Annotations

Recurrence of Symptoms Following Mitral Valvulotomy

Mitral valvulotomy is firmly established as effective therapy for mitral stenosis when mechani- cal obstruction is the major physiologic defect. Approximately 70 per cent of well-selected pa- tients can be expected to have subjective improvement after this procedure. It is becoming apparent, however, that improvement is often not sustained at its initial level. In a large series of patients who were followed up for 2 to 9 years by Ellis and associates,’ 30 per cent of those who were initially improved for at least 1 year showed subsequent deterioration, and a recent series reported upon from Russia has shown similar results. 2 The patients who were followed up postoperatively by Bruce and his colleagues3 have shown a perceptible diminution in the physical fitness index during the third year after operation.

There are multiple reasons for progressive cardiac disability after mitral valvulotomy. In the series studied by Ellis’ the percentage of mitral insufficiency found or produced at operation, and the percentage of technically unsatisfactory operations were higher among those who showed deterioration than among those who maintained improvement. However, the fact that many patients with mitral insufficiency or unsatisfactory procedures did maintain improvement in- dicates these are not the only factors associated with deterioration. Recurrent rheumatic fever was suspected in some of the patients. Restenosis of the valve undoubtedly occurs, but seems to be, after 10 years of experience with valvulotomy, a relatively rare phenomenon when a technically satisfactory operation has been performed. Restenosis is certainly much more rare than recurrence of symptoms.

Hemodynamic data obtained after valvulotomy have been helpful in understanding the recurrence of symptoms in some patients. Resting pulmonary arterial and wedge pressures are usually significantly reduced by valvulotomy, but these pressures may rise strikingly with exer- cise.486 This is often true even in patients who have experienced excellent symptomatic results. Left heart catheterizationa*’ usually reveals a reduction in the pressure gradient across the mitral valve, but this gradient is seldom abolished. The studies of Donald and co-workers4 indicate that cardiac output in relation to oxygen consumption remains below normal, both at rest and during exercise. Thus, it appears that valvulotomy even when successful in relieving symptoms does not necessarily restore normal hemodynamics. As long as the heart and lungs continue to function under an increased pressure load, progressive disability in some patients is to be expected,

It is extremely important to differentiate patients with recurrence of symptoms due to re- stenosis who may be improved by additional surgery from those with recurrence of symptoms due to mitral insufficiency, rheumatic myocarditis, or the progression of cardiac disease due to abnormal hemodynamics despite a “surgically” satisfactory valvulotomy. Left heart catheterization with demonstration of a significant gradient across the mitral valve is the most satisfactory method available for identifying cases of restenosis. For this purpose, base-line studies of the mitral gradient shortly after valvulotomy would be extremely valuable; however, the risk of this procedure must be considered in relation to the frequency of the problem of restenosis of the valve.

Robert Gilbert, M.D. Syracuse, N. Y.

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ANNOTATIONS 659

REFERENCES

1. Ellis, L. B., Harken! D. E., and Black, H.: A Clinical Study of 1,000 Consecutive Cases of Mitral Stenosis Two to Nine Years After Mitral Valvuloplasty, Circulation 19:803, 1959.

2. Putov, N. V.: Late Results of Surgical Treatment in Patients With Mitral Stenosis, Vestnik khir. 83:11, 1959 (abstracted in J.A.M.A. 172:387, 1960).

3. Bruce, R. A., Merendino, K. A., Pampush, J. J., Bergy, G. G., and Brock, L. L.: Functional Evaluation of Mitral Valvulotomy, Am. J. Med. 20:755, 1956.

4. Donald, K. W., Bishop, J. M., Wade, 0. L., and Wormald, P. N.: Cardiorespiratory Function Two Years After Mitral Valvotomy, Clin. SC. 16:325, 1957.

5. Lyons, W. S., Tompkins, R. G., Kirklin, J. W., and Wood, E. H.: Early and Late Hemody-

6. namic Effects of Mitral Commissurotomy, J. Lab. & Clin. Med. 58:499, 1959.

Samet, P., Litwak, R. S., Bernstein, W. H., Frerer, E. M., and Silverman, L. M.: Clinical and Physiologic Relationships in Mitral Valve Disease, Circulation 19517, 1959.

7. Coelho, E., Bordalo e Sa, A., Maltez, J., de Pavia, E., Amram, S. S., Luiz, A. S., Coelho, E. M., and Tavares, V.: Postoperative Physiopathologic Results in Mitral Stenosis, =Im. J. Cardiol. 4:163, 1959.

The Electrocardiographic Diagnosis of Right Ventricular

Hypettrophy: Correlation With the Anatomic Findings

The ability to diagnose right ventricular hypertrophy (RVH) from the electrocardiogram is of considerable clinical importance in cases of congenital and acquired heart disease. Just how reliable and specific are the currently employed electrocardiographic criteria for the diagnosis of anatomic RVH? If there is electrocardiographic RVH, can it be concluded that there is definite anatomic RVH? If the electrocardiogram does not exhibit RVH, can significant anatomic hyper- trophy of the right ventricle be excluded?

The answers to these questions are best secured from electrocardiographic-pathologic corrcla- tion studies.1

The more commonly employed electrocardiographic criteria for RVH may be listed: right axis deviation (RAD) of +llO” or more; R in Lead Vr 7 mm. or greater; R in Lead Vr plus S in Lead Vs (V,) greater than 10.5 mm.; R/S ratio greater than 1 in Lead Vr (V~R, V4a); R/S ratio in Lead Vs (V,) of 1 or less; delay in the onset of the intrinsicoid deflection in Lead Vr (Via) 0.035 to 0.055 sec.; S-T segment depression and T-wave inversion in right precordial leads; R in Lead aVa of 5 mm. or greater; Q/R ratio in Lead aVR of 1 or less; qR pattern in Lead Vr (Vaa); rSR’ in Lead Vr (V~R) with R’ of 10 mm. or greater (QRS duration less than 0.12 sec.).

Because of the normal right ventricular dominance in infancy and early childhood, the electro- cardiographic criteria for RVH in this age group must be modified somewhat. The absolute height of the R waves and the R/S ratio in the right precordial leads, as listed above, cannot be employed. RAD must be +120” or greater to be significant in this age group. Positive T waves in the right precordial leads in infants, after the first 48 hours of life, are indicative of RVH.

The accuracy of the electrocardiographic diagnosis of RVH has ranged from 23 to 100 per cent in various autopsy-controlled series. The diagnosis of RVH is most accurate in cases of congenital heart disease (86 to 100 per cent), moderately accurate in cases of RVH secondary to mitral stenosis and car pulmonale (7.5 per cent or less), but commonly undetected in cases of right heart enlargement secondary to left ventricular failure.1 The frequently mare striking evidence of electro- cardiographic RVH in congenital than in acquired heart disease may be related to several factors: RVH develops at an earlier age, often when physiologic right ventricular dominance is still present; the right ventricular pressures and pulmonary vascular resistances are often greater; the degree of anatomic RVH is often more marked; left ventricular enlargement is commonly not present: there may be an actual increase in the number of myocardial fibers (hyperplasia).‘*z

No correlation has been found by most workers between right ventricular thickness, total heart weight, left ventricular/right ventricular (LV/RV) thickness ratio, and any specific electro- cardiographic pattern of RVH.’ It has been found, however, that electrocardiographic evidence of RVH occurs more frequently as the thickness of the right ventricle increases3 Carouso and