LAHRS Celebrates 5 Years

El 20 de Mayo de 2017, se llevó a cabo en la sede de la Sociedad Uruguaya de Cardiología la ASAMBLEA CONSTITUTIVA de la Sociedad Latinoamericana del Ritmo Cardíaco/ Latin American Heart Rhythm Society (LAHRS).
En dicho acto, se realizó la inscripción jurídica de la sociedad, hasta entonces llamada SOLAECE, renombrada como LAHRS, considerando este nombre más apropiado para la inserción en el marco de Sociedades Científicas referentes a nivel mundial tales como HRS, EHRA y APHRS (Asia-Pacific Heart Rhythm Society).

Desde entonces, LAHRS se encuentra en pleno crecimiento, institucional, societario y científico.

Mensaje del Dr. Marcio Figueiredo, presidente LAHRS

Compartimos con todos ustedes un breve video que resume los logros y principales actividades de nuestra sociedad.

A message on or use of messages

When we read the research carried out by Guerra et al. (1) Regarding the use of electronic means in medical practice, we were curious to know what the situation was in Latin America. We intuitively knew that technological advances and, mainly, the need to work remotely due to the pandemic catalyzed their use, but we did not quantify them. We also made it important that the LAHRS become institutionally involved in the matter (2).

A large majority of those interviewed send (89%) and receive (98%) clinical data from patients through two instant message applications. That allows us to affirm that it is an integral part of medical practice. The instruments that we use are the ones that are more widespread in the region and the data obtained is more of an assessment of the situation of the digital market. The type of information shared is expected according to the specialties of the two doctors surveyed. At the top of the list are the different recording modalities of cardiac electrical activity. A majority of two electrophysiologists (71%) stated that they send the information without using the patient’s affiliation data, but 51% stated that they receive clinical information with data that would allow their identification. In that difference we see an important aspect to be reflected. In addition, it is believed that the legal regulations relating to the exchange of sensitive information are not known and, therefore, it is possible that they are not a cause for concern.

The work does not inquire about the use of new technologies that are used between patients and their doctors. This aspect is also an important issue. The heterogeneity in use is probably even greater and may be the cause of inequity in care. They also generate situations of potential risk for patients and doctors. To the former, in their quality of assistance and to the latter in the legal medical field. Another actor involved is the assistance institutions. During the pandemic they were forced to look for alternatives to face-to-face care and this has introduced instruments that will probably last after the emergency. Here are added labor relationship issues with health personnel, which often have not been formally resolved.

It is undeniable that the new information and communication technologies are here to stay. Medical deontology and ethics are also evolving, but not at the same speed. In many respects today they are being challenged. The legislation on the subject in each country can vary and in many it is non-existent. We insist that the survey carried out shows the lack of knowledge we have about this aspect.

In all countries there are codes of medical ethics that we cannot ignore. We also have the code of medical ethics of the World Medical Association (3). There it is established that we have the obligation to “respect the patient’s right to confidentiality. It is ethical to disclose confidential information when the patient gives consent…”. It also says that the physician must “when medically necessary, communicate with colleagues caring for the same patient” and “This communication must respect the patient’s confidentiality and be limited to necessary information”.

These precepts are prior to the existence of new technologies. The question is when and how much should we update them.


Dr. Alejandro N. Cuesta Holgado PhD FESC
Cardiologist – Pediatric Cardiologist – Electrophysiologist
Prof. Adj. University Cardiovascular Center, Clinic Hospital, UdelaR
Head of the Arrhythmia Service, Institute of Integral Cardiology, MUCAM, Montevideo
Pro-Treasurer LAHRS

References:

  1. Guerra, F., Linz, D., Garcia, R., Kommata, V., Kosiuk, J., Chun, J., Boveda, S., Duncker D. Use and misuse of instant messaging in clinical data sharing: the EHRA-SMS survey. Europace. 2021 Aug 6;23(8):1326-1330. doi: 10.1093/europace/euab063

  2. de Oliveira Figueiredo, M. J., Cuesta, A., Duncker, D., Boveda, S., Guerra, F., Márquez, M. F. Use of instant messaging in electrophysiological clinical practice in Latin America: a LAHRS survey. Europace. 2022 Jun 21:euac080. doi: 10.1093/europace/euac080
  3. https://www.wma.net/es/policies-post/codigo-internacional-de-etica-medica/

New perspectives in Cardiogenetics

xpert Consensus Statement EHRA/HRS/APHRS/LAHRS on the State of Genetic Testing for Cardiac Diseases

Knowledge about the genetic basis of cardiovascular diseases has made significant progress in recent decades, with the incorporation of new technologies in molecular diagnosis, functional characterization efforts, artificial intelligence, and strengthening of the genotype-phenotype association. The reduced cost of genetic sequencing allowed for widespread access to testing, making it an important part of clinical practice in cardiology. Eleven years after the first document published by Ackerman et al, (1) concepts and recommendations were updated, with multicontinental participation, including the Latin American Heart Rhythm Society (LAHRS). (2)

The basic principle for the use of clinical genetic tests is the understanding that the genes evaluated must have strong scientific evidence of association with the disease (for classification, see https://clinicalgenome.org/). In 2015, the American College of Medical Genetics and Genomics (3) provided a standard criteria-based approach to interpreting genetic variants in clinical trials. The sum of the tests leads to a classification of the variant in a probabilistic range of categories: pathogenic (pathogenic, P), probably pathogenic (probably pathogenic, LP), variant of uncertain significance (VUS), probably benign (probably benign, LB) and benign (benign, B). The VUS classification represents the challenge of current clinical practice when the experience of specialized and multidisciplinary centers is even more necessary.

