Research Methodology Chapter: Communication Research

Research Methodology Chapter: Communication Research One communication-related aspect of the engagement debate concerns the fundamental nature of engagement and whether it can be considered an attitude, a psychological or motivational state, or a personality trait. The nature of engagement is a significant issue for corporate communicators since they are well-placed to influence workplace attitudes and stimulate employee motivation. Kahn (1990) presents engagement as a three-component construct influenced by three psychological states. Robinson et al. (2004) define the concept as a positive attitude. Conversely, Saks (2006) argues that engagement is not an attitude but a psychological state, while others (Sparrow and Balain, 2010) believe that engagement is an attitude. Macey and Schneider (2008a) regard engagement as a complex network encompassing trait, state, and behavioural constructs. Kahn (2010) contrasts his conception of dynamic engagement with steady-state (trait) views of motivation. Kahn describes engagement as both delicate and fragile, and quite resilient. So, Kahns view of engagement exhibits a mixture of attitudinal-type states together with more fixed steady-state predisposition traits. This complex state and trait view of engagement is useful for communicators since it highlights a need for employee communication to understand and serve internal stakeholders core (trait) communication needs, as well as surface (state and attitude) communication needs. Moreover, internal communication represents one of the organisational conditions that facilitate engagement. Pugh and Dietz (2008) consider leadership as a precursor of organisation engagement and organisational effectiveness as a consequence. The communication abilities of leadership teams are recognised as important in driving engagement (Wiley et al., 2010). Communication has been identified also as an underlying factor associated with employee engagement (Kahn, 1992). Likewise, MacLeod and Clarke (2009) highlight communication as a critical factor for enhancing performance through employee engagement. They argue that good quality internal communication enhances engagement as they emphasise that employees need clear communication from senior management to understand how their own roles fit with the organisation vision. Unsurprisingly, they cite poor communication as a barrier to engagement and a cause of disengagement. However, contributions from the professionals on communication disciplines are surprisingly meager given that internal communication is an organisational level interventio n which can positively impact employee engagement. Internal communication in any organisation has been stated to have a correlation with employee feeling of self-satisfaction and their productivity (Clampitt and Downs, 1992). High communication effectiveness is linked to better financial performance and organizational stability (Internal communication effectiveness enhances bottom-line results, journal of organizational excellence, Summer 2006, pp 71-71) Van Riel (1998, pp. 8-27) gives an overview of the elements of corporate communication as all the communication within an organisation, such as managerial communication, organisational communication, and marketing communication. This informs the employees willingness to meet the strategic mission, vision, and objectives of the organisation which creates a competitive advantage of the organisation. Research Design This section will discuss the research framework proposed for use in this study. This methodological framework is influenced by the research onion model develop by Saunders (2012) pp 128 which include general information regarding the research design and strategy, method of data collection, measurement of variable and data analysis as well as evaluate the credibility and validity of the study. There would be an examination of merits and demerits of the chosen methods use in this study, a consideration of ethical issues, as a result, the limitations. Research Design Available literature considers basically five different approaches ranging from experimental, case study, longitudinal, cross-sectional to comparative design (Bryman and Bell, 2011; Saunders et al, 2009). In view of the aim of this research, there will be a combination of approaches also known as a mixed method in the investigation of the research theme (Saunders et al, 2009). Also, a set of quantifiable data will be collected to help establish the relationship between