Myocardial Infarction in a Young Woman with Isolated Coronary Arteritis

without evidence of primary valvular disease.v" Brody and Criley2 suggest that an abnormal sequence of contraction resulting in poor apposition of the mitral leaflets may account for acute regurgitant flow. In the case presented here, resting posterior ventricular hypokinesis was demonstrated. During transient ischemia (ST flattening), the anterior wall became hypolcinetic and the patient developed acute mitral regurgitation with concomitant dyspnea, increased intensity of murmur, and an 8 3 gallop. A soft holosystolic murmur persisted during periods of compensated function, suggestive of posterior waIl and/or postero-medial papillary muscle dysfunction. Periodic compromise of the anterior waD and papillary muscle may have accounted for the dramatic worsening of the mitral regurgitation. It is also possible that an increase in vascular resistance upon discontinuation of therapy with nitroprusside accounted for severe mitral regurgitation. The response of the heart failure to vasodilator drugs was anticipated on the basis of previous studies which have shown that a combined decrease in both left ventricular preload and afterload results in decrease in left ventricular filling pressure (LVFP) and an increase in stroke volume.vt In mitral regurgitation specifically, hemodynamic studies have shown an increase in forward stroke volume and decrease in regurgitant volume with vasodilator therapy.s Additionally, decreasing left ventricular volume decreases the size of the mitral orifice, In summary, we have presented angiographic documentation of intennittent severe mitral regurgitation in a patient with single-vessel coronary artery disease, These episodes and the resulting left ventricular decompensation were adequately controlled on medical therapy consisting of an appropriate inotropic agent and vasodilator. ACKNOWLEDGMENT: We wish to acknowledge the expert secretarial assistance of Ms. Pamlette Kinsey.

1 Cederqvist L, Soderstrom J. Papillary muscle rupture in myocardial infarction. Acta Med Scand 1964; 176:287-92 2 Brody W, Criley J. Intermittent severe mitral regurgitation. N Engl J Med 1970; 283:673-76 3 Bauman DJ, Sutton RB. Unusual hemodynamic response during exercise-induced angina pectoris. Chest 1975; 68:365-67 4 Coiba NH, Cohn IN, Mikulic E, Franciosa JA, Constantinos CR. Treatment of refractory heart failure with infusion of nitroprusside. N Engl J Med 1974; 291:587-92 5 Mehta J, Iacona M, Feldman R, Pepine CJ, Conti CR. Comparative hemodynamic effects of intravenous nitroprusside and oral prazosin in refractory heart failure. Am J Cardiol 1978; 41:925-30 6 Chatterjee K, Parmley WW. The role of vasodilator therapy in heart failure. Prog Cardiovasc Dis 1977; 19:301-25 7 Mehta J, Feldman RL, Wilmer WN, Pepine CJ, Conti CR. Acute hemodynamic effects of oral prazosin in severe mitral regurgitation. Br Heart J 1980; 43:446-60

378

Myocardial Infarction in a Young

Woman with Isolated Coronary Arteritis· Robert A. Pick, LCDR, MC, USNR; Matthew U. Glover, LCDR., Me, USNR.; and w. V. R. Vieweg, Capt, USN (Ret), FCCP

A 26-year-old black woman preseDted with a febrile IBDess aad subseqaeDtly sust8ined an lDferior myocardl8l lDfarctiOD with chest paID, CPK-MB elevatioD _d KeG changes. Left veDtriculography revealed iDferior wall hypoldaesls, ad coroaary ....ography demoDStrated multiple aneurysms of the coronary arteries. FlDdlDlI on visceral ....ography of multiple orpas normaL Varlo_ etiologies were considered; however, her dInIad course was felt to be most consistent with periarteritis nodosa and steroid therapy was instituted.

w.

