Cardiac amyloidosis presenting with elevations of cardiac troponin I and angina pectoris

R. V. Cantwell, R. J. Aviles, J. Bjornsson, R. Scott Wright, W. K. Freeman, Jae Kuen Oh, James Hoyer, Svetomir Nenad Markovic, Allan S Jaffe

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

We present the case of a 43-year-old male who was initially evaluated for angina pectoris and dyspnea. His CK, CK-MB, and cTnI were all elevated following a blood transfusion and he underwent coronary arteriography, which demonstrated no luminal obstructions. After several months, he was transferred to Mayo Clinic where diagnoses of fulminant cardiac amyloidosis and systemic multiple myeloma were established. The cTnI remained elevated despite normalization of the CK and CK-MB. Despite aggressive treatment, the patient died. Postmortem analysis demonstrated amyloid cardiac deposition including involvement of the coronary microvasculature. Electron microscopy revealed myocyte compression injury from amyloid infiltration. We believe this is the first report of elevated troponin I in a patient with cardiac amyloidosis. The electron microscopy in our case confirms cardiac damage as the mechanism for cTnI elevation. This observation strengthens our knowledge about the specificity of cTnI for the detection of cardiac injury.

Original languageEnglish (US)
Pages (from-to)33-37
Number of pages5
JournalClinical Cardiology
Volume25
Issue number1
StatePublished - 2002

Fingerprint

Troponin I
Angina Pectoris
Amyloidosis
Amyloid
Electron Microscopy
Wounds and Injuries
Microvessels
Multiple Myeloma
Blood Transfusion
Dyspnea
Muscle Cells
Angiography
Therapeutics

Keywords

  • Angina pectoris
  • Cardiac amyloidosis
  • Myocardial infarction
  • Troponin

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Cardiac amyloidosis presenting with elevations of cardiac troponin I and angina pectoris. / Cantwell, R. V.; Aviles, R. J.; Bjornsson, J.; Wright, R. Scott; Freeman, W. K.; Oh, Jae Kuen; Hoyer, James; Markovic, Svetomir Nenad; Jaffe, Allan S.

In: Clinical Cardiology, Vol. 25, No. 1, 2002, p. 33-37.

Research output: Contribution to journalArticle

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AU - Aviles, R. J.

AU - Bjornsson, J.

AU - Wright, R. Scott

AU - Freeman, W. K.

AU - Oh, Jae Kuen

AU - Hoyer, James

AU - Markovic, Svetomir Nenad

AU - Jaffe, Allan S

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AB - We present the case of a 43-year-old male who was initially evaluated for angina pectoris and dyspnea. His CK, CK-MB, and cTnI were all elevated following a blood transfusion and he underwent coronary arteriography, which demonstrated no luminal obstructions. After several months, he was transferred to Mayo Clinic where diagnoses of fulminant cardiac amyloidosis and systemic multiple myeloma were established. The cTnI remained elevated despite normalization of the CK and CK-MB. Despite aggressive treatment, the patient died. Postmortem analysis demonstrated amyloid cardiac deposition including involvement of the coronary microvasculature. Electron microscopy revealed myocyte compression injury from amyloid infiltration. We believe this is the first report of elevated troponin I in a patient with cardiac amyloidosis. The electron microscopy in our case confirms cardiac damage as the mechanism for cTnI elevation. This observation strengthens our knowledge about the specificity of cTnI for the detection of cardiac injury.

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