Evidence Of Right Ventricular Hypertrophy Research Articles

Abnormal fibrinolysis in familial pulmonary hypertension

The familial occurence of pulmonary hypertension is well documented, but the pathogenesis of this disease remains relatively obscure. Recurrent pulmonary embolization with impaired fibrinolytic mechanisms has been postulated as a possible etiologic factor. Data have been obtained from 10 members of a kindred comprising 4 generations. Of the 10, 5 have had electrocardiographic evidence of right ventricular hypertrophy. Of the five, four underwent cardiac catheterization and were found to have pulmonary hypertension. Coagulation studies were made in 7 of the 10 members. Factors 5, 7, 8, 9, 10, 12, antithrombin 3, plasminogen, platelet aggregation, fibrinogen and antiurokinase were within normal limits. In all these seven and in one additional family member, antiplasmin levels were abnormally elevated (p < 0.001). These findings suggest that the increased incidence of pulmonary hypertension in this family may be related to an impaired ability to lyse postulated, but not documented, recurrent pulmonary microemboli.

Right ventricular anomalous muscle bundle. Clinical and laboratory presentation and natural history.

Eighteen patients with right ventricular anomalous muscle bundles associated with ventricular septal defect and one patient with isolated anomalous muscle bundle were studied. The clinical differentiation of these patients from those with isolated ventricular septal defects or tetralogy of Fallot was difficult. Eleven patients were asymptomatic at the time of diagnosis; eight had various degrees of dyspnea on exertion, with three of these having cyanosis. A physiologically split second sound with a pulmonic component of normal intensity and a diffuse thrill and holosystolic murmur maximal at the lower left sternal border suggest the diagnosis. Chest X-rays and electrocardiograms usually show evidence of right ventricular hypertrophy, but may suggest left ventricular hypertrophy in the presence of a large left-to-right shunt. However, the diagnosis is best made by cardiac catheterization with measurement of a pressure gradient in the body of the right ventricle and by selective angiography with the demonstration of a wedge-shaped filling defect in the right ventricle. Progressive obstruction by the muscle bundle occurred in four of seven patients who had repeated catheterization associated with the development of electrocardiographic changes of right ventricular hypertrophy. To date, 11 patients have had surgery; one died before surgery; and surgery is being planned for the remaining patients.

The vectorcardiogram in mitral valve disease.

The Frank system vectorcardiogram has been studied in 61 patients with severe mitral valve disease to determine the value of the vectorcardiogram in the recognition of the relative degree of left and right ventricular hypertrophy in this situation. The appearance of the usual evidence of right ventricular hypertrophy is delayed in mitral valve disease by the vertical electrical position of the heart which may be due to alterations in the intrathoracic electrical field produced by left atrial enlargement. Voltage criteria for the recognition of isolated left or right ventricular hypertrophy in the vectorcardiogram are not applicable to combined ventricular hypertrophy in mitral valve disease. The present analysis is based on the spatial pattern of the QRS loop. The vectorcardiograms show a continuous gradation from posterior to anterior direction, the extremes indicating dominant left and right ventricular hypertrophy, respectively. Five groups are recognized from the appearance in the horizontal plane. Long posterior loops (Fig. 1) are associated with severe left ventricular hypertrophy, open posterior loops (Fig. 2) with left ventricular dominance, and wide posterior loops (Fig. 3) with moderate hypertrophy of both ventricles. Wide crossed loops (Fig. 4) indicate right ventricular dominance, and anterior clockwise loops (Fig. 5) are found with severe right ventricular hypertrophy. The vectorcardiogram rarely showed large QRS voltages in left ventricular hypertrophy, though these changes were often evident in the conventional electrocardiogram. The vectorcardiogram appeared to be more successful than the electrocardiogram in the recognition of severe right ventricular hypertrophy. An unusual rightwards displacement of the QRS loop was found in patients with tricuspid valve disease. It is concluded that the vectorcardiogram gives useful additional information for the recognition of ventricular hypertrophy that is not evident in the conventional electrocardiogram in mitral valve disease.

The Frank vectorcardiogram in coal miner's pneumoconiosis

Summary The relationship of the Frank vectorcardiogram to right ventricular hypertrophy in 22 coal miners with simple pneumoconiosis was investigated. Assessment of subjects without overt evidence of right ventricular enlargement was performed to delineate initial hemodynamic changes in the right ventricle as reflected in the vectorcardiogram. The parameters chosen failed to show evidence of right ventricular hypertrophy when right ventricular peak systolic pressures ranged from 20–38 mm.Hg. The results indicate that anatomic right ventricular enlargement is detected in the vectorcardiogram after pressure overloading of the right ventricle and not after the earlier stage of volume overloading.