Family counseling plays a fundamental role in providing guidance on the clinical impact of genetic tests for the testers and their relatives, being recommended before and after molecular diagnosis, in centers of experience in cardiovascular genetics. The clinically actionable outcome (presence of LP/P variants) can provide diagnostic, prognostic, and therapeutic information for the tester, depending on the disease investigated (Table 1). The main benefit of genetic testing is family cascade screening, i.e. accurately identifying family members who are carriers of LP/P variants, who benefit from specialized medical care, and non-carrier family members who are unlikely to develop the disease. Progress in genetic testing in inherited cardiovascular diseases has also increased understanding of oligogenic and polygenic diseases through the development of polygenic scores.

Table 1. Impact of genetic test for the tester

Illness

Diagnosis

Prognosis

Therapeutic

Arrhythmic syndromes

SQTL

+++

+++

+++

TVPC

+++

+

+

SBr

+

+

+

DPSC

+

+

+

SQTC

+

+

+

DNS

+

FA

+

Rep precoce

Cardiomyopathies

     

CMH

+++

++

++

CMD

++

+++

++

CMA

+++

++

++

MNC

+

+

CMR

+

+

+

Congenital cardiopathies

Syndromic

+++

++

Non syndromic

+

Familiar

++

SQTL: long QT syndrome, TVPC: catecholaminergic polymorphic ventricular tachycardia, Br: Brugada syndrome, DPSC: progressive wasting system disease, SQTC: congenital short QT syndrome, DNS: sinus node disease, AF: atrial fibrillation, Early Rep: early repolarization, CMH: hypertrophic cardiomyopathy, CMD: dilated cardiomyopathy, CMA: arrhythmogenic cardiomyopathy, MNC: non-compaction myocardium, CMR: restrictive cardiomyopathy.

The consensus provides disease-specific information organized into a disease summary, genes with strong and moderate association with phenotype (suggestion of which panel to order), as well as therapeutic and prognostic implications of genetic testing for the tester and their relatives. In family counseling, the recommended age to perform the genetic test is also specific to the diagnosis and age of clinical presentation in the family. In general, in channelopathies such as long QT syndrome (LQTS), catecholaminergic polymorphic ventricular tachycardia (CPVT), and Brugada syndrome, genetic testing is indicated from birth, since there are strategies for the prevention and treatment of life-threatening arrhythmias. In cardiomyopathies, on the other hand, the suggested age for genetic screening is between 10-12 years, due to age-dependent penetrance, unless there is a family history of a phenotype developed in childhood.

Long QT syndrome represents the disease with the highest performance and usefulness of genetic tests, when the pre-test clinical probability is high (Schwartz score 3.5), helping in the classification of subtypes 1 to 3, in the identification of syndromic forms. (Jervel Langue-Nilsen, Andersen Tawil, Thimoty and Triadin knockout) and calmodulinopathies (CALM1, CALM2 and CALM3). In hypertrophic cardiomyopathy, the distinction between sarcomeric disease and phenocopies such as Danon, Fabry, amyloidosis, and PRKAG2 syndrome can also guide specific medical follow-up and influence treatment.

Unlike the 2011 consensus, (1) atrial fibrillation (AF), progressive conduction system disease, and sinus node disease appear to be more based on a context of monogenetic inheritance or associated with other channelopathies/cardiomyopathies (overt or No). Another significant change in the current consensus was the weight of the genetic test in arrhythmogenic and dilated cardiomyopathies, since molecular diagnosis allows a more precise clinical stratification, with the development of new risk calculators, contributing to therapeutic decisions such as the indication of an implantable cardioverter-defibrillator (ICD).

The current consensus also provides recommendations for genetic testing in congenital heart disease. When congenital heart disease is diagnosed by fetal ultrasound (CHD), genetic testing of fetal tissue (chromosomal microarray or CNV sequencing) should be offered for pregnancy monitoring and genetic counseling.

It is easy to understand, therefore, that “genetic cardiology” is a new field of medicine, with specialists involved in the translation of genetic findings, reflecting on better clinical care. New gaps are emerging, and old challenges remain, including the accurate classification and interpretation of variants. The prospect is the development of gene therapy together with the precise identification of the disease-causing substrate, allowing not only genotype-guided therapies, but also gene-specific therapies, including variant-specific therapies.

Link: https://lahrs.org/guias/test-genetico-en-cardiopatias/

Dra. Luciana Sacilotto
MD, PhD, arrhythmologist focused on inherited Cardiac disease at University of Sao Paulo

Biobliography

1. Ackerman MJ, Priori SG, Willems S, Berul C, Brugada R, Calkins H, et al. HRS/EHRA expert consensus statement on the state of genetic testing for the channelopathies and cardiomyopathies: this document was developed as a partnership between the Heart Rhythm Society (HRS) and the European Heart Rhythm Association (EHRA). Europace. 2011 Aug;13(8):1077-109. PubMed PMID: 21810866. eng.

