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(Circulation Research. 2004;94:1530.)
© 2004 American Heart Association, Inc.

Editorials

Cardiac Angiotensin Is Upregulated in the Hearts of Unstable Angina Patients

Friedrich C. Luft

From Medical Faculty of the Charité, Franz Volhard Clinic at the Max Delbrück Center for Molecular Medicine, HELIOS Klinikum-Berlin, Berlin, Germany.

Correspondence to Friedrich C. Luft, Medical Faculty of the Charité, Franz Volhard Clinic at the Max Delbrück Center for Molecular Medicine, HELIOS Klinikum-Berlin, Wiltberg Strasse 50, 13125 Berlin, Germany. E-mail luft@fvk-berlin.de

Key Words: unstable angina • acute coronary syndromes • angiotensin • renin • aldosterone

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Patients with acute coronary syndromes commonly harbor multiple complex coronary plaques. Plaque instability is probably a widespread inflammatory process throughout the coronary vessels.¹ Such a notion makes selection of the "culprit lesion" difficult. A recent clinical example from our coronary care unit is shown in the Figure. The patient is a 62-year-old man who experienced his first episode of severe anterior chest pain. The initial electrocardiogram showed an acute ST segment elevation anterior myocardial infarction. The emergency physician selected thrombolytic therapy and the patient was referred to our coronary care unit. His ST segments reverted to baseline. Early that same afternoon, a second episode of chest pain occurred. This time, his electrocardiogram showed a shift in axis and ST segment elevation in the inferior leads. At cardiac catheterization, the left anterior descending coronary artery was open, albeit diseased. The right coronary artery was occluded but could be opened. The second episode of ST segment elevation resolved as well. What is responsible for the generalized plaque instability in patients with an acute coronary syndrome? How does inflammation contribute? What role does the renin-angiotensin-aldosterone system (RAAS) play, and can the system operate locally? The study by Neri Serneri et al in this issue may provide some mechanistic answers.² They tested the notion that the RAAS acts locally to cause generalized inflammation in the smaller coronary vessels of patients with unstable angina pectoris.

View larger version (131K): [in this window] [in a new window]   The patient had crushing anterior chest pain when the electrocardiogram on the left was performed. He received recombinant tissue . . . [Full Text of this Article]

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