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Spasm of the Left Anterior Descending Coronary ~ r t e r ~ * Frank 1- Rose, M.D.,** A h . D. Johnson, M-D-,t and Rfchrd A. Carleton, M.D.3 F.C.C.P. * ~ * twith -t whose e - a c data 4 a rlgM cornruterg ksion wps tormd at coronary angiography to have transient spasm of the left wedor descendiq cornMild atherosclerotic dhPerse app& to .a a m b s w for the kcalized coronary spasm. m. Since the original description by Prinzmetal,' the anatomic substratum of variant angina pectoris has been felt to be significant focal coronary atherosclerosis. However, the unusual characteristics of the syndrome gave rise to early speculation that coronary arterial spasm might coexist and be causally related. Recently, coronary arterial spasm in the setting of variant angina has been well documented, especially in the carefully studied case reported by Oliva, Potts, and Pluss,z and in the direct observation of MacAlpin and co-workers.8 A patient is described with variant angina in whom transient spasm of the left anterior descending coronary artery was demonstrated. A 46-year-old Caucasian man, an athletic coach, was in apparent good health until September 1973. At that time., 'From the Cardiology Section, Department of Medicine, Universitv of California San Diem. - , and the Veterans Administration H ital. S& Diego. **Cardiology F X W , Cardiology Division, University of California. thsistant Professor of Medicine, University of California; Director. Cardiac Catheterization Laboratorv. Veterans Administration H ital, San Diego. $F'rofessor of ~ z c i n eUniversity , of California; Chief, Cardiology Section, Veterans Administration Hospital, San Diego. Presently at Dartmouth Medical College, Hanover, New Hampshire. Reprint requests: Dr. Carleton, Dartmouth Medical School, Hanwer, New Hampshire 03755 .. hypertension (160/110mm Hg) was documented during a routine examination; an electrocardiogram demonstrated only left axis deviation. Diuretic therapy was begun, and subsequent blood pressures were normal. Approximately two weeks later, the patient experienced an episode of lower retrosternal chest pain while restfully seated. The pain lasted approximately two minutes and was associated &th diaphor&is; there- was no shortness of breath, nausea, or vomiting. Several episodes of similar pain occurred during the succeeding weekeach without relationship to mid~eptember,an -bode of pain lasting approximately one half hour occurred and the patient was placed in a coronary care unit. The admission electrocardiogram demonstrated left axis deviation. During the following day, while in bed, the lower retrosternal pressure sensation recurred. The e l d o g r a m monitor showed sinus bradycardia and frequent premature ventricular contractions. Subsequendy, an e l e c t d o g r a m demonstrated complete heart block, a junctional escape rhythm, and occasional Dremature ventricular contractions. Leads 2. 3. and aVF Lmonstrated marked ST segment elevation '(Fig 1 ) . The precordial R-wave progression was less well developed than on the prior tracing. Atropine and isoproterenol were infused; a junctional tachycardia at a rate of 95 per minute appeared. The ST segment elevation increased to approximately 1.1 mv and the drugs were discontinued. Within two hours, the patient had returned to a sinus rhythm with normal ST segmenis but with residual T wave inversion in Vz.4. The patient was referred to the San Diego Veterans Administration Hospital for further evaluation, where cardiovascular examination was unremarkable save for the presence of a fourth heart sound. E l d o g r a p h i c monitoring demonstrated transient ST segment elevation and premature ventricular contractions in coniunction with each of two e~isodesof chest pain. ~eithe; serial enzymes nor elec&adiograms suggested myocardial infarction. With a clinical diagnosis of variant angina, cardiac catheterization was performed. Atxial pacing to a rate of 150 per minute produced neither pain, e l d o g r a p h i c changes, nor abnormalities of pulmonary artery wedge or left ventricular end diastolic pressure. Left ventriculography demonstrated a normal contraction