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Acute myocardial infarction due to proximal aortic dissection in giant cell aortitis Thomas K. Nordt, MD, Bernhard Rauch, MD, Torsten Mattfeldt, MD, Rainer Zimmermann, MD, Maria Eberlein-Gonska, MD, Wolfgang Kiibler, MD, and Christoph Bode, MD. Heidelberg, Germany From Medizinische Universitiitsklinik, Abteilung III (Kardiologie). Reprint requests: Dr. Thomas Nordt, Medizinische Universitiitsklinik, Abteilung III (Kardiologie), Bergheimer Strasse 58, W-6900 Heidelberg Germany. 414131334

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In the majority of cases,acute myocardial infarction (AMI) is ultimately causedby thrombotic occlusionsof artherosclerotic coronary arteries. Other primary causesof AM1 like hemorrhagic dissections,coronary emboli, Takayasu’s disease,or primary dissectingcoronary aneurysms’are less frequent but often give a very poor prognosis. In the presentreport, we describethe clinical courseaswell asthe angiographic and morphologic findings of a large AM1 causedby spontaneousdissection of the ascendingaorta that extended to the main left coronary artery (LCA). A 70-year-old womanwasadmitted to the intensive care unit with severechestpain that had abruptly begun 1 hour before and wasaccompaniedby severedyspneaat rest. The patient’s history revealed neither coronary risk factors nor recurrent chest pain or symptoms of heart failure. Physi-

Fig. 1. A, Angiogram of the LCA in the right anterior oblique projection. The contrast medium is not drained out. 6, Angiogram of the LCA in the right anterior oblique projection. The main LCA hasdisappeared almost completely shortly after the injection of contrast medium.

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Fig. 2. A, The site of proximal aortic dissection. On the left and right side, aortic media is visible; in the center a wide dissection cleft is found containing blood and fibrin. Even at low magnification (45 power), a giant cell can be clearly seen in the lower right corner. (Paraffin section, Ladewig stain.) B, Giant cell granuloma in the proximal aorta. In addition to multinucleated giant cells, there are someplasma cells,lymphocytes, and macrophages.There is disruption of elasticfibers by the inflammatory infiltrate. (Paraffin section, Ladewig stain; final magnification: X 720.)

cal examination showeda 60 kg, 160 cm tall, pale woman with wet crackles over both lungs. Heart rate wasaccelerated (90beats/min) and blood pressurewasin the low range (110/80 mm Hg). Other physical findings were normal apart from a third heart sound. Laboratory findings obtained immediately after admissionrevealed normal creatine kinase (39 U/L), but elevated levels were found for creatinine (1.5 mg/dl) and blood glucose(237 mg/dl). The electrocardiogram disclosedthe typical signs of a large acute anterior myocardial infarction with ST segmentelevations of 2 to 6 mm in leadsI, aVL, and Vs to Vs. In the chest x-ray film the heart wasnot enlarged, but the aorta waselongatedand sclerotic. Marked pulmonary congestion with Kerley’s B lines was present. Thrombolytic therapy was started 1% hours after the onset of symptoms and

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consistedof 5000 IU of heparin given as a bolus intravenously and the simultaneousintravenous application of 12 mg recombinant tissue-type plasminogenactivator (given within 30 minutes) and 48 mg prourokinase (40 minutes).’ The clinical course was complicated by a sudden fall of blood pressure,occurrence of pulmonary edema,and respiratory failure. Therefore artificial respiration had to be initiated and intravenous epinephrine was applied. Becausewe assumedfailure of the thrombolytic therapy, coronary angiography was performed 60 minutes after the start of thrombolytic treatment. The right coronary artery as well as the left anterior and circumflex branch of the LCA showedno significant alterations. However, the contrast medium did not drain out of the LCA (Fig. 1, A), and the main stem of t,he LCA disappearedalmost completely shortly after injection of contrast medium (Fig. 1, B). Intermittent occlusionof the main LCA by arterial dissection wassuspectedfor the first time. For lack of therapeutic alternatives, coronary angioplasty wastried, but permanent revascularization could not be achieved. The patient died in cardiogenicshock 3 hours after admission.Autopsy disclosedonly moderate coronary artherosclerosis.However, proximal aortic dissectionstarting 1.5cm distal of the aortic valve, with a 1 cm long, diagonally oriented intimal tear, was detected. The dissection extended backward to the main LCA, thereby occludingits origin and leading to acute anterior myocardial infarction. Part of the dissectioncleft was filled with blood. The histologic examination of the proximal thoracic aorta showedflorid giant cell inflammation of the media (Fig. 2). Giant cell aortitis has been found in 0.4’~’ of 20,000 autopsies3Among the currently classifiedentities of vasculitis, giant cell arteritis and Takayasu’sarteritis typically involve the aortic arch.4 Whereas the latter primarily occursin young womenand rarely leadsto aortic dissection, giant cell arteritis is preferably seenin elderly patients, showingan aortic affection in about 14p1.3 Complications including aneurysm, aortic regurgitation, dissection, and rupture were found at autopsy in up to 50”; of these patients.3x5 Nevertheless, AM1 is regarded as an unusual complication, and an epidemiologicstudy did not showan increased prevalence of cardiac diseasein patients with giant cell arteritis.6 In the present case,thrombolytic therapy was started assuminga thrombotic origin of the large anterior AMI. Neither the patient’s history nor the clinical signsgave any evidence of aortic dissection.This wasonly suspectedfor the first time during coronary angiography, and it was confirmed at autopsy. Histologic examination revealed a giant cell aortitis asthe underlying disease.This caseclearly showsthat myocardial infarction can be caused by quite different mechanisms,which-apart from thrombotic occlusion--do not respond to thrombolytic therapy. Mechanical means,e.g., a coronary stent (which was not available to usat that time), could beregarded asan option in treating these cases. REFERENCES

