our preference for the terms doubly committed and juxta- (or sub) arteria1.2,3Once this single anatomic fact is recognized, all the apparent D. hby-kh, MD confusion discussedby Ludomirsky Leeds, United Kingdom et al’ with regard to distinction 12 March 1991 from obstruction in the outflow tract of the right ventricle is dis1. Caterina R, D’Ascanio A, Mazzone A, pelled. Gazzetti P, Bernini W, Neri R, BombarRobartn. -, m. 0K chieri S. Prevalence of anticardiolipin London, United Kingdom antibodies in coronary artery disease. Am 12 March 1991
defining seropositivity in the laboratory and allow accurate studies on associateddiseasepatterns to be performed.5
J Cardiol 1990;65:922-923. 2. Klemp P, Cooper RC, Strauss FJ, Jordaan ER, Przybojewki JZ, Nel N. Anticardiolipin antibodies in ischaemic heart disease. Clin Exp Immunol1988;14:254251. 3. Hamsten A, Bjorkholm M, Nonberg R, de Faine U, Holm G. Antibodies to cardiolipin in young survivors of myocardial infarction: an association with recurrent cardiovascular events. Lancer 1986; 2:1353-1356. 4. Keane A, Woods R, Dowding V, Roden D, Barry C. Anticardiolipin antibodies in rheumatoid arthritis. Brit J Rheumatol 1987;26:346-350. 5. Hughes GRV. Vascular disease, thrombosis and recurrent abortion. Br &fed J 1988;247:700-701.
Diagnosing and Differentiating a Doubly Committed Ventricular Septal Defect from Obstruction in the Oufflow Tract of the Right Ventricle It was with some surprise that I noted that comments on the fact that “approximately 5% of ventricular septal defects are located high in the right ventricular outflow tract between the crista supraventricularis and the pulmonic valve”’ referenced one of my published studies2 In that study, my colleagues and I pointed to the confusion that could occur when “supracristal” was used as a descriptor for such defects. In reality, the key to diagnosis of these defects is the observation that the entirety of the muscular outlet septum, together with the “septal” aspectof the muscular subpulmonary infundibulum, is totally lacking. Because of this, the leaflets of the pulmonary valves are in fibrous continuity with those of the aortic valve, and the interventricular communication sits beneath both outflow tracts: hence,
1. Ludomirsky A, Tani L, Murphy DJ, Huhta JC. Usefulness of color-flow Dopp ler in diagnosing and in differentiating supracristal ventricular septal defect from right ventricular outflow tract obstruction. Am J Cardiol 1991;67:194-198. 2. Anderson RH, Lenox CC, Zuberbuhler JR. The morphology of ventricular septal defects. Perspect Pediatr Pathol 1984;8:235-268. 3. Baker E, Leung MP, Anderson RH, Fischer DR, Zuberbuhler JR. The crosssectional anatomy of ventricular septal defects: a reappraisal. Br Heart J 1988; 59:339-351.
Natural History of Cardiac Rhabdomyoma I read with interest the article by Smythe et al’ and agree with their comments concerning the invariable spontaneousregression of cardiac rhabdomyoma. In 1987 my colleaguesand I described a caseof cardiac rhabdomyoma diagnosed and followed up prenatally and for 2 years after delivery by Doppler echocardiography. Spontaneous regression of multiple tumor masseswas documented, thus adding another case to the 15 patients cited by Smythe et al with evidence of tumor regression. More important, I wish to highlight the significant contribution of repeated Doppler examinations in the hemodynamic evaluation and management of such patients, which can help to avoid repeated cardiac catheterizations and unnecessary surgery. Doppler detection of mitral and pulmonary regurgitation was consequent to tumor massesinterfering with valve closure. Pulmonary regurgitation disappeared concomitantly with tumor massregression. Thus I consider the Dopp ler modality, not alluded to in your
article, to be more important and cost-effective than “magnetic resonance imaging” to “assist in charting the course of the lesion.” Edward0. Ablnubr, MD Haifa, Israel 28 March 1991 1. Smythe JF, Dyck JD, Smallhorn JF, Freedom RM. Natural history of cardiac rhabdomyoma in infancy and childhood. Am J Cardiol 1990;66: 1247-l 249. 2. Abinader EG, Goldhammer I, Sharf M, Reiter A, Berger A. The usefulness of Doppler echocardiography in the management of rhahdomyoma diagnosed prenatally. Eur Heart J 1987;8:1146-1152.