Multiple aneurysms of the small and medium-sized arteries are the diagnostic hallmarks of periarteritis nodosa (PAN). There are no other specific laboratory markers for this disease; therefore, angiography, (typically of the abdominal viscera), is employed to demonstrate evidence of arteritis.v" Coronary artery aneurysms are commonly described at autopsy;S-& however, coronary arteriograms of patients with PAN have not been published previously. Reported is a patient who demonstrated a necrotizing form of isolated coronary arteritis most consistent with PAN. CASE REPoRT

A 26-year-old black woman was admitted to an outlying hospital because of fever and chest pain. There was no previous history of cardiac symptoms. She had been admitted to the same hospital five months before because of peptic ulcer disease with gastrointestinal bleeding. On examination, the blood pressure was 140/74 mm Hg. The pulse was 80 beats/minute. Temperature was 100°F (37.7°C). Tachypnea was present. There was no jugular venous distention. The lungs were clear to auscultation. No murmur, gallop or friction rub was present. The chest x-ray film showed normal findings. The initial electrocardiogram demonstrated ST segment elevation in leads 1, 2, 3, aVF and VS-6. The serum creatine kinase was 305 IU (normal 0-110 IU), and the lactate dehydrogenase was 278 IU (normal up to 200 IU). A subsequent creatine kinase determination was 178 IU with a 16 percent MB fraction. A hemogram disclosed a normochromic, normocytic anemia (hematocrit 30 percent). The erythrocyte sedimentation rate -From the Cardiology Branch, Deparbnent of Internal Medicine, and the CliniCal Investigation Center, Naval Regional Medical Center, San Diego. Supported in part by the Bureau of Medicine and Surgery, C1UUcal Investigation Program Project No 8-16-1139. The opinions or assertions expressed in this pa~ are those of the authors and are not to be construed as ofBcial or as necessarily reft~ the views of the Department of the Navy or the naval service at large. Bsprint reqfMl8t8: LeDR Pick, Naval Regional MedictJl Cenfer, StIR Diego 9!134 Myocardial Infarction In a Young Woman (Pick, Glove" Vlew.g)

was 58 mm/hr (Westergren method). Results of urinalysis were normal. Chest pains continued. Serial electrocardiograms revealed T-wave inversion followed by normalization of the ST segments. On the second day, a fever was noted which persisted throughout her hospitalization in the range of 99100°F (37 .2°-37.7°C). On the sixth hospital day, a systolic murmur was heard. Additional laboratory data, which were normal or negative, include multiple blood cultures, a white blood cell count, serology for syphilis, antinuclear antibody, rheumatoid factor, cold agglutinins, a direct Coomb's test, blood urea nitrogen, creatinine, and multiple urinalyses. On the 22nd hospital day, she was transferred to our hospital. A detailed interview disclosed no history of mucocutaneous lesions, ocular lesions, digital swelling, arthritis, or lymphadenopathy. Prior drug abuse was denied. The blood pressure was 120/66 mm Hg. A grade 2/6 short ejection-type murmur was heard along the upper left sternal border. Chest pains, which were pleuritic/ pericardial by description, continued. A bone marrow examination revealed changes consistent with chronic inflammation. Erythrocyte sedimentation rates were as high as 120 mm/hr. Additional normal or negative tests included hepatitis B antigen and renal function studies. Cardiac catheterization was performed. The left ventriculogram showed mild inferior wall hypokinesis. The ejection fract ion was 61 percent. There was no mitral regurgitation. Coronary arteriograms demonstrated numerous aneurysms involving both the epicardial and intramyocardial segments of the left anterior descending, left circumflex, and right coronary arteries (Fig 1 and 2). In the region of hypokinesis, the right coronary artery and its branches contained several large aneurysms, and the vessels distal to these lesions were "pruned" in appearance . A muscle biopsy and angiography of the renal, superior mesenteric, coeliac, cerebral and lower extremity arteries were normal. The clinical course and coronary angiograms were judged to be consistent with a necrotizing arteritis of the PAN type. COMMENTS

