Krzysztof Błaszyk

The Management of Supraventricular Tachyarrhythmias in Patients with Pulmonary Arterial Hypertension.

BACKGROUNDnAtrial remodelling in pulmonary arterial hypertension (PAH) may lead to higher incidence of supraventricular arrhythmias (SVA). The purpose of this study was to evaluate the efficiency and safety of various methods for treatment of SVA in this group.nnnMETHODSnThis was a single centre study. Forty-eight patients (33 women and 15 men) aged 19-77 years (median 49 years) were enrolled. There were 30 patients with idiopathic PAH, 10 had PAH associated with connective tissue disease, and eight with congenital heart disease. A retrospective analysis was performed to estimate the prevalence and type of supraventricular arrhythmias, as well as efficiency and safety of treatment methods. Mean follow-up period was 28.8±17.7 months.nnnRESULTSnSupraventricular arrhythmias occurred in 17 patients (35%) and appeared to be atrial fibrillation, flutter or tachycardia. Supraventricular arrhythmias coexisted with elevated mean right atrial pressure in 75%. Four patients had more than one type of SVA. A flutter-like macro-reentrant form of atrial tachycardia dependent on cavo-tricuspid isthmus was found in four cases. The treatment of SVA included typical methods: antiarrhythmic drugs, direct current cardioversion (DCC), and radiofrequency (RF) ablation. All of the therapeutic methods were effective in managing acute arrhythmia. Three patients required re-ablation. Overall mortality: 14 patients (29%) in the whole study group, including six in SVA group (35%) and eight without SVA (26%).nnnCONCLUSIONSnIn patients with PAH DCC, pharmacological cardioversion and RF ablation can be applied safely and effectively. Flutter-like macro-reentrant atrial tachycardia dependent on cavo-tricuspid isthmus is observed in this group. It is more challenging, but possible, to successfully treat this arrhythmia with RF ablation.

Correlation of ST-segment depression during ambulatory electrocardiographic monitoring with myocardial perfusion and left ventricular function

To assess the relation between silent ischemia and objective markers of ischemia we compared ambulatory electrocardiographic (AECG) monitoring, exercise stress testing, and technetium-99m methoxyisobutyl isonitrile single-photon emission computed tomography (SPECT) in 68 patients with coronary artery disease. ST-segment depression at AECG monitoring occurred in 40%, exercise testing was positive in 88%, and SPECT was abnormal in 98% of patients. Patients with ST-segment depression had a higher incidence of 3-vessel disease (70% vs 45%, p = 0.04), shorter duration of exercise (267 +/- 109 vs 416 +/- 167 seconds, p < 0.01), lower workload achieved (5.1 +/- 1.9 vs 7.6 +/- 2.8 METs, p < 0.0002), and a greater extent of ischemia at scintigraphy (p = 0.01). Patients with a total ischemic time of >30 minutes in a 24-hour period had a lower ejection fraction (48 +/- 21% vs 70 +/- 9%, p = 0.001), a higher perfusion index at rest (2.4 +/- 0.6 vs 1.6 +/- 0.6, p = 0.001), and a greater number of segments with fixed perfusion defects (4.1 +/- 3.7 vs 1.3 +/- 1.8, p = 0.02) in comparison with those who had a shorter ischemic time. We conclude that AECG monitoring fails to identify a substantial proportion of patients with objective markers of ischemia; however, ST-segment depression reflects more significant disease. Longer total ischemic time correlates with the area of myocardial damage but not with other markers of ischemia.

Double atrial potentials in left-sided accessory pathways are associated with paroxysmal atrial fibrillation

Muscular connections between the coronary sinus (CS) and left atrium probably impact distribution of electrical activity. Double atrial potentials (DP) may be their presentation.

Should we implant a permanent pacemaker in patients with left bundle branch block and PQ prolongation following transcatheter aortic valve implantation

Corresponding author: Prof. Krzysztof Błaszyk MD, PhD, Department of Cardiology, Poznan University of Medical Sciences, 1/2 Długa St, 61-848 Poznan, Poland, phone: +48 602 222 143, fax: +48 61 854 90 94, e-mail: kblaszyk5@gmail.com Received: 23.09.2016, accepted: 10.11.2016. Should we implant a permanent pacemaker in patients with left bundle branch block and PQ prolongation following transcatheter aortic valve implantation?