2. Wilde AAM, Semsarian C, Márquez MF, Sepehri Shamloo A, Ackerman MJ, et al. European Heart Rhythm Association (EHRA)/Heart Rhythm Society (HRS)/Asia Pacific Heart Rhythm Society (APHRS)/Latin American Heart Rhythm Society (LAHRS) Expert Consensus Statement on the State of Genetic Testing for Cardiac Diseases. Heart Rhythm. 2022 Apr 4:S1547-5271(22)01697-6. doi: 10.1016/j.hrthm.2022.03.1225.

3. Sue R, Nazneen A, Sherri B, David B, Soma Das et al. Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology. Genet Med. 2015 May;17(5):405-24. doi: 10.1038/gim.2015.30. Epub 2015 Mar 5.

The revival of verapamil in atrial fibrillation

Summary of the study:

Koldenkof et al published in Europace the work entitled “Rate control differs in the prevention of progression in atrial fibrillation” 1. It is a sub-analysis of the RACE 4 study. Only patients without using antiarrhythmics were included. Investigators included 666 patients over 18 years of age with a diagnosis of paroxysmal atrial fibrillation (AF) of recent diagnosis. They classified subjects into three groups, those who used heart rate (HR) control with verapamil, those who used beta-blockers (BB) and one group who did not use any drug for rate modulation. It is important to note that those patients who presented symptoms of heart failure decompensation and patients with acute coronary syndrome within 3 months prior to screening were excluded. Of 666 study participants, 47 (7%) used verapamil, 383 (57.5%) used BB, and 236 (35.4%) received no treatment for HR control. The primary endpoint was a combined of need for first electrical cardioversion, pharmacological cardioversion and pulmonary vein isolation due to AF, while the secondary points included major cardiovascular events such as decompensated heart failure, acute coronary syndrome, hospitalization for arrhythmias, major bleeding, thrombotic events embolic or adverse effects of the drugs administered. After a 37-month follow-up, the analysis showed that the primary composite endpoint occurred in 17% of the subjects in the group that used verapamil compared to 33% in the groups that used BB or those that did not use HR control, with a statistically significant P value of 0.038. Authors concluded that the use of verapamil, a non-dihydropyridine calcium antagonist, was associated with a lower probability of progression of AF, in patients recently diagnosed with this condition1.

Editorial comment:

The published results of this substudy are really interesting. They show the advantages of the initial use of calcium antagonists not only as a HR control strategy but also as a preventive therapy to avoid progression of the disease in patients with newly diagnosed AF compared to other pharmacological drugs such as the most commonly used BB. From a pathophysiological point of view, this benefit is easily understandable since it is well known that the release of significant amounts of calcium from the sarcoplasmic reticulum is fundamental for the perpetuation and, therefore, the progression of the substrate responsible for the onset of atrial fibrillation2,3,4. It is known that calcium overload participates in signaling silencing and the progression of more calcium leak during diastole causing afterdepolarizations and therefore, helping to the development of an electrical substrate that perpetuates atrial fibrillation5, 6.If we take into consideration electrophysiological factors such as heterogeneous refractory periods favor the start of fibrillatory conduction waves and abnormal electrical activity that leads to the progression of atrial fibrillation because the calcium reduces the atrial refractory periods5.Therefore, the early implementation of a non-dihydropyridine calcium antagonist therapy, such as verapamil, would be justified, as it not only is associated with a lower need for pharmacological or electrical cardioversion, but it also reduces the need for invasive procedures such as pulmonary veins isolation7. On the other hand, it would be interesting to define the exact role of the autonomic nervous system and what is its participation in the pathophysiology of this condition, especially the role of the adrenergic pathways in the perpetuation and sustaining of AF8. BB therapy may be limited in many patients because it is associated with lower HR in those with concomitant sinus node disease.

What are the limitations of this publication?

We must keep in mind that these benefits are the result of an early diagnosis and a timely establishment treatment. Once AF has progressed to its persistent or permanent presentations, maybe it would not be possible to obtain these advantages. On the other hand, we must highlight that the number of patients who were in the verapamil group (n=47, only 17% of the study sample) was much lower compared to the other groups (i.e., BB were used in 383 patients [57.5%])1.Therefore, a prospective and controlled study is needed to confirm these results. Such study could provide with a more balanced groups, with the same clinical and demographic characteristics, including the HATCH score that was lower in the verapamil group than in the beta-blocker group9.In such prospective study, emphasis in contraindications for the use of verapamil should be taken into account as it may result in a lower number of candidates for such therapy. Adverse events must be clear registered. A sufficient sample size should be calculated to detect significant differences in mortality. Another consideration to be made is that other non-dihydropyridine calcium antagonists should probably also be studied, like diltiazem10.

Final remarks:

Verapamil has been studied in Ibero-America since many years ago11-14. With this new information presented by Koldenhof et al, the early use of non-dihydropyridine calcium antagonists such as verapamil, in patients with newly diagnosed atrial fibrillation, can be beneficial in those who do not have contraindications. Its use could be associated with less progression of this condition. We must keep in mind that these benefits may be restricted by the exclusion criteria mentioned above, so the selection of patients according to their comorbidities is of vital importance prior to the initiation of this pharmacological agent. The study of Koldenhof et al could represent the “revival” of an old drug, verapamil, in AF.