1. Mattfeldt Necropsy

T, Schwarz evaluation

F, Schuler G, Hofmann in seven patients with

M, Kiibler W. evolving acute

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myocardial infarction treated with thrombolytic therapy. Am J Cardiol 1984;54:530-4. Bode C, Schuler G, Nordt T, Schiinermark S, Baumann H, Richardt G, Dietz R, Gurewich V, Kiibler W. Intravenous thrombolytic therapy with a combination of single-chain urokinase-type plasminogen activator and recombinant tissue-type plasminogen activator in acute myocardial infarction. Circulation 1990;81:907-13. Klein RG, Hunder GG, Stanson AW, Sheps SG. Large artery involvement in giant cell (temporal) arteritis. Ann Intern Med 1975;83:806-12. Perruquet JL, Davis DE, Harrington TM. Aortic arch arteritis in the elderly. An important manifestation of giant cell arteritis. Arch Intern Med 1986;146:289-91. Garret R. Chronic diffuse giant cell mesaortitis, with dissecting aneurysm and rupture. Am J Clin Path01 1962;38:406-14. Huston GA, Hunder GG. Giant cell (cranial) arteritis: A clinical review. AM HEART J 1980;100:99-107.

Transient severe mitral regurgitation during percutaneous transluminal coronary angioplasty Peter J. Macander, MD, PhD,

Gary S. Roubin, MD, PhDF Ming C. Hsiung, MD,b and Navin C. Nanda, MD.b Birmingham, Ala.

An 83-year-old asthenic male with classIV anginapectoris of recent onset wasreferred to our institution for percutaneoustransluminal coronary angioplasty (PTCA). He had c previously sustainedan inferior myocardial infarction but had no history of murmur, paroxysmal nocturnal dyspnea, orthopnea, rheumatic heart disease,mitral valve prolapse, or congestive heart failure. Although examination at an emergency room during presentation with a prolonged episodeof angina accompanied by shortnessof breath 5 days prior to admissionhad revealed a grade l/6 systolic apical murmur with summationgallop, repeat examination during asymptomatic admissionto our hospital revealed no murmur, Ssgallop, parasternal lift, jugular venous distension, pronounced A or V wave, or edema.An Sqsoundwas detected and pulseswereof normal amplitude and contour. The electrocardiogram, suggestinga possible inferior inFig. 1. Left coronary arteriograms. A, Anteroposterior farction of indeterminate age,showednormal sinusrhythm and B, 45-degree RAO/caudal 14-degree views before of 83 beats/min with normal mean frontal QRS axis and PTCA demonstrate a severe, proximal stenosisin a large, intervals. bifurcating first diagonal branch (large arrow). Small One day following an initial presentation for prolonged arrow indicatesthe proximally occluded circumflex artery. rest onset angina, the patient underwent coronary arteriography, which discloseda proximally occludednondominant left circumflex coronary artery, a 60% midvessel stenosisinvolving a smallfirst obtusemarginal branch, and a 90% proximal stenosisin an extensive, bifurcating first diagonal branch (Fig. 1). The left main, left anterior From the Division of Cardiovascular Disease, %terventional Cardiology descending,and right coronary arteries werewidely patent. and bCardiac Ultrasonography-Graphics Laboratories, University of AlaThe right posterior descendingbranch had a midvessel,rebama at Birmingham Medical Center. canalized chronic total occlusion with no angiographic Reprint requests: Peter J. Macander, MD, PhD, Interventional Cardiology, evidence of collateralization. Cine left ventriculogram UAB Medical Center, LHRB 316, UAB Station, Birmingham, AL 35294. revealed moderately severe, inferobasal segmental hypo4/4/30568