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Correspondence

Subarachnoid Hemorrhage and Acute Myocardial Infarction

N Engl J Med 1996; 335:1320October 24, 1996

Article

To the Editor:

In their Clinical Problem-Solving article (June 6 issue),1 Pine and Tierney describe a 52-year-old man who was admitted to the hospital because of headache, lethargy, and heartburn. A 12-lead electrocardiogram showed extensive and persistent ST-segment elevation in the anterolateral leads. Because a computed tomographic scan of the head revealed subarachnoid hemorrhage, no thrombolytic therapy was administered, and the patient was treated only with nitrates, metoprolol, and nimodipine. Acute myocardial infarction was then confirmed by the detection of increased cardiac enzymes, wall-motion abnormalities on echocardiography, and finally, cardiac catheterization.

Although the authors present an excellent discussion of the somewhat difficult interpretation of ischemia-like electrocardiographic changes during subarachnoid hemorrhage, they do not comment on the possible therapeutic strategies in patients with acute myocardial infarction occurring at the same time as intracranial disease. The patient's electrocardiographic changes on admission were highly suggestive of acute myocardial infarction requiring immediate reperfusion therapy, but with obvious contraindications to thrombolysis. Yet in the event of an absolute contraindication to lytic therapy, prompt coronary reperfusion can be achieved with primary angioplasty, if an experienced team can be assembled rapidly.2 Although the relative risks and benefits of primary angioplasty as an alternative to thrombolytic regimens are still uncertain,3 the role of primary angioplasty in patients with contraindications to thrombolytic therapy seems well established. Thus, since subsequent coronary angiography showed a persistently occluded left anterior descending artery with apical dyskinesis on echocardiography, the patient could have been an ideal candidate for primary angioplasty, probably resulting in a smaller infarct and better left ventricular function.

Vincenzo Pasceri, M.D.
Università Cattolica del Sacro Cuore, 00168 Rome, Italy

3 References
  1. 1

    Pine DS, Tierney L Jr. A stressful interaction. N Engl J Med 1996;334:1530-1534
    Full Text | Web of Science | Medline

  2. 2

    The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. Acute myocardial infarction: pre-hospital and in-hospital management. Eur Heart J 1996;17:43-63
    Web of Science | Medline

  3. 3

    Michels KB, Yusuf S. Does PTCA in acute myocardial infarction affect mortality and reinfarction rates? A quantitative overview (meta-analysis) of the randomized clinical trials. Circulation 1995;91:476-485
    Web of Science | Medline

Author/Editor Response

The authors reply:

To the Editor: As the suspicion grew that our patient's subarachnoid hemorrhage was accompanied by a painless anterior infarction, he was immediately transferred to a hospital with expertise in neurosurgery and invasive cardiology. Multiple factors were considered in deciding that the circumstances were less than optimal for angioplasty. It was thought that the need to avoid using heparin or aspirin before the patient's probable ruptured cerebral aneurysm had been identified and treated would jeopardize the potential benefit of angioplasty. The location of the occlusion of the left anterior descending artery — after the origin of the first diagonal and all septal perforator vessels — reduced the area of myocardium at risk. The demonstration of good collateral flow to the distal left anterior descending artery from ipsilateral and right coronary arterial sources supported this belief. Finally, cardiac catheterization did not begin until 11 hours after the patient arrived in the emergency department, because of the combined delays of evaluation and hospital transfer.

The case for primary angioplasty without heparin would have been more compelling if there had been occlusion of the left main artery, more proximal occlusion of the left anterior descending artery, or cardiogenic shock. As reported in our article, the patient fared well, with follow-up echocardiography showing only limited apical dyskinesis and normal overall left ventricular function. He subsequently underwent a craniotomy for wrapping of the aneurysm and is currently asymptomatic taking metoprolol and aspirin.

Daniel S. Pine, M.D.
Thomas A. Ports, M.D.
University of California, San Francisco, School of Medicine, San Francisco, CA 94143

Citing Articles (1)

Citing Articles

  1. 1

    Josef Zander. (1999) Current Opinion in Anaesthesiology 12:5, 503-509
    CrossRef

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