Andrés Ricardo Pérez Riera

Queen's University, Kingston, Ontario, Canada

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Publications (53)82.77 Total impact

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    ABSTRACT: We report a case of a 68-year-old man admitted to the emergency department with syncope preceded by rapid palpitations. His admission ECG demonstrated a sustained ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT). This report highlights the importance of distinguishing ventricular tachycardia caused by arrhythmogenic right ventricular dysplasia (ARVD) from the more benign idiopathic RVOT-VT. Furthermore, we demonstrate the utility of the Fontaine leads placement in increasing the sensitivity for uncovering epsilon waves, a highly specific electrocardiographic feature that increases diagnostic accuracy in patients with ARVD.
    Annals of Noninvasive Electrocardiology 03/2014; · 1.08 Impact Factor
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    ABSTRACT: Brugada phenocopies (BrP) have emerged as new clinical entities that are etiologically distinct from true Brugada syndrome (BrS). BrP are characterized by an ECG pattern that is phenotypically identical to true BrS (type 1 or type 2); however, BrP are caused by various other factors such as mechanical mediastinal compression, myocardial ischemia, pericarditis, myocarditis, pulmonary embolism, and metabolic disturbances. We report a case of an electrocardiographic BrP in a patient with pectus excavatum deformity in the absence of true BrS using currently defined BrP diagnostic criteria. A systematic review of ECG manifestations associated with pectus excavatum is also discussed.
    Annals of Noninvasive Electrocardiology 09/2013; 18(5):415-20. · 1.08 Impact Factor
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    ABSTRACT: Congenital short QT syndrome (SQTS) is a rare inherited channelopathy without structural heart disease. It is an autosomal dominant primary electrical disorder with a low degree of penetrance. It has a characteristic clinical-electrocardiographic-electrophysiological phenotype consisting of irregular palpitations due to the frequent episodes of paroxysmal atrial fibrillation, dizziness and/or sudden cardiac death (SCD). Affected individuals usually have a positive family history of syncope or SCD in first-or second degree young relatives (younger than 40 years of age) with autopsy negative SCD. Resting electrocardiograms (ECGs) have very short and uniform QT/QTc intervals (QTc interval ≤330 ms with the exception of the calcium-dependent variants 4 and 5), absent or minimal ST segments, interval from J point to T wave peak (Jp-Tp) measured in the precordial lead with the T wave of greatest amplitude.
    Cardiology journal 05/2013; · 1.15 Impact Factor
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    ABSTRACT: Brugada syndrome is an inherited heart disease without structural abnormalities that is thought to arise as a result of accelerated inactivation of Na channels and predominance of transient outward K current (I(to)) to generate a voltage gradient in the right ventricular layers. This gradient triggers ventricular tachycardia/ventricular fibrillation possibly through a phase 2 reentrant mechanism. The Brugada electrocardiographic (ECG) pattern, which can be dynamic and is sometimes concealed, being only recorded in upper precordial leads, is the hallmark of Brugada syndrome. Because of limitations of previous consensus documents describing the Brugada ECG pattern, especially in relation to the differences between types 2 and 3, a new consensus report to establish a set of new ECG criteria with higher accuracy has been considered necessary. In the new ECG criteria, only 2 ECG patterns are considered: pattern 1 identical to classic type 1 of other consensus (coved pattern) and pattern 2 that joins patterns 2 and 3 of previous consensus (saddle-back pattern). This consensus document describes the most important characteristics of 2 patterns and also the key points of differential diagnosis with different conditions that lead to Brugada-like pattern in the right precordial leads, especially right bundle-branch block, athletes, pectus excavatum, and arrhythmogenic right ventricular dysplasia/cardiomyopathy. Also discussed is the concept of Brugada phenocopies that are ECG patterns characteristic of Brugada pattern that may appear and disappear in relation with multiple causes but are not related with Brugada syndrome.
    Journal of electrocardiology 09/2012; 45(5):433-42. · 1.08 Impact Factor
