Novel CineECG Derived From Standard 12-Lead ECG Enables Right Ventricle Outflow Tract Localization of Electrical Substrate in Patients With Brugada Syndrome

Background: In Brugada syndrome (BrS), diagnosed in presence of a spontaneous or ajmaline-induced type-1 pattern, ventricular arrhythmias originate from the right ventricle outflow tract (RVOT). We developed a novel CineECG method, obtained by inverse electrocardiogram (ECG) from standard 12-lead ECG, to localize the electrical activity pathway in patients with BrS. Methods: The CineECG enabled the temporospatial localization of the ECG waveforms, deriving the mean temporospatial isochrone from standard 12-lead ECG. The study sample included (1) 15 patients with spontaneous type-1 Brugada pattern, and (2) 18 patients with ajmaline-induced BrS (at baseline and after ajmaline), in whom epicardial potential duration maps were available; (3) 17 type-3 BrS pattern patients not showing type-1 BrS pattern after ajmaline (ajmaline-negative); (4) 47 normal subjects; (5) 18 patients with right bundle branch block (RBBB). According to CineECG algorithm, each ECG was classified as Normal, Brugada, RBBB, or Undetermined. Results: In patients with spontaneous or ajmaline-induced BrS, CineECG localized the terminal mean temporospatial isochrone forces in the RVOT, congruent with the arrhythmogenic substrate location detected by epicardial potential duration maps. The RVOT location was never observed in normal, RBBB, or ajmaline-negative patients. In most patients with ajmaline-induced BrS (78%), the RVOT location was already evident at baseline. The CineECG classified all normal subjects and ajmaline-negative patients at baseline as Normal or Undetermined, all patients with RBBB as RBBB, whereas all patients with spontaneous and ajmaline-induced BrS as Brugada. Compared with standard 12-lead ECG, CineECG at baseline had a 100% positive predictive value and 81% negative predictive value in predicting ajmaline test results. Conclusions: In patients with spontaneous and ajmaline-induced BrS, the CineECG localized the late QRS activity in the RVOT, a phenomenon never observed in normal, RBBB, or ajmaline-negative patients. The possibility to identify the RVOT as the location of the arrhythmogenic substrate by the noninvasive CineECG, based on the standard 12-lead ECG, opens new prospective for diagnosing patients with BrS.

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Longer Repolarization in the Epicardium at the Right Ventricular Outflow Tract Causes Type 1 Electrocardiogram in Patients With Brugada Syndrome

Journal of the American College of Cardiology ◽

10.1016/j.jacc.2007.10.059 ◽

2008 ◽

Vol 51 (12) ◽

pp. 1154-1161 ◽

Cited By ~ 51

Author(s):

Satoshi Nagase ◽

Kengo Fukushima Kusano ◽

Hiroshi Morita ◽

Nobuhiro Nishii ◽

Kimikazu Banba ◽

...

Keyword(s):

Right Ventricular ◽

Brugada Syndrome ◽

Right Ventricular Outflow Tract ◽

Ventricular Outflow Tract ◽

Outflow Tract ◽

The Right

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Right ventricular function and dyssynchrony in Brugada syndrome: Highlighting the importance of the mechanical substrate in the right ventricular outflow tract

International Journal of Cardiology ◽

10.1016/j.ijcard.2021.03.014 ◽

2021 ◽

Author(s):

Cristina Mitroi ◽

Eusebio García-Izquierdo ◽

Inés García-Lunar ◽

Victor Castro-Urda ◽

Jorge Toquero-Ramos ◽

...

Keyword(s):

Right Ventricular ◽

Ventricular Function ◽

Right Ventricular Function ◽

Brugada Syndrome ◽

Right Ventricular Outflow Tract ◽

Ventricular Outflow Tract ◽

Outflow Tract ◽

The Right

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Left Axis Deviation in Brugada Syndrome: Vectorcardiographic Evaluation during Ajmaline Provocation Testing Reveals Additional Depolarization Abnormalities

International Journal of Molecular Sciences ◽

10.3390/ijms22020484 ◽

2021 ◽

Vol 22 (2) ◽

pp. 484

Author(s):

Martijn H. van der Ree ◽

Jeroen Vendrik ◽

Jan A. Kors ◽

Ahmad S. Amin ◽

Arthur A. M. Wilde ◽

...

