Successful Surgical Resection of a Chronic False Aneurysm of the Left Ventricle

that no contrast material is trapped distal to the embolus, such an occurrence could easily escape detection and the usual pattern of pain immediately following an injection for no apparent cause could easily obtain. The findings in this case suggest that embolization with fresh soft thrombus lodging distally (particularly in patients with normal coronary arteries) may not only be compatible with life but the lesion may resolve without as much as a myocardial scar recognizable to external scrutiny. The lack of a full-thickness infarct pattern on the electrocardiogram might suggest a subendocardial infarct but the enzyme abnonnalities are compatible with more extensive damage. In consequence, not only may the outlook for complete recovery be optimistic for this complication but the incidence of coronary thromboembolism could be considerably higher than previously believed. Measures to avoid this hazard have been reported. 2,3 Cheng 4 lists eight recommendations aimed at reducing the opportunity for embolus formation. Others have resorted to withdrawing and Hushing the catheter between each injection, heparin-filling all left heart catheters and guide-wire holders prior to catheterization and pressureHushing coronary catheters with the tip in the arch of the aorta. Following the experience with the patient presented here, two further precautionary measures have been introduced. All left heart catheters are prepared prior to beginning the catheterization by filling with heparin. The guide-wire holder is similarly filled, and after use and cleaning the wire is returned to its heparin environment. When the coronary catheters are introduced, a test dose of 3 to 5 ml of diatrizoate (Hypaque) is injected at full pressure with the catheter tip in the arch of the aorta. Eyer 5 has reported the elimination of thromboembolic complication with the use of 50 to 100 mg heparin given intravenously following the arterial puncture and neutralized at the end of the procedure with an equal quantity of protamine sulfate. The effectiveness of such systemic heparinization is both supported 3 and denied in the literature. ACKNOWLEDGMENT: We thank Drs. Marcial Cerruti and Serge Jomain, who performed the mitral valve replacement, for their examination of the heart during surgery. REFERENCES

1 Adams DF, Fraser DB, Abrams HL: The complications of coronary arteriography. Circulation 48:609-618, 1973 2 Takaro T, Hultgren HN, Littmann D, et al: An analysis of deaths occurring in association \vith coronary arteriography. Am Heart J 86:587-597, 1973 3 Judkins MP, Gander MP: Prevention of complications of coronary arteriography. Circulation 49:599-602, 1974 4 Cheng TO: Fatal thromboembolism following selective coronary arteriography. Chest 62: 1, 1972 5 Eyer KM: Complications of transfemoral coronary arteriography and their prevention using heparin. Am Heart J 86:428, 1973

CHEST, 67: 3, MARCH, 1975

Successful Surgical Resection of a Chronic False Aneurysm of the Left Ventricle* Richard W. Harper, M.D.oO Groome Sloman, M.D.,t and George Westlake, M.D.:

The case of a patient with a chronic false aneurysm of the left ventricle diagnosed three years after a documented myocardial infarction is reported. The patient presented with a mass seen on the chest x-ray examination. The correct diagnosis was made by ventriculography and the aneurysm was successfully resected. of the heart is a relatively uncommon compliRupture cation of acute myocardial infarction and is rarely

compatible with life. 1 Occasionally a patient may survive an episode of cardiac rupture because dense adhesions between the pericardiallayers confine the bleeding and prevent cardiac tamponade. When this occurs the blood clot organizes with subsequent fonnation of a false (pseudo) aneurysm of the left ventricle. 2 This report describes a successful surgical resection of a chronic false aneurysm of the posterior wall of the left ventricle diagnosed three years after a documented myocardial infarction. CASE REPORT