two or more variables (Bryman and Bell, 2011). Research Strategy The strategy to be adopted for this research will be quantitative in nature, this is because will be formulation and testing of hypotheses which are tentative suppositions or proposed explanations made based on limited evidence as a starting point for further investigation which on the face of empirical evidence could hold true or false and as such be graduated to be theory or otherwise. According to Saunders et al, (2009) quantitative research is a strategy that lay emphasis on quantification in data collection and analysis that provides solid scientific fact of knowledge on the basis of positivism. Furthermore, Bryman and Bell, (2011) suggested that the application of a quantitative research strategy has the latent for statistical generalization as against qualitative research employed in many social and natural sciences academic disciplines which are more descriptive. This method of approach, therefore, is more useful to achieve the set aims and objectives of this research stated herein. Data Collection There will be the use of both primary and secondary data collection sources to collect appropriate and relevant data that will enable credible, complete and valid conclusions in accordance with the aims and objectives of the research. Primary data will include the conduct of interview of some members of the management team of the case study organisation and a questionnaire of other concerned employees. The use of these two methods is hoped to balance some of the limitations inherent in each. In addition, this research will use the content analysis approach which is a strategy for the review and analysis of relevant secondary documents from Abellio. Data Analysis All data collected for the purpose of this research will be careful analysis and tested against the theories with the aid of IBM SPSS statistical program. IBM SPSS Statistics is an integrated software product that addresses the entire analytical process, from planning to data collection to analysis, reporting, and deployment (Gaskin, J, 2012). It provides a range of statistical procedures suitable for many problems, including crosstabs, linear regression, Monte Carlo simulation, geospatial analytics, and the ability to extend built-in capabilities with Python, R, or Java code (IBM.com). I have opted for IBM SPSS statistical program for its effectiveness in data analysis and presentation quality of custom tables to help users and analysts to interpret data which could then be tested against the theoretical statements that could, in turn, lead to further generalisation statements (Bryman and Bell, 2011). Limitations of Study The following limitations are anticipated: 1. Data collected is based on interviews and questionnaires administered and as such respondents may not give the actual situation for fear that management of reprisal action against them 2. The data collected by the observation technique may be very limited. 3. The case study organisation has a large number of employees consequently, only one hundred of the affected will be sampled through the rank and file. 4. Equally important is the problem of time as the research will only be conducted within given three-month period. Frankenstein | Analysis Frankenstein | Analysis Frankenstein was a man whose ambition led to a disaster; and his actions led to evil. These are outcomes for which he is solely responsible. Is Frankenstein an innocent? In my opinion, he was not an innocent. The meaning of innocent is to free from evil or guilt. The word Frankenstein is defined in the Encarta dictionary as a creator of something that causes ruin or dest ruction, or brings about a personal downfall, this shows that his name was quite well suited. A common quotation is that One is innocent until proved guilty, If this quotation is applied to Victor Frankenstein, he would be innocent, however my argument is that he was not innocent, it was his fault his family suffered, he brought on his own destruction and was responsible for creating a human, which was morally and contextually incorrect; He would be innocent for allowing the murders of William, Justine, Elizabeth and Clerval to take place. It may be true that Frankenstein did not physically murder, however, he is the main cause, and the reason they died. Frankenstein never admitted to his families what he had done; he never took responsibility for his actions. The so called monster murdered for companionship, not to seek revenge from his victims, but to seek revenge from