Keyword(s):

Sodium Channel ◽

Brugada Syndrome ◽

Right Ventricular Outflow Tract ◽

Ventricular Outflow Tract ◽

Conduction Delay ◽

Channel Blockers ◽

Axis Deviation ◽

Provocation Testing ◽

The Right

Patients with Brugada syndrome (BrS) can show a leftward deviation of the frontal QRS-axis upon provocation with sodium channel blockers. The cause of this axis change is unclear. In this study, we aimed to determine (1) the prevalence of this left axis deviation and (2) to evaluate its cause, using the insights that could be derived from vectorcardiograms. Hence, from a large cohort of patients who underwent ajmaline provocation testing (n = 1430), we selected patients in whom a type-1 BrS-ECG was evoked (n = 345). Depolarization and repolarization parameters were analyzed for reconstructed vectorcardiograms and were compared between patients with and without a >30° leftward axis shift. We found (1) that the prevalence of a left axis deviation during provocation testing was 18% and (2) that this left axis deviation was not explained by terminal conduction slowing in the right ventricular outflow tract (4th QRS-loop quartile: +17 ± 14 ms versus +13 ± 15 ms, nonsignificant) but was associated with a more proximal conduction slowing (1st QRS-loop quartile: +12[8;18] ms versus +8[4;12] ms, p < 0.001 and 3rd QRS-loop quartile: +12 ± 10 ms versus +5 ± 7 ms, p < 0.001). There was no important heterogeneity of the action potential morphology (no difference in the ventricular gradient), but a left axis deviation did result in a discordant repolarization (spatial QRS-T angle: 122[59;147]° versus 44[25;91]°, p < 0.001). Thus, although the development of the type-1 BrS-ECG is characterized by a terminal conduction delay in the right ventricle, BrS-patients with a left axis deviation upon sodium channel blocker provocation have an additional proximal conduction slowing, which is associated with a subsequent discordant repolarization. Whether this has implications for risk stratification is still undetermined.

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Dormant conduction in the right ventricular outflow tract unmasked by adenosine in a patient with Brugada syndrome

Journal of Cardiovascular Electrophysiology ◽

10.1111/jce.14974 ◽

2021 ◽

Vol 32 (4) ◽

pp. 1182-1186

Author(s):

Tsukasa Kamakura ◽

Josselin Duchateau ◽

Frédéric Sacher ◽

Pierre Jais ◽

Michel Haïssaguerre ◽

...

Keyword(s):

Right Ventricular ◽

Brugada Syndrome ◽

Right Ventricular Outflow Tract ◽

Ventricular Outflow Tract ◽

Outflow Tract ◽

Dormant Conduction ◽

The Right

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Sudden Cause of Cardiac Death—Be Aware of Me: A Case Report and Short Review on Brugada Syndrome

Case Reports in Medicine ◽

10.1155/2010/823490 ◽

2010 ◽

Vol 2010 ◽

pp. 1-3 ◽

Cited By ~ 3

Author(s):

Jagadeesh K. Kalavakunta ◽

Vishwaroop Bantu ◽

Hemasri Tokala ◽

Mihas Kodenchery

Keyword(s):

Brugada Syndrome ◽

Past History ◽

Short Review ◽

Case Presentation ◽

St Segment Elevation ◽

First Case ◽

St Segment ◽

The Right ◽

Malignant Arrhythmias

Introduction. Brugada syndrome accounts for about 4% of sudden cardiac deaths (SCD). It is characterized by an ST-segment elevation in the right precordial electrocardiogram (EKG) leads.Case Presentation. We describe a 39-year-old healthy Caucasian man who was admitted to the intensive care unit after being cardioverted from ventricular fibrillation (VF) arrest. His past history was significant for an episode of syncope one month prior to this presentation for which he was admitted to an outlying hospital. EKG during that admission showed ST elevations in V1 and V2 leads, a pattern similar to Type 1 Brugada. A diagnosis of Brugada syndrome was missed and the patient had a cardiac arrest a month later. We discuss a short review of Brugada syndrome and emphasize the need to look for it in patients presenting with SCD and malignant arrhythmias.Conclusion. Physicians should always consider Brugada syndrome in the differential diagnosis of ST-segment elevation in anterior precordial leads of EKG and associated VT/VF. Although more than 17 years have passed since the first case was reported, increased awareness of this syndrome is needed to identify patients with EKG changes and treat them accordingly to prevent incidence of (SCD) and its deleterious complications.