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    ABSTRACT: There are fibers in the left ventricle (LV) (LV middle network) that in around one third of cases may be considered a true septal fascicle that arises from the common left bundle. Its presence and the evidence that there are 3 points of activation onset in the LV favor the quadrifascicular theory of the intraventricular activation of both ventricles. Since the 70s, different authors have suggested that the block of the left middle fibers (MS)/left septal fascicle may explain different electrocardiographic (ECG) patterns. The 2 hypothetically based criteria that are in some sense contradictory include: a) the lack of septal "q" wave due to first left and later posteriorly shifting of the horizontal plane loop and b) the presence of RS in lead V(2) (V(1)-V(2)) due to some anterior shifting of the horizontal plane vectorcardiogram loop. However, there are many evidence that the lack of septal q waves can be also explained by predivisional first-degree left bundle-branch block and that the RS pattern in the right precordial leads may be also explained by first-degree right bundle-branch block. The transient nature of these patterns favor the concept that some type of intraventricular conduction disturbance exists but a doubt remains about its location. Furthermore, the RS pattern could be explained by many different normal variants. To improve our understanding whether these patterns are due to MF/left septal fascicle block or other ventricular conduction disturbances (or both), it would be advisable: 1) To perform more histologic studies (heart transplant and necropsy) of the ventricular conduction system; 2) To repeat prior experimental studies using new methodology/technology to isolate the MF; and 3) To change the paradigm: do not try to demonstrate if the block of the fibers produces an ECG change but to study with new electroanatomical imaging techniques, if these ECG criteria previously described correlate or not with a delay of activation in the zone of the LV that receives the activation through these fibers or in other zones.
    Journal of electrocardiology 09/2012; 45(5):454-60. · 1.08 Impact Factor
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    ABSTRACT: Acquired long QT (LQT) interval is thought to be a consequence of drug therapy and electrolyte disturbances. We characterize the potential effects of polypharmacy in a case series of acquired LQT and torsades de pointes (TdP) in order to determine whether multiple risk factors play a role in the development of LQT. The case series consisted of 11 patients presenting to 4 tertiary care hospitals with LQT and ≥ 2 risk factors for developing LQT. Clinical characteristics, medications, electrolyte disturbances, and course in hospital were analyzed. Mean age was 49.1 ± 5.8 years. Eight patients were female. Four had hypertension, 1 had a history of dilated cardiomyopathy, and 1 patient demonstrated complete atrioventricular block. Average QTc interval at presentation was 633.8 ± 29.2 ms. Nine patients developed TdP. In 3, LQT was not initially detected and amiodarone was administered, followed by development of TdP. Patients were taking an average of 2.8 ± 0.3 QT-prolonging medications-an antidepressant in 6 cases and a diuretic in 8 cases. All patients had an electrolyte abnormality; 8 patients presented with severe hypokalemia (<3.0 mmol/L). Average serum potassium and magnesium were 2.82 ± 0.10 mmol/L and 0.75 ± 0.03 mmol/L, respectively. There were no deaths. This case series highlights the risks of polypharmacy in the development of LQT and TdP. It illustrates the importance of early detection of LQT in patients with multiple risk factors in ensuring appropriate treatment.
    Clinical Cardiology 09/2011; 34(9):577-82. · 1.83 Impact Factor
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    ABSTRACT: Several factors are known to interfere with electrocardiogram (ECG) sensitivity when diagnosing Left Ventricular Hypertrophy (LVH), with gender and cardiac mass being two of the most important ones To evaluate the influence of gender on the sensitivity of some of the criteria used to detect LVH, according to the progression of ventricular hypertrophy degree. According to gender and the degree of LVH at the echocardiogram, the patients were divided in three groups: mild, moderate and severe LVH. ECG sensitivity to detect LVH was assessed between men and women, according to the LVH degree. Of the 874 patients, 265 were males (30.3%) and 609, females (69.7%). The [(S + R) X QRS], Sokolow-Lyon, Romhilt-Estes, Perugia and strain criteria showed high discriminatory power in the diagnosis of LVH between men and women in the three groups with LVH, with a superior performance in the male population and highlighting the importance of the [(S + R) X QRS] and Perugia scores. Conclusion: The diagnostic sensitivity of the ECG increases with the cardiac mass. The examination is more sensitive in men, highlighting the importance of the [(S + R) X QRS] and Perugia scores. The diagnostic sensitivity of the ECG increases with the cardiac mass. The examination is more sensitive in men, highlighting the importance of the [(S + R) X QRS] and Perugia scores.
    Arquivos brasileiros de cardiologia 08/2011; 97(3):225-31. · 1.32 Impact Factor
  • International journal of cardiology 07/2011; 151(3):374-5. · 7.08 Impact Factor
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    ABSTRACT: Lead aVR is the only lead in the surface ECG that does not face the "typically" relevant walls of the left ventricle. Historically, its value has been neglected most likely due to its unusual configuration and direction, which appeared to have little correlation with other more congruous and easily diagnostic frontal leads. The isolation of the unipolar leads in the Standard surface ECG presentation may also have played an important role. Even with this "unfair" neglect, we know nowadays that it is very sensitive to locate obstructed epicardial coronary arteries. Besides helping distinguishing the culprit lesion of an infarct, lead aVR also helps recognizing other conditions that could be of clinical significance such as pericarditis, Brugada syndrome, fascicular blocks of the right branch, ectopic left atrial rhythms, etc. The purpose of this review is to revise the clinical value of lead aVR in the recognition of frequent and not so frequent clinical conditions.
