ECG-manifest and ECG-silent dipyridamole technetium-99m sestamibi SPET perfusion defects in patients with ischaemic heart disease

Michele Galli, Claudio Marcassa, Enzo Bosimini, Orazio Zoccarato, Fabio Comazzi, Pantaleo Giannuzzi

Research output: Contribution to journalArticle

Abstract

At dipyridamole myocardial scintigraphy, perfusion defects are seldom backed up by significant ECG changes. This would suggest myocardial blood flow heterogeneity rather than true ischaemia, as the cause of the scintigraphic abnormalities. Electrocardiographic surface mapping has been documented to be more accurate than standard 12-lead ECG in the detection of provoked ischaemia. Thus, to investigate the relationship between ECG changes and perfusion abnormalities, body surface maps were recorded during dipyridamole infusion in 55 subjects (11 normals and 44 patients with ischaemic heart disease) undergoing dipyridamole technetium-99m sestamibi single-photon emission tomography (SPET). All had a normal resting ECG. The extent and severity of the sestamibi defect were quantified. New negative areas in the isointegral maps and rest-dipyridamole map differences > 2 SD from normal limits were considered abnormal. After dipyridamole in normals, neither perfusion defects nor ≤ 1 mm ST segment depression on 12-lead ECG nor new negative areas in isointegral maps occurred. In patients, dipyridamole induced new perfusion defects in 35 (80%) but ST segment depression in only 18 (41%, P <0.001). Of the 35 patients with perfusion defects, 17 (49%, group 1) showed ST segment depression, while the other 18 (51%, group 2) did not. Abnormal body surface maps were found in 100% of group 1 and 88% of group 2 patients (NS). In group 1, the provoked hypoperfusion was of greater extent (P = 0.007) and severity (P = 0.01) and the onset of map abnormalities was significantly earlier (P <0.001) than in group 2; time to map abnormalities was also significantly shorter than time to ST segment depression (P = 0.01). In the 35 patients with complete scintigraphic, body map and angiographic data, the severity of reversible perfusion defect proved to be the strongest correlate of ST segment depression upon logistic regression analysis. Thus, sestamibi SPET abnormalities after dipyridamole are almost always associated with electrical changes on body surface maps, suggesting myocardial ischaemia as their cause. The much less common 12-lead ECG changes are slower to appear and reflect a more severe hypoperfusion.

Original languageEnglish
Pages (from-to)160-169
Number of pages10
JournalEuropean Journal Of Nuclear Medicine
Volume24
Issue number2
DOIs
Publication statusPublished - 1997

Fingerprint

Technetium Tc 99m Sestamibi
Dipyridamole
Photons
Myocardial Ischemia
Electrocardiography
Perfusion
Tomography
Ischemia
Myocardial Perfusion Imaging
Logistic Models
Regression Analysis

Keywords

  • Coronary artery disease
  • Dipyridamole
  • Myocardial ischaemia
  • Technetium-99m sestamibi single-photon emission tomography

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging

Cite this

ECG-manifest and ECG-silent dipyridamole technetium-99m sestamibi SPET perfusion defects in patients with ischaemic heart disease. / Galli, Michele; Marcassa, Claudio; Bosimini, Enzo; Zoccarato, Orazio; Comazzi, Fabio; Giannuzzi, Pantaleo.

In: European Journal Of Nuclear Medicine, Vol. 24, No. 2, 1997, p. 160-169.

Research output: Contribution to journalArticle

@article{b7b04fb24a1f4c58ab09b3c05e44f15d,
title = "ECG-manifest and ECG-silent dipyridamole technetium-99m sestamibi SPET perfusion defects in patients with ischaemic heart disease",
abstract = "At dipyridamole myocardial scintigraphy, perfusion defects are seldom backed up by significant ECG changes. This would suggest myocardial blood flow heterogeneity rather than true ischaemia, as the cause of the scintigraphic abnormalities. Electrocardiographic surface mapping has been documented to be more accurate than standard 12-lead ECG in the detection of provoked ischaemia. Thus, to investigate the relationship between ECG changes and perfusion abnormalities, body surface maps were recorded during dipyridamole infusion in 55 subjects (11 normals and 44 patients with ischaemic heart disease) undergoing dipyridamole technetium-99m sestamibi single-photon emission tomography (SPET). All had a normal resting ECG. The extent and severity of the sestamibi defect were quantified. New negative areas in the isointegral maps and rest-dipyridamole map differences > 2 SD from normal limits were considered abnormal. After dipyridamole in normals, neither perfusion defects nor ≤ 1 mm ST segment depression on 12-lead ECG nor new negative areas in isointegral maps occurred. In patients, dipyridamole induced new perfusion defects in 35 (80{\%}) but ST segment depression in only 18 (41{\%}, P <0.001). Of the 35 patients with perfusion defects, 17 (49{\%}, group 1) showed ST segment depression, while the other 18 (51{\%}, group 2) did not. Abnormal body surface maps were found in 100{\%} of group 1 and 88{\%} of group 2 patients (NS). In group 1, the provoked hypoperfusion was of greater extent (P = 0.007) and severity (P = 0.01) and the onset of map abnormalities was significantly earlier (P <0.001) than in group 2; time to map abnormalities was also significantly shorter than time to ST segment depression (P = 0.01). In the 35 patients with complete scintigraphic, body map and angiographic data, the severity of reversible perfusion defect proved to be the strongest correlate of ST segment depression upon logistic regression analysis. Thus, sestamibi SPET abnormalities after dipyridamole are almost always associated with electrical changes on body surface maps, suggesting myocardial ischaemia as their cause. The much less common 12-lead ECG changes are slower to appear and reflect a more severe hypoperfusion.",
keywords = "Coronary artery disease, Dipyridamole, Myocardial ischaemia, Technetium-99m sestamibi single-photon emission tomography",
author = "Michele Galli and Claudio Marcassa and Enzo Bosimini and Orazio Zoccarato and Fabio Comazzi and Pantaleo Giannuzzi",
year = "1997",
doi = "10.1007/BF02439548",
language = "English",
volume = "24",
pages = "160--169",
journal = "European Journal of Pediatrics",
issn = "0340-6199",
publisher = "Springer Berlin Heidelberg",
number = "2",

