Peripheral venospasm associated with signs of transient myocardial ischemia

Peripheral venospasm associated with signs of transient myocardial ischemia

Peripheral of transient venospasw associated myocardial with signs ischemia Gilles R. Dagenais, M.D.” Wulter D. Gundel, M.D.“* C. Richard Conti...

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Peripheral of transient

venospasw

associated

myocardial

with

signs

ischemia

Gilles R. Dagenais, M.D.” Wulter D. Gundel, M.D.“* C. Richard Conti MD. .‘** Balt~imore, ,Ud~

ince 1950, there have been several extensive surveys of the potential hazards and complications of more than 25,000 cardiac catheterizationsl-8 A few procedures have been associated with retrosternal pain and ischemic electrocardiographic changes, occurring mostly during manipulation of a catheter in the cardiac chambers or coronary ostia. We have recently observed a patient who developed simultaneous peripheral venospasm and clinical and electrocardiographic signs of acute myocardial ischemia during the insertion of a venous catheter for a right heart catheterization. To our knowledge, such an observation has not been reported in the literature. Case report A t5-year-old Caucasian female student, with the clinical diagnosis of tetralogy of Fallot was referred for cardiac catheterization before anticipated total surgical correction. A cardiac murmur was noted at the age of 5 days, and subsequently cyanosis appeared, particularly during crying and exertion. At age 4, a right end-to-side Blalock-Taussig anastoFrom the Department of Medicine, The Johns This work was supported in part by United Grant HE-05689 from the National Heart Received for publication Aug. 18, 1969. Reprint requea to: Dr. Gilles R. Dagenais, Ijniversity School of Medicine, Baltimore, *Fellow of the Canadian Heart Foundation. *Wellow of the Heart Association of Maryland. ***Assistant Professor of Medicine and Director

544

American Heart Journal

cnojis was cun~tructed aud the patient became asymptomatic. The patient, at age 13, was treated successfully for subacute ‘bacterial endocarditis. She experienced occasional dyspnea on moderate exertion but denied chest pain, syncope, orthopnea, or ankle edema. The pertinent physical findings of ihis girl who was 5 feet, 4 inches tall and weighed 114 pounds were blood pressure 110/70 (left arm) and 90/50 (right arm) and slight nail clubbing, withuut peripheral cyanosis. There was a right ventricu‘ar heave and SZ was single. A grade 4/6 ejection systolic murmur was heard maximally over the left lower sternal border, and a grade 2/6 continuous murmur was located at the aortic area. Multiple nematocrits were recorded in the range of 43 to 47 ml. per 100 ml. from 1963 to 1968, Chest x-rays revealed a slight “coeur en sabot” with mild right ventricular enlargement and the pulmonary vascularure was slightly increased on the right side. The electrocardiogram disclosed a previously documented sinus rhythm, right axis, and incomplete right bundle branch block (Fig. 1). Thirty minutes before cardiac catheterization, the patient received morphine, 6 mg. intramuscularly (I.M.), atropine, 0.5 mg. I.M., Nembutal, 100 mg. orally, and Benadryl, 50 mg. orally. Under local anesthesia w-ith infiltration of Xylocaine 1 per cent, an incision was made in the right antecubital fossa, and a deep vein near the brachial artery was isolated. The patient did not experience pain during this

Hopkina University States Public Health Institute. Department Md. 21205.

of Medicine,

of the Cardiac

School of Medicine Service Research

and Hospit& Grant HE-05584

Cardiovascular

Catheterization

Laboratory.

Division,

Baltimore, Md. and Training

The Johns

Hopkins

Yolume Number

80 4

Lpe~iphera~ venospusm and myocurdial

ischemia

545

AVi

Fig. 1. ECG before branch block.

cardiac

catheterization

demonstrating

procedure, and when the vein was opened, blood flowed freely from the vessel. A No. 7 RodriguezAlvarez catheter, tilled previously with heparinized 5 per cent dextrose in water, was introduced into the vein but could not be advanced more than ‘2 cm. The operator then attempted to withdraw the catheter and found that this was impossible, the catheter being firmly fixed in one position in the vein by spasm of the vein wall. No attempt was made to aspirate or flush the catheter or to do further manipulation. At this moment, when it was clear that the catheter was entrapped in a collapsed vein, the patient experienced retrosternal squeezing pain. Simultaneously, the electrocardiogram revealed S-T elevation in Leads II, III, and aVr, and atrioventricular dissociation (Fig. 2). There was no hypotension or cyanosis and no change in the findings on cardiac auscultation. No medication was given and, after 2 minutes, the chest pain and arrhythmia disappeared, the S-T segments became isoelectric, and the peripheral venospasm was no longer present.

normal

sinus

rhythm

and

incomplete

right

bundle

The catheter could then be advanced easily in the same vein, and the patient experienced no further pain or electrocardiographic changes during the remainder of the procedure. The atrioventricular dissociation with periods of sinus arrest returned after ventriculography. Hemodynamic and angiographic data were consistent with tetralogy of Fallot with moderate valvular and infundibular stenosis (right ventricle pressure, 120 mm. Hg, and pulmonary artery pressure, 27 mm. Hg), and a functioning right BlalockTaussig shunt. The arrhythmia persisted intermittently during the following 5 days (Fig. 3). The serum glutamic oxalacetic transaminase (SGOT) (normal below 40 units) was 41 and 20 units, 5 and 20 hours, respectively, after catheterization. Three days after this procedure, the patient underwent total surgical correction, and the coronary arteries were carefully examined and found to be normal to inspection and palpation. Two months later, the patient was well, and on exercise electrocardiogram did not reveal any sign of ischemia or arrhythmia.

