up to 49.1% of patients in EHP were treated with ACE inhibitors, however, left ventricular ejection fraction < 40% warranting feasibility of this treatment was achieved only in 26.7% of patients. Nitrates were administered to 62% of patients in EHP, of this number intravenously to 37.4% of patients. Calcium channel blockers were given only to 7.3% of patients. Treatment with heparin was performed in 90.9% of patients. 14.3% of patients received during EHP antiarrhythmics of class I and 2.7% of patients of class III. MgSO4 was used in 26.4% of patients in EHP. CONCLUSIONS: The reported PS of AUDIT Project gives for the first time information on the state of the pharmacotherapy of patients with AMI in Slovak Republic. Some results are relatively encouraging, however, others can not be a reason for satisfaction. The fact, that in Slovakia, adequate number of patients with AMI receive acetylosalicylic acid (Anopyrin) and that Slovakia belongs to countries with the smallest proportion of patients with AMI treated with calcium channel blockers and antiarrhythmics during EHP is encouraging. On the other hand, the use of TLT and betablockers is dissatisfactory. Requirement to increase the proportion of thrombolysed patients with AMI and the necessity for substantially more frequent use of betablockers, especially intravenous, in EHP in these patients result from these findings. In Slovakia, inadequately large proportion of patients with AMI is treated with ACE inhibitors, heparin, and partially also nitrates administered per os during EHP. (ABSTRACT TRUNCATED)

[Reperfusion arrhythmias]. / Reperfúzne arytmie.

Reperfusion arrhythmias originate as a consequence of the complex of cellular and humoral reactions accompanying the opening of coronary artery. As the primary cause of their generation are considered the chemically defined substances that are produced and accumulated in myocardium during reperfusion. The key role is ascribed to free oxygen radicals but of importance are also other substances such as calcium, thrombin, platelet activating factor, inositol triphosphate, angiotensin II and others. These chemical mediators of reperfusion arrhythmias operate as modulators of cellular electrophysiology causing the complex changes at the level of ion channels. It is supposed that in the genesis of reperfusion arrhythmias unlike ischemic arrhytmias operate nonreentrant mechanisms such as abnormal or enhanced automacy and triggered activity due to afterdepolarizations. As a typical reperfusion arrhythmia is considered an early (within 6 hours after start of thrombolysis), frequent (> 30 episodes/hour) and repetitive (occurring during > 3 consecutive hours) accelerated idioventricular rhythm (AIVR). AIVR with such characteristics has a high specificity and positive predictive accuracy but relative low sensitivity as a predictor of reperfusion. Thus, in occurrence of AIVR, recanalization of infarction-related coronary artery is very probable, but in absence of AIVR, reperfusion is still not excluded. The following arrhythmias are regarded also as markers of reperfusion: frequent premature ventricular complexes (> twofold increase in frequency within 90 minutes after the start of thrombolysis), a significant increase of episodes in nonsustained ventricular tachycardia, sinus bradycardia and probably also high-degree atrioventricular blocks. At present, there is no definite evidence, as to whether sustained ventricular tachycardia and especially ventricular fibrillation can be caused by reperfusion. Reperfusion arrhythmias are an important noninvasive marker of successful recanalization of infarction-related coronary artery. However, they are also a sign of reperfusion injury and a finding which may limit the favourable effect of reperfusion. In account of that, there is a very intensive search for pharmacologic interventions which could protect or attenuate the reperfusion injury and thereby also the genesis of reperfusion arrthythmias. Although promising results were obtained with many substances antagonizing the effects of mediators of reperfusion injury, there is no definite recommendation for their use under clinical conditions. However, the results from the latest clinical trials with ACE inhibitors are very promising. These trials render relative conclusive evidence, that ACE inhibitors could have a protective effect against reperfusion arrhythmias. (Ref. 89, Tab. 1.)

[Supraventricular arrhythmias and disorders of atrioventricular and intraventricular conduction in patients with acute myocardial infarct]. / Supraventrikulárne arytmie a poruchy atrioventrikulárneho a intraventrikulárneho vedenia u chorých s akútnym infarktom myokardu.

