Biomedical subjects

B Lüderitz

Publications and source records attributed to B Lüderitz.

At least 37 records · Page 2Linked to original sources

PubMed2003

[Biventricular thrombi dissolution and antibody development with lepirudin therapy].

HISTORY AND ADMISSION FINDINGS: A 50-year-old patient presented with clinical symptoms of heart failure with orthopnoe and edema (NYHA IV). INVESTIGATIONS: Echocardiography revealed a dilated left ventricle with severely reduced left ventricular function and biventricular floating thrombi, due to dilatative cardiomyopathy. TREATMENT AND COURSE: With a heart failure medication clinical symptoms reduced and body weight decreased > 10 kg in 3 weeks. Due to the high-risk constellation, anticoagulation was performed with lepirudin and the biventricular thrombi were dissolved within 17 days. At this point in time, the patient suffered from petechial bleedings, hemoptysis and gross hematuria. Despite breaking anticoagulation and substitution of PPSB with not measurable fibrinogen, subarachnoid hemorrhage occurred leading to exitus letalis. CONCLUSION: Lepirudin is a highly effective anticoagulant, that can induce severe hemorrhagic side effects in individual cases. The present case report demonstrates an immunological reaction as a rare cause with activation of prothrombin and formation of fibrin.

Antibody Formation↗

PubMed2003

[History of atrial fibrillation].

The authors review the history of atrial fibrillation, the most frequent clinically observed cardiac arrhythmia. A French "clinicopathologist", Jean Baptist de Sénac (1693-1770), was the first who assumed a correlation between "rebellious palpitation" and a stenosis of the mitral valve. From an analysis of simultaneously recorded arterial and venous pressure curves, the Scottish Sir James Mackenzie (1853-1925) demonstrated that a presystolic a wave cannot be seen on the jugular phlebogram during "pulsus irregularis perpetuus". The first human ECG depicting atrial fibrillation was published by Willem Einthoven (1860-1927) in 1906. The proof of a direct connection between absolute arrhythmia and auricular fibrillation was established by two Viennese physicians, Rothberger and Winterberg. The major discoveries relating to the pathomechanism and the clinical features of atrial fibrillation in the 20(th) century stemmed from the scientific activities of Karel Frederik Wenckebach, Sir Thomas Lewis, Gordon Moe, and Maurits Allessie.

Atrial Fibrillation↗

PubMed2003

The patient's informed consent for pacemakers and ICD implantation: how to write and how to explain it.

Written informed consent for pacemaker and ICD patients should be easy to understand and provided in written form in the patient's language. Comprehensiveness is required. It is essential to address driving and running machines, complication rates, benefits in appropriate hierarchical order and future necessary interventions. Eventually potential risks, e.g., flying, sports, sexual activity should be mentioned. It is important to explain pacemaker systems and ICD devices in details including cardiac resynchronization therapy (CRT) for heart failure. One of the main aspects concerns protection of human subjects participating in clinical studies. Informed consent necessitates a statement that the study involves research. This statement should include explanation of the purposes of the study, expected duration, description of the procedures, identification of experimental procedures, description of foreseeable risks or discomforts, and disclosure of alternative procedures. Further information should be given on psychological concerns, sexual activity, driving and quality of life in pacemaker and ICD patients.

Adult↗

PubMed2003

[Chlamydial and human heat shock protein 60 homologues in acute coronary syndromes. (Auto-)immune reactions as a link between infection and atherosclerosis].

