Coexistent aortic and subaortic stenosis—II

LETTERS

TO

THE

EDITOR

Coexistent Aortic and Subaortic Stenosis-II \vC

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inaccurate stntemcnt that could lend to inadvisable thernpeutir m:in:qement. On pngr 311, the st:rtemcnt is made, “Ar can be seen from Table IV, tlte 3 patients who were studied with an infusion of isoprotercnol (3 mgm/500 cc of 5 percent glucose in water) showc~d the typirnl rcsl)onae diagnostic of functional the left ventrifulnr c:ivitJ liypertrophic, subnortic stenosis: prrssurc ros:(s while the periplicrnl arterial systolir pressure frll (Fig. S I.” \Vr wo111d expect isoproterenol to increase the systolic pre.qsurc gradient across the aortic v:rlvc in pure valvulnr aortir stenosis without sccondnry subnortic niuscutar hypert rophy because ( I ) ixoproterenol increases cardiac output; (2) the incrcnsed blood flow across the fiscd rrsistnnce of :I rtenotic aortic valve causes increased left ventricular llrrssure: (3) isoproterenol causes decreased total peripheral vascular resistance resulting in a fall in peripheral arterial pressure. Braunwald et al.” have reported that isoprotrrrnol administration to patients with val\-iilar nortic stenosis proclurcs an inrrcnse in cardiac output and an inrreasc in left vcntriciil:~r-:irtcri:ll pressure gradient, without a decrease in aortic orifice size.

Reply to Massing

WC do not intend to deny the l)ossil)lr importance of identifying serondary muscular sulxiortica Ii\-pertrophy di1c1 to vnlvular nortir stenosis. WC, do, IiowvcLver,wish to prevent, its fnlrr diagnosis hnsetl solrly on an incre:isrd lrft vcantrirutar-art&d systolic gradient protluc~cd 1)~ isolrrotc~renol ii~fusion. This could lead to the improper ll,Gr of proprnnolol or improper surgical approach in thfa trcntmrnt of l)“rc valvutar aortic stenosis. GEORGE MASSING, MD Cleveland Metropolitan General Hospital Cleveland, Ohio JEROME LIEBMAN, MD, FACC Case Western Reserve University School of Medicine Cleveland, Ohio January 7, 1970 References 1.

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Parker DP, Kaplan MA, Connolly JE: Coexistent am-tic valvular and functional hypertrophic subaortic stenosis. Clinical, physiologic and angiographic aspects. Amer J Cardiol 24:307. 1969 Braunwsld E. Ebert PA: Hemodvnamic alterations in idiooathic hypertrophic subaortic stenosisinduced by sympathom~metic drugs. Amer J Cardiol 10:489, 1962

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and Liebman

We agree that isoproterenol increases the pressure gradient across the nortir valve in pure aortic vnlvular stenosis. However, the nortic systolic pressure should increase along with the increase in left ventricular systolic pressure in the presence of :I fired size to the nortir orifice. This sequence of events is the result of the inotropic action of the drug on the myocnrdiuni itself and the attendant increase in cardiac output. If the I)eriphernl vasodilnting effect of isoprotercnol takes prccedcnce over its inotropir effect, in any given case, then both peripl~rral nrt,erinl and intraventriculnr pressures fall. In our experience, the vnsodilnting effect appears first and is super,sedod by the inotropir effect as more of the driig is administered: we 11:~~~not observed both actions at the samr time in term:: of prrs~urc gxdient arros:: thr left vrntrirulnr olitflow tract. In Cnw 4 of the paper quoted,’ we believe either that there was unrecognized subnortic ohstrwtion along with aortic \alvnlar stenosis or that cnt.lieter entrapment or

cavity obliteration accounts for the divergent intraventrirutar and aortic pressures. Finally, we hnvr devised a !untllem:ltic:11-t,lectri~:~l analog2 which simulates the hemodynnmic conditions observed whrn both fised aortir vnlvulnr stenosis and functional hypertrophic subnortic stenosis coexist or w11e11 either lesion i:: present alone. This model clearly corroboratc.~ the hemodynamic ohservntions discusecd. MARVIN A. KAPLAN, MD DAVID P. PARKER, MD JOHN E. CONNOLLY, MD January 26, 1970 References 1.

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Hemodynamic alterations in idiopathic Braunwald E. Ebert PA: hypertrophic subaortic stenosis induced by sympathomimetic drugs. Amer J Cardiol 10:489. 1962 Kaplan MA, Parker DP. Sherwood J, et al: Coexistent aortic valvular and functional hypertrophic subaortic stenosis. An electrical analog simulating the physiologic observations. J Ass Advance Med Instrum, in press

Concealed Extrasystoles I believe that Friedberg completely misses the boat in his article concerning concealed extrasystoles in the August) issue of thr Jo~txnl.’ Far be it from me to deny the existence of concealed ronduction that has been so aptly described 1)~ Langrdorf, Pick and others. In the particular nrrhythmin strip representrd in Figurr 2 of the article, however, concealed conduct,ion does not exist. Friedberg is completely overlooking two rather obvious phenomena that are occurring. The first is the obvious sinus arrhythmia that can he recognized by a speeding up and a slowing down of the I’ waves. The second is the lrss well known but firmly catnhlished phenomenon of the changing refractory period :IC-

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1970

rording to cycle length, or the so-c:rll(~d .4,~lim:in ptienomrnon. Acknowledging thrse two factors, one can cq~lain rvrr: item in the tracing without having to conjllrc 1111conce:ilrd conduction. First of all in etril) A we first see :I simlr rh\.thm A4 with second degree A-T? blork with 2: 1 .4-V condurtion. premature ventricular contraction intcrrrq+ ttii,< seqiK9rc and represents the fifth beat in the strip. The sixth beat is again conducted from the sinlls. Then th(xre is :I ii: 1 ,4-j: conduction surrounding the sisth beat instead of 2:l. This is because the sisth beat now 1~ a much longer rrfrartor! period than the previous 2:l beat? sincr tlic ryrlt, length betwern the premature ventricular rontrartion and thr

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