Predictors of slow flow during primary percutaneous coronary intervention: An intravascular ultrasound-virtual histology study

Jang Ho Bae, T. G. Kwon, D. W. Hyun, C. S. Rihal, Amir Lerman

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

Objectives: Slow flow phenomenon is a serious complication of percutaneous coronary intervention (PCI) and is associated with a poor prognosis. We sought to evaluate the characteristics of lesions predisposing to the slow/no-reflow phenomenon during primary PCI in patients with acute myocardial infarction. Methods: The study subjects consisted of 57 consecutive patients (mean age 58.5 (SD 14.5) years, 45 males) who underwent primary PCI for acute myocardial infarction and intravascular ultrasound-virtual histology (IVUS-VH) examination. Slow flow was defined as ≤ thrombolysis in myocardial infarction grade 2 after PCI. Results: Slow flow developed in 12 patients (eight males). Patients with slow flow were likely to be older (67.5 (13.8) years vs 56.2 (13.9) years, p = 0.015), had more cardiogenic shock (16.7% vs 2.2%, p = 0.046), larger fibrofatty volume over the entire lesion length (36.7 (25.5) mm3 vs 18.0 (18.6) mm3, p = 0.006), higher remodelling index (1.10 (0.17) vs 0.99 (0.16), p = 0.043), larger plaque area (16.2 (5.4) mm2 vs 12.5 (4.9) mm2, p = 0.025), fibrous area (8.0 (3.3) mm2 vs 5.4 (3.0) mm2, p = 0.014) and fibrofatty area (2.7 (2.2) mm2 vs 1.3 (1.6) mm2, p = 0.016) at the minimal lumen site than those without slow flow (37 males). Multivariate analysis revealed that the fibrofatty volume over the entire lesion length was the only independent factor (β = 0.359, 95% confidence interval 0.002 to 0.012, p = 0.006) for slow flow during primary PCI. Conclusions: This study suggests that slow flow may be dependent on the tissue characterisation (fibrofatty volume) of the underlying lesion at the time of the primary PCI for acute myocardial infarction.

Original languageEnglish (US)
Pages (from-to)1559-1564
Number of pages6
JournalHeart
Volume94
Issue number12
DOIs
StatePublished - Dec 2008

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Percutaneous Coronary Intervention
Histology
Myocardial Infarction
No-Reflow Phenomenon
Cardiogenic Shock
Multivariate Analysis
Confidence Intervals

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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Predictors of slow flow during primary percutaneous coronary intervention : An intravascular ultrasound-virtual histology study. / Bae, Jang Ho; Kwon, T. G.; Hyun, D. W.; Rihal, C. S.; Lerman, Amir.

In: Heart, Vol. 94, No. 12, 12.2008, p. 1559-1564.

Research output: Contribution to journalArticle

Bae, Jang Ho ; Kwon, T. G. ; Hyun, D. W. ; Rihal, C. S. ; Lerman, Amir. / Predictors of slow flow during primary percutaneous coronary intervention : An intravascular ultrasound-virtual histology study. In: Heart. 2008 ; Vol. 94, No. 12. pp. 1559-1564.
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abstract = "Objectives: Slow flow phenomenon is a serious complication of percutaneous coronary intervention (PCI) and is associated with a poor prognosis. We sought to evaluate the characteristics of lesions predisposing to the slow/no-reflow phenomenon during primary PCI in patients with acute myocardial infarction. Methods: The study subjects consisted of 57 consecutive patients (mean age 58.5 (SD 14.5) years, 45 males) who underwent primary PCI for acute myocardial infarction and intravascular ultrasound-virtual histology (IVUS-VH) examination. Slow flow was defined as ≤ thrombolysis in myocardial infarction grade 2 after PCI. Results: Slow flow developed in 12 patients (eight males). Patients with slow flow were likely to be older (67.5 (13.8) years vs 56.2 (13.9) years, p = 0.015), had more cardiogenic shock (16.7{\%} vs 2.2{\%}, p = 0.046), larger fibrofatty volume over the entire lesion length (36.7 (25.5) mm3 vs 18.0 (18.6) mm3, p = 0.006), higher remodelling index (1.10 (0.17) vs 0.99 (0.16), p = 0.043), larger plaque area (16.2 (5.4) mm2 vs 12.5 (4.9) mm2, p = 0.025), fibrous area (8.0 (3.3) mm2 vs 5.4 (3.0) mm2, p = 0.014) and fibrofatty area (2.7 (2.2) mm2 vs 1.3 (1.6) mm2, p = 0.016) at the minimal lumen site than those without slow flow (37 males). Multivariate analysis revealed that the fibrofatty volume over the entire lesion length was the only independent factor (β = 0.359, 95{\%} confidence interval 0.002 to 0.012, p = 0.006) for slow flow during primary PCI. Conclusions: This study suggests that slow flow may be dependent on the tissue characterisation (fibrofatty volume) of the underlying lesion at the time of the primary PCI for acute myocardial infarction.",
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T1 - Predictors of slow flow during primary percutaneous coronary intervention