Roentgenology of tetralogy of Fallot

If the patient is cyanotic and has EKG evidence of right ventricular hypertrophy, tetralogy can be suggested from the plain chest film. The characteristic plain film findings are a slightly enlarged heart with an elevated apex, a prominent aorta, an inconspicuous pulmonary artery and decreased pulmonary vascularity. Helpful associated findings are a right aortic arch and disproportionate decrease in left pulmonary vascularity. If the heart is large, an additional anomaly, especially atrial defect, should be suspected. Angiography is often needed to distinguish tetralogy from pseudotruncus, truncus, transposition, single ventricle and double outlet right ventricle. Angiography is vital for alerting the surgeon to the anatomy of the obstruction. Obstruction to right ventricular outflow may be demonstrated at any one or combination of five levels: the infundibulum, pulmonary valve, valve ring, main pulmonary artery or left pulmonary artery.

Partially obstructed total anomalous pulmonary venous return

Three cases of partially obstructed total anomalous pulmonary venous return are described to illustrate the plain radiographic findings. There are nodular and reticular changes in the lung fields due to pulmonary congestion and oedema but the heart is usually normal in size and shape. The diagnosis should always be considered in cyanosed dyspnoeic newborn infants showing this radiological picture and can be confirmed by finding clinical evidence of right ventricular failure and electrocardiographic evidence of right ventricular hypertrophy. Right heart angiocardiography will demonstrate the obstructed anomalous venous drainage.

Supravalvular mitral stenosis

Two children with suprawalvular mitra stenosis are reported. The first child, in addition to his cardiac malformation, had a perculiar facies, musculoskeletal deformities, and genitourinary anomalies. The clinical features were severe retardation of growth, microcytic hypochronic anemia, loud midsystolic ejection click over the pulmonary area, and electrocardiographic evidence of right ventricular hypertrophy. The second patient had intractable congestive heart failure, progressive cardiac enlargement, and severe right ventricular hypertrophy on electrocardiogram. In both patient, the angiocardiograms were found to be diagnostic in that showed shelflike structure above the mitral valve.

Mitral stenosis: Hemodynamic, electrocardiographic, and vectorcardiographic studies

The data of transseptal left heart and right heart catheterization were correlated with the phonocardiographic, electrocardiographic, and vectorcardiographic findings in 75 patients with significant mitral stenosis. Measurement of the rate of the “y” descent in the first tenth of a second after the opening of the mitral valve was helpful in detecting the presence of significant mitral stenosis. In the absence of tachycardia, the value of the formula P 1-P 2 MLAP was 0.3 or less among patients who had predominant mitral stenosis. No significant difference was seen between patients with normal sinus rhythm and those with atrial fibrillation. In the 54 available phonocardiograms, Q-1 minus 2-O.S. was equal to or greater than 0 in all but 7 patients. The electrocardiograms revealed evidence of right ventricular hypertrophy in 26 instances, whereas the vectorcardiograms revealed evidence of right ventricular hypertrophy in 31 instances. Forty-one patients had neither electrocardiographic nor vectorcardiographic evidence of isolated right ventricular hypertrophy. Both the electrocardiogram and vectorcardiogram failed to show patterns typical of right ventricular hypertrophy in 15 patients despite the significantly elevated resting right ventricular pressure. There were 9 patients who had posterior displacement of the QRSsÊ loop.

HYPOTHYROIDISM AND ALVEOLAR HYPOVENTILATION.

THE PATIENT with a hypoventilation syndrome1generally complains of easy fatigability, hypersomnolence, and morning headaches and exhibits irritability and mental deterioration. Dyspnea is rarely prominent unless lung disease is present. On examination, tremor, twitching, cyanosis, and irregular respiration may be observed. The irregularity in respiration is particularly apparent during sleep. There may be evidence of right ventricular hypertrophy which can be confirmed by roentgenograms of the chest and/or the electrocardiogram. Polycythemia without leukocytosis or thrombocytosis and an elevated serum bicarbonate are common. The essential finding is an elevated arterial carbon dioxide tension (paCO2). Although hypoxemia is usually present, normal arterial oxygen tensions may be recorded if the patient has hyperventilated immediately prior to the study. With such an increase in ventilation, hypoxemia is reversed quickly, but the carbon dioxide retention is corrected more slowly. The etiology of this syndrome is varied (Fig 1). Most frequently it is the