Metoprolol as Antihypertensive
Drug
We read with interest the article of Schrader et al’ on the comparison of the antihypertensive efficiency of nitrendipine, metoprolol, mepindolol and enalapril using ambulatory 24-hour blood pressure monitoring. Although the investigators demonstrated in an elegant way the effectivenessof the antihypertensive drugs, they overlooked the potential hazards of using /3blocking drugs, such as metoprolol, for the treatment of arterial hypertension. It is now widely accepted that this drug doeshave deleterious effects on the lipid metabolism, which could eventually be more harmful to the patient.2,3 Significant increase in triglycerides, total cholesterol and the atherogenic index as estimated by the ratio LDL/HDL cholesterol concentrations together with a decrease in HDL cholesterol are some of the most altered metabolic parameters that deserverecognition, becausein some casesthese might counteract the possiblebenefit of a reduction in blood pressure or the prevention of coronary artery disease. In contrast to the observations of White et aL4 nitrendipine reduced the average daily blood pressure, one of the important predictors of hypertensive heart diseases. Becauseantihypertensive therapy implies continued and prolonged drug administration, agents with neutral or favorable effects on lipid metabolism such as nitrendipine,5 READERS’COMMENTS 831
1. Wikstrand J, Warnold J, Olsson G, Tuomilehto J, Elmfeldt D, Berglund G. Primary prevention with metoprolol in patients with hypertension. JAMA 1988; 259:1976-1982.
pi
Chol. = cholesterol;
TG = triglycerides.
in adequate dose, should therefore be recommended. Dirk hk!U, Klaus Gohle,
MD MD
Brussels,Belgium 23 January 1991 1. Schrader J, Schoel G, Buhr-Schinner H, Kandt M, Warneke G, Armstrong VW, Scheler F. Comparison of the antihypertensive efficiency of nitrendipine, metoprolol, mepindolol and enalapril using ambulatory 24-hour blood pressure monitoring. Am J Cardiol 1990;66:967972. 2. Ferrara LA, Marotta T, Scilla A, Manstranzo P, Strazullo P, Mancini M. Effect of oxprenolol and metoprolol on serum lipid concentration. Eur J Clin Pharmaco1 1984;26:331-334. 3. Nilsson A, Hanson BG, H&felt B. Effect of metoprolol on blood glycerol, free fatty acids, triglycerides and glucose in relation to plasma catecholamines in hypertensive patients at rest and following submaximal work. Eur J Clin Pharmacol 1978;13:5-8. 4. White WB, Smith VE, McCabe EJ, Meerean MK. Effects of chronic nitrendipine on casual (office) and 24-hour ambulatory blood pressure. Clin Pharmacol Ther 1985;38:60-64. 5. Ferrara LA, Soro S, Fasano ML. Effects of nitrendipine on glucose and lipid serum concentrations. Curr Ther Res 1985;37:614-618.