    Annals of Noninvasive Electrocardiology 07/2011; 16(3):295-302. · 1.08 Impact Factor
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    ABSTRACT: Several publications considering anatomical, histological, pathological, electrocardiographic, vectorcardiographic, and electrophysiologic studies have shown that the left bundle branch splits into three fascicles or in a "fan-like interconnected network" in the vast majority of human hearts. The left His system is trifascicular with a left anterior, a left posterior, and a left septal fascicle (LSF). Consequently, the classic term "hemiblock," to describe the block of one of the fascicles, established several decades ago by the Rosembaum's school, should be updated. Electrovectorcardiographic changes resulting from conduction abnormalities of the left anterior and left posterior fascicles are commonly diagnosed, mainly by their changes in the frontal plane. However, the existence of conduction defects of the LSF remains controversial. The ECG/VCG hallmark of LSF block is prominent anterior QRS forces (PAF) on the horizontal plane. This ECG/VCG phenomena should be distinguished from other conditions that also produce anterior QRS shift in the HP as: normal variants, right ventricular enlargement, misplaced precordial leads, lateral myocardial infarction, right bundle branch block, Wolff-Parkinson-White, obstructive and nonobstructive forms of hypertrophic cardiomyopahty, diastolic left ventricular enlargement, endomiocardial fibrosis, Duchenne muscular dystrophy, and dextroposition. The two highly frequent etiologies of LSFB are ischemia (coronary artery disease (CAD) with critical proximal obstruction of the left anterior descending coronary artery) and, in Latin America, Chagas' cardiomyopathy. The aims of this review are to revise the evidence of the existence of a trifascicular left Hissian system and to help in the ECG/VCG recognition of the LSFB.
    Annals of Noninvasive Electrocardiology 04/2011; 16(2):196-207. · 1.08 Impact Factor
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    ABSTRACT: Exogenous catalase influences neural control of cardiovascular system; however, we do not know yet if its inhibition into the fourth cerebral ventricle (4(th) V) influences baroreflex regulation. We evaluated the effects of central catalase inhibition on baroreflex in conscious Wistar rats. We used males Wistar rats (320-370 g), which were implanted with a stainless steel guide cannula into 4(th) V. The femoral artery and vein were cannulated for mean arterial pressure (MAP) and heart rate (HR) measurement and drug infusion, respectively. After basal MAP and HR recordings, the baroreflex was tested with a pressor dose of phenylephrine (PHE, 8 μg/kg, bolus) and a depressor dose of sodium nitroprusside (SNP, 50 μg/kg, bolus). Baroreflex was evaluated before 5, 15, 30 and 60 minutes after 3-amino-1, 2, 4-triazole (ATZ, 0.001 g/100 μL) injection into the 4(th) V. Vehicle treatment did not change baroreflex responses. ATZ attenuated bradycardic peak and reduced HR range at 30 minutes. ATZ into the 4(th) V reduced bradycardic and tachycardic reflex responses to increase and decrease MAP, respectively (p<0.05) 30 minutes after its microinjection without significantly changing the basal MAP and HR. In conclusion, central catalase inhibition influenced the highest parasympathetic response to MAP increase in conscious Wistar rats without change baroreflex gain.
    Journal of Integrative Neuroscience 03/2011; 10(1):1-14. · 1.15 Impact Factor
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    ABSTRACT: Myotonic dystrophy (DM), the commonest dystrophy in adults, is an autosomal dominant disease characterized by a variety of multisystemic features. Two main genetically distinct forms of DM have been identified: type 1 (DM1), the classic form first described by Steinert, and type 2 (DM2), identified by Ricker. DM1 is caused by trinucleotide expansion of cytosine- -thymine-guanine (CTG) in the myotonic dystrophy protein kinase gene, whereas in DM2 the expansion of tetranucleotide repeats (CCTG) in the zinc finger protein 9 gene was identified. Both mutations are dynamic and are located in non-coding parts of the genes. Phenotype variability of DM1 and DM2 is caused by a molecular mechanism due to mutated RNA toxicity. DM1 is characterized by myotonia and multi-organ damage with major cardiac involvement. The disease is usually slowly progressive and life expectancy is reduced by the increased mortality associated with cardiopulmonary complications. Sudden death can occur as a consequence of cardiac-conduction abnormalities. We present the ECG of a 26 year-old male with DM1 and progressive conduction system disturbance characterized by syncopal episodes.
    Cardiology journal 01/2011; 18(3):322-5. · 1.15 Impact Factor
  • Medicina 01/2011; 71(2):166. · 0.42 Impact Factor