Recent studies provide evidence that infectious agents play a causal role in the pathogenesis of atherosclerosis. In this respect, a chronic persistent Chlamydia pneumoniae infection, indicated by the presence of chlamydial heat shock protein 60 (cHSP 60), is of central interest. Both cHSP60 and endogenous human (h) HSP60 are upregulated under stress conditions in intimal cells and serve as a target for cross-reactive cytotoxic HSP-serum-antibodies. Therefore, the present study evaluates the expressions of both HSP60 homologues in advanced human coronary lesions and a correlation between intimal tissuebound protein and serum antibodies (Ab) to HSP65. Coronary atherectomy specimens retrieved from 114 primary target lesions of patients with acute coronary syndrome (ACS; n=46) or stable angina (SA; n=68) were assessed immunohistochemically for the presence of cHSP60 and hHSP60. Chronic persistency of Chlamydia pneumoniae was additionally examined by transmission electron microscopy. Blood samples from30 patients were tested for anti-Chlamydia pneumoniae-IgG/IgA- and anti-HSP65-Ab titers and for serum CRP levels. Coronary plaques revealed immunoreactive cHSP60 in 47% and hHSP60 in 57% of the lesions colocalized within macrophages/foam cells. Chlamydia in foam cells most often presented ultrastructural patterns that pointed to the persistency of the pathogen. Intact, non-atherosclerotic vessels showed no signals. Mean expressions were 3.1% for cHSP60 and 3.3% for hHSP60. As a central finding, the expression of both HSP homologues was significantly (each p<0.001) higher in ACS lesions compared to SA lesions (cHSP60: 6.2 vs 1.0%, and hHSP60: 7.2 vs 0.7%). Moreover, we found positive correlations between both determinants in ACS and SA lesions (r=0.41, r=0.37; p<0.01). Most interestingly, cHSP60 revealed no relationship with anti-Chlamydia pneumoniae-IgG/IgA titers, whereas expression of cHSP60 as well as that of hHSP60 correlated with anti-HSP65-Ab titers (r=0.50, p<0.01, and r=0.42, p<0.05, respectively).cHSP60 and hHSP60 colocalize within coronary primary atheroma, most prevalent in lesions associated with ACS. For the first time, our data demonstrate a significant correlation between the intimal expression of these HSP60 homologues and serum HSP65 antibodies, thereby suggesting that humoral immune reactions to bacterial and human HSPs may play an important role in coronary atherosclerosis and plaque instability.

Acute Disease↗

PubMed2003

[Prevalence of intimal pathogen burden in acute coronary syndromes].

Increasing evidence supports a link between serological evidence of prior exposure to infectious pathogens, pathogen burden, and the risk for future myocardial infarction and death in patients with coronary artery disease. Based on this concept, we evaluated the intimal presence of four pathogens in human coronary atheroma, clinically associated with acute coronary syndromes (ACS) and stable angina (SA), and the effect of pathogen burden on the expression of human heatshock protein 60 (hHSP60), a key protein in (auto-)immune pathogenesis of atherosclerosis. Coronary atherectomy specimens retrieved from 53 primary target lesions of patients with ACS (n=33) or SA (n=20) were assessed immunohistochemically for the presence of Chlamydia pneumoniae (C. pn.), Helicobacter pylori (H.p.), Cytomegalovirus (CMV) and Epstein-Barr Virus (EBV), and for the expression of hHSP60. Chlamydia pneumoniae was present in 74%, Helicobacter pylori in 32%, CMV in 13% and EBV in 42%. Exclusively C.pn. revealed a prevalence in ACS (91%) vs SA (45%; p<0.001). Immunohistochemical analysis revealed 6 lesions without, 21 lesions with 1, 17 lesions with 2, 6 lesions with 3 and 3 lesions with 4 infectious agents. As an important finding, the mean value in ACS lesions was significantly increased compared to those in SA (1.9 vs 1.1; p<0.01). ACS-subgroup analysis revealed the highest mean value in patients with pain at rest within the last two days (Braunwald class III). In addition, expression of hHSP60 was significantly higher in ACS (8.7%) compared to SA (1.3%; p<0.001). Pathogen burden correlated highly significant (p<0.01) with the expression of hHSP60 (r=0.44).Our data demonstrate the impact of intimal pathogen burden in plaque instability, and suggest the presence of (auto-)immunoreactions against upregulated hHSP60 as an important pathomechanism that may contribute to acute coronary syndromes.

Acute Disease↗

PubMed2003

Amiodarone-associated "torsade de pointes". Relevance of concomitant cardiovascular medication in a patient with atrial fibrillation and structural heart disease.

A 69 year old female with history of coronary heart disease, myocardial infarction and paroxysmal atrial fibrillation suffered from occipital apoplexy. Under treatment with amiodarone 600 mg daily and concomitant medication with beta-acetyldigoxine (0.1 mg daily) and bisoprolole (1.25 mg daily), significant QT-prolongation (max. 700 ms; QTc: 614 ms) could be documented. Out of normofrequent sinus rhythm but as well out of bradycardia, the patient developed repetitive short-lasting "torsade de pointes" tachycardias (320 bpm) which terminated spontaneously. Serum electrolytes, plasma levels of digoxine (1.76 ng/ml) and amiodarone (1.9 mcg/ml) were within therapeutic range. This case report is the first to describe induction of amiodarone-associated "torsade de pointes" tachycardia during concomitant beta-blocker and digitalis medication in a patient with atrial fibrillation and structural heart disease. This points towards an elevated risk for proarrhythmia under this triple therapy.