REPLY: We appreciated the comments by Deleu and Bohle. The aim of our randomized study was to examine whether different drugs that show similar antihypertensive effects as assessedby casual blood pressure measurements possess comparable antihypertensive efficacy during ambulatory monitor-
832
ing. On the basis of this study it is not possible to give comments on the effects of treatment with the chosendrugs on patients’ prognosis. We can only state that different antihypertensive regimens do not confer the samedegree of 24-hour ambulatory control. As mentioned by Deleu and Bohle, p blockers are said to have unfavorable effects on lipid metabolism. In our study, measurements of fasting triglycerides and total cholesterol were also performed. No group had significant changes in lipids, although there might have been a slight tendency toward a minor elevation of triglycerides during P-blocker therapy (see table above). We doubt that the effects of p blockers on lipid metabolism are of prognostic importance. In contrast, it has clearly been shown that /3 blockers were able to improve prognosis of hypertensives. This has not been shown for the drugs recommended by Deleu and Bohle. It should also be noted that the /$-selective blocker metoprolol had no negative effects on lipids during the MAPPHY study, although a significant reduction of total mortality was achieved.’ We believe that general recommendations for the selection of antihypertensive drugs should not be based on changes of single laboratory parameters before a prognostic advantage has been proven in clinical trials. Joachim Schrader, MD Gerhard kheel. MD Goettingen, Germany
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68
3 April 1991
SEPTEMBER 15, 1991
Bidirectional ST Shift in lschemic Right Ventricle
I read with interest the Brief Report, “Is ST Elevation the Only Electrocardiographic Response of the Ischemic Right Ventricle?” by Krueger et al.’ The authors state that ST elevation may be the only electrocardiographic response of the ischemic right ventricular free wall. I call the attention of the authors and readers to my publication on this subject. We2previously had a caseof pure right ventricular ischemia in which not only ST-T elevation but also ST depressionand a Twave inversion were documented during angioplasty for proximal right coronary artery disease. The depressedST segment and inverted T wave were considered to reflect subendocardial right ventricular ischemia beneath the leads as the samemechanism in left ventricular subendocardial infarction. Therefore, it is difficult to accept the conclusion that “ST elevation is the only electrocardiographic response of the ischemic right ventricle.” Of course, it seemsthat ST depression in response to the ischemic right ventricle should only rarely ha pen. Hajime Katao t: a,
MD
Oita, Japan 2 April 1991 1. Krueger DW, Morrison DA, Buckner JK, Kelly K, Lindenfeld J. Is ST elevation the only electrocardiographic response of the ischemic right ventricle? Am J Cardiol 1991;67:643-645. 2. Kataoka H, Mikuriya Y, Nasu M. Bidirectional precordial ST-T wave changes in pure right ventricular ischemia. Am Heart J 1988;116:1631-1632.
defining seropositivity in the laboratory and allow accurate studies on associateddiseasepatterns to be performed.5
J Cardiol 1990;65:922-923. 2. Klemp P, Cooper RC, Strauss FJ, Jordaan ER, Przybojewki JZ, Nel N. Anticardiolipin antibodies in ischaemic heart disease. Clin Exp Immunol1988;14:254251. 3. Hamsten A, Bjorkholm M, Nonberg R, de Faine U, Holm G. Antibodies to cardiolipin in young survivors of myocardial infarction: an association with recurrent cardiovascular events. Lancer 1986; 2:1353-1356. 4. Keane A, Woods R, Dowding V, Roden D, Barry C. Anticardiolipin antibodies in rheumatoid arthritis. Brit J Rheumatol 1987;26:346-350. 5. Hughes GRV. Vascular disease, thrombosis and recurrent abortion. Br &fed J 1988;247:700-701.
Diagnosing and Differentiating a Doubly Committed Ventricular Septal Defect from Obstruction in the Oufflow Tract of the Right Ventricle It was with some surprise that I noted that comments on the fact that “approximately 5% of ventricular septal defects are located high in the right ventricular outflow tract between the crista supraventricularis and the pulmonic valve”’ referenced one of my published studies2 In that study, my colleagues and I pointed to the confusion that could occur when “supracristal” was used as a descriptor for such defects. In reality, the key to diagnosis of these defects is the observation that the entirety of the muscular outlet septum, together with the “septal” aspectof the muscular subpulmonary infundibulum, is totally lacking. Because of this, the leaflets of the pulmonary valves are in fibrous continuity with those of the aortic valve, and the interventricular communication sits beneath both outflow tracts: hence,
1. Ludomirsky A, Tani L, Murphy DJ, Huhta JC. Usefulness of color-flow Dopp ler in diagnosing and in differentiating supracristal ventricular septal defect from right ventricular outflow tract obstruction. Am J Cardiol 1991;67:194-198. 2. Anderson RH, Lenox CC, Zuberbuhler JR. The morphology of ventricular septal defects. Perspect Pediatr Pathol 1984;8:235-268. 3. Baker E, Leung MP, Anderson RH, Fischer DR, Zuberbuhler JR. The crosssectional anatomy of ventricular septal defects: a reappraisal. Br Heart J 1988; 59:339-351.