Cardiac manifestations of PAN are common. In Holsinger's series,' 51 of 65 patients had cardiovascular features including hypertension, tachycardia, cardiomegaly, congestive heart failure, murmurs, pericardial friction rubs and arrhythmias. A disturbance in the conduction system has been described by others." Myocardial infarction results from vasculitis and thrombosis with significant atherosclerotic lesions being found in some cases. According to Arkin's clinicopathologic review," the development of aneurysms is seen during the second stage of PAN when there is a transmural spread of the inHammatory process. Toward the end of this stage, aneurysms may rupture and bleed into surrounding tissues. Coronary aneurysms may rupture and cause hemopericardium. 7 Diffuse aneurysmal dilatation of small and mediumsized arteries is most often seen with PAN. Similar lesions are occasionally seen in systemic lupus erythematosis," thrombotic thrombocytopenic purpura," and Wegener's granulomatosis.t? A necrotizing angiitis, which is clinically and angiographically identical to

FIGURE 1. Shallow right anterior oblique projection of the left coronary artery. There are numerous large and small aneurysms of epicardial and intramyocardial arteries. PAN, has also been observed in drug abusers.!' Methamphetamine is the drug involved. A pathologically similar vasculitis may occur in patients with mucocutaneous lymph node syndrome. First described by Kawasaki et al,11 this entity occurs almost exclusively in infants and children five years or less in age. However, the syndrome has also been described in a 28-year-old man.P Although generally regarded to have a benign course, a small number of patients have had vasculitis with coronary artery involvement. Aneurysms of the larger epicardial arteries, thrombosis, and myocardial infarction have been described at autopsy and with angiography.w'w Several investigators,15,18 have noted that infantile periarteritis (age 24 months or less) is indistinguishable from fatal cases of Kawasaki's disease; however, most experts would agree that beyond the age of 24 months, distinguishing features are present. In PAN there is a more protracted course with more extensive renal and gastrointestinal involvement. If the coronary arteries are affected in PAN, medium-sized and small-vessel disease is present, rather than large epicardial coronary artery involvement

FIGURE 2. Left anterior oblique projection of the right coronary artery . The entire course of the vessel has a beaded appearance. There is a paucity of vessels beyond the large aneurysms in the distal segment of the artery. CHEST / 82 / 3 / SEPTEMBER , 1982

379

as in Kawasaki's disease. Our patient's age, and the absence of mucocutaneous manifestations and lymphadenopathy precluded a diagnosis of Kawasaki's syndrome. In spite of the divisions just described, it may not always be possible to separate these diseases. Kitamura et al1 7 have recently reported a 26-year-old Japanese man with a myocardial infarction who had multiple epicardial coronary artery aneurysms. Because of a previous acute febrile illness with arthralgias at age 14, PAN or the mucocutaneous lymph node syndrome was considered the likely cause of his disease. Coronary arteritis may be a manifestation of several multisystemic diseases. In the absence of either clinical or laboratory markers of mucocutaneous lymph node syndrome, systemic lupus erythematosis, lues or drug abuse, a diagnosis of periarteritis nodosa was made. Isolated coronary arteritis, we feel, represents a distinctly unusual presentation for PAN and raises the question of a previously undescribed fonn of arteritis with an aBnity for the coronary arteries. Classification of patients with vasculitis into etiologic subgroups appears clinically useful, but at times may be somewhat arbitrary, as our patient demonstrates. REFERENCES

1 Fleming RJ, Stem LZ. Multiple intraparenchymal renal aneurysms in polyarteritis nodosa. Radiology 1965; 84: 100-03 2 Bron KM, Strott CA, Shapiro AP. The diagnostic value of angiographic observations in polyarteritis nodosa. Arch Intern Med 1965; 116:450-54 3 Arkin A. A clinical and pathological study of periarteritis nodosa. Am J Patho} 1930; 6:401-26 4 Holsinger DR, Osmundson PJ, Edwards JE. The heart in periarteritis nodosa. Circulation 1962; 25:610-18

