Gastrointestinal symptoms of progressive myocardial disease

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AMER!(L~N ! H~;A]~? J O U R N A L

v e n t r i c u l a r rate and ])y increasing ~he possibility ()i ~Vlta/ systemic embo]i would seem imperat[ve. The factors ~, he eonsider~i ,-~'e eonlplex, a~d w i l l be dealt with in anothec st~dy:

Auricular fibrillation in associatio:,~ with myocardial inf~x~li<)n i~ a series of eighty-four patienl;s at; the l~os A~)~'eies (,~om~i.y (~enl'ral !i<)s!)ilai ~ a s a hazard as regards both mort:ality rate ~l'~,~ ~hc incident(, oi systemic e~nho]i. REFEII,t,~NCES 1~ Master, A, M., Daek~ S., and Jaff G H . L . : Disturbances of }gate and R h y t h m ir~ Acute Coronary A r t e r y Thrombosis, Ann. I ~ t Med. 11: 7:~5~ 1937. 2. t~osenbaum, F. F., and Levine, S . A . : Prognostie Value of V~l.~'ions C~inieai a~d Nleet~'oeardiographie Features of Aeut:e Myoeardiai ]nfareti(:~;; I m m e d i a t e Prognosis, Arch° Int. Ned. 68: 913~ 1941. ;I. lgathe~ H . W . : Myocardial Infaretion~ C~i~iiea~ Features am~ Prognosis, J A 2d',.A. t20: 99, 1942. 4. Wood~ F. C., Wo]fert] b C. C., and BelleL So: ~nfaretion of t:he Laterai Wall of ~he Left Ventricle; Electrocardiographic (?haraeteristicS~ A~I:. l~[~;Aa~pJ~ 1t3: 387~ 1938. 5. Thomson~ H. W , and Feil, H.: Infare, tion o~ t]~e Lateral Wal! of the L e f t Ver~triek3; Pathologic and Electrocardiographic Study~ Am. J. M Se. 207: 588~ 1.044. (L Smith, J. R., and Wilson, K . S . : Studies on t:he Produetio~ a~d Mair~te~mn,!e of F]xperimental Auricular Fibrillation, AM;, H~;Aa,r J. 27: 176, 194L 7. Ilobinson, (}. C.: The Infiuenee of the Vagus Nerves on the F'~radized At~rieles i~ lbe Dog*s Heart, J. Exper. Med. 17: 429, I!)13o 8. Sigler, L. H.: Hyperae{;ive Cardio-inhibi~ory Carotid Sinus ~eflex; Possiilie Aid i!i Diagnosis of Coronary Disease, Arch° 1at° Med. t37: 177, ~!}4/i. 9. 1~evine, S. A.: Coronary T h r o m b o s i s ~ts Various (~Hnieai V~s,tures, B~l~imore~ ~929, Williams & Wiikins Company

( ~ A S T R ( ) I N T E S T I N A L S Y M P T O M S ()F P]~()(~RESSIVlq MYOCARDIA[~ 1)IS E A S E ROBT. I,. MC~IILLAN, M.I)., FRED ]~]. (+~0WI)EN, :Mfl).. AND . l }~. REINHART, M.i}.

WINS'rON-Sat,~:,,~, N. (7. T A T E M E N T S can be found in medieai literature to ~he effect tha.t gastrointestinal symptoms are of common occurrence in ) r i m a r y hear~; disease, ~md that these symptoms m a y largely overshadow the more typical symp~;oms oi heart failure. Thus, in 71892, ()sler ~ made the observation ~hat "cases of ~
S

I~rom the Department of Inter'nal Medicine, t~owman Gray SebooI of Medicine .af Wake Forest College, and the North Carolina. Baiotist H()si)itM, X~rinston-S~?em N~ C ]{eeeived for publication July 27, 1944.

full clinical application or led to more illuminating studies. It is, 1herefor*e, our purpose to review briefly the lit:tomach, and vice versa (b) Nausea and vomiting are not, uncommon symptoms of cardiac disease, espe Gaily disease resulting from inadequate coronary flow. (c) These symptom may, under certain conditions at least, be induced reflexly from the heart itself The following case seems 1-o illnstrate these srveral points.