In addition to ventricular arrhythmias, various forms of supraventricular arrhythmias (SVA) and atrioventricular (AV) and intraventricular (IV) conduction disturbances occur also in acute myocardial infarction (AMI). In the setting of AMI, SVA may be caused by relevant atrial ischemia or infarction. SVA complicate the course especially that of inferior, posterior and lateral AMI. SVA occur frequently also in the right ventricular myocardial infarction and in pericarditis. SVA appearing in the late phase of AMI are caused particularly by hemodynamic factors especially those of both left and right ventricular dysfunctions. Atrial dilatation and the increase of intraatrial pressure are also important factors in the genesis of SVA. The autonomous nervous system, electrolyte disturbances, acidosis and global hypoxia may operate as modulating factors in the development of SVA. AV conduction disturbances are significantly more frequent in patients with inferior than with anterior AMI. In inferior AMI, they are frequently caused by reflex parasympathetic activation. In the genesis of AV conduction disturbances, a significant role may be played also by the following mechanisms: ischemia or necrosis of AV node or AV junction and the negative dromotropic effect of adenosine and potassium which are released to a great extent during myocardial ischemia and reperfusion. A high-degree AV block complicating the course of inferior AMI has a significantly better prognosis than that occurring in the setting of anterior AMI. In inferior AMI, AV block is frequently reversible, whereas in anterior AMI, it is persistent and irreversible. Early AV conduction disturbances, appearing within 24 hours of AMI have a better prognosis than those occurring in the late phase of AMI. Bundle branch blocks (BBB) complicating the course of AMI are caused by occlusion of bundle-related coronary artery or by serious ischemia in its bed. BBB is frequently a marker of a multivessel disease. New BBB appearing in AMI especially the right bundle branch block is considered as an predictor for the development of a complete AV block. Frequent and repetitive SVA as well as serious AV and IV conduction disturbances are frequently associated with a significantly worse clinical course of AMI and with increased mortality, with that of especially hospital mortality. However, this is usually not caused by SVA or AV and IV conduction disturbances per se. The major cause of death in these patients are heart failure, cardiogenic shock and malignant ventricular arrhythmias due to larger AMI, significant reduction of left ventricular function and advanced coronary heart disease. Complex SVA as well as serious AV and IV conduction disturbances are usually considered as markers, but not as independent predictors for both increased hospital mortality and in some cases also for that of posthospital mortality. Their occurrence in AMI may help to identify the patients at great risk who require a very intensive treatment including aggressive management of extensive coronary heart disease. (Ref. 62.)

Reperfuzne arytmie.

Reperfusion arrhythmias originate as a consequence of the complex of cellular and humoral reactions accompanying the opening of coronary artery. As the primary cause of their generation are considered the chemically defined substances that are produced and accumulated in myocardium during reperfusion. The key role id ascribed to free oxygen radicals but of importance are also other substances such as calcium, thrombin, platelet activating factor, inositol triphosphate, angiotensin II and others. These chemical mediators of reperfusion arrhythmias operate as modulators of cellular electrophysiology causing the complex changes at the level of ion channels. It is supposed that in the genesis of reperfusion arrhythmias unlike ischemic arrhythmias operate nonreentrant mechanisms such as abnormal or enhanced automacy and triggered activity due to afterdepolarizations. As a typical reperfusion arrhythmia is considered an early (within 6 hours after start of thrombolysis), frequent (> 30 episodes/hour) and repetitive (occurring during > 3 consecutive hours) accelerated idioventricular rhythm (AIVR). AIVR with such characteristics has a high specificity and positive predictive accuracy but relative low sensitivity as a predictor of reperfusion. Thus, in occurrence of AIVR, recanalization of infarction-related coronary artery is very probable, but in absence of AIVR, reperfusion is still not excluded. The following arrhythmias are regarded also as markers of reperfusion: frequent premature ventricular complexes (> twofold increase in frequency within 90 minutes after the start of thrombolysis), a significant increase of episodes in nonsustained ventricular tachycardia, sinus bradycardia and probably also high degree atrioventricular blocks. At present, there is no definite evidence, as to whether sustained ventricular tachycardia and especially ventricular fibrillation can be caused by reperfusion. Reperfusion arrhythmias are an important noninvasive marker of successful recanalization of infarction-related coronary artery. However, they are also a sign of reperfusion injury and a finding which may limit the favourable effect of reperfusion. In account of that, there is a very intensive search for pharmacologic interventions which could protect or attenuate the reperfusion injury and thereby also the genesis of reperfusion arrhythmias. Although promising results were obtained with many substances antagonizing the effects of mediators of reperfusion injury, there is no definite recomendation for their use under clinical conditions. However, the results from the latest clinical trials with ACE inhibitors are very promising. These trials render relative conclusive evidence, that ACE inhibitors could have a protective effect against reperfusion arrhythmias. (Ref. 89, Tab. 1.)