}

TY - JOUR

T1 - ECG-manifest and ECG-silent dipyridamole technetium-99m sestamibi SPET perfusion defects in patients with ischaemic heart disease

AU - Galli, Michele

AU - Marcassa, Claudio

AU - Bosimini, Enzo

AU - Zoccarato, Orazio

AU - Comazzi, Fabio

AU - Giannuzzi, Pantaleo

PY - 1997

Y1 - 1997

N2 - At dipyridamole myocardial scintigraphy, perfusion defects are seldom backed up by significant ECG changes. This would suggest myocardial blood flow heterogeneity rather than true ischaemia, as the cause of the scintigraphic abnormalities. Electrocardiographic surface mapping has been documented to be more accurate than standard 12-lead ECG in the detection of provoked ischaemia. Thus, to investigate the relationship between ECG changes and perfusion abnormalities, body surface maps were recorded during dipyridamole infusion in 55 subjects (11 normals and 44 patients with ischaemic heart disease) undergoing dipyridamole technetium-99m sestamibi single-photon emission tomography (SPET). All had a normal resting ECG. The extent and severity of the sestamibi defect were quantified. New negative areas in the isointegral maps and rest-dipyridamole map differences > 2 SD from normal limits were considered abnormal. After dipyridamole in normals, neither perfusion defects nor ≤ 1 mm ST segment depression on 12-lead ECG nor new negative areas in isointegral maps occurred. In patients, dipyridamole induced new perfusion defects in 35 (80%) but ST segment depression in only 18 (41%, P <0.001). Of the 35 patients with perfusion defects, 17 (49%, group 1) showed ST segment depression, while the other 18 (51%, group 2) did not. Abnormal body surface maps were found in 100% of group 1 and 88% of group 2 patients (NS). In group 1, the provoked hypoperfusion was of greater extent (P = 0.007) and severity (P = 0.01) and the onset of map abnormalities was significantly earlier (P <0.001) than in group 2; time to map abnormalities was also significantly shorter than time to ST segment depression (P = 0.01). In the 35 patients with complete scintigraphic, body map and angiographic data, the severity of reversible perfusion defect proved to be the strongest correlate of ST segment depression upon logistic regression analysis. Thus, sestamibi SPET abnormalities after dipyridamole are almost always associated with electrical changes on body surface maps, suggesting myocardial ischaemia as their cause. The much less common 12-lead ECG changes are slower to appear and reflect a more severe hypoperfusion.

AB - At dipyridamole myocardial scintigraphy, perfusion defects are seldom backed up by significant ECG changes. This would suggest myocardial blood flow heterogeneity rather than true ischaemia, as the cause of the scintigraphic abnormalities. Electrocardiographic surface mapping has been documented to be more accurate than standard 12-lead ECG in the detection of provoked ischaemia. Thus, to investigate the relationship between ECG changes and perfusion abnormalities, body surface maps were recorded during dipyridamole infusion in 55 subjects (11 normals and 44 patients with ischaemic heart disease) undergoing dipyridamole technetium-99m sestamibi single-photon emission tomography (SPET). All had a normal resting ECG. The extent and severity of the sestamibi defect were quantified. New negative areas in the isointegral maps and rest-dipyridamole map differences > 2 SD from normal limits were considered abnormal. After dipyridamole in normals, neither perfusion defects nor ≤ 1 mm ST segment depression on 12-lead ECG nor new negative areas in isointegral maps occurred. In patients, dipyridamole induced new perfusion defects in 35 (80%) but ST segment depression in only 18 (41%, P <0.001). Of the 35 patients with perfusion defects, 17 (49%, group 1) showed ST segment depression, while the other 18 (51%, group 2) did not. Abnormal body surface maps were found in 100% of group 1 and 88% of group 2 patients (NS). In group 1, the provoked hypoperfusion was of greater extent (P = 0.007) and severity (P = 0.01) and the onset of map abnormalities was significantly earlier (P <0.001) than in group 2; time to map abnormalities was also significantly shorter than time to ST segment depression (P = 0.01). In the 35 patients with complete scintigraphic, body map and angiographic data, the severity of reversible perfusion defect proved to be the strongest correlate of ST segment depression upon logistic regression analysis. Thus, sestamibi SPET abnormalities after dipyridamole are almost always associated with electrical changes on body surface maps, suggesting myocardial ischaemia as their cause. The much less common 12-lead ECG changes are slower to appear and reflect a more severe hypoperfusion.

KW - Coronary artery disease

KW - Dipyridamole

KW - Myocardial ischaemia

KW - Technetium-99m sestamibi single-photon emission tomography

UR - http://www.scopus.com/inward/record.url?scp=0030998637&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030998637&partnerID=8YFLogxK

U2 - 10.1007/BF02439548

DO - 10.1007/BF02439548

M3 - Article

C2 - 9021113

AN - SCOPUS:0030998637

VL - 24

SP - 160

EP - 169

JO - European Journal of Pediatrics

JF - European Journal of Pediatrics

SN - 0340-6199

IS - 2

ER -