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The acute anatomic and valvular consequences of radiofrequency catheter ablation of accessory pathways were evaluated in 62 patients by means of serial echocardiographic examinations. Semiquantitative assessment of valvular incompetence and classification into one of four grades according to the width and the extension of the jet from the valvular orifice were carried out. Segmental wall motion abnormalities were evaluated semiquantitatively with four grades of severity (normal, hypokinesia, akinesia, or dyskinesia). New echocardiographic abnormalities were observed in five patients. One thrombus on the ventricular aspect of the mitral valve, three hemodynamically insignificant pericardial effusions, and one increase in severity of tricuspid incompetence were found 1 day after radiofrequency catheter ablation. We conclude that echocardiographic changes after radiofrequency ablation of accessory pathways are rare and of minor significance. These findings confirm the safety of the procedure.

A left parasternal lift is usually attributed to right ventricular hypertrophy. In a previous communication,l we have shown that the high-amplitude, late systolic lift of the left parasternal region which occurs in severe mitral incompetence (MI) is due to systolic enlargement of the left atrium (Fig. 6, 0. As a logical follow-up to these studies, we have now investigated the high-amplitude left parasternal lift in severe tricuspid incompetence (TI) to define its precise character. There are several good descriptions of the precordial movement in TL2-* but these are not widely known. The object of this paper is to draw attention to the clinical importance of bedside observation by combined palpation and auscultation of the chest wall. We hope to show that the left parasternal lift of severe TI is of high amplitude, diastolic in time, and has its peak on or about the first heart sound On the other hand, the lift of right ventricular hypertrophy is systolic in time as is the left atria1 lift of mitral incompetence. The instrumental tracings shown are designed only to validate the bedside findings which we consider to be valuable diagnostic pointers.

Two infants with isolated congenital tricuspid incompetence appeared to have associated right ventricular outflow tract obstruction at diagnostic evaluation, including catheterization and cineangiography. One infant died during surgery; the other improved rapidly and survived with medical therapy. We discuss the problem of establishing the presence of patency of the right ventricular outflow tract in infants with massive tricuspid incompetence and outline an approach to the management of infants whose diagnosis remains unclear even after careful evaluation.

Between January, 1963, and June, 1985, 67 patients underwent corrective surgery for this complex anomaly. Symptoms and signs of atrial septal defect were dominant in the majority of subjects. History of rheumatic fever (46%), paroxysmal nocturnal dyspnea (33%), presence of an opening snap, mitral diastolic murmur, or pansystolic murmur provided clinical clues to document associated mitral valve disease. Open mitral valvotomy was accomplished in 39 subjects, while in the remainder (28 subjects) the valve required replacement. Partial anomalous venous connection was encountered in 12 subjects. Recognition and attention to the associated tricuspid incompetence is a high priority, and 21 subjects underwent concomitant annuloplasty. The overall hospital mortality was 13.4%, with no deaths in the last 22 consecutive patients. The period of follow-up ranged from 1 year to 22 years, with a mean +/- SD of 9.34 +/- 6.61 years. We believe, with other authors, that since the hemodynamic and therapeutic considerations are very similar, both the stenotic and regurgitant lesions should be included in the same syndrome.

Four patients of our own observation and 63 cases from the literature were reviewed, illustrating the association of IASD and pericardial effusion, adhesion, or constriction. In three of our four patients, pericardial disease had assumed dimensions of clinical importance or intensified progressive cardiac decompensation. One patient was of particular interest because of unusual persistence of a pericardial friction rub which has been present for now five years. Pericardial disease appears to be relatively common in IASD, as has occasionally been indicated in the literature, and it is probably more frequent than chance relationship could account for. We have suggested that right atrial enlargement and chronic elevation of intra-atrial pressure may play an important, yet ill-defined role in the genesis of pericardial effusion. Recurrent pulmonary infections, common in conditions with augmented pulmonary blood flow, and rheumatic heart disease provide opportunity for pericarditis to develop. This may be an important factor. Chronic heart disease, especially mitral and tricuspid incompetence or stenosis, was frequently seen in the suses reviewed; this may relate to the supposed mechanisms linking IASD and pericardial disease. The condition may be of considerable clinical importance and its recognition is essential for successful management and well-planned surgical intervention.

D I A S T O L E REFERENCES 1. Freedom RM, Culham G, Moss F, Olley PM, Rowe RD. Differentiation of functional and structural pulmonary atresia: role of aortography. Am J Cardiol 1978;41:914. 2. Smallhorn JF, Izukawa T, Benson L, Freedom RM. Noninvasive recognition of functional pulmonary atresia by echocardiography. Am J Cardiol 1984;54:925. 3. Berman W, Whitman V, Stanger P, Rudolph AM. Congenital tricuspid incompetence simulating pulmonary atresia with intact ventricular septum: a report of two cases. AM HEART J 1978;96:655. 4. Silberbach GM, Ferrara B, Berry JM, Einzig S, Bass JL. Diagnosis of functional pulonary atresia using hyperventilation and Doppler ultrasound. Am J Cardiol 1987;59:709. 5. Kutsche LM, Van Mierop LHS. Pulmonary atresia with and without ventricular septal defects: a different etiology and pathogenesis for the atresia in the two types? Am J Cardiol 1983;51:932. 6. Allan LD, Crawford DC, Tynan MJ. Pulmonary atresia in prenatal life. J Am Coll Cardiol 1986;8:1131.

The coupling of the heart beats in digitalis intoxication may be used to demonstrate the expansile nature of the hepatic pulsation of tricuspid incompetence, since ventricular extrasystoles produce pulsations of the liver without corresponding arterial pulsation, with the result that two hepatic pulsations may be felt for each arterial pulsation.

In two patients with chronic rheumatic carditis with mitral stenosis (and in one patient with aortic regurgitation) there were large venous pulsations limited to the base of the neck. These pulsations consisted of very large “a” waves in the phlebogram. It is probable that these pulsations were due to tricuspid stenosis without failure and without dynamically active tricuspid incompetence.

1. 1. Five cases of severe mitral stenosis with associated tricuspid incompetence that masqueraded as mitral insufficiency are presented. 2. 2. They were suspected of having significant mitral insufficiency chiefly because of a loud systolic murmur in the apical area. 3. 3. The systolic murmur which was loudest along the lower left sternal border and xiphoid region, and which increased in intensity on deep inspiration, was due to tricuspid incompetence rather than mitral insufficiency. 4. 4. In addition to the tricuspid murmur, other features commonly present were: atrial fibrillation, advanced right heart failure, loud functional pulmonic murmurs, and other physical evidence of tricuspid incompetence. Cardiomegaly was greater than usual in mitral stenosis because of more advanced right ventricular hypertrophy. 5. 5. At surgery, severe mitral stenosis without insufficiency was discovered, and operation was followed by uniformly good results. 6. 6. They represent a group of incapacitated patients that often are denied surgery for mitral stenosis when they could be benefited.