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Fig. 2. Continuous ECG recording at the time of chest pam. Numbers on the left indicate the time in seconds and the leads are identified on the right. The tracing reveals progressive S-T &vdtiOn during the first 70 seconds. The record had returned to normal by 120 seconds. Intermittent atrioventricular dissociation is also noted. The tracings are not standardized to 1 mv. per centimeter of deflection.

Discussion

During the course of cardiac catheterization, a U-year-old girl developed severe chest pain and transient electrocardiographic changes characteristic of myocardial ischemia in association with an episode of severe peripheral venospasm. A number of possible explanations must be considered for this unusual situation. It was considered possible, although unlikely, that this young woman had coronary artery disease. The basic diagnosis of congenital heart disease suggested the possibility of a congenital malformation of distribution or a stenosis in the coronary arterial system. Acquired coronary artery disease secondary to an inborn error of

metabolism was also considered. Anatorltic abnormalities of the coronary arteries appear to have been excluded by direct inspection of the vessels at surgery, the negative electrocardiographic exercise test in the postoperative period, the subsequent course, and the absence of any evidence of manifestations of metaboiic disorders known to be associated with premature coronary artery disease. Thromboembolism is suggested by the temporal association of the ischemic episode with the catheter insertion in the peripheral vein. It is possible that a thrombus, liberated at the peripheral site, lodged in the coronary arteries, having reached the systemic circulation by way of the right-to-

Ydwme Number

80 4

Fin. 3. ECG right bundle

Peripheral

tracing branch

obtained block.

24 hours

after

catheterization

left intracardiac shunt. The presence of free bleeding from the proximal segment of the vein when it was first opened is against this explanation. The catheter was advanced 2 cm. before it became fixed and later could be moved freely through the same vein to the heart. This suggests that spasm, not thrombosis, was responsible for the obstruction. The possibility of coincidental embolization from another source at the time of venous catheterization, unrelated to the peripheral venospasm, seems unlikely but cannot be eliminated. No right-sided endocardial thrombi were disclosed at the time of open-heart surgery. The short duration of the chest pain and electrocardiography abnormalities (2 minutes) plus the absence of other evidence of peripheral thromboembolism make coronary thromboembolism from any source unlikely. Air embolism must also be considered and has been reported in association with the opening of a vein. This usually occurs with the jugular vein in which the pressure may fall below atmospheric in association

venospasm‘ and myocardial

showing

atrioventricular

&hernia

dissociation

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and inc zomplete

with negative intrathoracic pressure.g Air in the right side of the heart will collect in the right ventricular outflow tract, but in the presence of a right-to-left shunt at this level, air embolism to the coronary circulation is possible. In our patient, the presence of a spontaaeous backflow after venous incision indicates that the peripheral venous pressure exceeded atmospheric pressure and therefore minimizes the likelihood of spontaneous aspiration of air from the open antecubital vein. Air might possibly have been introduced via the catheter but this seems unlikely because the venous catheter was filled with heparinized 5 per cent dextrose in water and was neither aspirated nor flushed prior to the time of the observed electrocardiographic change. We feel, therefore, that air embolism from the antecubital vein can be (excluded as a likely cause of the chest pain and electrocardiographic abnormalities in the patient. This conclusion is further supported by the absence of auscultatory changes (including a “millwheel murmur”) and the inability to detect

air in any cardiac chamber during Hueroscopy. A final possibility remains that the patient developed myocardial ischernia secondary to coronary artery spasm. Similar episodes of myocardial ischemia, manifested by pain and electrocardiographic change, have occurred during manipulation of catheters in atria or ventricIes,e-* Similar findings have been recorded during coronary arteriography, and transient narrowing of a coronary artery has been visualized and temporarily associated with chest pain and electrocardiographic abnormalities”-“1s which are often S-T segment elevations as described by Prinzmetal and associates.‘0 During coronary arteriography the spasm appears to be induced by mechanical stimulation associated with manipulation of the catheter in the coronary ostium.4 I-Iowever, in one of the patients described by Demany and colIeagues,5 coronary spasm was observed with the catheter tip in the ascending aorta indicating that remote contact with the wall of the vascular system may be responsible. S-T segment elevation has been observed following ingestion of ice water’l; this might represent another example of coronary spasm, although the local direct effect of temperature on repolarization is another possibility. In any case there is some evidence to suggest that coronary spasm may occur as a response to stimuli other than direct contact with the wall of the coronary arteries. Venospasm is most often induced by trauma,12 and in the present patient, the insertion of the catheter seems the most likely course. Venospasm may be associated with a neurogenic discharge causing an increase in both venous and arterial tone.12 Experimental work on isolated coronary and peripheral veins’” arterial segment+ suggests that constriction of these vessels occurs in response to adrenergic alpha receptor stimulation. In the present patient, the simultaneous occurrence of peripheral venospasm and evidence of coronary spasm seem more than coincidental and suggest that both events represent manifestations of intense alpha-receptor stimulation. The distribution of the electrocardiographic changes suggests that the coronary spasm involved the right coronary artery