Autores:

Dr. Manlio F. Márquez Murillo

Médico Adscrito al Servicio de Electrocardiología del Instituto Nacional de Cardiología Ignacio Chávez.

Académico Titular de la Academia Nacional de Medicina de México.

Vocal del Comité de Investigación del Instituto Nacional de Cardiología Ignacio Chávez

Secretario del Consejo Mexicano de Cardiología

Coordinador de la Alianza contra la Muerte Súbita, una Iniciativa de la Sociedad Interamericana de Cardiología

Sistema Nacional de Investigadores SNI II

Dr. Manlio F. Márquez Murillo
Médico Adscrito al Servicio de Electrocardiología del Instituto Nacional de Cardiología Ignacio Chávez.
Académico Titular de la Academia Nacional de Medicina de México.
Vocal del Comité de Investigación del Instituto Nacional de Cardiología Ignacio Chávez
Secretario del Consejo Mexicano de Cardiología
Coordinador de la Alianza contra la Muerte Súbita, una Iniciativa de la Sociedad Interamericana de Cardiología
Sistema Nacional de Investigadores  SNI  II

Dr. Angelo Columna Capellán
Dr. Angelo Columna Capellán
Médico Residente de Electrofisiología del Instituto Nacional de Cardiología Ignacio Chávez

References

  1. Koldenhof T, Wijtvliet PEPJ, Pluymaekers NAHA, Rienstra M, Folkeringa RJ, Bronzwaer P, Elvan A, Elders J, Tukkie R, Luermans JGLM, van Kuijk SMJ, Tijssen JGP, van Gelder IC, Crijns HJGM, Tieleman RG. Rate control drugs differ in the prevention of progression of atrial fibrillation. Europace. 2022 Mar 2;24(3):384-389.

  2. Márquez MF, Gómez-Flores J, Aranda-Faustro A, Cazares-Campos I, Cárdenas M. Avances recientes en la fisiopatología de la fibrilación auricular [Recent advances in the pathophysiology of atrial fibrillation]. Arch Cardiol Mex. 2009 Dec;79 Suppl 2:18-25. Spanish.

  3. Jost N, Kohajda Z, Kristof A, Husti Z, Juhasz V, Kiss L et al. Atrial Remodeling and Novel Pharmacological Strategies for Antiarrhythmic Therapy in Atrial Fibrillation. Current Medicinal Chemistry. 2011;18(24):3675-3694.

  4. Dagres N, et al. European Heart Rhythm Association (EHRA)/Heart Rhythm Society (HRS)/Asia Pacific Heart Rhythm Society (APHRS)/Latin American Heart Rhythm Society (LAHRS) expert consensus on arrhythmias and cognitive function: what is the best practice?. Europace 2018;20(9):1399-1421.

  5. Márquez MF (Ed.) “Fibrilación Auricular”. 2nd Ed. Sociedad Mexicana de Cardiología, PyDESA Editorial, Mexico City, 2018.

  6. Rodríguez-Diez G, Márquez MF, Iturralde-Torres P, Molina-Fernández de L LG, Pozas-Garza G, Cordero-Cabra A, Rojel-Martínez U. Joint Mexican position document on the treatment of atrial fibrillation. Arch Cardiol Mex. 2020;90(1):69-76.

  7. Márquez MF, González Hermosillo JA, Cárdenas M. Guía para el diagnóstico y tratamiento de la fibrilación auricular [Guidelines for the diagnosis and treatment of atrial fibrillation]. Arch Cardiol Mex. 2006 Apr-Jun;76(2):231-6. Spanish.

  8. de Vos C, Pisters R, Nieuwlaat R, et al. Progression From Paroxysmal to Persistent Atrial Fibrillation. J Am Coll Cardiol. 2010 Feb, 55 (8) 725–731.

  9. https://doi.org/10.1016/j.jacc.2009.11.040Hu WS, Lin CL. Comparisons of HATCH, HAVOC and CHA2DS2-VASc scores for all-cause mortality prediction in atrial fibrillation: a real-world evidence study. Postgrad Med J. 2022 Jan 24:postgradmedj-2021-141147. doi: 10.1136/postgradmedj-2021-141147. Epub ahead of print. PMID: 35074802.

  10. Luciardi H, Berman S, Santana M, Monteros L. Diltiazem por vía intravenosa en la conversión a ritmo sinusal de taquiarritmias supraventriculares [Intravenous diltiazem in the reversion to sinus rhythm in supraventricular tachyarrhythmias]. Arch Inst Cardiol Mex. 1996 Nov-Dec;66(6):505-9. Spanish.

  11. De Soldati L, Stritzler G, Balassanian S, Fuksman A, Mario Krasnov C, Rosental R, Chutlian A, Fabregas R. Ensayos de desfibrilación auricular con la asociación quinidina-verapamil por vía oral [Trials of auricular defibrillation with the quinidine-verapamil combination by oral route]. Prensa Med Argent. 1972 May 26;59(17):665-70. Spanish. PMID: 5048460.

  12. Shapiro M, Malo R, Férez S, Martínez-Ríos MA, Salazar E. Effectos antiarrítmicos del verapamil [Antiarrhythmic effects of verapamil]. Arch Inst Cardiol Mex. 1976 May-Jun;46(3):305-16. Spanish. PMID: 1088854.