Supraventrikularne arytmie a pouchy atrioventrikularneho a intraventrikularneho vedenia u chorych s akutnym infarktom myokardu.

In addition to ventricular arrhythmias, various forms of supraventricular arrhythmias (SVA) and atrioventricular (AV) and intraventricular (IV) conduction disturbances occur also in acute myocardial infarction (AMI). In the setting of AMI, SVA may be caused by relevant atrial ischemia or infarction. SVA complicate the course especially that of inferior, posterior and lateral AMI, SVA occur frequently also in the right ventricular myocardial infarction and in pericarditis. SVA appearing in the late phase of AMI are caused particularly by hemodynamic factors especially those of both left and right ventricular dysfunctions. Atrial dilatation and the increase of intraatrial pressure are also important factors in the genesis of SVA. The autonomous nervous system, electrolyte disturbances, acidosis and global hypoxia may operate as modulating factors in the development of SVA. AV conduction disturbances are significantly more frequent in patients with inferior than with anterior AMI. In inferior AMI, they are frequently caused by reflex parasympathetic activation. In the genesis of AV conduction disturbances, a significant role may be played also by the following mechanisms: Ischemia or necrosis of AV node or AV junction and the negative dromotropic effect of adenosine and potassium which are released to a great extent during myocardial ischemia and reperfusion. A high-degree AV block complicating the course of inferior AMI has a significantly better prognosis than that occurring in the setting of anterior AMI. In inferior AMI, AV block is frequently reversible, whereas in anterior AMI, it is persistent and irreversible. Early AV conduction disturbances, appearing within 24 hours of AMI have a better prognosis than those occurring in the late phase of AMI. Bundle branch blocks (BBB) complicating the course of AMI are caused by occlusion of bundle-related coronary artery or by serious ischemia in its bed. BBB is frequently a marker of a multivessel disease. New BBB appearing in AMI especially the right bundle branch block is considered as an predictor for the development of a complete AV block. Frequent and repetitive SVA as well as serious AV and IV conduction disturbances are frequently associated with a significantly worse clinically course of AMI and with increased mortality, with that of especially hospital mortality. However, this is usually not caused by SVA or AV and IV conduction disturbances per se. The major cause of death in these patients are heart failure cardiogenic shock and malignant ventricular arrthythmias due to larger AMI, significant reduction of left ventricular function and advanced coronary heart disease. Complex SVA as well as serious AV and IV conduction disturbances are usually considered as markers, but not as independent predictors for both increased hospital mortality and in some cases also for that of posthospital mortality. Their occurrence in AMI may help to identify the patients at great risk who require a very intensive treatment including aggressive management of extensive coronary heart disease. (Ref. 62.).

[Ventricular arrhythmias and sudden cardiac death in acute myocardial infarct in the era of thrombolytics]. / Komorové arytmie a náhla srdcová smrt pri akútnom infarkte myokardu v trombolytickej ére.