The patient, a 60-year-old man, had a history of a posterior myocardial infarction in June 1967 and a lateral \vall infarction in November 1970. He had been a heavy smoker all his life. Following the second infarction the patient developed cardiac failure which was treated with digitalis. In August 1973 the patient noticed increasing exertional dyspnea and was admitted to Ballarat Base Hospital after an episode of paroxysmal nocturnal dyspnea. He had suffered no recent chest pain and an electrocardiogram taken soon after admission showed no change from the previous tracing obtained in 1970. During this admission, the serum enzymes were not elevated and a chest x-ray picture revealed a large mass in the left lower zone occupying the cardiophrenic angle (Fig 1) which had not been present on the chest x-ray film in 1970. This mass was regarded as a neoplasm of the lung. Although a bronchoscopic examination did not reveal any abnormality, cytologic examination of the sputum showed cells with a metaplastic change. In September 1973 a left lateral thoracotomy was performed, and at operation the mass was found to be within the pericardium. The chest was closed without further exploration and the patient was subsequently transferred to the Royal Melbourne Hospital. A clinical diagnosis of ventricular aneurysm was made and cardiac studies performed. The left ventricular angiogram in the left anterior oblique projection demonstrated a large false aneurysm communicating with the pos°From the Cardiac Department, Royal Melbourne Hospital, Victoria, Australia. oOCardiology Registrar. tDirector, Cardiac Laboratory. tCardiac Surgeon. Reprint requests: Dr. Sloman, Cardiac Department, Royal Melbourne Hospital, Melbourne, Victoria 3050, Australia

SUCCESSFUL RESECTION OF FALSE ANEURYSM 359

FIGURE 1. Chest x-ray film in the PA and lateral projections (with barium swallow). The false aneurysm is indicated by the arrows. The lateral projection demonstrates that the false aneurysm is posterior to the barium filled esophagus. terior wall of the left ventricle via a narrow neck (Fig 2). In view of the severity of the cardiac failure and the possibility of rupture, it was decided to surgically resect the aneurysm. At operation, there were dense adhesions between the pericardium and the left ventricle and these were divided revealing a large fibrous aneurysm containing a considerable amount of blood clot and communicating with the left ventricle by a relatively narrow neck. Under cardiopulmonary bypass the aneurysm was resected and the edges. of the resulting defect which consisted of tough fibrous tissue, were sewn together. Histology of the resected aneurysm showed that the wall consisted of dense hyaline material without any identifiable myocardial elements. Postoperatively the patient made a good recovery and was discharged 14 days after surgery. Subsequently he has been reviewed three months after the operation and was found to be well with no evidence of cardiac failure.

FIGURE 2. Left ventriculogram in the left anterior oblique projection showing the false aneurysm filling with dye from a narrow neck as indicated by the arrows.

360 HARPER, SLOMAN, WESTLAKE

DISCUSSION

The anatomic characteristics of a false aneurysm are generally considered to be: (1) The mouth of the aneurysm is small compared to the diameter of the fundus of the aneurysm; (2) the parietal pericardium is adherent to the outer surface of the false aneurysm; (3) the false aneurysm is walled by fibrous tissue devoid of myocardial elements; and (4) the junction of the aneurysm and the left ventricular wall shows a sudden interruption in the continuity of myocardial tissue. 3 In our patient the first three criteria were present but we were unable to tell if the fourth criteria was fulfilled because the base of the aneurysm was not completely resected. In comparison with true aneurysms of the left ventricle which are a relatively common complication of acute myocardial infarction 4 false aneurysms are extremely rare and are not often diagnosed antemortem. 5 In a review of 40 pathologic specimens obtained from seven different hospitals, Van Tassel and Edwards 3 found nine cases of false aneurysm formation. In four of the nine cases rupture of the false aneurysm occurred and in only one of these four cases was the diagnosis made prior to death. The authors mentioned that in two of the nine cases successful surgical resection of the false aneurysm was performed but no further details were provided. Despite an extensive search of the literature we were able to find only one other case report where a preoperative diagnosis of a false aneurysm was made and successful surgical resection occurred. Our case is unusual in two other aspects. Firstly, the plain chest x-ray appearance was more suggestive of a lesion in the lung fields than in the cardiac structures. Secondly, the false aneurysm probably occurred at the time of the patient's second myocardial infarction in 1970 and had been present for over three years before a diagnosis was eventually made.

