- Email: [email protected]
Therapy for mild systemic hypertension
May 1, 1984
who found equal changes in mouth pressure and esophageal pressure during Mueller maneuvers in dogs. We agree that during normal respiration the change in transpulmonary pressure could contribute to pulmonary edema, hut our study was concerned with the potentially high pulmonary hydrostatic pressure produced by negative pressure inspiration. The relative importance for fluid accumulation of each of these factors has yet to be determined. Sheklon A. Magder, MD Samuel Llchtenstein, MD Allan G. Adelman, MD Montreal, Quebec, Canada
APICAL HYPERTROPHIC CARDIOMYOPATHY We read the letter by Abinader and the reply by Maron regarding apical hypertrophic cardiomyopathy.“‘** Recently we encountered 3 men in their early fifties who presented with all the classic features of this syndrome, as described by Yamaguchi et al.“*4 Two patients were Indian and the third was Malay in ethnic origin. Their electrocardiograms showed marked asymmetrical T-wave inversion >lO mm (24 mm in 1 patient) and tall precordial R waves from leads Vz to Vs. The left ventricular angiograms revealed the typical spade-like configuration described by Yamaguchi et al. Coronary angiograms showed normal coronary arteries. We agree with Abinader that this syndrome as exemplified by Yamaguchi and our own cases is very different from the cases described by Maron et al. In the latter situation, although the hypertrophy is most apparent at the apex, left ventricular angiog“atypical” findings-a shows raphy midventricular constriction, instead of a spade-like configuration. The second major difference is that no patients in Maron’s study showed marked T-wave inversion. Thus, this syndrome would appear to be most frequently seen in Japan, hut may not he uncommon in other Asian countries. To date3r5 1 case each was reported in Israel and Singapore and 17 in Iram The only case reported in the USA was that of a 55-year-old Korean woman.7 The only Caucasian patient reported was a 32-year-old man from South Africa.6 Because of its occurrence outside of Japan, the proposed terminology of “apical hypertrophic cardiomyopathy of the Japanese type” as was suggested by Maron appears inappropriate. Because most patients reported have been Asian, a more suitable term would be “Asian apical hypertrophic cardiomyopathy.” Alternatively, the term “apical hypertrophic cardiomyopathy,” which was first proposed by Yamaguchi and coworkers and which has the merit of simplicity, could he preserved for this specific syndrome.4 6. L. Chla, MB Lenny K. Tan, MB Singapore 1. Abtn8dw EG. Apical hypartrophic cardiomyopathy It&tar). Am J Cardfol 1983:53:1570. 2. Maron BJ. Apical hypertrophic cardiomyopathy (reply
THE AMERICAN JOURNAL OF CARDIOLOGY
to letter). Am J Cardiol 1983;53:1570. 3. Chia BL, NS R, Dh V, Ee B, Tan L. Apical hyperirophic cardiomyopathy in an Indian male. Sing Mad J 1981; 22:298-301. 4. YamaSuchl M, khknura 1, Nishlyama S, Nagasaki F, Nakankhf S, Takalsu F, Nfshfjo T, Urnads T, Mach8 K. l-iypartqzhic nonobsbuctia cardiiopathy with giant na@iia T waves (apical hypartrophy): vantriiaphic and echocardiogaphic features in 30 patients. Am J Cardiol 1979;44:401-412. 5. Abhadsr EG. Rauchfkisch S, Naschitz J. Hypartrophic apical cardiomyopathy: a subtype of hypertrophic cardiomvcmathv. lsr J Mad Sci 1982:18:1005-1009. 6. Shelkhiadeh A, GhabusslP. A &w?y of uncommon forms of coronary arteries. Jpn Heart J 1982;23:725731. 7. Kerelakas W, Anderson DJ, Crows L, Chalterjaa K. Apical hypwtrophic cardiomyopathy. Am Heart J 1983;105:855-856. 8. SteIngo L, Dansky R, Pocock WA, Barlow JB. Apical wwbstw6i cardiomyopathy. Am Heart hywrvti J 1982;104:635-837
CARDIOKYMOGRAPHY DURING EXERCISE TESTING We read with interest the article by Weiner et al,* but wish to point out that a diagnostic cardiokymograph (CKG) can only be recorded 2 to 3 minutes after cessation of exercise. Their article entitled, “CKG During Exercise Testing” is, therefore, somewhat misleading. In our experience, and also that of Vas2 and Silverberg et aL3 CKG record during treadmill exercise is technically unsatisfactory because of: (1) the patient’s inability to hold his breath; (2) interference with the electromagnetic field by chest wall motion; (3) inability to keep a CKG transducer, which weighs 14 oz, in the preexercise position unchanged during upright exercise; and (4) droplets of perspiration on the chest wall beneath the transducer distorting an induced electromagnetic field. We believe that the application of CKG during treadmill exercise is impossible until a newly designed, suitable CKG transducer is available. Peiliang Kuan, MD Myrvin H. Elleeied, MD Long Beach, California Welnar DA, McCaba CH, Da~osthm 0, Calfar BB, Ryan TJ. Cardiokymography during exercise testing. Am J Cardiol 1983;51:1307-1311.