  13. Ronderos R, Escudero EM. Efectos del verapamilo en la fibrilación auricular [Effects of verapamil in atrial fibrillation]. Medicina (B Aires). 1985;45(3):247-51. Spanish. PMID: 3841935.

  14. Sobrino JA, et al. Combinación de quinidina y verapamil en la fibrilación auricular. Rev Esp Cardiol 1989;42(4):262-266.

EP Fellowship Program

The Latin American Heart Rhythm Society (LAHRS) announces the Registration to the Fourth Edition (2023-2024) of its Cardiac Electrophysiology Training Program at McGill University (Montreal, Canada)

Director: Dr. Vidal Essebag – Head of Electrophysiology – McGill University

Vacancies: one (1)

Duration: two (2) years

Start: July 1, 2023

LAHRS SCHOLARSHIP: Includes salary of $60,000 CAD per year, and tuition fees to McGill University. Does not include costs of transportation (air) and accommodation.

Registration closes: September 1, 2022

Those interested must meet the following 2 application requirements:

1) SEND MOTIVATION LETTER and CURRICULUM VITTAE BY EMAIL to info@lahrs.org and vidal.essebag@mcgill.ca(before August 15, 2022)

2) COMPLETE THE McGill ONLINE APPLICATION by accessing the following webpages for detailed instructions (deadline for COMPLETE application by September 1, 2022). The registration fee will be discounted by LAHRS in future activities (will be informed shortly).

  1. For information pertaining to the Fellowships admission requirements:

http://www.mcgill.ca/pgme/admissions/prospective-fellows

  1. A step-by-step guide to help candidates successfully navigate through the admissions process can be found under the Menu: Application Process that includes an Applicant Guide

  1. Candidates will have to choose the following for your program selection:

a. Faculty/School: Postgraduate Medicine

b. Program: Post Residency Fellowship

c. Major or subject: Residency Program (Cardiology)

d. Concentration or area of ​​specialization: Fellowship Program: (Cardiac Electrophysiology Fellowship – 2 years)

  1. A description of the EP fellowship can be found at: https://www.mcgill.ca/pgme/fellowships/fellowship-programs/internal-medicine-cardiology by accessing the link for Cardiac Electrophysiology Fellowship (2 year program)

Contact Information:

a. Dolly Rabbath 1-514-398-8264, email: pgfellows.med@mcgill.ca

Admissions Manager, Postgraduate Medical Education, Faculty of Medicine

and Health Sciences

b. Ms. Mathushni Suntaram: pgcoordinator.med@mcgill.ca

c. Ms. Lisa Campbell: fellowshipspg.fmhs@mcgill.ca

Important: in the “proof of funding” field write LAHRS-McGill Scholarship Award

Selection Procedure: The candidate will be selected by a committee of members from LAHRS and McGill University, who will evaluate the technical and academic excellence of the candidate, and their career goals, through the curriculum vitae. Cardiology degree is a prerequisite and additional training in electrophysiology is desirable. The acceptance of admission to the program by the candidate implies the commitment to develop their subsequent professional activity within the Latin American territory for a minimum period of 2 years.

LAHRS Congress 2022

After two years of social distancing, important to contain the spread of COVID-19, finally it’s time to resume face-to-face activities!

The return will be in great style: as on other occasions, our Society will hold the Congress together with a large national scientific society of specialty. As one of the most important, because of the number of colleagues and because of the great scientific production, this year the face-to-face Congress will be in Brazil, along with SOBRAC!

LAHRS board, as well as the Scientific Committee, is working hard and developing a scientific program that includes members of associated societies, such as the Heart Rhythm Society (HRS), the European Heart Rhythm Association (EHRA), the Asia Pacific Heart Rhythm Society (APHRS), SOMEEC, SADEC, Colombian College of Electrophysiology, among others.

We hope that you join us in this experience and that together we can build a great event.

Get connected with LAHRS 2022!

Visit the official site: https://sobrac.org/sobrac2022/?page_id=397&lang=es

Marcio Figueiredo
LAHRS President

Ulises Rojel
Vicepresident

Nestor López Cabanillas
Secretary

Sebastian Massaferro
Treasurer

Patients with ischemic heart disease and VT. Drugs or ablation as a first-line treatment?

Heart attacks leave areas of scars mixed with healthy myocytes, generating areas of slow conduction within the scars, giving rise to a favorable environment for the origination of ventricular tachycardia (VT) by reentry mechanism. We all agree that in this type of scenario the implantable cardioverter-defibrillator (ICD) effectively prevents sudden death1,2. However, ICD does not prevent TV generation. In turn, each adequate shock is not only a traumatic and painful situation for the patient, but also affects their quality of life, reduces device longevity, and is associated with reduced ventricular function and, possibly, increased mortality. Therefore, when faced with a patient with ICD and symptomatic VT, it is essential to offer something more.