CHEST, 67: 3, MARCH, 1975

REFERENCES

CASE REPORT

1 Gould SE: Pathology of the Heart (2nd ed). Springfield, III., Charles C Thoma~, 1960 2 Eisek RA, Chisler E, Koins ME, et aI: Spontaneous rupture of a false ventricular aneurysm following myocardial infarction. Am Heart J 77:677-680,1969 3 Van Tassel RA, Edwards JE: Rupture of the heart complicating myocardial infarction. Chest 61: 104-116, 1972 4 Alford WC, BumlS GR, Stoney WS, et al: The spectnun of ventricular aneurysms. Heart and Lung 2:211-217,1973 5 Gueron M, Husch M, Venderman K, et al: Pseudoaneurysm of left ventricle. Report of a case diagnosed by angiography and successfully repaired. Br Heart J 35:663665, 1973

This 71-year-old man was referred to Saint Luke's Hospital for evaluation of exertional dyspnea, weakness and vague anterior chest discomfort. These symptoms had progressed in the three years prior to admission. The history was suggestive of childhood rheumatic fever. Physical examination revealed a blood pressure of 106/60 mm Hg and atrial fibrillation at 68 per minute. Auscultation confirmed mitral stenosis with no insufficiency. A "scratchy" murmur was heard along the left sternal border occurring during midsystole. The electrocardiogram revealed atrial fibrillation, left axis deviation, and poor R wave progression in leads VI to V4. Generalized cardiomegaly, interstitial congestion, left atrial enlargement and calcium in the area of the left atrial appendage were seen on x-ray films. Complete blood count and biochemical screen findings were within normal limits. The clinical impression was mitral stenosis, moderately severe. At cardiac catheterization, severe mitral stenosis with no mitral regurgitation was demonstrated. The aortic valve was normal. Coronary arteriograms showed total occhlSion of the right system 2 cm distal to the conus artery and advanced disease in the proximal anterior descending and circumflex arteries. Immediately proximal to the major obstruction in the anterior descending artery, a "channel" approximately 2 mm in diameter coursed cephalad and entered the left atrium (Fig 1). Operation was performed while maintaining total cardiopulmonary bypass. The left atrium was opened, revealing a large amount of adherent clot and a stenotic mitral valve, which was estimated to be .8 em square. A very hard calcified mass was noted in the left lateral wall of the left atrium near the appendage. Near the center of this mass was a 1 mm-sized orifice, from which blood could be seen entering the left atrium. This opening was closed, the mitral valve was replaced and saphenous bypass graft to the anterior descending artery was performed.

Coronary Artery to Left Atrial Fistula in Association with Severe Atherosclerosis and Mitral Stenosis: Report of Surgical Repair* Spencer B. King, Ill, M.D., °° and Fred W. Schoonmaker, M.D., F.C.C.P.t

Not uncommonly, atherosclerosis may be found associated with rheumatic heart disease. The combination of atherosclerosis, rheumatic heart disease and corooary fistula is an unusual combination of hemodynamic and disease states. We report a patient with advanced mitral stenosis and atherosclerosis who also had a fistula from the left coronary artery into the left atrium. Surgical approach: combined valve replacement, bypass grafting and closure of the fistula in an attempt to relieve the pathophysiologic abnormalities.

I

t has been postulated recently that coronary-cameral fistulae may "open up" as a consequence of severe coronary atherosclerosis. 1 Coronary arteriography revealed abnormal shunting of blood from the left coronary artery to the left atrium in a 71-year-old man with severe atherosclerosis of the left anterior descending artery. Because of the age of the patient, the small size of the fistula, the rarity with which congenital fistulae enter the left atrium and the lack of dilatation of the proximal left coronary, it is felt that this shunt may represent an acquired fistula due to severe atherosclerosis. This patient is also interesting because of associated severe mitral stenosis requiring valve replacement. This is the first direct surgical demonstration of a coronary-to-Ieftatrial-fistula in atherosclerosis and the first report of ligation of a coronary-cameral fistula combined with saphenous vein bypass grafting. A combined operation was performed in an attempt to relieve both pathophysiologic insults to the coronary circulation. °From the Departments of Medicine and Radiology °°, Emory University School of Medicine, Atlanta. tDepartment of Cardiology, St. Luke's Hospital, Denver. Reprint requests: Dr. King, Emory University Clinic, Atlanta 30322

CHEST, 67: 3, MARCH, 1975

DISCUSSION

Symptoms of congenital coronary-eameral fistulae are commonly characterized by a continuous precordial murmur. If drainage is into the right side of the heart,

FIGURE 1. Left anterior oblique view of right coronary artery, which is totally occluded distal to conus artery.

CORONARY ARTERY TO LEFT ATRIAL FISTULA 361