Vas R, Dfamand GA, Wyatf HL, daLuz PL, Swan HJC, Forreslar JS. Noninvasiva anatysii of regional myocardial wall motion: cardiokymography. AmJ Cardial 1977:233:700-706. Bilvarbar~ RA, DIamaad GA, Vas R, Tzlvoni D, Swan HJC, Farador JB. NonInvasive diagnosis of coronary artery disease: the cardiokymoQaDhic stress test. Circulat& 1980:61:579-589: -
PRECISE SCIENTIFIC MEANINGS ADVOCATED The editorial by Tzivoni et al’ attempts to differentiate torsades de pointes (TdP) from polymorphous ventricular tachycardia (VT) on a clinical basis. Their definition of TdP is dependent on its association with an ahnorma1 QT-syndrome interval. The clinical evidence they present is clear, although the mechanisms underlying the presumably different clinical entities represented by TdP and polymorphous VT is still uncertain. Nevertheless, from a semantic point of view such a distinction is unwise. This type of classification allows for the definition of VT
Volume 53
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or ventricular fibrillation or other electrocardiographic patterns as such only when they are associated with a long QT interval in the preceding sinus beat or some other clinical characteristic. The electrocardiographic patterns of TdP and polymorphous VT cannot be descriptively separated. Whether one prefers to designate this pattern by its French or English nomenclature is of little consequence. To differentiate the clinical significance one can simply use the added qualifier, “with or without long QT interval.” Scientific language requires precision of meaning to assure universal understanding. The definitions suggested by Tzivoni et al are shortcuts that erode such precision. When mechanisms have been established for these electrocardiographic patterns, the adopted terms may have to be revised. Many can attest to the arduous task required to extirpate old terms from common usage. Benjamin J. Bcherlug, MD Oklahoma City, Oklahoma 1. Tzfw4 D, Kew A, Stem S. Torsades ds pointes versus polymorphous ventricular 1983:52:639-640.
tachycardia. Am J Cardiol
THERAPY FOR MILD SYSTEMIC HYPERTENSION Kaplan advocates withholding antihypertensive drugs from patients with a diastolic blood pressure (BP) in the 90 to 100 mm Hg range who are otherwise at relatively low risk for at least 6 months while encouraged to follow nondrug therapy, including weight reduction for the obese, moderate sodium restriction for all, and relaxation therapy for those who are willing. (Am J Cardiol 1983; 51:621). His suggestion is puzzling. Those who adhere to a low-salt diet or who lose weight will attain a lower BP. Some will have a lower BP when treated with placebo. The central question is not whether a short-term improvement in BP can be seen, but whether these forms of therapy favorably affect the mortality associated with hypertension. I write from the perspective of a community practitioner with a particular interest in hypertension. A nurse practitioner works with me. One of her responsibilities is to track patients with hypertension whom we have not seen in the last 3 months. I have a pretty clear idea of the frequency with which my patients give up even simple treatment that involves 1 pill a day. I treat patients with diabetes, a disease for which weight reduction is a major treatment. However, although my prescribed weight reduction is reinforced by community expectation, I can count on the fingers of 1 hand the obese adult-onset patients who have dieted to an ideal weight and kept their weight off for more than 6 months. Does Kaplan have a different experience? Can he work with patients and persuade them to change their lifestyles, their body habitus, their sodium intake and their patterns of reacting to stress on a lifelong basis, with sufficient confidence in patient compliance so that he can justify this as a prime form of therapy? J. Walden Retan, MD Birmingham, Alabama
who found equal changes in mouth pressure and esophageal pressure during Mueller maneuvers in dogs. We agree that during normal respiration the change in transpulmonary pressure could contribute to pulmonary edema, hut our study was concerned with the potentially high pulmonary hydrostatic pressure produced by negative pressure inspiration. The relative importance for fluid accumulation of each of these factors has yet to be determined. Sheklon A. Magder, MD Samuel Llchtenstein, MD Allan G. Adelman, MD Montreal, Quebec, Canada
