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The frequent association of pulmonary hypertension with symptomatic mitral stenosis has stimulated much investigation concerning its significance and the mechanism of its production. Two types are now recognized: passive hypertension, where the increased pressure in the left atrium and pulmonary veins and capillaries produced by the stenosed mitral valve is transmitted to the pulmonary artery; and active hypertensions, where much higher levels of pulmonary arterial pressure are due to an increased vascular resistance in the lungs (Bayliss et al., 1950a;Eliasch, 1952;Lewis et al., 1952). The causes of this increase in vascular resistance are not fully understood, but Parker and Weiss (1936), Larabee et al. (1949), Henry (1952), and Harrison (1953) have found thickening of the walls of the small pulmonary arteries, while Dexter et al. (1950), Holling (1952), and Ball et al. (1952 have suggested that reversible vasoconstriction may also occur. Angio-cardiography has demonstrated narrowing and irregularity of the smaller pulmonary arteries in patients with symptomatic mitral stenosis (Goodwin et al., 1952;Actis-Dato et al., 1952). The present investigation was undertaken to determine the significance of these changes, whether they could be detected on plain radiographs, and whether they were proportional to the pulmonary arterial pressure. The value of the symptoms, physical findings, and electrocardiographic signs, in estimating pulmonary arterial pressure was assessed by comparing them with the pressures measured by cardiac catheterization. An attempt was made to determine which of these methods provided the best estimate of the pressure. METHODSFifty-one patients suffering from mitral stenosis of varying severity were studied. The series included patients with normal pulmonary arterial pressures and with all degrees of pulmonary hypertension. Thirty-five patients had aortic valve disease, but in all these mitral valve disease was the dominant lesion. Mitral incompetence, in association with stenosis, was diagnosed in 10 subjects, and in 4 of these was thought to be of greater hlmodynamic importance than stenosis. One patient had systemic hypertension in addition to mitral stenosis. Dyspncea was graded according to the classification of the New York Heart Association (1939).The clinical classification of pulmonary hypertension was as follows. Grade 0: normal left ventricular impulse, normal second sound in the pulmonary area. Grade I: tapping impulse, gentle sternal lift, narrow splitting of the second heart sound with slight accentuation of the pulmonary element. Grade II: tapping impulse, marked sternal heave, narrow splitting of the second heart sound with more accentuation of the pulmonary element. A systolic murmur over the pulmonary area and a triple rhythm were not found frequently enough to be of diagnostic value. 393 group.bmj.com on June 4, 2015 -Published by http://heart.bmj.com/ Downloaded from

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The use of the electrocardiogram as an aid in the diagnosis of right ventricular hypertrophy is a comparatively recent advance. It has been suggested that an electrode placed in a similar position to V4 but to the right of the sternum (V4R) would be of additional value in that it would record right ventricular patterns more accurately than the present chest leads. We have been recording this lead (V4R) routinely for the last year and have frequently had difficulty in assessing the significance of the patterns found, mainly because complexes with secondary R waves often occurred in both normal and abnormal tracings. There is no agreed terminology for describing these patterns but the different terms used and the theories underlying them have been comprehensively reviewed by Katz et al. (1950). The complexes have been termed RSR1 or denoted as showing the presence of an " embryonic r wave " or " incomplete right bundle branch block." A more recent suggestion is that the pattern occurs as the result of " defective intraventricular conduction " which may be " focal " or more widespread (Segers, 1949). The confusion in nomenclature is well illustrated by the term " physiological incomplete right bundle branch block" which aptly reflects the uncertainty as to the significance of this type of pattern.It was decided to record V4R in a series of normal subjects in order to determine the variations that might be found. In addition, it was felt that a study of records taken from other positions over the right chest might help determine the significance of complexes with secondary R waves.Material and Methods. Fifty subjects (30 men and 20 women) were studied, their ages ranged from 10 to 75 years. None had symptoms of cardiovascular or pulmonary disease, all had blood pressures within the normal range and their hearts were normal on clinical examination.All the records were taken on an Elmqvist three-channel recorder.The leads taken from the right of the chest were initially V5R, V4R, V3R, and Vl. V5R, V4R, and V3R were recorded with electrodes placed in similar positions to V5, V4, and V3 but to the right of the sternum. At first these leads were recorded in different phases of respiration, but then it was realized that complexes with secondary R waves were more often found when further leads were taken from the intercostal spaces above and below V5R, V4R, V3R, and VI with the patient breathing normally. The standard and unipolar limb leads and V3, VS, and V7 were also recorded in each patient. RESULTSIn V4R, the S wave was always greater than either R deflection; in over half the subjects (52%) the pattern was RSR1 or RSR1S1 and in the remainder was rS. We would stress the necessity of placing the electrode in the correct position, because occasionally we found that small changes in electrode position caused important changes in the configuration of the QRS complex. The incidence of patterns with secondary R waves in the additional leads was also high (Table I) and in 42 of our 50 subjects (84%) RSR1 or RSR1S1 complexes ...