Frankenstein. The circumstances forced Frankensteins monster to do so, Victor was the instigator of these circumstances. My first thought was to discover what I knew of the murderer and cause instant pursuit to be made. But I paused when I reflected on the story I had to tell, this shows that Victor had the knowledge that he was the reason William was dead. He said my first thought, showing the clearness of his knowledge and that this thought had been lingering in his mind, he knew what he was doing. Frankenstein didnt need to know about the murderer, because he indirectly was the murderer, through the circumstances he created for the monster, as I mentioned briefly before. Which is why he paused half way through his thought and realised he was exactly who the murderer was, even though he blamed the creature. Frankensteins reason for creating the creature was his interest in his studies, which led him to the idea of bettering mankind. Victor thought he was doing a service to humanity by creating a new human. A new species would bless me as its creator and source; many happy and excellent natures would owe their being to me. I might in process of time (although I now found it impossible) renew life where death had apparently devoted the body to corruption. This quote shows his ego behind these plans. He wanted to conquer death, something the average human could not do. He wanted this creature to revere him highly by as he was supposedly beautiful and perfect creature. According to him, it may have been acceptable to play the role of god; maybe his being a scientist is why he didnt think of what was morally correct, and he didnt think of how the society would react to his actions. However, having said that, he didnt admit his doings to his family, perhaps he knew they wouldnt accept it, or the deaths in the family could have a higher weightage in terms of being more important than letting his parents know the truth. If they did know the truth, they wouldnt be happy with him creating the creature. The quote does show that right from the start, Victor had an idea of how he would somewhat be stepping into the shoes of a godlike figure, he outlines the fact that he would be superior, and he would have the power to renew the dead. This proves that he had no innocence, or naivety in terms of knowing precisely what he was doing and what it would lead to. I, the miserable and the abandoned, am an abortion, to be spurned at, and kicked, and trampled on. Is what the creature says after being shunned, on the basis of aesthetics. This shows his faults, and how he was wrong to shun the creature. He may have shunned it because he already conquered death, so in his view, he may have already obtained the status of god, or a superior power, something no one had achieved. He didnt think about anything past the ugliness of the creature, or his personal benefits. His selfishness is what ultimately destroyed him and others as well. The creature he created is more like a project to Frankenstein, his aim is to conquer death, and once he has done so, the project is over. Not once does he consider the fact that he has simply given birth to a new human being, with feelings and emotion, a live creature who has to be taught the ways of life as if it is a baby. Frankensteins abandonment of the creature is another factor that proves him guilty, and not an innocent, as shown in the quote I previously mentioned, with the creatures emotions towards being shunned. Its his own fault that the creature comes back saying I may die; but first you, my tyrant and tormentor, shall curse the sun that gazes on your misery. Beware; for I am fearless, and therefore powerful. The creature was deprived of the companionship, which he could only get from his creator. The creature figures that the only way he can get some attention, is by threatening his creator. This could be compared to a situation with a child and a parent. Frankenstein is somewhat the parent of his creature. His job is to nurture him, but because of his own ego, he runs away. If it were a parent and a child, the child would be defenceless because it hasnt even developed physically, however the creature is an example where he is an uneducated child, with a higher physical strength. Frankensteins creature thinks through intuition, as any child who hasnt learnt anything would do. He doesnt know whats right and wrong, so he doesnt know its wrong to threaten; he doesnt know its wrong to kill. Blaming him is like blaming a child for breaking a valuable, such as a vase. You cant blame