predominantlyU ‘The right ventricle, supplied by the righ:: coronary artery, would be especially susceptible to ischemia in this patient because of the right ventricular hypertension and hypertrophy. The right coronary artery is usually the predominant vessel, probably giving off the artery to the X-V node and the sinus node; this might also explain the simultaneous arrhythmia. Similar rhythm disturbances have been I-eported with ischemic electrocardiographic !.;hanges5~10and also with catheter manipulation in cardiac chambers.15~18 The increase in SGOT after catheterization may be due io the coronary artery spasm but is not tmusual after hemodynamic and angiographic studies.17 This suggested reflex may prove to be of significance in patients with angina pectoris and normal coronary arr.eriograms. urnmary A young patient with tetralogy of Fallot developed clinical electrocardiographic evidence of myocardial ischemia in association with intense peripheral venospasm. Several mechanisms are discussed, but it seems most likely that the ischemic changes were !he result of coronary artery spasm.

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Thompson, H. Ii., Jr., Sleeper, j”. C., a11d MCTntosh, Ii. D.: Coronary occlusion during right heart catheterization, Amer. J. Cardiol. 10:110, 1962. Tsitouris, G.: Right coronary artery occlusion during retrograde left heart catheterization complicated by rare arrhythmias, Angiology B6:748, 1965. Gensini, G. G., DiGiorgio, S., Serra, C., Coskum, 0.. and Black, A.: Coronary angiography, Vast. Dis. 1:34, 1964. Sones, F. WI.: i>a Hurst, .I. W., and Logue, R. B., editors: Cine coronary arteriography in the heart. vol. 33. New York. 1966. McGraw-Hill Book’Compa&, Inc., p. 203. Demany, M. A., Tambe, A., and Zimmerman, H. A.: Coronary arterial spasm, Dis. Chest 53:714, 1968. Hager, It::., and Orth, H. I;.: Fluchtige ST und T l-eranderungen in Electrocardiogramm bei der Katheterisierung des linken Herzens, Cardiologia 45:299, 1964. \\Tennevold, A., Christiansen, I., and Lindeneg, 0. : Complications in 4,413 catheterizations of the right side of the heart, AMER. HEART j. 69:173, 1965. Sraunwald, E., aud Swan, H. J. C., editors:

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Pevipherul

Cooperative study on cardiac catheterization, Circulation 37:Suppl. 3, 1968. 9. Zeft, H. J., Harley,.A., Whalen, R. E., and MCIntosh. H. D.: Pulmonarv air embolism duringinsertion of a permanent transvenous cardiac pacemaker, Circulation 36:4.56, 1967. 10. Prinzmetal, M., Kennamer, R., Merliss, R., Wada, T., and Bor, N.: Angina pectoris. I. A variant form of angina pectoris, Amer. J. Med. 27~375, 1959. 11. Hical, H., and Massumi, R.: Variant angina pectoris, Amer. J. Cardiol. 19:607, 1967. 12. Alexander, R. S.: The peripheral venous system. in Hamilton. W. F.. and Dow. P.: Handbook of physiology, Section 2, Circulation, 31, Washington, D. C., 1963, vol. 2, p. 1086, American Physiological Society. 13. Moran, N. C.: Adrenergic receptor drugs and

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the cardiovascular system, Mod. Cont. Cardiovasc. Dis. 35:99, I966. Webb-Peploe, M. M., and Shepherd, J. T.: Veins and their control, New Eng. J< Med. 278:317, 1968. Black, J. F. S., Moore, A. A. S., Cortes, S., and Lambert, E. C.: Atrioventricular block as a complication of cardiac catheterization, Circulation 30 (Suppl. 3):48, 1964. Gault, J. H., Ross, J., and Braunwald, E.: Persistent atrioventricular dissociation with block and nodal rhythm after cardiac catheterization, AMER. HEART J. 71:690, 1966. Adrouny, Z. A., Stephenson, M. J., Strouke, K. R., Dotter, C. T., and Griswold, H, E.: Effect of cardiac catheterization and angiocardiography on serum glutamic oxaloacetic transaminase, Circulation 27:565, 1963.