were depressed; S-T, was elevatetl; T, anil T, were upright; and T, anti T, were inverted. Diagnosis: Sinus tachycardia. The record suggested myoeardial disease with fairly recent myocardial infarction, probably of the Ilosterior type. Fluoroscopic examination of the chest showed mark&i cardiac enlargement due to hypertrophy :!nd dilatatiou, without characteristic configuration. The amplitud? of the The fluoroscopic examination was repealed three cardiac contractions was greatly reduced. Gastrointestinal roentgcnologic studies two weeks after admission, Imt no change was xecn. weeks after admission were negative. The basal metabolic rate t3’i per cent. The venous pressure soon after atlmission mas .Xl cm. of saiiue. The circulation time (arm-to-tongue, using calcium glueonate) was 45 secontls, ant1 the vital cnpwitp was 2.23 liters. Clini& Cowse.-The pxticnt was given digitalis and, later, squill continued t,o complain constantly of SP~I’(: nausea, am1 vomited frequently. never fell below 116 per minute, and 11e continually hat1 :I, 1wlsr pressure mm. of mercury. On April 10, 1940, all 0~11 mellical-ions except sedatives wfw Idiscontinued in the lratient ‘s condition. On hpri! 17, he began to show pitting eclenia sntl, on April 19, of hi; ankles. Hecnuse there was evitlence of ascites, centesis was performed; this yielded only 100 C.C. of thirk callow fluid, which fifteen minutes. The specific gravity of this fluid was 1.014.

(Urginin). Ile The pulse rate of 0nIy 10 to 20 without over his abdominal congealed

change sacrmn, parawithin

The patient began to rxpectorate bright ret1 blootl on April 23, and, on April 25, his temperature rose to 38.5 0. The hlootl pressure hat1 fallen slowly since admission, and was ll(i/lOO at this time. The nest (lap he complained of pain in tlw right side of his chest, :rml shoTvet marked temlerness to pexussion over the right hemlthorax anteriorly from the costal margin to the precortlinm. RBlrs had been heard over ihe lower lohe of the right A diagnosis of infarction of the lung, and signs of consolirlation ap1Iearetf in that area. lung was made because of signs of consolidation plus marked tenderness over the area.14 Ralyrgxn and aminophylline rvere given intrnvenously without effeet. 13ecxuse of Ilie persistent nausea an,11 rolrliting, fluids were given large amounts of thiamine hy~lrochlori~lc ant1 liver extract intramuscularly. vomiting were constant complaints. At times the patient becwne quite was obtained only by sedatives. On April 27, 1943, he became unable to void, ant1 catheterization had become severe, but the lungs were relatively clear except for in the lower half of the right lung.

the

parenterally, The nausea irrationitl.

with ant! Relief

was necessary. Edema signs of consolitlation

On the morning of April 29, 194::, the patient ‘9 pulsa became small and rapid, ant1 the blood pressure was imperceptible. He ww irrational, coverwl with cold clammy swat, am1 presented a picture of peripheral am1 rentral circulatory collapse, with pulmonary o~lema. Only terminally did the patient tlevelop any orthopnea ; until then he was able to lie relatively flat in bed without respiratory tlistress. The puhcondry edema became more severe, nirrl the patient tlietl at noon on April 29, 1943. The autopsy observations were as follows : The peritoneal and right pleural cavities contninetl, respectively, 1,330 and 700 C.C. of straw-colored, clear fluid with a specific gravity of 1.015. Several infarcts Q-rcre fount1 in the lower lobe of the right lung, and ant?-mortem b!ood clots occluded the luminn of the pulmonary arteries which supplied these areas. The liver, which meighed 1,650 grams, was congested. The lieart weighed 450 grams. The rhxmbers of the right side were dilatctl, and the wall of the left ventricle was hypertrophied. The homogeneous gray color of the subendothelial tissue of the left ventricle was in striking contrast to the reddish-brown colol, of the inner surface of the right ventriclp. A mural thrombus 2.5 cm. in (liameter was attached to the left anterior wall, and the musculature in that area was softened a!ld dark brown in color. Section of the left ventricular wall revealed a thin subendothelial zone and extensive patcll,y areas of fibrosis involving eq)eci~l~y the interventricular septum and the posterior wall. Exrminatioo of the coronary arteries revealed numerous athwosclerotic plaques which ha11 prot1uee.d varying degrees of narroming of the Iumina of these vessels. The right main eoronwv artery contained a fresh thrombns which completely occluded its lumen 2 ml. from its orifice at the sinus of Valsalva. On microscopic examination, the kidneys, xdwnal giamls, pancreas, ant1 myocardium showed marked arteriolar sclerosis. The mural thrombus was in an early phase of organization. The subendothelial tissue of the nlyocartliunl >\-a~ swollen and hyalinize~l. Focal areas of filbrosis of variable maturation, ant1 acute and chronic i-nflammatory reactions W~TD evidence of repeated occlusions of small branches of the coronary arteries. The older and