Sudden cardiac death (SCD) in the setting of acute myocardial infarction (AMI) remains an actual problem. There is a very close relationship between ventricular arrhythmias and SCD in AMI. Malignant ventricular arrhythmias, such as ventricular fibrillation and ventricular tachycardia are the major causes of SCD in coincidence with AMI. Frequent and complex ventricular arrhythmias are also important predictors of the risk of SCD in coincidence with and after AMI. In this article the authors emphasize the importance of the complexity of pathophysiological mechanisms responsible for the genesis of ventricular arrhythmias in coincidence with AMI. The necessity of taking into account the current knowledge about pathophysiology in prevention and therapy of separate forms of ventricular arrhythmias is also emphasized. The incidence and time course of ventricular arrhythmias and SCD in coincidence with AIM in prethrombolytic and thrombolytic periods is described. The importance of separate forms of ventricular arrhythmias in coincidence with AMI with regard to short and long-term prognoses is described. There are discussed also the possible mechanisms of thrombolytic and adjuvant therapies that affect the incidence and frequency of ventricular arrhythmias. The authors recommend the optimal therapy for each form of ventricular arrhythmia and the following management of patients with AMI. In the prevention and therapy of ventricular arrhythmias in the setting of AMI the authors emphasize the importance of early recanalization and prevention of re-occlusion of the infarction-related coronary artery. Great importance is attributed also to other adjuvant measures directed to the restriction of the size of infarction, myocardium protection, prevention and attenuation of remodelling of the left ventricle and thereby to the prevention of heart failure and attenuation of adverse effects of the sympathetic nervous system. An early administration of beta-blockers which favourable effect in and after AMI was documented with conclusive evidence is considered as one of the most important measures in prevention and therapy of malignant ventricular arrhythmias and SCD. The occurrence of malignant ventricular arrhythmias in the setting of heart failure and/or 24-48 hours after AMI should be an indication for aggressive management directed to arrhythmia (programmed ventricular stimulation, electrophysiologically guided pharmacologic or nonpharmacologic therapy) as well as to underlying coronary heart disease (coronary angiography and revascularization).

[Anti-arrhythmia agents in the prevention of sudden cardiac death after myocardial infarct]. / Prevencia náhlej srdcovej smrti u chorých po infarkte myokardu antiarytmikami.

Heart rhythm disturbances represent one of the most important causes of cardiovascular mortality and, in particular, sudden cardiac arrhythmic death. The persistent actuality of arrhythmias is currently characterized by: 1) better knowledge of pathogenetic mechanisms of arrhythmias and their modulating factors, 2) improved diagnostic possibilities of arrhythmias, 3) availability of a large number of effective antiarrhythmics, as well as of nonpharmacologic therapeutic approaches too. Despite the narrowing spectrum of indications to pharmacologic treatment, both chronic and prophylactic antiarrhythmic therapies have nor become less complicated, but on the contrary they are even more problematic. The most actual and at the same time most controversial question of everyday clinical practice is the long-term antiarrhythmic prevention of sudden cardiac death. The author's aim is to review: 1) survey of studies which have influenced in a more decisive manner the management of patients after myocardial infarction and preventive antiarrhythmic therapy, 2) current antiarrhythmic prevention of sudden cardiac death, 3) the importance of programmed ventricular stimulation regarding the antiarrhythmic therapy and risk stratification in patients after myocardial infarction.

[Non-pharmacologic prevention of sudden cardiac death]. / Nefarmakologická prevencia náhlej srdcovej smrti.