APICAL HYPERTROPHIC CARDIOMYOPATHY We read the letter by Abinader and the reply by Maron regarding apical hypertrophic cardiomyopathy.“‘** Recently we encountered 3 men in their early fifties who presented with all the classic features of this syndrome, as described by Yamaguchi et al.“*4 Two patients were Indian and the third was Malay in ethnic origin. Their electrocardiograms showed marked asymmetrical T-wave inversion >lO mm (24 mm in 1 patient) and tall precordial R waves from leads Vz to Vs. The left ventricular angiograms revealed the typical spade-like configuration described by Yamaguchi et al. Coronary angiograms showed normal coronary arteries. We agree with Abinader that this syndrome as exemplified by Yamaguchi and our own cases is very different from the cases described by Maron et al. In the latter situation, although the hypertrophy is most apparent at the apex, left ventricular angiog“atypical” findings-a shows raphy midventricular constriction, instead of a spade-like configuration. The second major difference is that no patients in Maron’s study showed marked T-wave inversion. Thus, this syndrome would appear to be most frequently seen in Japan, hut may not he uncommon in other Asian countries. To date3r5 1 case each was reported in Israel and Singapore and 17 in Iram The only case reported in the USA was that of a 55-year-old Korean woman.7 The only Caucasian patient reported was a 32-year-old man from South Africa.6 Because of its occurrence outside of Japan, the proposed terminology of “apical hypertrophic cardiomyopathy of the Japanese type” as was suggested by Maron appears inappropriate. Because most patients reported have been Asian, a more suitable term would be “Asian apical hypertrophic cardiomyopathy.” Alternatively, the term “apical hypertrophic cardiomyopathy,” which was first proposed by Yamaguchi and coworkers and which has the merit of simplicity, could he preserved for this specific syndrome.4 6. L. Chla, MB Lenny K. Tan, MB Singapore 1. Abtn8dw EG. Apical hypartrophic cardiomyopathy It&tar). Am J Cardfol 1983:53:1570. 2. Maron BJ. Apical hypertrophic cardiomyopathy (reply
THE AMERICAN JOURNAL OF CARDIOLOGY
to letter). Am J Cardiol 1983;53:1570. 3. Chia BL, NS R, Dh V, Ee B, Tan L. Apical hyperirophic cardiomyopathy in an Indian male. Sing Mad J 1981; 22:298-301. 4. YamaSuchl M, khknura 1, Nishlyama S, Nagasaki F, Nakankhf S, Takalsu F, Nfshfjo T, Urnads T, Mach8 K. l-iypartqzhic nonobsbuctia cardiiopathy with giant na@iia T waves (apical hypartrophy): vantriiaphic and echocardiogaphic features in 30 patients. Am J Cardiol 1979;44:401-412. 5. Abhadsr EG. Rauchfkisch S, Naschitz J. Hypartrophic apical cardiomyopathy: a subtype of hypertrophic cardiomvcmathv. lsr J Mad Sci 1982:18:1005-1009. 6. Shelkhiadeh A, GhabusslP. A &w?y of uncommon forms of coronary arteries. Jpn Heart J 1982;23:725731. 7. Kerelakas W, Anderson DJ, Crows L, Chalterjaa K. Apical hypwtrophic cardiomyopathy. Am Heart J 1983;105:855-856. 8. SteIngo L, Dansky R, Pocock WA, Barlow JB. Apical wwbstw6i cardiomyopathy. Am Heart hywrvti J 1982;104:635-837
CARDIOKYMOGRAPHY DURING EXERCISE TESTING We read with interest the article by Weiner et al,* but wish to point out that a diagnostic cardiokymograph (CKG) can only be recorded 2 to 3 minutes after cessation of exercise. Their article entitled, “CKG During Exercise Testing” is, therefore, somewhat misleading. In our experience, and also that of Vas2 and Silverberg et aL3 CKG record during treadmill exercise is technically unsatisfactory because of: (1) the patient’s inability to hold his breath; (2) interference with the electromagnetic field by chest wall motion; (3) inability to keep a CKG transducer, which weighs 14 oz, in the preexercise position unchanged during upright exercise; and (4) droplets of perspiration on the chest wall beneath the transducer distorting an induced electromagnetic field. We believe that the application of CKG during treadmill exercise is impossible until a newly designed, suitable CKG transducer is available. Peiliang Kuan, MD Myrvin H. Elleeied, MD Long Beach, California Welnar DA, McCaba CH, Da~osthm 0, Calfar BB, Ryan TJ. Cardiokymography during exercise testing. Am J Cardiol 1983;51:1307-1311.