the child because their knowledge hasnt developed, they havent yet learnt. However in the childs case, after making such a mistake, the child would be taught not to do so again, creating a basis of how it is wrong, this does not take place for the creature. It could be argued that the creature shou ld know through Victors fear, but does a child learn anything when it senses fear? No, it anything, it will only learn to keep intimidating. Frankensteins faults of his creation, or you could say his faults in parenting, were completely his responsibility. Frankensteins creature is described as having dark black hair, yellow skin, black lips and eyes sunk into his sockets (Shelly 56). Its quite ironic that Frankenstein feared his own creation, he is the one who hand-picked the features his so called perfect man would have. For him to say breathless horror and disgust filled my heart(56), towards a creation of his own, just shows his tendency towards aesthetics, and how backward he is in terms of being accepting, yet how forward he is in terms of doing something new. He is responsible for the way the creature turned out. This once more, proves his irresponsibility, and his view to the creation as a project. His attitude towards the creature is why he was incapable of acting the right way. He wasnt serious enough, or perhaps he wasnt ready to face negative consequences, seeing as he was a perfectionist. The background Frankenstein created in terms of nurture is what caused his creature to murder. Victor admitted to creating the monster, but he denied that he drove the monster to commit murder. He wouldnt admit to anyone; not himself, not his family, that he was the one who allowed the murders to take place. He allowed Clerval, his wife Elizabeth, his brother William and Justines death to take place because he didnt take the blame for his actions. If he had admitted to his actions earlier, less deaths would have been caused, if he had been responsible, and given the creature what it needed, he would not be guilty of four murders. In the end, Frankenstein was at loss of everything close to him, he blamed the monster, but it was his fault. He had a faint idea that it was his fault, although no one could possibly be able to admit to murdering the people close to them. The only way he could be innocent, is for not literally taking a knife and stabbing his relatives. However the pain he got from his creature was his own fault. Innocence lies in having no sense of guilt for any action of yours, this, Victor did clearly not have. The creature couldnt stop himself from destroying Victor, because Victor couldnt stop himself from creating the creature. The creature was an innocent; it only reacted to the actions of society. Victor was guilty in every way. Arrhythmogenic Right Venticular Dysplasia | Case Report Arrhythmogenic Right Venticular Dysplasia | Case Report Arrhythmogenic Right Venticular Dysplasia – A Rare case report from tribal zone of Central India Dr. Prakash Khunte, Dr. P. Beck, Dr. K. Yadav ABSTRACT Arrhythmogenic right ventricular dysplasia (ARVD) is under diagnosed cardiomyopathy which commonly presents in young adults with ventricular tachycardia or sudden death. It is characterized pathologically by progressive fibrofatty replacement of the myocardium, primarily of the right ventricular free wall. Clinically, it presents with life-threatening malignant ventricular arrhythmias which may lead to sudden death, most often in young people and athletes. ARVD/C is difficult to diagnose, although standardized diagnostic criteria have been proposed, based on the presence of major and minor criteria encompassing electrocardiographic, arrhythmic, morphofunctional, histopathologic, and genetic factors. Case report A 30 year male patient named Heeralal Diwakar R/o Baloda Bazar (C.G.) was admitted in department of Medicine, Intensive cardiac Coronary Unit at Pt. J. N. M. Medical College Dr .B.R.A.M. Hospital Raipur with the complain of palpitation ,dizziness, dyspnoea on exertion and left sided chest pain, cough with expectorant distension of abdomen since 8 days.patient having severe palpitation and dizziness in recent hours. Patients having similar complain and admitted two time in hospital in last two year and patient had episode of PSVT and had given DC shock and patient on aspirin,amidaron,metoprolol. There is no family history of sudden cardiac death and any heart disease. Patient was former by occupation and having addiction to tobacco and occasionally alcoholic. On admission patient on general