LETTERS

VENTRICULAR TACHYCARDIA INDUCED BY ATRIAL STIMULATION I read with interest the paper by German et al1 on “Ventricular Tachycardia Induced by Atria1 Stimulation in Patients Without Symptomatic Cardiac Disease.” In 4 of their patients with idiopathic ventricular tachy- cardia of a right bundle branch block mor- phology and left-axis deviation, they noted that intravenous verapamil slowed and ter- minated the tachycardia. This observation and the suggestion that such patients may correspond to a unique electrocardio- graphic-electrophysiologic entity were first made by our group2 and confirmed by Lin et al3 However, these papers are not referenced by German et al.

Bernard Belhaeeen, MD Tel Aviv, Israel

1. German LD, Packer DL, Bardy GH, Gallagher JJ. Ventricular tachycardia induced by atrial stimulation in patients without symptomatic cardiac disease Am J Cardiol 1983.52.1202-1207.

2. Belhaaaan 6, Rotmensoh HH, Lanlado S. Response Of recwrent sustained ventricular tachycardia to wrapemil Br Heart J 1981;46:679-682.

3. Lift FC. Flnley CD, Rahlmtoola SH, Wu D. ldiopathrc paroxysmal ventriwlar tachycardia with a QRS pattern of rroht bundle branch block and left-axis deviation: a && clinical entity with specific properties. Am J Cardiol 1983:52:96-100.

REPLY: We greatly appreciate the interest of Belhassen in our article. We are aware of the case report by Belhassen et al, but we believe that the claim for priority properly belongs to Zipes et al (our reference 7) and Wellens et al (our reference lo), who first reported patients with this form of arrhyth- mia and its response to verapamil. We were also interested in the excellent article by Lin et al (Am J Cardiol 1983;52:96-loo), which appeared after our manuscript had been submitted for publication and therefore was not referenced by us.

Lawrence D. German, MD Durham, North Carolina

LATERAL SYSTOLIC PULSATION OF THE EARLOBE: A SIGN OF

TRICUSPID REGURGITATION It is well recognized that pulsatile anterior movement of the head and neck (head bobbing) is characteristic of aortic regurgi- tation. The enlarged deep jugular systolic V wave is a prominent feature of tricuspid regurgitation (TR), as observed in the region of the sternocleidomastoid muscle with the patient at a 45’ elevation. Tricuspid regur- gitation also is usually present when lat- eral systolic pulsations of the earlobes are present, even if the typical deep jugular V waves are not prominent. This earlobe pul- sation may occur when the TR is not severe enough to produce the more easily recognized deep jugular vein systolic V wave. This sign, in my experience, has not been seen with any other type of cardiac dysfunction and is very possibly pathognomonic of TR. The deep

Before submitting a letter for publication, please reed the “Letters” section in the “Instructions to Authors” in this issue.

jugular vein runs deep to the earlobe, and therefore its pulsation should produce lateral pulsation of the earlobe by virtue of its location.

M. Daniel Byrd, MD Atlanta, Georgia

CALCIUM-CHANNEL BLOCKERS FOR CHRONIC CONGESTIVE

HEART FAILURE We read the recent report by Elkayam et al1 on the hemodynamic effects of oral nifedipine in severe chronic congestive heart failure (CHF). We simultaneously published a sim- ilar study elsewhere.2 Our findings are com- parable with many of the findings of Elkayam et al in that oral administration of nifedipine is associated with rapid and sustained arterial vasodilatation, with marked reductions in systemic and pulmonary vascular resistance at 30 minutes. However, improvements in cardiac index were more marked in our pa- tients (37 vs 25% at peak response) and more uniform (9 of 9 patients vs 8 of 11 patients). Finally, the duration of action was shorter, as many of the effects had dissipated by 2 hours. As calcium-channel blockers can have nega- tive inotropic effects, the differences in car- diac output responses may be a dose-related phenomenon. However, preliminary reports are conflicting. Bellocci et al3 demonstrated acute and long-term (2 months) improvement with a 20-mg dose of nifedipine administered every 6 hours. Brooks and et al4 identified a decrease in cardiac output when doses of 20 to 30 mg were administered acutely. Two preliminary reports compared nifedipine with “equipotent” doses of hydralazine5 and nitroprusside.6 These data also suggest a primary arteriolar vasodilating effect of ni- fedipine, and raise the issue of a potential negative inotropic effect. In both studies the dose of nifedipine was larger than in our study. Thus, it is pcesible that beneficial after- load reduction occurs with a lo-mg dose, but that negative inotropic effects are increas- ingly important with doses of 20 to 40 mg.