Fig. Z.-An 1 are in varying ?ly obliterated

area

of myocardial scarring. stages of degeneration. by eubendothelial connectire

Fig. 3.-In this ions, degenerating 11 thrombosis.

photomicrograph, myocardial

fibers

made are

The

A4t the edges lumen of the tissue deposits.

of a section seen together

through with

of the small

photomicrograph, artery is almost

one of endocardial

the

myocardia thickening

thn corn-

MC

MILLAN

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GASTROI?jTESTIS~lL

SWdp’L’OXIS

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The condition presented involves a patient who, after coronary occlusion, developed heart failure, the primary symptoms of which were nausea and vomiting, and in whom the significant pathologic changes were multiple areas of As a result of the experiences with this and other similar myocardial fibrosis. cases and a review of the literature, the following concl-asions are drawn : 1. When nausea and vomiting are dominant symptoms in a case of heart failure, one should consider as possible factors not only drugs, congestion of the abdominal viscera, and disorders of the blood meta.bolites (such as occur in uremia), but should also entertain the possibility that progressive myocardial disease may be the cause of the symptoms. 2. The mechanism of the nausea and vomiting induced by progressive myocardial disease is believed to be analogous to that caused by digitalis, which has been shown to be due to a reflex arising in the heart itself. 3. When coronary thrombosis occurs in a patient with pre-existing narrowing of the smaller coronary arterial branches, a vicious cycle may ensue; the decline in cardiac output and small pulse pressure lead to further coronary insufficiency and progressive myocardial fibrosis, which bring about a further dccrease in cardiac output and perpetuation of the cycle. 4. In cases of heart failure in which there is a small pulse pressure with a high diastolic pressure, the outlook is poor because of the factors outlined. REFERFXCES

Practice of Medicine, ed. 2, New York, 1892, D. Appleton-Century Co., p. G27. 1. Osler, W.: 2. Herrick, J. B.: Clinical Features of Sutlrlen Obstruction of the Coronary Arteries, J. A. M. A. 59: 2015, 1912. 7< . Levine, S. A.: Management of Patients With Heart Failure, J. A. M. A. 115: 1713, 1940. 4. Harrison, T. R.: Failure of the Circulation, ed. 2, Baltimore, 1939, Williams & Wilkins Co., p. 361. Osler’s Principles and Practice of Xedicine, ed. 13, New York, 1944, 5. Christian, H. A.: D. Appleton-Century Co., p. 1032. 6. Tice, F.: General Treatment of Chronic Myoearditis and Valvular Disease, in Tice, F.: Practice of Medicine, Hogerstown, MCI., 1941, W. F. Prior Company, Inc., vol. 6, p. 346. 7. Hatcher, R. A., and Weiss, 8.: Mechanism of Vomiting, Physiol. Rev. 4: 479, 1924. 8. Hatcher, R. A., and Weiss, 8.: Studies on Vomiting, J. Phsrmacol. & Exper. Therap. 22: 139, 1923. 9. Hatcher, R. A., and Weiss, S.: Seat of Emetic Action of Digitalis Bodies, Arch. Int. Med. 29: 690, 1922. 10. Sutton, D. C., and King, W. W.: Physiological Effects of Temporary Occlusion of Coronary Vessels, Proe. Sot. Exper. Biol. & Med. 25: S42, 1925. 11. Manning, G. W., Hall, G. E., and Banting, F. 6.: Vagus Stimulation and Production of Myocardial Damage, Cacad. M. A. J. 37: 314: 1937. 12. Gilbert., N. C., Fenn, G. K., ad LeRoy, G. V.: Effect of Distension of Ab~lominal Viscera on Coronary Blood Flow and on Angina Pectoris, J. A. M. A. 115: 1962, 1940. 13. Levy, H., and Boas, E. P.: Angina Pectoris and the Syndrome of Peptic Ulcer, Arch. Int. Med. 71: 301, 1943. 14. McMillan, R. L. : A New Physical Sign in Tnfarction of the Lung, North Carolina M. J. 3: 642, 1942. 15. Smith, J. J., and Fbrth, J.: Fibrosis of the Emlocxrdium and Myocardium With Maral Thrombosis, Notes on Its Relation to Isolated (Fiedler’s) Myocarditis and to Beriberi Heart, Arch. Int. Med. 71: 602, 1943.