examination pulse -100/min regular.blood pressure was 100/70 mmhg, height -161 cm,weight 58 kg,BMI- 22.39,Iteric ,no cyanosis, oedema were present .on systemic examination bilateral crepitatition present in infrascapular area ,apex beat present on 5 th intercosta space on midclavicular lines,s1 soft.s2 present,s3,s4 absent .No thrill ,murmur,parasternal heave were present. On investigation E.C.G. ST segment elevation seen in lead II,III,aVf, ST segment depression in lead I,Avl,Twave inversion in v1-v6, epsilon wave in V1-v3. Troponin card test was positive and patient diagnosed as acute inferior wall Myocardial Infraction with congestive cardiac failure. Other investigation were random blood sugar was 120 mg/dl, urea 90 mg/dl, creatinine 2 mg/dl,s.billirubin 3.7 mg/dl , direct billirubin 2.3 mg/dl,S.G.O.T S.G.P.T were high,alkaline phosphatase 12877 mg/dl ,sodium 130 mg/dl, potassium 4.9 mg/dl.s. protein 7 g/dl,serum albumin 4 gm/dl,s. cholesterol 114 mg/dl, triglyceride 64 mg/dl,LDL 84 MG/DL,VLDL 13 mg/dl,HDL-17 mg/dl. TLC count were 34000/cumm,Hb 14.5 gm/dl, platelet 222000 /cumm X ray chest cardiomegaly was present. On echocardiography Right ventricle dilated ,RV wall thickness 4 mm. Right Atrium dilated, severe non hypertensive TR , Right ventricle thinned out ,normal LV systolic function suggestive of Arrhythmogenic right ventricular dysplasia. Patient was advised to continue amiodarone ,aspirin ramipril and has been asymptomatic ever since. DISCUSSION The name arrhythmogenic right ventricular dysplasia(ARVD) was coined for the first time in 1978 by Frankand Fontaine. Arrythmogenic right ventricular (RV) cardiomyopathy (ARVC) is a cardiomyopathy characterized pathologically by fibrofatty replacement primarily of the RV and clinically by life-threatening ventricular arrhythmias in apparently healthy young people. The prevalence of the disease has been estimated at 1 in 5,000 individuals, although this estimate will likely increase as awareness of the condition increases among physicians. Arrythmogenic RV cardiomyopathy is recognized as a cause of sudden death during athletic activity because of its association with ventricular arrhythmias that are provoked by exercise-induced catecholamine discharge. Diagnosis may be difficult because many of the electrocardiographic abnormalities mimic patterns seen in normal children, and the disease often involves only patchy areas of the RV. he prevalence of ARVC in the general population is approximately 1 in 5,000 , but the disease is not widely recognized because of the difficulty in making the diagnosis . A familial predilection of the disease has been recognized since 1982 when Marcus et al. described 24 cases of ARVC, two in the same family. Subsequently, several groups have reported familial ARVC, and families with two or more affected individuals have been recognized in Asian, Japanese, Northern European, African and North American populations . Genectics The disease is typically inherited as an autosomal dominant trait with variable penetrance and incomplete expression. The genes responsible for ARVC have not been identified, but seven loci have been mapped to chromosomes 14 (14q23 to q24 and 14q12 to q22), 1 (1q42 to q43), 2 (2q32.1 to q32.2), 3 (3p23) and 10 (10p12 to p14) . The genetic products of these sites have not been easily identified because of incomplete penetrance and expression, age-related expression and difficulties with accurate diagnosis of the disease. Recently, plakoglobin has been identified as the first gene responsible for autosomal recessive ARVC . The gene was identified in Naxos disease where greater than 90% cosegregation of ARVC with cutaneous manifestations, woolly hair and keratodermia, facilitated case identification. Plakoglobin participates in forming cell-to-cell junctions. It is postulated that inadequate cell adherence damages the cardiac cell membranes leading to cell death and fibrofatty replaceme nt. The cardiac ryanodine receptor gene (RyR2) has also recently been implicated in ARVC and offers potential insight into the association of adrenergically mediated ventricular arrhythmias with this disease. The ryanodine receptor induces calcium release from the sarcoplasmic reticulum into the cytosol . The cardiac ryanodine receptor has also been identified as being responsible for catecholamine-induced ventricular tachycardia . Its skeletal muscle counterpart has been implicated in malignant hyperthermia and central core disease , a congenital myopathy, but the mechanisms by which mutations in the cardiac