We agree with Elkayam et al that barore- ceptor mediated reflex augmentation of @-adrenergic tone is not an important mech- anism for preservation of forward flow during nifedipine therapy. To document the range of sympathetic responsiveness in chronic CHF, we have previously described the reflex responses to head-up tilt7 and cold pressor stimu1ation.s In our evaluation of nifedipine by these techniques, we found no evidence of significant sympathetic augmentation that would account for the hemodynamic im- provement.

The beneficial vasodilator effects of cal- cium-channel blockers has prompted the use of nifedipine by many clinicians for the management of chronic CHF. However, ad- equate clinical studies of these agents have not been performed, so that the data base supporting the clinical efficacy of these agents is small, and the potential adverse effects are unknown. We therefore risk a repetition of the mistakes made with hy- dralazine and prazosin, in which clinical trials

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were performed (and are still under way) to determine clinical efficacy almost a decade after their initial use for CHF.

The present controversies with nifedipine, a prototype of numerous “second-generation” dihydropyridines, suggests that both dose- response studies and double-blind efficacy studies are mandatory, so that mechanisms of action, proper dosage, side-effect profile and long-term efficacy can be established.

Spencer H. Kubo, MD Robert J. Cody, MD

New York, NY

1. Elkaywn U, Wabar L, Tofkan B, Barman D, Rahlmtoola S. Acute herodynamIc effect of cfal nffedipina in severe chronic congestive heart failure, Am J Cardiol 1963; 52:1041-1045.

2. Prlda XE, Kubo SH, Laragh JH, Cody RJ. Evaluation of cafcium-madffted vawmnsfriction in chronic congestive heart failure. Am J Med 1983;75:795-800.

3. Balloool F, Anaakma 0, Sanlarelll P, Loparlldo F, Scabbla E, Zaochl P, Manzoll U. Oral nifedipine in the longterm management of severe chronic heart failwe J Cardiovasc Pharmacol 1962;4:647-855.

4. -8 N, Cafteg M, Pk&son J, B&on R. Unf~edictabfe response to nifedipine in severe cardiac failure. Br f&d J 1980;281:1324.

5. Elkayam U, Weber L, Rosa J, McKay C, Rahlmtoola S. Nffiins vs f@alazine tn the treatment of sevare heart failure: an evidence for a negative inotropic affect of nifedipine (abstr). Circulation 1963;68:suppl lll:lll-8.

6. Flfar MA, Coluool WS, Barry WH, Wynna J. LoraIl SH. Comparative hamcdynsmfc and netrfoamkrcrine effects of nftmpmssfde and nifadipins in heart fallwe. Clrcutation 1963:66:suppl lll:lll-8.

7. Knba SH, Cody RJ. Circulatory autoregulation in chronic congestive heart failure: responses to head-up bit in 41 patients. Am J Cardiol 1983;52:512-518.

6. Cody RJ, FrankIln KW, Kkfgar J, Laragh JH. fJecha- nisrns gowning ths postwal response, and baraaceptcw abnommlttfas in chronic cocgsstive haart fellwe: affects of acute and long-term converting enzyme inhibition. Circulation 1982;66:135-141.

REPLY: We agree with Kubo and Cody that further studies are needed before the full therapeutic spectrum of nifedipine in pa- tients with CHF can be understood. However, acute hemodynamic evaluations of this drug in patients with seuere chronic CHF have revealed that the intrinsic negative inotropic effect of nifedipine can play an important clinical role. This effect limits the hemody- namic benefits of arterial dilation with ni- fedipineQ and may even result in deleterious effecta.s*4 These findings should he taken into consideration when further evaluation of nifedipine in CHF is being planned or when nifedipine is being considered as a thera- peutic modality in patients with seuere CHF.

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Ekayam U, Wsbar L, Torkan B, McKay CR, Rahlmtoola SH. Comparison of hemcdynamic responses to nifadl- pinaarkfnRqm&dsinseveracfucnfccongsstivehaart failure. Am J Cardiol 1984;53:1321-1325. Elkayam U, Wabw L, Rosa J, McKay CR, Rahlmfoola SH. Nifsdipine vs hydrafasina in the treatment of sovare haart failure: an evidence for a negatffa inobcplc effect of nifedipine (abstr). Circulation 1983;68:111:18-8. Gllhner RI, Kark P. Pulmonary edema precipitated by nifedlpine. Br Med J 1980;280:1420-1421. &oaks K Catfell M, Pklgaon J, Bakat R. Unpredictable response to nifedipine in severe cardiac fallwe. Br Med J 1980;281:1324. Elksyam U, Webar L, MoKay C, Rahlmtoola SH. Vari- able, unpredictable, and deleterious hemodynamic re- sponsa to oral nifsdipine in *era chronic heart failure: an experience in 32 pattents (abstr) J Am Coil Cardiol, in press.

Uri Elkayam, MD Shehbudin H. Rahlmtoola, MD

Los Angeles, California