SURVIVE-VT 1 is a randomized trial, carried out in 9 centers in Spain. It compares catheter ablation (AC) versus antiarrhythmic drugs (AAD) as first-line treatment in patients with ischemic heart disease and symptomatic VT or ICD shocks. It included 145 patients (average age 70 years, 96% male, average FEY 34%) who were randomized to AC (n=71) or FAA (n=73). They all had chronic ischemic heart disease, a recent history of ICD shocks or symptomatic VT, and no antiarrhythmic pharmacological treatment. The primary endpoint was a composite of cardiovascular death, appropriate ICD shock, hospitalization for worsening heart failure, or serious treatment-related complications. Patients in the ablation group underwent substrate-guided ablation. Patients in the drug group could receive amiodarone alone, amiodarone plus beta-blockers, or sotalol. 86% received amiodarone.

After 24 months of follow-up, the primary endpoint was significantly reduced in the AC group by 28.2% vs 46.6% (Hazard Ratio [HR]: 0.52; P = 0.021). The number of patients to be treated to prevent a case with the primary endpoint was 4.6. The benefits in the AC group were mainly due to a significant reduction in treatment-related complications (9.9% vs 28.8% HR: 0.30; P = 0.006) and a non-significant trend towards fewer hospitalizations for heart failure (HR: 0.56; P = 0.198). There were no differences in mortality or ICD shocks.

The ad hoc analysis shows that in the AC group there was a significant reduction in the recurrence of slow VT not detected by the CD (1.4% vs 13.7% HR 0.18) and hospitalizations for VT. The crossover rate was higher in the FAA group (24.3% vs. 10.1%).

These results lead the authors to conclude that CA guided by substrate modification, performed in sinus rhythm and without the need for VT induction, reduces the primary point of safety and efficacy.

COMMENTS:

SURVIVE-VT tries to solve a very common clinical situation: a patient with ischemic heart disease with ICD who has VT. What do we do? Do we start pharmacological treatment and wait to see if there is a recurrence and then propose ablation? Or do we propose ablation as a first option? LAHRS Guidelines, carried out in conjunction with HRS/EHRA/APHRS, do not recommend ablation in these cases (indication IIb, level of evidence A), but in those who have recurrent VT despite treatment with amiodarone (indication I, level of evidence B-R )4.

The results obtained suggest that ablation, as a first line, would be better than pharmacological treatment, mainly due to the significant reduction in treatment-related complications (10% vs 29% HR 0.30 P=0.006). So, let’s focus on treatment and adverse effects.

In the FAA group, it was used mainly (86% with amiodarone), the most effective drug, but with the highest rate of adverse reactions. In the AC group, the substrate-guided ablation technique was used, which is based on the elimination of potential isolated sites to achieve scar homogenization, eliminating the transition zones between fibrosis and healthy myocytes. As there is no need to induce VT during the intervention, adverse reactions resulting from hemodynamic compromise due to repetitive VT induction are avoided. We could say that the ablation branch used the safest technique. We currently do not have solid data to support the use of one ablation technique over the other. In fact, the VISTA 5 study showed that substrate ablation, compared with clinical ablation, significantly reduced VT recurrence at 12 months and combined re-hospitalization and mortality.

Considering that the ablations were performed in centers with extensive experience in these procedures, 10% of complications is not a negligible number. And a separate debate requires a qualitative, not just quantitative, analysis of the complications between the two groups. In the ablation group, some of the complications were stroke and heart block. While in the pharmacological group, sinus bradycardia and hypothyroidism were quantified as serious complications.

It would have been expected that ablation would reduce the primary point by reducing VT recurrence. However, there was no reduction in ICD shocks, mortality or any type of VT (27% vs 29% P=0.42).

On a positive note, ablation significantly reduced slow TV episodes. And this is not a minor observation. Slow VT, as it is not detected and treated by the ICD, favors patient decompensation, increased hospitalizations and even requires external cardioversion. This could explain the trend towards a lower number of hospitalizations for heart failure observed in the AC group.

Finally, SURVIVE-VT highlights the high rate of adverse reactions to antiarrhythmics during follow-up and that catheter ablation “might” be considered first-line therapy in patients with ischemic heart disease and first-episode VT. We need more information to change “might” to “must”. The great advances in the field of ablation compared to the few advances in the field of antiarrhythmics make us very optimistic about the future.


Dr. Aldo Carrizo MTSAC, CEPS
Head of Electrophysiology Service
Clinica El Castaño
San Juan, Argentina
Founding Member, LAHRS

Bibliografía

  1. Arenal A, Ávila P, Jiménez-Candil J, et al. Substrate ablation vs antiarrhythmic drug therapy for symptomatic ventricular tachycardia. J Am Coll Cardiol. 2022;79:1441–1453.

  2. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002;346:877–83.

  3. Poole JE, Johnson GW, Hellkamp AS, et al. Prognostic importance of defibrillator shocks in patientswith heart failure. N Engl J Med. 2008;359:1009–1017.

  4. Cronin E, Bogun FM, Maury P et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias. Europace 2019; 21:1143–1144

  5. Di Biase L, Burkhardt JD, Lakkireddy D, et al. Ablation of stable VTs versus substrate ablation in ischemic cardiomyopathy. The VISTA randomized multicenter trial. J Am Coll Cardiol. 2015;66:2872–2882.