ryanodine receptor might mediate fibrofatty myocardial changes are not clear and will likely be the focus of future studies. Despite these advances, genetic analysis for ARVD is not clinically available and is restricted to research laboratories. Histopathology Characteristically, the RV in ARVC is replaced with a fibrofatty tissue. Morphologic alterations of ARVC usually begin in the subepicardium or mediomural layers of the RV and progress to the endocardium with fibrofatty replacement of myocytes and thinning of the wall. The regions of RV most frequently involved are the RV inflow area, the apex and the infundibulum. These three areas form â€Å"the triangle of dysplasia† . However, small amounts of fat are present in the epicardial layer and within the RV myocardium in normal subjects. Etiology In addition to a genetic cause of ARVC, disontogenetic, degenerative, infectious or inflammatory ( apoptotic and myocyte transdifferentiation theories have been proposed either as the cause of or as environmental factors facilitating gene expression. The disontogenetic theory is largely historical but suggests that ARVC is a milder form of â€Å"parchment RV† or Uhl’s anomaly a congenital hypoplasia of the RV myocardium, which presents in infancy as congestive heart failure (CHF) . The degenerative theory suggests that ARVC is a consequence of myocyte death due to an inherited metabolic or ultrastructural defect. A possible defect has been mapped to chromosome l4q23 to q24 . This area encodes for the alpha actinin gene, which shares structural homology with the amino terminal domain of dystrophin. This finding supports the concept of a genetically determined atrophy similar to that in patients with Duchenne’s or Becker’s muscular dystrophy. Some have suggested that ARVC should be considered as a â€Å"myocardial dystrophy† Furthermore, skeletal muscle involvement has been reported in a Swedish family with ARVC, and the defect has been tentatively localized to chromosome 10q22.3 The infectious or inflammatory theory maintains that the disease results from previous myocarditis. Inflammatory infiltrates are common in histologic specimens from patients with ARVC ECG The ECG in patients with ARVD/C usuallyshows sinus rhythm, QRS duration 110 ms in lead V1, a terminal deà ¯Ã‚ ¬Ã¢â‚¬Å¡ection within or at the end of the QRS complex (called epsilon wave) in leads V1–V3 (30% of patients), and inversion of T waves in the right precordial leads (50%–70% of patients). Complete right bundle branch block is found in approximately 15% of patients and incomplete right bundle branch block in 18% of patients with ARVD/C. In the presence of right bundle branch block pattern, selective prolongation of the QRS duration in leads V1–V3 compared with lead V6 (25 ms, parietal block) is an important hallmark of ARVD/C. . Additional ECG markers have been reported, such as the ratio of QRS duration in leads V1V2V3 vs V4V5V6 >1.2 and a prolonged S wave upstroke in V1–V3 >55 ms in the absence of right bundle branch block. Arrhythmia Left bundle branch block type VT on ECG, Holter monitoring, or during exercise testing Extrasystoles of more than 200 over a 24-h period. Echocardiography mild to Severe dilatation and reduction of right ventricular ejection fraction with no (or only mild) left ventricular impairment Localised right ventricular aneurysms (akinetic or dyskinetic areas with diastolic bulging) Severe segmental dilatation of the right ventricle. Radioisotope techniques Radionuclide angiography, by showing abnormal right ventricular function with left ventricular involvement, is usefulfor predicting subsequent cardiac death in ARVD/C.Myocardial perfusion scintigraphy allows noninvasive assessment of right ventricular damage in patients with arrhythmias due to ARVD/C This technique may distinguish patients with ARVD/C from those with idiopathic right ventricular outà ¯Ã‚ ¬Ã¢â‚¬Å¡ow tract tachycardias Cardiovascular magnetic resonance imaging This modality allows visualization of the right ventricle, not only anatomically and morphologically but also in functional and à ¯Ã‚ ¬Ã¢â‚¬Å¡ow dynamic terms. Functional ab normalities consist of right ventricular aneurysms, regional thinning, right ventricular dilation, failure of systolic thickening, and impaired global and diastolic right ventricularfunction. Clinical presentation The clinical presentation varies widely because ARVD/C includes a spectrum of different conditions rather than a single identity. Different pathologic processes may manifest a diversity of symptoms, such as