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    ABSTRACT: There is a direct relationship between the regression of left ventricular hypertrophy (LVH) and a decreased risk of mortality. This investigation aimed to describe the effects of anti-hypertensive drugs on cardiac hypertrophy through a meta-analysis of the literature. The Medline (via PubMed), Lilacs and Scielo databases were searched using the subject keywords cardiac hypertrophy, antihypertensive and mortality. We aimed to analyze the effect of anti-hypertensive drugs on ventricle hypertrophy. The main drugs we described were enalapril, verapamil, nifedipine, indapamina, losartan, angiotensin-converting enzyme inhibitors and atenolol. These drugs are usually used in follow up programs, however, the studies we investigated used different protocols. Enalapril (angiotensin-converting enzyme inhibitor) and verapamil (Ca(++) channel blocker) caused hypertrophy to regress in LVH rats. The effects of enalapril and nifedipine (Ca(++) channel blocker) were similar. Indapamina (diuretic) had a stronger effect than enalapril, and losartan (angiotensin II receptor type 1 (AT1) receptor antagonist) produced better results than atenolol (selective beta1 receptor antagonist) with respect to LVH regression. The anti-hypertensive drugs induced various degrees of hypertrophic regression.
    Clinics (São Paulo, Brazil) 07/2010; 65(7):723-8. · 1.59 Impact Factor
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    ABSTRACT: This anesthetic drug may cause a rare condition named propofol infusion syndrome, characterized by unexplained lactic acidosis, lipemia, rhabdomyolysis, cardiovascular collapse and Brugada-like electrocardiographic pattern or Brugada electrocardiographic phenocopy changes following high-dose propofol infusion over prolonged periods of time. Several articles have contributed to our understanding of the cause of the syndrome, and the growing number of case reports has made it possible to identify several risk factors. Uncertainty remains as to whether a genetic susceptibility exists. The favorable recovery profile associated with propofol offers advantages over traditional anesthetics in clinical situations in which rapid recovery is important. Propofol is a safe anesthetic agent, but propofol infusion syndrome is a rare lethal complication.
    Cardiology journal 01/2010; 17(2):130-5. · 1.15 Impact Factor
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    Mauricio Arce, Andrés Ricardo Pérez Riera, Francisco Femenía, Adrián Baranchuk
    Cardiology journal 01/2010; 17(5):525-7. · 1.15 Impact Factor
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    ABSTRACT: Previous events evidence that sudden cardiac death (SCD) in athletes is still a reality and it keeps challenging cardiologists. Considering the importance of SCD in athletes and the requisite for an update of this matter, we endeavored to describe SCD in athletes. The Medline (via PubMed) and SciELO databases were searched using the subject keywords "sudden death, athletes and mortality". The incidence of SCD is expected at one case for each 200,000 young athletes per year. Overall it is resulted of complex dealings of factors such as arrhythmogenic substrate, regulator and triggers factors. In great part of deaths caused by heart disease in athletes younger than 35 years old investigations evidence cardiac congenital abnormalities. Athletes above 35 years old possibly die due to impairments of coronary heart disease, frequently caused by atherosclerosis. Myocardial ischemia and myocardial infarction are responsible for the most cases of SCD above this age (80%). Pre-participatory athletes' evaluation helps to recognize situations that may put the athlete's life in risk including cardiovascular diseases. In summary, cardiologic examinations of athletes' pre-competition routine is an important way to minimize the risk of SCD.
    Sports Medicine Arthroscopy Rehabilitation Therapy & Technology 01/2010; 2:19.
  • Andrés Ricardo Pérez Riera, Augusto Hiroshi Uchida
    Cardiology journal 01/2010; 17(2):211-3. · 1.15 Impact Factor
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    ABSTRACT: Accelerated Idioventricular Rhythm (AIVR) is a ventricular rhythm consisting of three or more consecutive monomorphic beats, with gradual onset and gradual termination. It can rarely manifest in patients with completely normal hearts or with structural heart disease. It is usually seen during acute myocardial infarction reperfusion. This manuscript aims to review the history of the main discoveries that lead to the identification and comprehension of this fascinating arrhythmia.
    Indian pacing and electrophysiology journal 01/2010; 10(1):40-8.
  • Cardiology journal 01/2009; 16(6):592-3. · 1.15 Impact Factor

Publication Stats

920 Citations
82.77 Total Impact Points

Institutions

  • 2013
    • Queen's University
      Kingston, Ontario, Canada
  • 2011
    • Universidade Federal de São Paulo
      • Departamento de Medicina
      São Paulo, Estado de Sao Paulo, Brazil
  • 2010
    • Faculdade de Medicina do ABC
      Santo André, São Paulo, Brazil
  • 2007
    • University of Barcelona
      Barcino, Catalonia, Spain
    • University of São Paulo
      • Faculty of Medicine (FM)
      San Paulo, São Paulo, Brazil
  • 2005
    • University of Rochester
      • Division of Hospital Medicine
      Rochester, NY, United States
  • 2003–2004
    • Centro Universitário Fundação Santo André
      Santo André, São Paulo, Brazil
    • Masonic Medical Research Laboratory
      Utica, New York, United States