Early and late syncope: understanding the mechanisms

Bearing in mind that:

The most common cause of syncope is vasovagal (VVS), followed by orthostatic hypotension (OH) and cardiac causes, (1)

The tilt test is the study used for the diagnosis of VVS and OH, being recommended (class IIa, level of evidence B) in those cases with suspected reflex cause, OH, postural orthostatic tachycardia syndrome or psychogenic syncope (PS) after “initial assessment” (interrogation, physical examination including orthostatic blood pressure test and 12-lead ECG) did not identify the cause of the syncope (“unexplained syncope”) (1)

Epidemiological studies have shown a “bimodal” distribution of this symptom, with a peak between 15-20 years and another after 70, (2-4)

The etiology of syncope differs with age: most young people will have VVS, while OH and cardiac causes tend to be more prevalent in older adults, (2, 5)

Diagnosis is often challenging in older adults because prodromes tend to be short-lived or absent and possible amnesia for a loss of consciousness event, which may therefore mask your diagnosis as just a blackout. a “fall” (3, 6, 7)

• “Unexplained syncope” is associated with a poor prognosis, with increased mortality and increased cardiovascular morbidity (8),

Torabi P. et al. (9) propose in this work the need to know the causes of “unexplained syncope” in different age groups and the factors associated with a “final diagnosis” to establish effective diagnostic approaches.

As the “age of onset” of syncope has only been investigated in certain populations (e.g. it is a bimodal pattern of “first episode” age and the influence of “early” (<30 years) vs. “late” (≥60 years) onset years of this symptom on the clinical features and the “final diagnosis”.

After ruling out cardiac causes of syncope and non-traumatic causes of loss of consciousness (eg, epilepsy), 1,972 patients with “unexplained syncope” were evaluated between 2008 and 2018 in a syncope unit of a tertiary hospital. The “final diagnoses” after the tilt test were: VVS, HO, hypersensitivity/carotid sinus disease (HSC/CAD), complex syncope (2 or more diagnoses), non-diagnostic tilt test (TTND) and SP. Patients with TTND were recommended for further evaluation to rule out cardiac and non-cardiac causes of syncope and epilepsy. Finally, 1928 patients with available data on “age at first episode” were included in the analysis, comparing clinical features and “final diagnosis” in 3 groups according to age at onset: “early” (<30 years), 30 -59 years and “late” (≥60 years).

The first finding of this study was that the “age” of the “first episode of syncope” also shows a “bimodal” distribution in this patient population, with a first peak at 15 years and the second, less pronounced, at 70. assessment” peaked at its highest at age 75, followed by a lowest at age 20.

Clinical features and “final diagnosis” were different according to “age at first episode” (early vs. late). A significantly higher frequency of prodromes (64% vs 26%), palpitations (41% vs 15%), VVS (59% vs 19%) and SP (4% vs 0.2%) were observed in those with a first ‘early’ episode compared to those who had it “delayed.” In contrast, HO (23% vs 3%), HAC/ESC (9% vs 0.6%) and complex syncope (26% vs 14%) were significantly more frequent in those with a “late” first episode, compared to those who had it “early”. No significant differences were observed in the frequency of TTND between the 2 groups (initial 19% and late 23%).

Table 1: Clinical characteristics and diagnostic result of the tilt test with “first episode of syncope” <30 (“early”) and ≥60 years (“late”).

Results are expressed as a number (percentage), except * which are expressed as a median (interquartiles). HT: high blood pressure. VSV: vasovagal syncope. OH: orthostatic hypotension. CAH/ESC: carotid sinus hypersensitivity/disease. PP: psychogenic syncope. TTND: non-diagnostic tilt test

In the subgroup of 836 patients who were evaluated for syncope after age 60 years (Table 2), only 12% reported an “early” episode. The majority (70%) had their first “delayed” episode. VVS was significantly more frequent in those with an “early” first episode (39% vs 19%), while OH was significantly more frequent in those with a “late” onset (23% vs 7%). Prodromes were significantly less frequent in those with a “late” first episode (26% vs 52%). A “late” first episode was a predictor of HO and HAC/ESC (+31% and +26%, respectively, for every 10-year difference). In contrast, an “early” first episode was the occurrence of prodromes, VLS and complex syncope (+23%, +22% and +9% respectively, for each 10-year difference). Table 3.

Table 2: Clinical features and diagnostic result of the tilt test in patients aged ≥60 years at the time of evaluation.

Results are expressed as a number (percentage), except * which are expressed as a median (interquartiles). HTA: high blood pressure. VSV: vasovagal syncope. OH: orthostatic hypotension. HSC/ESC: carotid sinus hypersensitivity/disease. PP: psychogenic syncope. TTND: non-diagnostic tilt test

Table 3: Association between “final diagnosis” of syncope according to “age at first episode”: “early” (<30) vs “late” (≥60 years)

* OR: Probability ratios presented by 10-year increments in “age at first episode” of syncope

Although the large number of patients included is highlighted as strengths of this study, the authors mention as potential limitations of being a single-center study, the potential bias of including a selected population referred to a syncope unit to perform the tilt test, and the possible error in the determination of a clinical variable, such as the one analyzed in this study, which requires patients’ memory to recall the date of an event, which sometimes occurred many years before.

In conclusion, they highlight the diagnostic value of the “age” of the “first episode” of syncope as a relevant finding, due to its association with the clinical characteristics and the “final diagnosis”:

Shows a “bimodal” age pattern

In those over 60 years of age, most will have their first “late” episode (≥60 years) and they will have HO and ESC more often compared to those who had “early” syncope. On the contrary, when the first episode occurred “early” (<30 years), the occurrence of prodromes, SVV and complex syncope were more frequent.