Natural History of Cardiac Rhabdomyoma I read with interest the article by Smythe et al’ and agree with their comments concerning the invariable spontaneousregression of cardiac rhabdomyoma. In 1987 my colleaguesand I described a caseof cardiac rhabdomyoma diagnosed and followed up prenatally and for 2 years after delivery by Doppler echocardiography. Spontaneous regression of multiple tumor masseswas documented, thus adding another case to the 15 patients cited by Smythe et al with evidence of tumor regression. More important, I wish to highlight the significant contribution of repeated Doppler examinations in the hemodynamic evaluation and management of such patients, which can help to avoid repeated cardiac catheterizations and unnecessary surgery. Doppler detection of mitral and pulmonary regurgitation was consequent to tumor massesinterfering with valve closure. Pulmonary regurgitation disappeared concomitantly with tumor massregression. Thus I consider the Dopp ler modality, not alluded to in your
article, to be more important and cost-effective than “magnetic resonance imaging” to “assist in charting the course of the lesion.” Edward0. Ablnubr, MD Haifa, Israel 28 March 1991 1. Smythe JF, Dyck JD, Smallhorn JF, Freedom RM. Natural history of cardiac rhabdomyoma in infancy and childhood. Am J Cardiol 1990;66: 1247-l 249. 2. Abinader EG, Goldhammer I, Sharf M, Reiter A, Berger A. The usefulness of Doppler echocardiography in the management of rhahdomyoma diagnosed prenatally. Eur Heart J 1987;8:1146-1152.
Metoprolol as Antihypertensive
Drug
We read with interest the article of Schrader et al’ on the comparison of the antihypertensive efficiency of nitrendipine, metoprolol, mepindolol and enalapril using ambulatory 24-hour blood pressure monitoring. Although the investigators demonstrated in an elegant way the effectivenessof the antihypertensive drugs, they overlooked the potential hazards of using /3blocking drugs, such as metoprolol, for the treatment of arterial hypertension. It is now widely accepted that this drug doeshave deleterious effects on the lipid metabolism, which could eventually be more harmful to the patient.2,3 Significant increase in triglycerides, total cholesterol and the atherogenic index as estimated by the ratio LDL/HDL cholesterol concentrations together with a decrease in HDL cholesterol are some of the most altered metabolic parameters that deserverecognition, becausein some casesthese might counteract the possiblebenefit of a reduction in blood pressure or the prevention of coronary artery disease. In contrast to the observations of White et aL4 nitrendipine reduced the average daily blood pressure, one of the important predictors of hypertensive heart diseases. Becauseantihypertensive therapy implies continued and prolonged drug administration, agents with neutral or favorable effects on lipid metabolism such as nitrendipine,5 READERS’COMMENTS 831
1. Wikstrand J, Warnold J, Olsson G, Tuomilehto J, Elmfeldt D, Berglund G. Primary prevention with metoprolol in patients with hypertension. JAMA 1988; 259:1976-1982.
pi
Chol. = cholesterol;
TG = triglycerides.