Vas R, Dfamand GA, Wyatf HL, daLuz PL, Swan HJC, Forreslar JS. Noninvasiva anatysii of regional myocardial wall motion: cardiokymography. AmJ Cardial 1977:233:700-706. Bilvarbar~ RA, DIamaad GA, Vas R, Tzlvoni D, Swan HJC, Farador JB. NonInvasive diagnosis of coronary artery disease: the cardiokymoQaDhic stress test. Circulat& 1980:61:579-589: -
PRECISE SCIENTIFIC MEANINGS ADVOCATED The editorial by Tzivoni et al’ attempts to differentiate torsades de pointes (TdP) from polymorphous ventricular tachycardia (VT) on a clinical basis. Their definition of TdP is dependent on its association with an ahnorma1 QT-syndrome interval. The clinical evidence they present is clear, although the mechanisms underlying the presumably different clinical entities represented by TdP and polymorphous VT is still uncertain. Nevertheless, from a semantic point of view such a distinction is unwise. This type of classification allows for the definition of VT
Volume 53
1413
or ventricular fibrillation or other electrocardiographic patterns as such only when they are associated with a long QT interval in the preceding sinus beat or some other clinical characteristic. The electrocardiographic patterns of TdP and polymorphous VT cannot be descriptively separated. Whether one prefers to designate this pattern by its French or English nomenclature is of little consequence. To differentiate the clinical significance one can simply use the added qualifier, “with or without long QT interval.” Scientific language requires precision of meaning to assure universal understanding. The definitions suggested by Tzivoni et al are shortcuts that erode such precision. When mechanisms have been established for these electrocardiographic patterns, the adopted terms may have to be revised. Many can attest to the arduous task required to extirpate old terms from common usage. Benjamin J. Bcherlug, MD Oklahoma City, Oklahoma 1. Tzfw4 D, Kew A, Stem S. Torsades ds pointes versus polymorphous ventricular 1983:52:639-640.
tachycardia. Am J Cardiol
THERAPY FOR MILD SYSTEMIC HYPERTENSION Kaplan advocates withholding antihypertensive drugs from patients with a diastolic blood pressure (BP) in the 90 to 100 mm Hg range who are otherwise at relatively low risk for at least 6 months while encouraged to follow nondrug therapy, including weight reduction for the obese, moderate sodium restriction for all, and relaxation therapy for those who are willing. (Am J Cardiol 1983; 51:621). His suggestion is puzzling. Those who adhere to a low-salt diet or who lose weight will attain a lower BP. Some will have a lower BP when treated with placebo. The central question is not whether a short-term improvement in BP can be seen, but whether these forms of therapy favorably affect the mortality associated with hypertension. I write from the perspective of a community practitioner with a particular interest in hypertension. A nurse practitioner works with me. One of her responsibilities is to track patients with hypertension whom we have not seen in the last 3 months. I have a pretty clear idea of the frequency with which my patients give up even simple treatment that involves 1 pill a day. I treat patients with diabetes, a disease for which weight reduction is a major treatment. However, although my prescribed weight reduction is reinforced by community expectation, I can count on the fingers of 1 hand the obese adult-onset patients who have dieted to an ideal weight and kept their weight off for more than 6 months. Does Kaplan have a different experience? Can he work with patients and persuade them to change their lifestyles, their body habitus, their sodium intake and their patterns of reacting to stress on a lifelong basis, with sufficient confidence in patient compliance so that he can justify this as a prime form of therapy? J. Walden Retan, MD Birmingham, Alabama