pattern. Coronary arteriograms were performed by the Sones technique after premeditation with 1 mg of intravenous atropine and 0.4 mg of sublingual nitroglycerin. The initial injection into the left coronary artery showed minimal lumenal irregularity in the proximal left anterior descending coronary artery. The remeder of the left comnary artery was normal. The right coronary artery was dominant and gave rise both to the sinus nodal and AV nodal arteries. A small marginal = FIGURE1. Electrocardiogramduring an episode of chest pain. CHEST, 66: 6, DECEMBER, 1974 SPASM OF LEFT ANTERIOR DESCENDING CORONARY ARTERY 719 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20959/ on 05/05/2017 The nature and origin of coronary arterial spasm is unknown. In turn, the role of coronary arterial spasm in the production of some or, perhaps, mast instances of variant angina remains unclea~.~J~ Coronary arterial spasm has been demonstrated as a sequel to stimulation of the coronary ostium6by a catheter tip. In the present case, the catheter tip was never within 2 cm of the point of spasm. Coronary arterial spasm has also been demonstrated by Lange and his co-workers7 in individuals subjected to long-term industrial nitroglycerin exposure. The present patient had no such known exposure. However, the observations of Lange may have direct pertinence in the management of patients with coronary arterial spasm in the sense that it may be deleterious to attempt perpetual medication with nitrata in the event that therapy is suddenly withdrawn. The observation of mild atheromatous disease at the site of spasm in our patient supports the original notion of F'rinzmetal and co-workers' that spasm may contribute a reversible, obstructive, and transient factor in the setting of coexistent atheromatous disease. Further study will be needed to clarify the role of coronary arterial spasm >invariant and traditional angina pectoris, so that appropriate medical or surgical therapy can be designed. FIGURE 2. Left coronary injection one hour after nitroglycerin administration. Note segmental spasm in the proximal anterior descending vessel. branch of the right coronary artery had apparent plaquing; the remainder of the right comnary artery was normal. The absence of meaningful coronary obst~~ction and the variant character of the pain led to a dedsion to repeat the arteriograms 50 minutes later without the dmhistntim of atropine or nitroglycerin. Early total occlusion of the proximal left anterior descending ccnmary artery at the site of the previous minor lumenal irregularities was present (Fig 2). The right cvronary artery showed a minor deawure in c a l i i , but was otherwise not different. Sublingual nitroglycerin, 0.4 mg, was then administered and selective left amnrary arteriograms were repeated at intervals.The left anterior dsgoending coronary obstruction gradually disappeared until the appearance was identical to that seen on the initial study (Fig 3). It is notable that the patient experienced neither chest pain nor ST segment elevation during the procedure. The usual transitory T-wave inversions occurred during each coronary injection. The patient has subsequently been maintained on nitroglycerin as needed for chest discomfort. Several episodes of chest pain have occurred at rest, each subsiding promptly with nitroglycerin administration. The present case shows typical clinical and elechocardiographic features of variant angina. The initial presumption, based upon the associated arrhythmia, was that a lesion would be found in the right coronary artery. Instead, transitory left coronary arterial spasm was demonstrated in the absence of clinical symptoms or of electrocardiographic changes. We infer that this patient may, at other times, develop arterial spasm in the right coronary artery. 720 ROSE, JOHNSON, CARLETON ACKNOWLEDGMENT: The patient described in this case report was kindly referred after the initial excellent observations by Dm. Quentin L. Wood and Peter E. Pool of Solana Beach, California. 