Underdeveloped right ventricle and pulmonary stenosis ∗

There is a poorly documented cyanotic congenital malformation in which moderate underdevelopment of the right ventricle and hypoplasia of the tricuspid valve ring occur in association with pulmonary stenosis. Four patients with this malformation had characteristic signs which allow the diagnosis to be made on clinical grounds. Although they presented some findings consistent with severe pulmonary stenosis, in no case was there more than a slight right ventricular lift; the electrocardiogram showed little or no evidence of right ventricular hypertrophy; and in 3 cases splitting of the second heart sound behaved paradoxically with respiration. Cardiac catheterization data before and after correction of the malformation indicate that the right-to-left shunt at atrial level is caused by the abnormal filling resistance of the small right ventricle. The condition can be effectively treated by pulmonary valvotomy with cardiopulmonary bypass, excision of trabeculation in the right ventricle, and closure of the interatrial communication.

A comparative study of prosthesis applied to the outflow tract of the right ventricle

1. 1. A number of different kinds of prosthesis were inserted in the outflow tract of the right ventricles of fifty dogs. They were observed up to one year after surgery. 2. 2. Woven Teflon ® with its inner surface covered with autogenous pericardium proved the most satisfactory prosthesis. Autogenous pericardium, woven Teflon alone and diaphragmatic fascia follow in order as to their observed satisfactory response. 3. 3. Homogeneous aortas were the easiest to manipulate and satisfactory immediately after the surgery, but were unsatisfactory in the later periods. The application of this graft for clinical use is not recommended. 4. 4. Free transplantations of muscle tissue of diaphragm or chest wall were not satisfactory and have no clinical value. 5. 5. Five out of twenty-one dogs studied electrocardiographically showed evidence of right ventricular hypertrophy, believed caused by pulmonary valvular insufficiency.

The electrocardiogram in chronic bronchitis with generalized obstructive lung disease: Its relation to ventilatory function

The electrocardiogram has been studied in an autospy series of 30 patients with chronic bronchitis and obstruction of airways (one form of generalized obstructive lung disease), and in a clinical series of 58 patients with this disease. In the clinical series an analysis was made of the relationship between the electrocardiogram and the one-second forced expiratory volume (F.E.V. 1.0). P pulmonale and electrocardiographic evidence of right ventricular hypertrophy are uncommon until the F.E.V. 1.0 is less than 45 per cent of predicted normal. It is at approximately this point that ventilatory capacity becomes inadequate to maintain normal blood gases. Positional changes in the P wave axis occur when ventilatory capacity is relatively well preserved and are believed to be positional in origin due to the increased residual volume of the lungs. Left ventricular hypertrophy unexplained by hypertension or myocardial ischemia was found in half of the autopsy cases. There was often no electrocardiographic evidence of its presence. Unexplained T wave changes are also common. Both these changes are thought to result from hypoxemia.

The electrocardiogram in diffuse interstitial disease of the lung and its relation to pulmonary function

The electrocardiogram has been studied in 45 cases of diffuse interstitial disease of the lungs, 21 with asbestosis and 24 with chronic diffuse interstitial fibrosis of unknown etiology. Seven patients had electrocardiographic evidence of right ventricular hypertrophy; three P pulmonale alone; and one both. The presence of these changes was related to the diffusing capacity since the majority occurred in patients in whom the D co was less than 40 per cent of normal. The P wave axis was usually normal. This finding is in contrast to the findings in chronic bronchitis with obstruction of airways in which the P wave axis is often +80 ° or more. It is suggested that the increase in residual volume of the lungs in the latter condition may account for this difference.

Mild pulmonic stenosis: a clinical and hemodynamic study of eleven cases.