Niewydolność serca i zapalenie płuc jako kliniczna maska guza lewego przedsionka

We present a case of heart failure and pneumonia which masked the tumour that filled the whole left atrium.

Cardiac and neurogenic syncope and atrial flutter misdiagnosed as ventricular tachycardia in a patient after myocardial infarction

A 61-year-old male presented with a history of transient ischaemic cerebral episode (ten years earlier), previous myocardial infarction (MI) treated with percutaneous coronary intervention of the left circumflex artery, and deployment of a drug-eluting stent (four years earlier). Initially, he was admitted to hospital because of retrosternal pain and recurrent syncope that followed a wide QRS complex tachycardia (WCT). The arrhythmia was originally diagnosed as ventricular tachycardia (VT) and reverted to sinus rhythm (SR) using a direct current cardioversion (DCCV) followed by an intravenous amiodarone infusion. Despite the treatment, the same arrhythmia reoccurred and was accompanied by two episodes of syncope and retrosternal pain. Therefore, he was referred to cardiology department as recurrent VT secondary to acute coronary syndrome (troponin I 0.25 ng/mL) was suspected. On admission, he reported fatigue, dizziness, and preor syncope episodes that started two days earlier. The electrocardiogram (ECG) revealed WCT (HR = 210 bpm) of left bundle branch block (LBBB) morphology (QRS = 140 ms) (Fig. 1A). Intravenous amiodarone bolus plus a gentle carotid sinus massage (CSM) produced significant vasovagal reaction revealing atrial flutter (AFl) wave (Fig. 1B). Ultimately, DCCV to SR was performed (100 J), but AFl recurred shortly. Echocardiography and coronary angiography documented no abnormalities. The patient was qualified to cavotricuspid isthmus (CTI) radiofrequency ablation. Anticlockwise AFl (CL = 217 ms) with 2:1 atrioventricular conduction was confirmed at invasive procedure. During the manipulation with the coronary sinus catheter introduced via the external jugular vein, accidental tapping of the right carotid sinus region produced a 14-second vasovagal syncope deteriorating to ventricular fibrillation (Fig. 1C). Immediate defibrillation (200 J) restored SR and a success ful CTI ablation was completed. No VT was induced with a programmed ventricular stimulation. The patient was sent for thoracic angio-magnetic resonance imaging. As well as fibrotic tissue, it revealed blood flow limitation at the right carotid sinus level. Ultimately, a dual-chamber pacemaker was implanted. No recurrent syncope or arrhythmias were observed during the subsequent 12 months. Syncope can precede cardiac arrest, especially in patients with organic heart disease. A male with previous MI and fast LBBB-WCT resulting in syncope must be suspected of VT requiring eventual implantation of a cardioverter-defibrillator. However, if excluded, it needs further differential diagnosis of WTC. Valsalva manoeuvre and CSM may be helpful in aberrated atrial arrhythmias that can be treated with radiofrequency ablation. In this patient, WCT initially misdiagnosed as VT could contribute to cardiac syncope. Moreover, in our case, the response to mild CSM was enormous, suggesting substantial carotid sinus hypersensitivity leading to neurocardiogenic syncope. The disease is also treatable, and symptoms may be resolved with implantation of a pacemaker. In the presented case the ECG diagnosis of WCT may be quite error-prone.

Dynamic variability of T wave polarity in 12-lead ambulatory ECG as a sign of imminent hypertrophic cardiomyopathy.

