READERS COMMENTS Disopyramide in Hypertrophic Cardiomyopathy Both articles by Pollick’** erroneously suggest a too prominent role of the outflow tract pressure gradient in the management of patients with hypertrophic obstructive cardiomyopathy. In both the invasive and noninvasive study disopyramide is advocated as an ideal drug for reduction of the left ventricular outflow tract obstruction as represented by a pressure gradient. Both studies strongly suggest that “de-obstruction” of the outflow tract by eliminating the pressure gradient invariably results in a beneficial effect for the heart and the patient. However, neither study yields convincing evidence that the reported beneficial effects can be ascribed only to the reduction of the pressure gradient. First, after disopyramide, systolic emptying does not increase for cardiac output or heart rate; thus stroke volume remains unchanged (Table I, Figure 2A, page 1249: Table II. naee 1250). The same stroke volume of 56 ml is now expelled in a shorter ejection time; however, it is at the expense of a significant reduction in ejection fraction as estimated from the ratio of the preejection period and ejection time in the hemodynamic study (Table II, page 1250). Second, the small decrease in left ventricular end-diastolic pressure may only be appreciated as beneficial in conjunction with a simultaneously measured increase in end-diastolic volume. However, data from Table II (page 12.53)indicate that the end-diastolic volume as calculated from the left ventricular end-diastolic dimension does not increase even despite a supposed reduction in mitral reflux. Third. we314and other@ did find a normal or low systolic wall stress as representative of afterload in hypertrophic cardiomyopathy (HC). Depending on the severity of the pressure gradient, peak systolic wall stress only differs in timing, not in magnitude. Thus we cannot support the suggestion that a reduction of the pressure gradient is followed by a further reduction of a normal ventricular afterload. Fourth, the small but significant increase in exercise duration in the noninvasive study may be ascribed to a more uniform and coordinated pattern of relaxation due to the calcium antagonistic effect of disopyramide rather than to the reduction of the pressure gradient, an effect similar to that of verapamil. In this regard Letters (from the United States) concerning a particular article in the Journal must be received within 2 months of the article’s publication, and should be limited (with rare exceptions) to 2 double-spaced typewritten pages. Two copies must be submitted.

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it would be interesting to investigate the effect of disopyramide in the nonobstructive form of HC. In conclusion. the results of both studies do not permit the focus on the pressure gradient as a prime determinant in left ventricular dysfunction and management of hypertrophic obstructive cardiomyopathy. 2. van der War, MO

Groningen, The Netherlands 15 February 1989 1. Pollick C, Kimball B, Hendersoh M, Wigle ED. Disopyramide in hypertrophic cardiomyopathy I. Hemodynamic assessmentafter intravenous administration. Am J Cardiol 1988,62:

inotrope favorably alters wall stress via a reduction in the pressure gradient. By using disopyramide instead of verapamil, which appears to have a greater effect on the pressure gradient, perhaps all 6 patients would have developed a “nonobstructive” stress curve. Fourth, his point is well taken that there may be other reasons that contribute to the increase in exercise duration such as a more uniform and coordinated left ventricular relaxation. Charlee

i’dlick,

MB

Toronto, Canada 3 March 1989

1248-1251. 2. Pollick C. Disopyramide in hypertrophic car-

diomyopathy II. Noninvasive assessment after oral administration. Am J Cardiol 1988;62; 1252-l 255. 3. Blanksma PK. Pressure-volume and stress-

strain relationshipsin hypertrophic cardiomyouathv. In: Van der Wall E, Lie KI. eds. Recent Viewson Hypertrophic Cardiomyopathy. Dordrecht: Martinus Nijhoff, 1985:53-69. 4. Van der Wall E. Recent views on left ventricular function in hypertrophic cardiomyopathy: hemodynamic concepts and their clinical implications.In: Van der Wall E, Lie KI, eds. Recent Views on Hypertrophic Cardiomyopathy. Dordrecht: Martinus Nijhofj 1985:71-99. 5. Pouleur H, Rousseau MF, van Eyll C, Brasseur LA, Charlier AA. Force-velocity-length relations in hypertrophic cardiomyopathy: evidence of normal or depressed my%ardial contractility. Am J Cardiol 1983;52:813-817.

6. Strauer BE. Myocardial oxygen consump tion in chronic heart disease: role of wall stress, hypertrophy and coronary reserve. Am J Cardiol 1979;44:730-740. REPLY: I thank van der Wall for his interest and comments. First, he remarks that there is a significant reduction in the ejection fraction, which he implies as being harmful although he does not say why. Most of these patients, however, have “supernormal” ejection fractions and disopyramide could be conceived as “normalizing” the ejection fraction. Second, the interpretation of left ventricular compliance from left ventricular end-diastolic pressure alone is clearly somewhat limited. While the exact meaning of the disopyramide-induced decrease in left ventricular end-diastolic pressure is debatable, it is nevertheless presumably of benefit. In contrast, an increase in left ventricular end-diastolic pressure would have been considered deleterious. Third, in his study of 19 patients3 van der Wall clearly showed that 8 of 12 of the obstructive patients had an abnormal wall stress curve (type A), consisting of a definite increase in wall stress after obstruction. Three of 6 patients showed a change in the wall stress curve to a “nonobstructive” (type B) curve after verapamil. Thus I believe that his own data could well be interpreted as suggesting that a negative

THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 65

Magnesium Sulfate Is the Treatment for Torsadeb de Pointes if the Right Dose Is Given We were delighted to read about magnesium as a treatment of ventricular arrhythmias in the report of Rodeni in the recent symposium on magnesium deficiency. In the section “Long QT-Related Arrhythmias,” in the paragraph dealing with the effectiveness of magnesium as a treatment for torsades de pointes, we were surprised to find that we were misquoted by the investigator on a critical point addressing the dose of magnesium that should be used. According to our published data,* magnesium sulfate is a very effective therapy for torsades de pointes. It was administered to 12 patients with this arrhythmia as a 2-g intravenous bolus within 1 to 2 minutes. In 9 patients the torsades de pointes was immediately abolished after the initial dose. Three other patients who did not respond completely to the first magnesium sulfate bolus received a second bolus of 2 g within 5 to 15 minutes after the first bolus. Most patients received additional magnesium sulfate infusions at rates of 3 to 20 mg/min for as long as 7 to 48 hours. until the OT interval was shortened to

Disopyramide in hypertrophic cardiomyopathy.

READERS COMMENTS Disopyramide in Hypertrophic Cardiomyopathy Both articles by Pollick’** erroneously suggest a too prominent role of the outflow tract...
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