Acetyldigoxins↗

PubMed2003

Potential device interaction of a dual chamber implantable cardioverter defibrillator in a patient with continuous spinal cord stimulation.

Spinal cord or thalamic deep brain stimulation with a pacemaker is becoming more important in the treatment of drug refractory pain due to peripheral vascular disease, angina pectoris and intractable tremor in patients with neurologic disorders such as Parkinson's disease. An additional indication for a cardiac pacemaker or implantable cardioverter defibrillator raises concerns about possible interactions between the implanted electrical devices. We report on a patient with existing spinal cord stimulation who survived sudden cardiac death and received a dual chamber cardioverter defibrillator capable of delivering tiered therapies in both the atrium and ventricle.

Aged↗

PubMed2003

Atrial fibrillation: relation between clinical risk factors and transoesophageal echocardiographic risk factors for thromboembolism.

OBJECTIVE: To correlate clinical risk factors for thromboembolism with transoesophageal echocardiography (TOE) markers of a thrombogenic milieu. DESIGN: Clinical risk factors for thromboembolism and TOE markers of a thrombogenic milieu were assessed in consecutive patients with non-rheumatic atrial fibrillation. The following TOE parameters were assessed: presence of spontaneous echo contrast, thrombi, and left atrial appendage blood flow velocities. A history of hypertension, diabetes mellitus, or thromboembolic events, patient age > 65 years, and chronic heart failure were considered to be clinical risk factors for thromboembolism. SETTING: Tertiary cardiac care centre. PATIENTS: 301 consecutive patients with non-rheumatic atrial fibrillation scheduled for TOE. RESULTS: 255 patients presented with clinical risk factors. 158 patients had reduced left atrial blood flow velocities, dense spontaneous echo contrast, or both. Logistic regression analysis showed that a reduced left ventricular ejection fraction and age > 65 years were the only independent predictors of a thrombogenic milieu (both p < 0.0001). The probability of having a thrombogenic milieu increased with the number of clinical risk factors present (p < 0.0001). 17.4% of the patients without clinical risk factors had a thrombogenic milieu whereas 41.2% of the patients presenting one or more clinical risk factors had none. CONCLUSION: There is a close relation between clinical risk factors and TOE markers of a thrombogenic milieu. In addition, TOE examination allows for the identification of patients with a thrombogenic milieu without clinical risk factors.

Aged↗

PubMed2002

[Cardiac resynchronization therapy by biventricular pacing. How many patients with left ventricular dysfunction are eligible?].

BACKGROUND AND OBJECTIVE: Cardiac resynchronization therapy by multisite biventricular pacing presents an additive therapeutic option in the treatment of severe congestive heart failure. The objective of the study was to evaluate how many patients with left ventricular dysfunction may potentially benefit from this therapy. METHODS: A total of 975 patients were screened for the prevalence of left ventricular dysfunction. Patients with a left ventricular ejection fraction (LVEF) <45 % were included into the investigation. Potential benefit of biventricular pacing was presumed in the presence of: LVEF < 35 %, severe heart failure (NHYA class III or IV), intrinsic left bundle branch block pattern with QRS interval > 150 ms and the absence of atrial fibrillation in the last 3 months before study inclusion. RESULTS: In 203 patients (168 male, 35 female, mean age: 64 +/- 11) an LVEF <45 % was found. A total of 12 of these patients (6 %) or 12 of 113 patients (11 %) with an LVEF <35 % were identified as appropiate candidates for biventricular resynchronization therapy. CONCLUSIONS: Cardiac biventricular pacing currently serves as a therapeutic option for a relatively small subgroup of patients with left ventricular dysfunction. Focusing on estimations that the incidence of heart failure in Germany amounts to more than 100.000 cases per year our results suggest that after all more than 6.000 patients per year may potentially benefit from electric resynchronization therapy. This number may increase substantially if prospective studies can prove that patients with heart failure and atrial fibrillation or left ventricular conduction delay due to univentricular pacing also benefit from cardiac resynchronization therapy.

Aged↗

PubMed2002

[Association between progression of untreated coronary lesions and in-stent restenosis].