A 27-year-old male had suffered from eight episodes of exercise-induced syncope since he was seven years old. He had professionally trained for soccer and judo. His mother had died aged 46 of dilated cardiomyopathy. ECG revealed: sinus rhythm (SR), rSr’ pattern in V1, flat negative T waves in II, III, aVF, V5–V6, left ventricular hypertrophy (LVH) criteria not met. 12-lead ambulatory ECG revealed: major variability of T wave polarity, particularly in inferolateral leads; inverted T waves of various amplitude observed by day, completely normalised at night. Tilt test was negative. Echocardiography revealed: minor LVH (≤ 12 mm), normal LV function referred to as ‘athletic hypertrophy’. Exercise treadmill test (ETT) revealed: achieved predicted workload, then blood pressure (BP) drop to 90/60 mm Hg at heart rate (HR) of 180 bpm, followed by progressive HR slowing to 15 bpm with ultimate pauses (≤ 6.1 s) over next 2 min (Fig. 1). Subsequently, SR at 70 bpm and BP of 130/80 mm Hg restored. Coronary angiography revealed no abnormalities. Exercise-induced neurocardiogenic syncope was diagnosed and a dual-chamber pacemaker was implanted. Further professional training was discouraged. He remained asymptomatic for the next 4.5 years. Progressive LVH (IVS 16 mm) allowed for a diagnosis of hypertrophic non-obstructive cardiomyopathy (HNOC) and the pacemaker was upgraded to implantable cardioverter-defibrillator. Two months later, a dual-chamber pacemaker was implanted to his brother (normal resting ECG, four syncopes and Mobitz type II AV block in Holter ECG). Early hypertrophic cardiomyopathy (HCM) diagnosis and prediction of life-threatening events is still challenging and the prognostic importance of ECG-based modalities remains unclear due to their relatively low sensitivity (Baggish A et al. Heart, 2009; 95: 345–347; Erice B et al. Scand J Med Sci Sports, 2009; 19: 356–363). In this report, the diagnostic investigation initially focused on reproducing the syncopal episodes. Ambulatory ECGs and tilt test failed. However, routine ETT revealed the pathomechanism of exercise-induced syncope, allowing for implantation of a pacemaker that protected against future syncope. Nevertheless it could diminish further diagnostic alertness by documenting a neurocardiogenic cause of syncope. At that stage there was no concrete rationale for further investigation for cardiomyopathy. The subtle LVH was, at that time, being linked to the physiological hypertrophy observed in athletes. The marked T wave variability observed in 12-lead ambulatory ECG is intriguing. Negative T waves in II, III, aVF, V5–V6 in the resting ECG were qualified nonspecific. However, T wave variability, i.e. inverted T waves by day (mostly sympathetic modulation) and then normalised during night sleep (predominating parasympathetic tone) is most probably a specific ECG picture of an initial stage of HCM. Normalisation of T waves persisting at night actually excludes new myocardial ischaemia. Also, no chest pain was reported on ETT. It seems that this day-to-night dynamic variability of T wave polarity may be a distinct diagnostic sign of an early stage of HNOC that could add to a differential diagnosis with athletic LVH.

Unresectable cardiac pseudoneoplasms causing ventricular tachycardia.

Cardiac pseudoneoplasms are rare and benign. According to World Health Organization, they are classified as tumor-like lesions. We report two patients with recurrent ventricular tachycardia (VT) in whom magnetic resonance imaging revealed a pathological mass occupying a large part of the left ventricle. The localization of both tumors precluded the possibility of resection; thus, only surgical biopsy was performed. After deducting the prospect of malignancy of the tumors, we treated both patients with amiodarone and implantation of a cardioverter-defibrillator [implanted cardioverter/defibrillator (ICD)]. VT is one of many probable symptoms indicating a tumor within the heart; therefore, treatment with an ICD should only be considered after a more thorough diagnosis.

[Unusual epicardial location of ventricular ectopy in left ventricular outflow tract, cured with RF ablation from the great cardiac vein].

The case report refers to a 54-year-old woman with a drug-refractory premature ventricular contractions (total number of ventricular ectopy: 40,851 beats/24 h) where an ectopy focus was localised in epicardial part of the left ventricular outflow tract. Successful radiofrequency ablation with the open-irrigated-tip catheter was performed at the site of earliest activation in the great cardiac vein.