fatigue, atypical chest pain, syncope, or acute coronary syndrome .ARVD/C is a disease that may have a temporal progression, and the disease may present differently according to the time of presentation There may be (1) a symptomatic form with transient or sustained ventricular tachycardia of left bundle branch block configuration, although right bundle branch block configuration also can be observed; (2) an asymptomatic form consisting of ventricular ectopic beats (1,000/24 hours); (3) right ventricular failure with or without arrhyth mias; and (4) a masked form in which sudden death, usuallyduring exercise, is the first clinical presentation. Overall, judging the accurate position of the patient on the time scale of the spectrum is difficult, and some patients may remain stable for several decades. Diagnosis A definite diagnosis of ARVD/C is based on histologic demonstration of transmural fibrofatty replacement of right ventricular myocardium at either autopsy or surgery. In 1994, McKenna et al established the criteria for diagnosing ARVD/C in a Task Force report on ARVD/C Criteria for Diagnosis of ARVD/C 1. Family history Major Familial disease confirmed at necropsy or surgery. Minor Family history of premature sudden death (,35 years of age) due to  suspected ARVD/C. Family history (clinical diagnosis based on present criteria). 2. ECG depolarization/conduction abnormalities Major Epsilon waves or localized prolongation (.110 ms) of QRS complex in  right precordial leads (V1–V3). Minor Late potentials on signal-averaged ECG. 3. ECG repolarization abnormalities Minor Inverted T waves in right precordial leads (V2 and V3) in people. 12  years of age and in absence of right bundle branch block. 4. Arrhythmias Minor Sustained or nonsustained left bundle branch block–type ventricular  tachycardia documented on ECG or Holter monitoring or during  exercise testing. Frequent ventricular extrasystoles (.1000/24 h on Holter monitoring). 5. Global or regional dysfunction and structural alterations* Major Severe dilatation and reduction of RV ejection fraction with no or mild  LV involvement. Localized RV aneurysms (akinetic or dyskinetic areas with diastolic  bulgings). Severe segmental dilatation of RV.   Minor Mild global RV dilatation or ejection fraction reduction with normal LV. Mild segmental dilatation of RV. Regional RV hypokinesia. 6. Tissue characteristics of walls Major Fibrofatty replacement of myocardium on endomyocardial biopsy. *Detected by echocardiography, angiography, magnetic resonance imaging,  or radionuclide scintigraphy. Modified from McKenna et al. Therapy Because clinical findings that predict long-term outcomeof patients with ARVD/C are incompletely known, no precise guidelines exist to select patients who should be treated with b-blockers, antiarrhythmic drugs, or a Implantable cardioverter-defibrillator. r. Management of patients with ARVD/C is individualized, and strategies are based on local experience of the different centers. References Siddiq I. Khalil), Amjad Kamal, Shakeel Ahmad Department of Medicine and Cardiology, Almana General Hospital, PO Box 10366,Jubail 31961, Saudi Arabia. Eur J Echocardiography (2004) 5, 394e398. Carol Gemayel, MD*; Antonio Pelliccia, MD† ; Paul D Thompson, MD J Am Coll Cardiol. 2001;38(7):1773-1781.doi:10.1016/S0735-1097(01)01654-0. Cristina Basso, Domenico Corrado, Frank I Marcus, Andrea Nava, Gaetano Thiene Lancet 2009; 373: 1289–1300 University of Padua Medical School, Padua, Italy. Philippine Kià ¨s, MD, Marianne Bootsma, MD, PhD, Jeroen Bax, MD, PhD,  Martin J. Schalij, MD, PhD, Ernst E. van der Wall, MD, PhD Heart Rhythm, Vol 3, No 2, February 2006,Department of Cardiology, Leiden University Medical Centre, Leiden, The Netherlands. Domenico Corrado, Guy Fontaine, Frank I. Marcus, William J. McKenna, Andrea Nava, Gaetano Thiene and Thomas Wichter, Circulation. 2000;101:e101-e106, doi: 10.1161/01.CIR.101.11.e101 Frank R, Fontaine G. Electrocardiologie de quatre cas de dysplasia ventriculaire droite arythmogene. Arch Mal Coeur Vaiss 1978;71:963–972. Rampazzo A, Nova A, Malacrida S, Beffagua G, Bauce B, Rossi V, et al. Mutation in human desmoplakin domain binding to plakoglobin causes a dominant form of arrhythmogenic right ventricular dysplasia. Am J Hum Genet 2002;71(5):1200e6 Bauce B, Rampazzo A, Basso C, Bagattin A, Daliento L, Tiso N, et al. Screening of ryanodine receptor type 2 mutations in families with effort induced polymorphic ventricular rhythmias and sudden death: early diagnosis of asymptomatic carrier. JACC 2002;40(2):341e9.