5 Roberts FB, Fettennan GU. Polyarteritis nodosa in infancy. J Pediatr 1963; 63:519-29 6 Thiene G, Valente M, Rossi L. Involvement of the cardiac conducting system in panarteritis nodosa. Am heart J 1978; 95:716-24 7 Sinclair W, Nitsch E. Polyarteritis nodosa of the coronary arteries. Am Heart J 1949; 38:898-04 8 Longstreth PL, Korobkin M, Palubinskus AJ. Renal microaneurysms in a patient with systemic lupus erythematosis. Radiology 1974 ;113:65-66 9 Sraer JD, Beaufils P, Morel-Moroger L, Richet G. Vascular nephropathies with acute renal failure. In: KincaidSmith P, Matthew TH, Becker EL, eds. Glomerulonephritis : morphology, natural history and treabnent, Vol. 2. New York: Wiley and Sons, 1973: 1035-46 10 Baker SB, Robinson DR. Unusual renal manifestations of Wegener's granulomatosis. Am J Med 1978; 64:883-89 11 Citron BP, Halpern M, McCarron M, Lundberg GD, McCormick R, Pinus IJ, et aI. Necrotizing angiitis associated with drug abuse. N Eng} J Med 1970; 283: 1003-11 12 Kawasaki T, Kosaki F, Okawa S, Shigematsu I, Yanagawa H. A new infantile acute febrile mucocutaneous lymph node syndrome ( MLNS ) prevailing in Japan. Pediatrics 1974; 54:271-76 13 Glanzer JM, Galbraith WB, Jacobs JP. Kawasaki disease in a 28-year-old man. JAMA 1980; 244:1604-06

14 Kato H, Koike S, Yamamoto M, Ito Y, Yano E. Coronary aneurysms in infants and young children with acute febrile mucocutaneous lymph node syndrome. J Pediatr 1975; 86:892-98 15 Landing BH, Larson EJ. Are infantile periarteritis nodosa with coronary artery involvement and fatal mucocutaneous lymph node the same? Comparison of 20 patients from North America with patients from Hawaii and Japan. Pediatrics 1977; 59:651-62 16 Ahlstrom H, Lundstrom N, Mortensson W, Ostberg G, Lantorp K. Infantile periarteritis nodosa or mucocutaneous lymph node syndrome. A report of four cases and diagnostic considerations. Acta Paediatr Scand 1977; 66:193-98 17 Kitamura S, Kawashima Y, Miyamoto K, Kobayashi T, Matsuda H, Ohgitani N, et ale Multiple coronary artery aneurysms resulting in myocardial infarction in a young man. J Thorac Cardiovasc Surg 1975; 70:290-97

Massive Hemoptysis and Tension Pneumothorax following Pulmonary Artery Catheterization· Tudith A. CtJpe'PPer~ andJean E. RintJldo~

M.D.;t Margaret Setter, M.D.;t M.D.t

We report a c.e of mMSive hemoptysis and bilateral tension pneumothoru immediately following placement of a fiberoptic pulmonary artery catheter. We postulate air entry into a traumatic communication caused by the catbeter, traversllll. parenchymal autery, tile contiguous airspace and the intentltial space. Dissection of air through the perivasc...... sheath and Into tissue plaDes of the thorax and abdomen foDowed. ThIs sequence W8I rapidly fataL Tension pneumothorax should be CODsldered If dynamic respiratory system compliance remains poor despite aggressive evacuation of blood from the trachea of a patient with a recently Inserted baBoontype catheter.

M

assive hemoptysis following pulmonary artery:; catheterization is being reported with increasing frequency.vP In this case, fatal pulmonary hemorrhage followed pulmonary artery catheterization using the Oximetrix catheter, which contains an additional luminal channel for 6beroptic bundles permitting continuous monitoring of mixed venous oxygen saturation. At the time of massive hemoptysis, inability to inflate the lungs easily during cardiopulmonary resuscitation was thought to be due to partial obstruction of the endotracheal tube by clotted blood, but was in fact caused by bilateral tension pneumothoraces which appeared concurrently with massive hemoptysis. This diagnosis was not suspected antemortem. This is the 6rst report of fatal tension pneumothorax caused by -From the Departments of Anesthesiology and Internal

Medicin~e University of Pittsburgh School of Medicine, Pittsbur . tFellow, ritical Care Medicine. tAssistant Professor of Pulmonary Medicine. Reprint requests: Dr. RintJldo~ Pulf!&Ot1lJfll Medicine~ 440 Scaife Hall, University of Pittsburgh, Pitl8burgh 15261 M_lve Hemoptysis and Tension Pneumothorax (CUlpepper, Sener, Rlna/doJ