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Dynamic anatomical study of cardiac shunting in crocodiles using high-resolution angioscopy

Journal of Experimental Biology ◽

10.1242/jeb.199.2.359 ◽

1996 ◽

Vol 199 (2) ◽

pp. 359-365 ◽

Cited By ~ 4

Author(s):

M Axelsson ◽

C E Franklin ◽

C O Löfman ◽

S Nilsson ◽

G C Grigg

Keyword(s):

High Resolution ◽

Connective Tissue ◽

Right Ventricle ◽

Anatomical Study ◽

Systemic Circulation ◽

Outflow Tract ◽

Aortic Valves ◽

Aortic Blood Pressure ◽

The Right

Prolonged submergence imposes special demands on the cardiovascular system. Unlike the situation in diving birds and mammals, crocodilians have the ability to shunt blood away from the lungs, despite having an anatomically divided ventricle. This remarkable cardiovascular flexibility is due in part to three anatomical peculiarities: (1) an 'extra' aorta (the left aorta) that leaves the right ventricle and allows the blood from the right ventricle to take an alternative route into the systemic circulation instead of going to the lungs; (2) the foramen of Panizza, an aperture that connects the right and left aortas at their base immediately outside the ventricle; and (3) a set of connective tissue outpushings in the pulmonary outflow tract in the right ventricle. Using high-resolution angioscopy, we have studied these structures in the beating crocodile heart and correlated their movements with in vivo pressure and flow recordings. The connective tissue outpushings in the pulmonary outflow tract represent an active mechanism used to restrict blood flow into the lungs, thus creating one of the conditions required for a right-to-left shunt. We observed that the foramen of Panizza was obstructed by the medial cusp of the right aortic valve during most of systole, effectively differentiating the left and right aortic blood pressure. During diastole, however, the foramen remained open, allowing pressure equilibration between the two aortas. Contrary to current theories, we found that the left aortic valves were unable to cover the foramen of Panizza during any part of the cardiac cycle, supporting the reversed foramen flow hypothesis. This would ensure a supply of blood to the coronary and cephalic circulation during a complete shut-down of the left side of the heart, such as might occur during prolonged submergence.

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Intraoperative findings and the beginning of bleeding. The tumor could be dissected from the right ventricle and aorta. Subsequently, while dissecting the tumor from the pulmonary trunk, the forceps held by the assistant accidentally touched the tensed pulmonary trunk adjacent to the right ventricular outflow tract, causing massive bleeding (duration: 1 min 50 s)

ASVIDE ◽

10.21037/asvide.2021.044 ◽

2021 ◽

Vol 8 ◽

pp. 044-044

Author(s):

Noriaki Sakakura ◽

Aiko Nakai ◽

Hisao Suda ◽

Takeo Nakada ◽

Takuya Matsui ◽

...

Keyword(s):

Right Ventricle ◽

Right Ventricular ◽

Right Ventricular Outflow Tract ◽

Ventricular Outflow Tract ◽

Massive Bleeding ◽

Outflow Tract ◽

Pulmonary Trunk ◽

The Right

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Pressure segment length analysis of right ventricular function: influence of loading conditions

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.260.4.h1087 ◽

1991 ◽

Vol 260 (4) ◽

pp. H1087-H1097

Author(s):

J. E. Calvin

Keyword(s):

Right Ventricle ◽

Right Ventricular ◽

Ventricular Function ◽

Systolic Pressure ◽

Pressure Overload ◽

Outflow Tract ◽

Segment Length ◽

Stroke Work ◽

Volume Changes ◽

The Right

The purpose of this study was to determine whether segment lengths measured from the right ventricular inflow and outflow tract regions of the right ventricle would accurately reflect true volume changes of the right ventricle and to determine the response of the right ventricle to afterload increases induced by both constricting the pulmonary artery (PAC) and embolizing the pulmonary circulation with glass beads (GBE). Three excised hearts were instrumented with segment-length crystals attached to the inflow and outflow tract regions, and saline was instilled into a balloon implanted inside the right ventricular cavity. The experiments showed a high correlation (r greater than or equal to 0.90 in all cases) between static segment lengths and volume instilled. In open chest, open pericardial canine experiments, vena caval occlusion reduced end-diastolic segments lengths and right ventricular systolic pressure consistent with a reduction in right ventricular end-diastolic volume. In a separate group of animals, volume loading with dextran increased inflow and outflow end-diastolic segment lengths and increased cardiac output. In two further groups of animals, one of which was pretreated intravenously with propranolol (Inderal), both forms of pressure overload increased end-diastolic lengths in both regions. However, GBE increased right ventricular stroke work compared with PAC. We conclude that end-diastolic segment lengths reflect true volume changes of the right ventricle. Furthermore, during acute pressure overload, the right ventricle dilates to compensate for the afterload change. However, ventricular function is better maintained after GBE.

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