Will Imaging Assist in the Selection of Patients With Heart Failure for an ICD?
Myron C. Gerson, MD*, ,*,
Mouhamad Abdallah, MD*,
James N. Muth, MD, PhD*,
Alexandru I. Costea, MD*
* Division of Cardiovascular Diseases, University of Cincinnati College of Medicine, Cincinnati, Ohio
E. L. Saenger Radioisotope Laboratory, University Hospital of Cincinnati, Cincinnati, Ohio

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Figure 1 Pathologic and Cardiac Magnetic Resonance Demonstration of Myocardial Fibrosis in Nonischemic Cardiomyopathy
(A) Pathologic short-axis section through the left and right ventricles at mid-ventricular level showing mid-wall fibrosis (straight arrows) in the inferior, lateral, and septal walls from a patient with nonischemic dilated cardiomyopathy. (B) Sirius red staining confirming the presence of collagen in a microscopic section from the area of fibrosis in the pathologic section. (C) Premortem cardiac magnetic resonance image of the same myocardial slice illustrating the correlation of areas of late gadolinium enhancement with pathologic fibrosis. Reproduced with permission from Assomull et al. (10).
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Figure 2 Prediction of Sudden Cardiac Death by LGE
(A) Kaplan-Meier estimates for the combined end point of sudden cardiac death and sustained ventricular tachycardia with the presence (LGE+) or absence (LGE–) of LGE. (B) The same data adjusted for baseline differences in left ventricular ejection fraction. Reproduced with permission from Assomull et al. (10). LGE = late gadolinium enhancement.
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Figure 3 Prediction of Sudden Cardiac Death or Implantable Cardioverter-Defibrillator Therapy by Myocardial Ischemia
Kaplan-Meier curves indicating freedom from sudden cardiac death and appropriate implantable cardiac defibrillator therapy in patients with coronary artery disease at high risk for arrhythmic death. Risk is stratified by the presence or absence of myocardial ischemia detected by stress echocardiography. Independent predictors of events in the Cox multivariate model were a history of spontaneous sustained ventricular tachycardia (hazard ratio [HR]: 1.9; 95% confidence interval [CI]: 1.3. to 3.8; p < 0.01), inducible ventricular tachycardia on electrophysiologic study (HR: 1.7; 95% CI: 1.2 to 4.5; p < 0.01), and myocardial ischemia (HR: 2.1; 95% CI: 1.2 to 3.5; p < 0.01). Reproduced with permission from Elhendy et al. (17).
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Figure 4 Prediction of SCD From Combined Myocardial Ischemia and Scar
Relative contribution of the extent of myocardial ischemia plus scar to estimating sudden cardiac death (SCD) when compared with clinical risk factors and left ventricular ejection fraction (LVEF). When compared with the clinical index, LVEF contributes 48.3% of the prognostic model content for estimating SCD. By comparison, the combination of EF + summed stress score (SSS) contributes 51.6% of the prognostic model content for estimating SCD, with the addition of SSS providing only a modest improvement in information content (20).
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Figure 5 H/M Ratio of Sympathetic Nerve Activity From [123I]meta-iodobenzylguanidine
Example of the heart to mediastinum (H/M) ratio calculated from a [123I]meta-iodobenzylguanidine planar anterior image. (A) Image from a patient with severe heart failure (H/M ratio 1.02). (B) Image from a patient with moderate heart failure (H/M ratio 1.55). Reproduced with permission from Gerson et al. (23).
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Figure 6 Perfusion/Innervation Mismatch and VT Site of Origin
Correlation of perfusion/innervation mismatch location and site of earliest activation of ventricular tachycardia (VT) in an animal model of VT. (Left, top) Positron emission tomography polarmaps show regional distribution of perfusion with 13N-ammonia and of sympathetic innervation by 11C-epinephrine retention. (Left, bottom) Extent maps of reduced perfusion and innervation. (Right, bottom) The extent of denervation exceeds the region of hypoperfusion, producing a mismatch. (Right, top) Three-dimensional electroanatomic maps, depicted in an anterior projection, show reduced bipolar endocardial voltage in the apex and distal anteroseptal wall. Propagation maps show the earliest activation of VT in the infarct border zone in the distal anterior wall (red arrow). Reproduced with permission from Sasano et al. (25). LV = left ventricular; RV = right ventricle.
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Figure 7 Perfusion/Innervation Mismatch and Inducibility of VT
In experimental animals with a mid-left anterior descending artery occlusion, positron emission tomography perfusion and innervation defect size was not significantly different in animals inducible for ventricular tachycardia (VT) compared with animals that were not inducible. Animals that were inducible for VT had more extensive perfusion/innervation mismatch size compared with animals that were not inducible for VT (p = 0.019). Reproduced with permission from Sasano et al. (25).
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Figure 8 [123I]meta-iodobenzylguanidine Prediction of SCD
Sudden cardiac death (SCD)-free survival rate following adjustment for age, gender, and left ventricular ejection fraction based on [123I]meta-iodobenzylguanidine normal washout rate (WR) 27% versus abnormal washout rate >27%. Reproduced with permission from Tamaki et al. (51).
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Figure 9 [123I]meta-iodobenzylguanidine Prediction of Sudden Cardiac Death in Patients With Left Ventricular Ejection Fraction >35%
Sudden cardiac death rates by [123I]meta-iodobenzylguanidine washout rate (WR) >27% (abnormal) versus 27% (normal). (A) Patients with left ventricular ejection fraction >35%. (B) Patients with left ventricular ejection fraction 35%. Reproduced with permission from Tamaki et al. (51).
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