BACKGROUND AND OBJECTIVES: Progression of coronary artery disease is only incompletely understood regarding de-novo stenoses as well as in-stent restenoses (ISR) indicative of accelerated atherosclerosis. The objective of the present angiographic study was to prove an association between target lesion ISR and progression of primarily untreated coronary lesions. PATIENTS AND METHODS: A total of 179 high-grade native coronary stenoses (mean diameter stenosis 68+/-16 %) of 131 patients were treated by stent implantation. Additional 101 lesions remained untreated because of their moderate to intermediate diameter stenoses (>30 %). Quantitative coronary angiographic analysis was performed 6+/-2 months later to evaluate ISR (diameter stenosis > 50 %), coronary progression (>20 % increase in diameter stenosis) and regression (>20 % decrease), respectively. Angiographic, procedural and clinical characteristics were assessed for a possible association with ISR and/or coronary progression and regression, respectively. RESULTS: ISR was seen in 70 of 179 (39 %) stented target lesions. Presence of diabetes mellitus (p = 0.04) and cumulative duration of inflations (p = 0.01) as procedural determinant were predictive for ISR. Significant progression was found in ten of 101 (10 %) primarily untreated lesions. Progression of previously normal segments or regression were not seen. Progression of native plaques was associated with ISR presence in nine cases and with ISR absence in only one case (p = 0.01). Of note, smoking (p = 0.02) turned out to be predictive for plaque progression, whereas medication and procedural/angiographic parameters were not. CONCLUSIONS: The findings of the present pilot study demonstrate target lesion ISR associated with progression of other primarily untreated lesions and thereby suggest that both atherosclerosis types share common systemic pathogenetic mechanisms. With presence of ISR, coronary angiography should also include primarily untreated arteries, especially in case of preexisting plaques.

Adult↗

PubMed2002

[Noncompaction of the left ventricular myocardium. Case report and review of the literature].

Left ventricular non-compaction is an unclassified cardiomyopathy characterized by an excessively prominent trabecular meshwork due to an arrest in myocardial morphogenesis. We report on a 51-year-old female patient with abnormal myocardial trabeculations associated with a congenital mitral valve stenosis post commissurotomy at the age of 14. In the present case report, clinical manifestation of the disorder included impaired left ventricular systolic function and atrial fibrillation. Noncompaction was diagnosed by echocardiography and levocardiography. In addition, a review of the literature on this rare disorder is presented.

Adolescent↗

PubMed2002

[Neointimal hyperplasia by luminal cell recruitment and not be transmural migration. The role of Bcl-2 and HSP47 after balloon angioplasty].

Restenosis post angioplasty remains the major limitation of several therapeutic interventions including stent implantation. This explains the ongoing interest in its basic pathogenic mechanisms and factors. The aim of the present study was to assess the localization and maximal expression of Bcl-2, a central antiapoptotic protooncogene, and of heat shock protein 47 (HSP47), a marker of early collagen synthesis, in the context with hyperplastic neointima formation as well as concomitant transmural remodeling processes following angioplasty. 0, 4, 24 and 48 hours, 4, 7 and 14 days post balloon traumatization by use of a rat carotid artery model, specific vascular wall compartments were evaluated concerning area, cell density as well as Bcl-2 and HSP47 expression by immunohistochemistry and morphometry, supplemented by electron microscopy (TEM). Neointimal cell accumulation was detected 4 days post angioplasty, characterized by luminal cells adherent to the internal elastic lamina, associated with maximal Bcl-2 and HSP47 expression amounting to 49% and 41%, respectively. With ongoing neointimal formation, a luminal prevalence of both key determinants and a decreasing expression in basal neointimal areas were found. In the media, a temporally reduced cell density was observed significant at 48 hours post trauma. Constitutive HSP47 expression of the media was constant during the entire observation period, whereas sparse Bcl-2 signalling was induced post angioplasty maximal on day 2 with 3% and on day 14 with 5%. The adventitia demonstrated a transient structural separation between day 4 and 7, exhibiting an inner layer with sparse cellularity and an outer layer with extremely high cell density as well as pronounced neovascularization. In this outer adventitia layer, a high frequency of signals for both Bcl-2 and HSP47 were observed amounting to 29% and 57%, respectively. Complementary TEM analysis gave no evidence of transmural migratory events propagated by adventitial cells and thereby supports early neointimal formation by luminal cell recruitment and marked co-expression of anti-apoptotic Bcl-2 and matrix-generating HSP47 as important survival factors. Clinical implications of these findings may be seen in the integration of proapoptotic substances with temporal efficacy in order to prevent restenosis, e.g., by use of coated stents.