Article1 May 1960MILD PULMONIC STENOSIS: A CLINICAL AND HEMODYNAMIC STUDY OF ELEVEN CASESSTEPHEN M. AYRES, M.D., DANIEL S. LUKAS, M.D.STEPHEN M. AYRES, M.D.Search for more papers by this author, DANIEL S. LUKAS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-52-5-1076 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptWith recent widespread use of cardiac catheterization as a diagnostic tool, it has become increasingly apparent that isolated pulmonic stenosis, uncomplicated by defects of the septum, is a relatively common congenital anomaly. Of 750 patients with congenital heart disease in whom a definite diagnosis was established either clinically or by catheterization, Wood1 found that 13% had this anomaly. The older autopsy data are at variance with this experience. Abbott2 reported only nine examples of the condition in her series of 1,000 autopsied cases. Taussig,3 writing in 1947, described it as an extremely rare entity.In 1949 Greene and co-workers4could...Bibliography1. WoodMagidsonWilson POPA: Ventricular septal defect with a note on acyanotic Fallot's tetralogy, Brit. Heart J. 16: 387, 1954. CrossrefMedlineGoogle Scholar2. Abbott ME: Atlas of congenital cardiac disease, 1936, American Heart Association, New York. Google Scholar3. Taussig HB: Congenital malformations of the heart, 1947, The Commonwealth Fund, New York, p. 175. Google Scholar4. GreeneBaldwinBaldwinHimmelsteinRobCournand DGEdJSACEA: Pure congenital pulmonic stenosis and idiopathic dilatation of the pulmonary artery, Am. J. Med. 6: 24, 1949. CrossrefMedlineGoogle Scholar5. JoosYuLovejoyNyeSimpson HAPNFWREJH: Clinical and hemodynamic studies of congenital pulmonic stenosis with intact ventricular septum, Am. J. Med. 17: 6, 1954. CrossrefMedlineGoogle Scholar6. SobinCarsonJohnsonBaker SSMJJLCR: Isolated pulmonary stenosis, Am. Heart J. 48: 416, 1954. CrossrefMedlineGoogle Scholar7. GotzscheEskildsenHansen HPAT: Isolated pulmonary stenosis, Acta med. scandinav. 139: 431, 1951. CrossrefMedlineGoogle Scholar8. Campbell M: Simple pulmonary stenosis. Pulmonary valvular stenosis with a closed ventricular septum, Brit. Heart J. 16: 273, 1954. CrossrefMedlineGoogle Scholar9. SilvermanNadasWittenborgGoodaleGross BKASMHWTRE: Pulmonary stenosis with intact ventricular septum, Am. J. Med. 20: 53, 1956. CrossrefMedlineGoogle Scholar10. Torner-SolerMorato-PortellBalaguer-Vintro MJMI: Pulmonary stenosis with closed ventricular septum, Am. Heart J. 53: 213, 1957. CrossrefMedlineGoogle Scholar11. DowLevineElkinHaynesHellomsWhittenbergerFerrisGoodaleHarveyEppingerDexter JWHDMFWHKJWBGWTWDECL: Studies of congenital heart disease. IV. Uncomplicated pulmonic stenosis, Circulation 1: 267, 1950. CrossrefMedlineGoogle Scholar12. BlountKomesuMcCord SGSM: Asymptomatic isolated pulmonary stenosis, New England J. Med. 248: 5, 1953. CrossrefMedlineGoogle Scholar13. LukasDotter DSCT: Modifications of the pulmonary circulation in mitral stenosis, Am. J. Med. 12: 639, 1952. CrossrefMedlineGoogle Scholar14. GorlinGorlin RSG: Hydraulic formula for calculation of the area of the stenotic mitral valve, other cardiac valves, and central circulatory shunts. I. Am. Heart J. 41: 1, 1951. CrossrefMedlineGoogle Scholar15. LeathamVogelpoel AL: The early systolic sound in dilatation of the pulmonary artery, Brit. Heart J. 16: 21, 1954. CrossrefMedlineGoogle Scholar16. AlimurungLesterNadasMassell MMGJASBF: The unipolar precordial and extremity electrocardiogram in normal infants and children, Circulation 4: 420, 1951. CrossrefMedlineGoogle Scholar17. SokolowLyon MP: The ventricular complex in right ventricular hypertrophy as obtained by unipolar precordial and limb leads, Am. Heart J. 38: 519, 1951. Google Scholar18. AbrahamsWood DGP: Pulmonary stenosis with normal aortic root, Brit. Heart J. 13: 519, 1951. CrossrefMedlineGoogle Scholar19. ReinholdNadas JDAS: The role of auscultation in the diagnosis of congenital heart disease, Am. Heart J. 47: 405, 1954. CrossrefMedlineGoogle Scholar20. LeathamWeitzman AD: Auscultatory and phonocardiographic signs of pulmonary stenosis, Brit. Heart J. 19: 303, 1957. CrossrefMedlineGoogle Scholar21. JohnsonFerrerWestCournand JBMIJRA: The relation between electrocardiographic evidence of right ventricular hypertrophy and pulmonary arterial pressure in patients with chronic pulmonary disease, Circulation 1: 536, 1950. CrossrefGoogle Scholar22. BlountMunyanHoffman SGEAMS: Hypertrophy of the right ventricular outflow tract, Am. J. Med. 22: 784, 1957. CrossrefMedlineGoogle Scholar23. Brock R: Congenital pulmonary stenosis, Am. J. Med. 12: 706, 1952. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, N. Y.*Received for publication January 26, 1960.From the Department of Medicine and Cardio-Pulmonary Laboratory, New York Hospital-Cornell Medical Center, New York, N. Y.†Supported by grants from the National Heart Institute (H-3918), The American Heart Association and New York Heart Association.Requests for reprints should be addressed to Daniel S. Lukas, M.D., 525 East Sixty-eighth Street, New York 21, N. Y. 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The electrocardiogram in pulmonary stenosis with intact septa