T2 - An intravascular ultrasound-virtual histology study

AU - Bae, Jang Ho

AU - Kwon, T. G.

AU - Hyun, D. W.

AU - Rihal, C. S.

AU - Lerman, Amir

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N2 - Objectives: Slow flow phenomenon is a serious complication of percutaneous coronary intervention (PCI) and is associated with a poor prognosis. We sought to evaluate the characteristics of lesions predisposing to the slow/no-reflow phenomenon during primary PCI in patients with acute myocardial infarction. Methods: The study subjects consisted of 57 consecutive patients (mean age 58.5 (SD 14.5) years, 45 males) who underwent primary PCI for acute myocardial infarction and intravascular ultrasound-virtual histology (IVUS-VH) examination. Slow flow was defined as ≤ thrombolysis in myocardial infarction grade 2 after PCI. Results: Slow flow developed in 12 patients (eight males). Patients with slow flow were likely to be older (67.5 (13.8) years vs 56.2 (13.9) years, p = 0.015), had more cardiogenic shock (16.7% vs 2.2%, p = 0.046), larger fibrofatty volume over the entire lesion length (36.7 (25.5) mm3 vs 18.0 (18.6) mm3, p = 0.006), higher remodelling index (1.10 (0.17) vs 0.99 (0.16), p = 0.043), larger plaque area (16.2 (5.4) mm2 vs 12.5 (4.9) mm2, p = 0.025), fibrous area (8.0 (3.3) mm2 vs 5.4 (3.0) mm2, p = 0.014) and fibrofatty area (2.7 (2.2) mm2 vs 1.3 (1.6) mm2, p = 0.016) at the minimal lumen site than those without slow flow (37 males). Multivariate analysis revealed that the fibrofatty volume over the entire lesion length was the only independent factor (β = 0.359, 95% confidence interval 0.002 to 0.012, p = 0.006) for slow flow during primary PCI. Conclusions: This study suggests that slow flow may be dependent on the tissue characterisation (fibrofatty volume) of the underlying lesion at the time of the primary PCI for acute myocardial infarction.

AB - Objectives: Slow flow phenomenon is a serious complication of percutaneous coronary intervention (PCI) and is associated with a poor prognosis. We sought to evaluate the characteristics of lesions predisposing to the slow/no-reflow phenomenon during primary PCI in patients with acute myocardial infarction. Methods: The study subjects consisted of 57 consecutive patients (mean age 58.5 (SD 14.5) years, 45 males) who underwent primary PCI for acute myocardial infarction and intravascular ultrasound-virtual histology (IVUS-VH) examination. Slow flow was defined as ≤ thrombolysis in myocardial infarction grade 2 after PCI. Results: Slow flow developed in 12 patients (eight males). Patients with slow flow were likely to be older (67.5 (13.8) years vs 56.2 (13.9) years, p = 0.015), had more cardiogenic shock (16.7% vs 2.2%, p = 0.046), larger fibrofatty volume over the entire lesion length (36.7 (25.5) mm3 vs 18.0 (18.6) mm3, p = 0.006), higher remodelling index (1.10 (0.17) vs 0.99 (0.16), p = 0.043), larger plaque area (16.2 (5.4) mm2 vs 12.5 (4.9) mm2, p = 0.025), fibrous area (8.0 (3.3) mm2 vs 5.4 (3.0) mm2, p = 0.014) and fibrofatty area (2.7 (2.2) mm2 vs 1.3 (1.6) mm2, p = 0.016) at the minimal lumen site than those without slow flow (37 males). Multivariate analysis revealed that the fibrofatty volume over the entire lesion length was the only independent factor (β = 0.359, 95% confidence interval 0.002 to 0.012, p = 0.006) for slow flow during primary PCI. Conclusions: This study suggests that slow flow may be dependent on the tissue characterisation (fibrofatty volume) of the underlying lesion at the time of the primary PCI for acute myocardial infarction.

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