Angioplasty, Balloon, Coronary↗

PubMed2002

[C-reactive protein in coronary plaques -- prevalence with acute coronary syndrome].

Inflammatory mechanisms are central in human atherosclerosis. Although C-reactive protein (CRP) as a serum marker is highly predictive for cardiovascular events, the intimal expression of CRP in clinically relevant coronary lesions is unknown, in particular in acute coronary syndromes (ACS). Shown by reduced CRP serum values, statins have antiinflammatory and plaque-stabilizing effects. In the present study, the presence of CRP in coronary atheromas with ACS versus stable angina (SA) as well as its possible modification by chronic statin medication was assessed. Coronary atherectomy probes from 90 primary stenoses were immunohistochemically analyzed with regard to the presence and the localization of CRP. Intimal results of patients with ACS (n=36), categorized according to the Braunwald classification, were compared with those of patients with SA (n=54). In 40 of 90 lesions (44%), immunoreaction specific for CRP was observed demonstrating a mean CRP expression of 1.7%. CRP was focally localized in a maximum of 69% of all plaque cells, the most in macrophages/foam cells, infrequently in smooth muscle cells. CRP-positive plaques showed more thrombus than plaques without CRP (63% vs 41%). Intact non-atherosclerotic control tissue revealed no signaling. As a central finding, intimal presence and expression were higher (each p<0.001) with ACS (69% and 3.1%, respectively) compared to SA (28% and 0.8%, respective). Subgroup analysis of target lesions associated with ACS according to the clinical Braunwald classification showed an increase of intimal CRP with classes I-III. In the presence of statin medication, intimal CRP was significantly lower than that without statin therapy (29 and 1.3%, vs 61 and 2.6%, respectively; p<0.01), in particular in the subgroup of ACS patients. Intimal CRP is frequently found in coronary primary stenoses, very often with macrophages/foam cells, and shows a highly significant prevalence with ACS. In this subgroup of patients, statin therapy is associated with significantly reduced intimal CRP. Our in situ findings as shown might explain the well-known serum constellations with statin therapy.

Anticholesteremic Agents↗

PubMed2002

Insights into vascular pathology after intracoronary brachytherapy.

Post-angioplasty restenosis is a major limitation of interventional cardiology. A large body of evidence reveals that expression of myofibroblast activity promoters moves progressively from the neoadventitia to the neointima. Brachytherapy inhibits vascular cell activity (proliferation, migration), mitigates recruitment of intimal cells, and shows a favorable prophylactic effect on late vascular remodeling by preventing adventitial constriction at the injured site. These effects of brachytherapy are dose related. Clinical and experimental data demonstrate that restenosis is determined by the balance between arterial remodeling and intimal hyperplasia. Apparently, brachytherapy-induced positive remodeling plays the principal role in increasing the luminal diameter after PTCA and, in case of a lower dose or dose fall-off, to cause detrimental edge effects. With regard to clinical course, healing defects, endothelial dysfunction and stent-vessel wall malapposition are apparently important and possibly underestimated features of vascular pathology, since they may contribute to late thrombosis and delayed intimal hyperplasia in long-term course after intracoronary brachytherapy.

Angioplasty, Balloon, Coronary↗

PubMed2002

History of cardiac rhythm disorders.