The electrocardiograms of 100 patients with pure pulmonary stenosis studied by right heart catheterization were reviewed. For analysis, the subjects were grouped according to the systolic pressure in the right ventricle. The majority of patients showed evidence of right ventricular hypertrophy, the frequency increasing with the severity of the stenosis. No diagnostic pattern was established. The severity of the stenosis and the height of systolic pressure in the right ventricle cannot be gauged in the individual patient by the character of the tracing.

The Electrocardiogram and Vectorcardiogram in Right Ventricular Hypertrophy and Right Bundle Branch Block

It is the purpose of this paper to appraise certain applications of the electrocardiogram and vectorcardiogram to the diagnosis of right ventricular hypertrophy. The problems that are encountered in this area of electrocardiography are created by the similarity of the records seen in recognizable right ventricular hypertrophy to those that occur in normal infants and to those that are seen in right bundle branch block. The not infrequent failure of any kind of record of the cardiac potentials to reveal recognizable evidence of right ventricular hypertrophy when in fact it is proved to exist adds further confusion to this constellation of difficulties. For the purpose of this paper it has been deemed practical to ignore almost completely problems created by the coexistence of left ventricular hypertrophy and other conditions occurring frequently in rheumatic heart disease (which contribute to the difficulties that are encountered in this area of electrocardiography and vectorcardiography). Our material consists of 1) serial observations on a large group of normal infants some of whom are now five years of age; 2) observations of individuals with congenital heart disease; 3) observations of normal young adults; and 4) observations on an individual with varying degrees of right bundle branch block. In addition we have reviewed observations of other authors that fall in the first three of the above categories. At the outset it is necessary to clarify certain matters that frequently appear to become confused in the literature. In the individual case entirely satisfactory proof of the presence of right ventricular hypertrophy can be obtained only at autopsy. The inference that the right ventricle is hypertrophied when the intraventricular pressure is high and more especially, the inference that it is not hypertrophied when the intraventricular pressure is normal, must be rejected because of the lack of close correlation between the level of the intraventricular pressure and the degree of hypertrophy found at autopsy in individual cases. On the other hand, when one encounters a large group of cases of the same cardiac condition in which a characteristic electrocardiogram is observed, it is not illogical to relate the electrocardiographic findings in question to the presence of that condition. However, the mechanism by which the cardiac condition produces the characteristic electrocardiographic changes may still be open to question. The form of the electrocardiogram may depend upon alterations of the cardiac potentials due to such a structural change as right ventricular hypertrophy or, on the other hand, it may result from a func

Some clinical notes on patients with mitral valvular disease who have had mitral valvuloplasty. Part II

Some clinical notes on patients with mitral valvular disease who have had mitral valvuloplasty. Part II

Electrocardiographic Diagnosis of Ventricular Hypertrophy in the Presence of Right Bundle-Branch Block

Forty-nine autopsied cases of complete and incomplete right bundle-branch block were studied with correlation of the electrocardiographic and anatomic diagnosis of ventricular hypertrophy. Twenty-six (53 per cent) of the cases showed anatomic evidence of right ventricular hypertrophy. The cases were studied for right ventricular hypertrophy according to the criteria of Barker and Valencia and of Milnor. Milnor's criteria resulted in frequent overdiagnosis while those that met Barker and Valencia's criteria usually but not invariably showed anatomic right ventricular hypertrophy. The electrocardiographic diagnosis of left ventricular hypertrophy was masked by the bundle-branch block in anatomically proved cases.