in adequate dose, should therefore be recommended. Dirk hk!U, Klaus Gohle,
MD MD
Brussels,Belgium 23 January 1991 1. Schrader J, Schoel G, Buhr-Schinner H, Kandt M, Warneke G, Armstrong VW, Scheler F. Comparison of the antihypertensive efficiency of nitrendipine, metoprolol, mepindolol and enalapril using ambulatory 24-hour blood pressure monitoring. Am J Cardiol 1990;66:967972. 2. Ferrara LA, Marotta T, Scilla A, Manstranzo P, Strazullo P, Mancini M. Effect of oxprenolol and metoprolol on serum lipid concentration. Eur J Clin Pharmaco1 1984;26:331-334. 3. Nilsson A, Hanson BG, H&felt B. Effect of metoprolol on blood glycerol, free fatty acids, triglycerides and glucose in relation to plasma catecholamines in hypertensive patients at rest and following submaximal work. Eur J Clin Pharmacol 1978;13:5-8. 4. White WB, Smith VE, McCabe EJ, Meerean MK. Effects of chronic nitrendipine on casual (office) and 24-hour ambulatory blood pressure. Clin Pharmacol Ther 1985;38:60-64. 5. Ferrara LA, Soro S, Fasano ML. Effects of nitrendipine on glucose and lipid serum concentrations. Curr Ther Res 1985;37:614-618.
REPLY: We appreciated the comments by Deleu and Bohle. The aim of our randomized study was to examine whether different drugs that show similar antihypertensive effects as assessedby casual blood pressure measurements possess comparable antihypertensive efficacy during ambulatory monitor-
832
ing. On the basis of this study it is not possible to give comments on the effects of treatment with the chosendrugs on patients’ prognosis. We can only state that different antihypertensive regimens do not confer the samedegree of 24-hour ambulatory control. As mentioned by Deleu and Bohle, p blockers are said to have unfavorable effects on lipid metabolism. In our study, measurements of fasting triglycerides and total cholesterol were also performed. No group had significant changes in lipids, although there might have been a slight tendency toward a minor elevation of triglycerides during P-blocker therapy (see table above). We doubt that the effects of p blockers on lipid metabolism are of prognostic importance. In contrast, it has clearly been shown that /3 blockers were able to improve prognosis of hypertensives. This has not been shown for the drugs recommended by Deleu and Bohle. It should also be noted that the /$-selective blocker metoprolol had no negative effects on lipids during the MAPPHY study, although a significant reduction of total mortality was achieved.’ We believe that general recommendations for the selection of antihypertensive drugs should not be based on changes of single laboratory parameters before a prognostic advantage has been proven in clinical trials. Joachim Schrader, MD Gerhard kheel. MD Goettingen, Germany
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68
3 April 1991
SEPTEMBER 15, 1991
Bidirectional ST Shift in lschemic Right Ventricle
I read with interest the Brief Report, “Is ST Elevation the Only Electrocardiographic Response of the Ischemic Right Ventricle?” by Krueger et al.’ The authors state that ST elevation may be the only electrocardiographic response of the ischemic right ventricular free wall. I call the attention of the authors and readers to my publication on this subject. We2previously had a caseof pure right ventricular ischemia in which not only ST-T elevation but also ST depressionand a Twave inversion were documented during angioplasty for proximal right coronary artery disease. The depressedST segment and inverted T wave were considered to reflect subendocardial right ventricular ischemia beneath the leads as the samemechanism in left ventricular subendocardial infarction. Therefore, it is difficult to accept the conclusion that “ST elevation is the only electrocardiographic response of the ischemic right ventricle.” Of course, it seemsthat ST depression in response to the ischemic right ventricle should only rarely ha pen. Hajime Katao t: a,
MD
Oita, Japan 2 April 1991 1. Krueger DW, Morrison DA, Buckner JK, Kelly K, Lindenfeld J. Is ST elevation the only electrocardiographic response of the ischemic right ventricle? Am J Cardiol 1991;67:643-645. 2. Kataoka H, Mikuriya Y, Nasu M. Bidirectional precordial ST-T wave changes in pure right ventricular ischemia. Am Heart J 1988;116:1631-1632.