1 Primmetal M, Kennamer R, Merliss R, et al: Angina pectoris: I. A variant form of angina pectoris: Preliminary 1 FIGURE 3. Subsequent left coronary injection 30 minutes following sublingual nitroglycerin administration. CHEST, 66: 6, DECEMBER, 1974 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20959/ on 05/05/2017 report. Am J Med 27:375-388, 1959 2 Oliva PV, Potts DE, Pluss RG: Coronary arterial spasm in Prinzmetal angina: Documentation by coronary arteriography. N Engl J Med 288:745-751,1973 3 MacAlpin RN, Kattus AA, Alvaro AB: Angina pectoris at rest with preservation of exercise capacity. Circulation 47:948,1973 4 Carleton RA, Johnson AD: Coronary arterial spasm: A clinical entity? Mod Conc Cardiovasc Dis 43:87-91,1974 5 Demany MA, Tamb A, Zimmerman HA: Coronary arterial spasm. Dis Chest 53:714-721, 1968 8 O'ReiUy RJ, Spelberg RD, King TW: Recognition of proximal right coronary artery spasm during coronary arteriography. Radiology 95:305309, 1970 7 Lange RL, Reid MS, Tresch DD, et al: Nonatheromatous ischemic heart disease following withdrawal from chronic industrial nitroglycerin 7. Circulation 46:888878, 1972 The subject of this report is a 63-year-old woman who had been in good health until she developed typical episodes of variant angina pectoris, occasionally associated with high degree AV block and ventricular tachycardia. Third and fourth heart sounds were heard. Despite adequate medical therapy, increasingly frequent chest pain occurred; cardiac catheterization was performed. Two tapering areas of 50 percent narrowing were seen in the diagonal branch of the anterior descending and proximal portion of the circumflex arteries. These lesions were unchanged following nitroglycerin. The right coronary artery was initially widely patent (Fig 1A). During the procedure she spontaneously developed ST segment elevation and typical pain. Visualization of this vessel now revealed 95 percent luminal narrowing 3 cm distal to the ostium extending to, and including, the posterior descending branch (Fig 1B). Clinical improvement has occurred with use of nitroglycerin ointment. Prinzmetal's Angina with Extensive There is good evidence that coronary arterial spasm Spasm of the Right Coronary ~ r t e r ~ * exist~.6-~ Previously reported cases had spasm limited to Mark M . Applefield, M.D. and James A. R a n , Jr., M.D. A pntient with Prinmetclrs angina had extensive sp&m of the right coronary artery, demonstrated by coronary arteriogmphy. Additionally, then were kss severe narrowing~(50 percent) h the diagonal and circndex arteries probably due to atherosckmsk Improvement ha8 occurred on long-actingnitrite therapy. N - umerous cases of variant angina pectoris have been reported and the topic has been reviewed.'-' We have studied a patient with this syndrome who had spasm involving most of the length of the right coronary artery. 'From the Department of Medicine, Division of Cardiology, Georgetown University School of Medicine, Washington, D.C. This study was supported in part by U.S. Public Health Grant HE 05433-14, the Benjamin May Memorial Fund, the Metropolitan Heart Guild, and the Special Cardiac Research Fund. short arterial segments. Our patient had involvement of most of the length of the right coronary system. Therapy of coronary artery spasm seems to be medical rather than surgical because the artery distal to the obstruction may become spastic. Of six patients dethree have had bypass grafting. scribed thus far,l~5-~ One patient died six weeks postoperation during chest pain; the graft was patent. Both survivors, though pain free, have occluded grafts; one, an inferior infarction. All three patients treated medically are improved. Although myocardial infarction may occur in 25 percent of patients with this syndrome, in many cases pain either completely subsides or stabilizes after about three months.1.J 1 MacAlpin RN, Kattus AA, Alvaro DB: Angina pectoris at rest with preservation of exercise capacity. Circulation 47:948,1973 2 Whiting RB, Klein MD, Vanderveer J, et al: Variant WIVJ LLLWIJ, -V VEW. -8 -W 111uarmuzi main right V-1; short m, acute marginal branch. Note relative vessel sizes before (A, left) and during (B, rfght)vasospasm. rluunv a. ~UWL CHEST, 66: 6, DECEMBER, 1974 PRINZMETAL'S ANGINA WITH EXTENSIVE SPASM 721 Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20959/ on 05/05/2017