Finally, it is worth noting that, despite being evaluated in a syncope unit of a tertiary hospital, a significant proportion of patients (approximately 20%) persisted with the diagnosis of “unexplained syncope” (TTND) and the need for further evaluations or diagnoses. reevaluation.

Author:

Roberto Keegan, MD

LAHRS Co-Chair/Representative of the European Heart Rhythm Association (EHRA) Electrophysiology Certification Subcommittee 2020-2022

Former President of the Latin American Heart Rhythm Society (LAHRS) 2017-2018

Director of Electrophysiology – Hospital Privado del Sur and Hospital Español – Bahía Blanca – Argentina

References:

1. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J. 2018. http://dx.doi.org/10.1093/eurheartj/ehy037.

2. Colman N, Nahm K, Ganzeboom KS, et al. Epidemiology of reflex syncope. Clin Auton Res. 2004;14 Suppl 1:9-17. http://dx.doi.org/10.1007/s10286-004-1003-3.

3. Duncan GW, Tan MP, Newton JL, et al. Vasovagal syncope in the older person: differences in presentation between older and younger patients. Age Ageing. 2010;39(4):465-70. http://dx.doi.org/10.1093/ageing/afq039.

4. Cooke J, Carew S, Costelloe A, et al. The changing face of orthostatic and neurocardiogenic syncope with age. QJM. 2011;104(8):689-95. http://dx.doi.org/10.1093/qjmed/hcr032.

5. Ceccofiglio A, Mussi C, Rafanelli M, et al. Increasing Prevalence of Orthostatic Hypotension as a Cause of Syncope With Advancing Age and Multimorbidity. J Am Med Dir Assoc. 2019;20(5):586-8. http://dx.doi.org/10.1016/j.jamda.2019.01.149.

6. Parry SW, Kenny RA. Vasovagal syncope masquerading as unexplained falls in an elderly patient. The Canadian journal of cardiology. 2002;18(7):757-8.

7. Tan MP, Parry SW. Vasovagal syncope in the older patient. Journal of the American College of Cardiology. 2008;51(6):599-606. http://dx.doi.org/10.1016/j.jacc.2007.11.025.

8. Yasa E, Ricci F, Magnusson M, et al. Cardiovascular risk after hospitalisation for unexplained syncope and orthostatic hypotension. Heart. 2018;104(6):487-93. http://dx.doi.org/10.1136/heartjnl-2017-311857.

9. Torabi P, Rivasi G, Hamrefors V, et al. Early and late-onset syncope: insight into mechanisms. Eur Heart J. 2022. http://dx.doi.org/10.1093/eurheartj/ehac017.

10. Ganzeboom KS, Colman N, Reitsma JB, et al. Prevalence and triggers of syncope in medical students. Am J Cardiol. 2003;91(8):1006-8, A8. http://dx.doi.org/10.1016/s0002-9149(03)00127-9.

11. Sheldon RS, Sheldon AG, Connolly SJ, et al. Age of first faint in patients with vasovagal syncope. Journal of cardiovascular electrophysiology. 2006;17(1):49-54. http://dx.doi.org/10.1111/j.1540-8167.2005.00267.x.

Call for public comment – 2022 HRS/APHRS/LAHRS Guideline on Cardiac Physiologic Pacing for the Avoidance and Mitigation of Heart Failure

The LAHRS, APHRS and HRS invites interested stakeholders to submit comments on the draft recommendations of the 2022 HRS/APHRS/LAHRS Guideline on Cardiac Physiologic Pacing for the Avoidance and Mitigation of Heart Failure. This open public comment stage provides greater transparency in the clinical practice document development process and the opportunity for key stakeholders to offer feedback before the document’s finalization and publication. All comments will be reviewed, and recommendations edited as appropriate.

The clinical practice guideline is intended to provide comprehensive guidance to electrophysiologists, cardiologists, and other health care providers in the use of pacing in patients with bradycardia-only indications and those in heart failure without bradycardia indications.

Document goals:

  • Introduce the general concepts of cardiac physiologic pacing, which includes conductions system pacing and cardiac resynchronization therapies

  • Review indications for cardiac physiologic pacing to improve outcomes and reduce risk of unnecessary procedures

  • Discuss optimal approaches for pre-procedure, at the time of implant, and follow-up practices

  • Identify opportunities for shared decision making to improve patient outcomes and experiences

  • Provide recommendations for troubleshooting unfavorable responses

If you have questions or experience technical difficulties entering your comments, please contact clinicaldocs@hrsonline.org

Download the document: CPP Guideline_Public Comment_2022.03.18_0

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17th edition Arrhythmias Venice 2022

The next October 13-15th, the 17th edition of Venice Arrhythmias 2022 will take place, in Venice, Italy.
LAHRS will participate in a join session called “Topics in modern electrophysiology: A
Latin American perspective for a global health problem”
Drs. M. Figueiredo, J.C Pachón Mateos, E. Saad, M. Scanavacca, Manlio Marquez and D. Hachul.
For more information: https://www.venicearrhythmias.org/va2022-program