The history of cardiac rhythm disorders including antiarrhythmic drugs and electrotherapeutical tools is long and fascinating. In the beginning, there was not simply the anatomy and physiology of the heart, but also analysis of the pulse, which indicates the activity of the heart. Thus, like any other field of medicine, the study of arrhythmias has a distinctive past. Our current level of knowledge is not the result of a straight, linear progression any more than there is a static, established, monolithic body of thought dominating this field. Instead, our knowledge of arrhythmias today is the result of many competitive, sometimes serendipitous, scientific realizations, of which a few proved useful enough to pursue and eventually led to real advancements. Looking at the worldwide development of rhythmology it can be said that considerable contributions came from Germany in the last few centuries. Arrhythmology--past, present and future--includes clearly German investigators as pioneers of the field. The growing clinical importance of electric cardiac stimulation has been recognized and renewed as Zoll in 1952 described a successful resuscitation in cardiac standstill by external stimulation. The concept of a fully automatic implantable cardioverter-defibrillator system for recognition and treatment of ventricular flutter/fibrillation was first suggested in 1970. The first implantation of the device in a human being was performed in February 1980. By early 1997, 17 years after the first human implantation more than 100,000 ICD systems had been implanted worldwide. Further developments concern new pharmacological compounds, modern cardioverter-defibrillators, radiofrequency ablation, particularly pulmonary vein ablation in atrial fibrillation, innovative pacemakers including preventive pacing techniques, probably laser therapy and perhaps the automatic implantable pharmacological defibrillator. The advances in the field of therapeutic application of pharmacologic and electrical means as well as alternative methods will continue as rapidly as before in order to give us further significant aid in taking care of the patient.

Anti-Arrhythmia Agents↗

PubMed2002

[Micro-coil embolization of a fistula of the circumflex ramus in the coronary sinus. Case report, differential therapy and review of the literature].

A 45 year old male suffered from typical exercise-induced dyspnoea and angina. Crohn's disease treated with glucocorticoids was present for 18 years. Coronary angiography revealed small left anterior descending and right coronary arteries without reference to coronary artery disease, while the main stem and circumflex artery were severely dilated due to a fistula (diameter 5.5 mm) into the coronary sinus with a left/right shunt amounting to 35%. Haemodynamics, significant risk of endocarditis with chronic inflammatory bowel disease and obligatory glucocorticoid treatment were indications for fistula closure. As an alternative to surgical correction, the coronary fistula was totally occluded by antegrade micro-coil embolization. The present report offers a review on differential therapeutic considerations and specific treatment options including novel interventional modalities for coronary fistulas.

Arteriovenous Fistula↗

PubMed2002

[Chlamydia pneumoniae and cytomegalovirus in degenerative aortic valve stenoses].

Recent evidence suggests a causal relationship between inflammatory as well as infectious pathomechanisms and valvular degeneration. Based on the concept of chronic Chlamydia pneumoniae and cytomegalovirus (CMV) infections, and of variable stressors working on valvular microecology, the present study sought to assess the presence of the specific chlamydial heat shock protein (cHSP) 60, of CMV, of macrophages and of the human homologue hHSP60. Serial sections of high-grade degenerated native (n = 16) and prosthetic (n = 6) aortic valves were analyzed by immunohistochemistry for the presence of these determinants. Degenerated aortic valves revealed prevalence of Chlamydia pneumoniae in 41% (10 of 22) and CMV in 73% (16 of 22), while immunoreactive hHSP60 was present in 64% (14 of 22) and CD68 in 86% (19 of 22). Chlamydial HSP60, CMV and hHSP60 were predominantly found in valvular fibrosa; CMV showed a second predilection site at the ventricular luminal border. Both microorganisms revealed a strong correlation between each other (r = 0.73; p < 0.001) as well as with hHSP60 (cHSP60: r = 0.74; p < 0.001; CMV: r = 0.80; p < 0.001). Macrophage infiltration correlated with cHSP60 (r = 0.78; r < 0.001), CMV (r = 0.78; r < 0.001) and hHSP60 (r = 0.56; r = 0.007). Of note, the frequency of cHSP60, CMV and CD68 signaling was increased more than 5-fold in prosthetic valves compared to native valves (p = 0.017, p = 0.002 and p = 0.005). In summary, valvular infections of Chlamydia pneumoniae and of cytomegalovirus are frequently seen in degenerated aortic valves, irrespective of native or prosthetic origin. Colocalization of both HSP60 homologues and cytomegalovirus within macrophages in valvular fibrosa points to regional stressor effects that might be at least partly attributable to chronic persistent pathogen burden and molecular mimicry.

Aged↗

PubMed2002

Decremental intravenous pulse propagation during extrastimulus pacing: relevance for catheter ablation of focal atrial fibrillation.

We report a case study demonstrating delayed circumferential intrapulmonary-venous conduction characteristics during coronary sinus extrastimulus pacing. This phenomenon allowed the unmasking and discrimination of a localized left atrial to PV breakthrough from secondarily activated PV muscle in a common left-sided PV ostium. Thus, this pacing manoeuvre may serve to guide RF delivery in the treatment of focal AF.

Atrial Fibrillation↗