Join the 200th Anniversary Celebration

Correspondence

Case 11-1996: Atheroembolism of the Kidneys and Lungs

N Engl J Med 1996; 335:821September 12, 1996

Article

To the Editor:

In the clinical discussion of Case 11-1996 (April 11 issue),1 no mention was made of the possible role of anticoagulation in the patient's progressive illness. The patient had chronic renal insufficiency with marked proteinuria. Three months before admission, transient weakness developed in his right arm, and evaluation revealed a small atheromatous plaque at the right carotid bifurcation. Treatment with warfarin was begun. Progressive renal failure and pulmonary edema subsequently developed, and then hemoptysis. A renal biopsy revealed cholesterol microembolization as the cause of the renal failure. Open-lung biopsy also revealed atheromatous emboli in the pulmonary arteries.

Reports have linked warfarin therapy to worsening atheroembolic disease.2-5 Recently, Keen et al.5 reported a series of 100 patients with atheroembolic disease, including 11 with renal atheroemboli. Warfarin was a precipitating factor in 21 patients; 4 of 5 who had recurrent atheroembolic events after surgery were receiving warfarin at the time of recurrence. Anticoagulants may lead to embolization by preventing the formation of a protective thrombus or by causing subintimal hemorrhages.4 Cholesterol microembolization has also been associated with the administration of streptokinase in the treatment of myocardial infarction, most likely because of “dissolution of cholesterol-containing thrombi resulting in release of cholesterol crystals to the peripheral circulation.” 6

Roger Mallory, M.D.
Richard G. Appel, M.D.
Bowman Gray School of Medicine, Winston-Salem, NC 27157

6 References
  1. 1

    Case Records of the Massachusetts General Hospital (Case 11-1996). N Engl J Med 1996;334:973-979
    Full Text | Web of Science | Medline

  2. 2

    Hyman BT, Landas SK, Ashman RF, Schelper RL, Robinson RA. Warfarin-related purple toes syndrome and cholesterol microembolization. Am J Med 1987;82:1233-1237
    CrossRef | Web of Science | Medline

  3. 3

    Moldveen-Geronimus M, Merriam JC Jr. Cholesterol embolization: from pathologic curiosity to clinical entity. Circulation 1967;35:946-953
    Web of Science | Medline

  4. 4

    Dahlberg PJ, Frecentese DF, Cogbill TH. Cholesterol embolism: experience with 22 histologically proven cases. Surgery 1989;105:737-746
    Web of Science | Medline

  5. 5

    Keen RR, McCarthy WJ, Shireman PK, et al. Surgical management of atheroembolization. J Vasc Surg 1995;21:773-780
    CrossRef | Web of Science | Medline

  6. 6

    Queen M, Biem HJ, Moe GW, Sugar L. Development of cholesterol embolization syndrome after intravenous streptokinase for acute myocardial infarction. Am J Cardiol 1990;65:1042-1043
    CrossRef | Web of Science | Medline

Author/Editor Response

The discussants reply:

To the Editor: I appreciate the comments of Drs. Mallory and Appel concerning anticoagulation. The patient's renal function was clearly deteriorating six months before admission, whereas the warfarin was not started until three months before admission. This suggests that the disease process causing his renal failure (atheroembolic disease and possibly bilateral renal-artery stenosis) had begun before the start of anticoagulation. In this setting, I believe that the physicians caring for the patient at the time of the transient weakness in his arm appropriately began treatment with warfarin, since they had documentation of a plaque at the carotid bifurcation. Whether or not this treatment contributed to any of the ensuing events is speculative. Nevertheless, I certainly agree that it is important for physicians to remember that anticoagulation may worsen atheroembolic disease.

Robert C. Stanton, M.D.
Joslin Diabetes Center, Boston, MA 02215

Author/Editor Response

In my discussion of the pathology, I stated that pulmonary cholesterol embolism had not been described previously to my knowledge. That statement would still stand were it not for a kind letter and reprint 1 sent to me by C.E. Weigent, a pathologist retired from the Minneapolis Veterans Administration Hospital, who 18 years ago reported on a patient who had a large atherosclerotic abdominal aneurysm with a tear creating an aortocaval fistula. The fistula was closed with sutures and the aneurysm resected, but the patient died 15 days later after progressive respiratory failure. Autopsy showed that the cause of death was widespread atherosclerotic emboli from the aorta to the pulmonary circulation. The cholesterol-occluded arteries in Dr. Weigent's illustrations are the very image of those in the Case Records.

Eugene J. Mark, M.D.
Massachusetts General Hospital, Boston, MA 02114-2698

1 References
  1. 1

    Weigent CE. Pulmonary atheroembolism complicating repair of an atherosclerotic abdominal aneurysm. Minn Med 1978;61:15-16
    Medline

Trends: Most Viewed (Last Week)

More Trends