Non-pharmacologic therapy has revolutionized the management of arrhythmias and prevention of sudden cardiac death (SCD). Of particular importance is the introduction of radiofrequent catheter ablation (RFCA) and implantable cardioverter-defibrillator (ICD). RFCA is effective and useful in the treatment and prevention of SCD, especially in supraventricular tachyarrhythmias related to dual or accessory atrioventricular pathways. There are some limitations in using this method in the prevention of SCD in ventricular tachyarrhythmias. RFCA is very successful, particularly in the treatment of bundle branch reentrant ventricular tachycardia and ventricular tachycardia in patients without structural heart disease. RFCA can be used as a palliative treatment of incessant or frequent VT before and after ICD implantation. Antibradycardia pacing decreases SCD not only by the removal of serious bradyarrhythmias but also by prevention of the occurrence of malignant ventricular tachyarrhythmias induced by bradyarrhythmia. Antitachycardia pacing is used in the prevention of SCD only as a part of ICD device. Implantation of an antitachycardia pacemaker as an isolated permanent treatment of tachycardias is currently almost not used. This method was replaced by RFCA in supraventricular tachyarrhythmias and by ICD in ventricular tachyarrhythmias. ICD is a very perspective non-pharmacologic approach to SCD prevention, particularly as transvenous leads were introduced and device construction was simplified. ICD is indicated especially in patients with spontaneous sustained hemodynamically significant ventricular tachycardia/ventricular fibrillation and when antiarrhythmic drug treatment, RFCA or antitachycardia surgery are ineffective, intolerated, contraindicated or cannot be performed. ICD as the treatment of first choice instead of antiarrhythmic drugs as well as prophylactic ICD implantation in asymptomatic patients at high risk is a subject of discussion. ICD decreases the incidence of SCD significantly. However, the decrease in overall mortality was not verified. Antitachycardia surgery is less frequently used after RFCA, and ICD have been introduced. At present, this therapy is reserved only for the cases of failure of RFCA or the impossibility to use RFCA and ICD. Surgical therapy can be combined also with concommitant surgical correction of associated structural heart disease. Sympathectomy is used in prevention of malignant ventricular tachyarrhythmias and SCD in patients with congenital long Q-T syndrome. Selective left cardiac sympathetic denervation significantly reduces the risk of SCD in these patients but does not remove it completely. Heart transplantation is the last alternative of non-pharmacologic prevention of SCD. It is indicated in cases when all pharmacologic and non-pharmacologic approaches have been exhausted. Heart transplantation is the only effective modality for the improvement of long-term prognosis in patients with malignant ventricular tachyarrhythmias and advanced chronic heart failure.

Radiofrequency catheter ablation of a right atriofascicular (Mahaim) and two atrioventricular (Kent) accessory pathways in a single session.

This report describes the case of a 19-year-old patient with Ebstein's anomaly, who had an unusual combination of a right atriofascicular (Mahaim) and two ipsilateral right atrioventricular (Kent) accessory pathways participating in three types of antidromic and orthodromic reciprocating tachycardias in the absence of retrograde conduction over the bundle of His-atrioventricular node axis. All three pathways were ablated in a single session using temperature-guided radiofrequency current.

[Adjuvant therapy in patients with acute myocardial infarct]. / Podporná liecba u chorých s akútnym infarktom myokardu.

Besides the thrombolytic therapy several adjuvant therapeutic measures were identified which significantly improve the prognosis of patients with acute myocardial infarction (AMI). These measures include the treatment by means of acetylsalicylic acid (ASA), beta-blockers and ACE inhibitors. Early administration of ASA and beta-blockers are indicated in all patients with AMI who have no contraindications for this therapy. They are especially the patients with manifest heart failure or asymptomatic left ventricular dysfunction who benefit from ACE inhibitors. The effectivity of routine administration of other medicaments such as anticoagulants, nitrates, calcium channel blockers and magnesium, have not been convincingly proved. However, some selected patients with AMI can benefit from these medicaments. Intravenous administration of heparin is unambiguously justified only in thrombolysis with t-PA. Thrombolyses with streptokinase, urokinase, and anistreplase are justified only at high risk of thromboembolic complications. Their prevention and therapy include also the necessity to restrict the administration of pelentan. The use of nitrates is indicated in patients with AMI in case of sustaining stenocardia, arterial hypertension and manifest heart left ventricular failure. Until the definitive standpoint is gained regarding the effect of magnesium in patients with AIM, its administration remains especially indicated in cases of arterial hypertension, tachycardiac disturbances of the heart rhythm and states of assumed or proved hypomagnesiemia. In AMI cases when magnesium is used in order to protect the patient from reperfusion lesion, it must be administered prior to the reperfusion therapy. An intensive research in the field of therapeutical measures in patients with AMI still continues. It is certain that it will soon bring further knowledge which will in turn improve the prognosis and quality of life of patients with AMI. (Tab. 4, Ref. 133.)