The electrocardiogram in atrial septal defect: A study of twenty-four cases, with observations on the RSR'-V1 pattern

1. 1. In twenty-four patients with uncomplicated atrial septal defects, we have examined the electrocardiographic findings and their relation to the location and size of the defect, the degree of pulmonary hypertension and the ratio of pulmonic to systemic blood flow. The anatomic diagnosis was confirmed at autopsy in seven cases and at operation in seventeen cases. The septal defect was defined as persistent ostium primum in six cases and persistent ostium secundum in eighteen cases. 2. 2. Electrocardiographic evidence of right ventricular hypertrophy was present in twenty-two cases. Right axis deviation appeared in eighteen cases. 3. 3. Three patients had a persistent ostium primum, a cleft mitral leaflet and left as well as right ventricular hypertrophy, presumably due to mitral insufficiency. The electrocardiograms in these cases showed left axis deviation, with signs of both left and right ventricular hypertrophy. 4. 4. One patient, aged fifty-two years, with a persistent ostium primum, normal mitral valve and autopsy evidence of coronary insufficiency due to atherosclerosis, showed left axis deviation and complete right bundle branch block. 5. 5. An RSR'-V1 pattern was present in fifteen patients (63 per cent), two of whom had a QRS duration prolonged beyond 0.12 second. This confirms previous reports that this pattern occurs much more often with atrial septal defects than with other clinically similar lesions. The relatively high incidence of this pattern with any lesion which leads to right ventricular hypertrophy, however, and the lack of clear evidence as to its etiology suggest that it might be well to abandon the term “incomplete right bundle branch block” for the present. 6. 6. Prolongation of the PR interval was present in four of six patients with persistent ostium primum, and two of eighteen patients with persistent ostium secundum.

The ventricular patterns in the right precordial leads in mitral stenosis

1. 1. Routine 12-lead electrocardiograms were recorded in 173 patients with mitral stenosis, 136 of whom had right ventricular hypertrophy assessed clinically and radiologically. In fifty-five of these patients Leads V 1 and V 6 were recorded synchronously. 2. 2. A great variety of QRS patterns were obtained from precordial Lead V 1 and these fell into five groups: 2.1. A. Clinical and radiologic evidence of right ventricular hypertrophy was present in sixty-seven of the 104 patients who showed normal rS or S complexes in Lead V 1. 2.2. B. Rs complexes or single R waves occurred in Lead V 1 in twenty-one patients, all of whom had clinical evidence of right ventricular hypertrophy which was confirmed radiologically in fifteen cases. There was no relationship between the height of the R wave and the time of onset of the intrinsicoid deflection in these twenty-one cases, and the criteria for the electrocardiographic diagnosis of right ventricular hypertrophy were not completely fulfilled in any. 2.3. C. RSR′ patterns were obtained in thirty-six patients, all of whom had clinical and radiologic evidence of right ventricular hypertrophy, but in twenty the form of the complexes was similar to that sometimes obtained in normal subjects. In all patients there was delay in the intrinsicoid deflection and in two right bundle branch block was present. 2.4. D. A qR complex was recorded from V 1 in nine patients, all of whom showed clinical and radiologic evidence of right ventricular hypertrophy. Delay in the onset of the intrinsicoid deflection occurred in all. 2.5. E. Polyphasic complexes occurred in three patients who showed right ventricular hypertrophy on clinical and radiologic examination. 3. 3. It is probable that in many patients in this series, the degree of right ventricular hypertrophy was insufficient to produce forces capable of outweighing those incident to simultaneous left ventricular excitation. The absence of classical electrocardiographic signs of right ventricular hypertrophy in any patient in Groups 1 and 2 of the present series suggests that there is a need for the clear definition of the electrocardiographic signs of right ventricular hypertrophy in mitral stenosis. 4. 4. The lack of correlation between the height of the R wave and the time of onset of the intrinsicoid deflection in the V 1 Rs and R complexes suggests that delay in onset of the intrinsicoid deflection is not a reliable sign of right ventricular hypertrophy in mitral stenosis. 5. 5. Synchronous leads showed an essential similarity between RSR′ and qR complexes in Lead V 1. Evidence is presented to show that a qR pattern in right precordial leads in patients with mitral stenosis is not due to potentials derived from the left ventricle. 6. 6. The tall secondary R′ waves of RSR′ complexes and the R waves of qR complexes were considered to be due to the slow passage of the stimulus through the wall of the right ventricle when stimulation of the left ventricle was almost complete. It is suggested that in mitral stenosis the slow passage of the stimulus is related to the type of thickening of the right ventricular wall, which in this disease consists largely of hypertrophied trabeculae.