Methods

The study population consisted of patients referred for stress myocardial perfusion imaging (MPI) for clinical indications from August 2008 through May 2009. Inclusion criteria were (1) age >18 years, (2) normal QRS duration on 12-lead surface electrocardiogram at time of study, (3) normal MPI finding at rest or during stress (exercise or pharmacologic), and (4) end-stage renal disease (ESRD) on dialysis. Pregnant women, patients with hypertrophic cardiomyopathy or other congenital heart disease, left or right bundle branch blocking, ventricular pacing, atrial fibrillation, and any perfusion abnormality (fixed or reversible) were excluded. We also identified consecutive patients with a glomerular filtration rate >60 ml/min/m ² within the same time frame and who otherwise met the same inclusion criteria and served as a control group. Demographics and other pertinent data were extracted through chart reviews.

Gated single-photon emission computed tomography MPI was obtained at stress (exercise or pharmacologic) and rest with technetium-99m sestamibi according to American Society of Nuclear Cardiology guidelines as previously described. LV ejection fraction (EF), volumes, and mass were measured from gated studies at rest (because it was performed using a higher tracer dose of 30 to 45 vs 10 to 15 mCi for the stress study) based on a method described by Germano et al. HR was recorded at the time of gated single-photon emission computed tomographic acquisition at rest. Most studies were with 8 frames/cycle.

Phase SD and histographic bandwidth were measured as previously described and briefly summarized in this report. Three-dimensional count distributions were extracted from each LV short-axis dataset and subjected to Fourier phase analysis, thus generating a 3-dimensional phase distribution (0° to 360°) spanning the entire RR interval. The latter was displaced on a polar map and on a histogram. Two dyssynchrony indexes were derived: (1) phase SD, which represents the SD of the phase distribution, and (2) histographic bandwidth, which represents duration of the cardiac cycle during which 95% of the myocardium initiated contraction. These parameters are related to onset of mechanical contraction or systole and thus reflect systolic dyssynchrony.

A descriptive analysis was performed examining pertinent variables in the 4 cohorts of patients (ESRD and control with normal [≥50%] and abnormal [<50%] EFs). Furthermore, each group was divided into tertiles based on HR, and mean values in the first (slowest HR) and third (highest HR) tertiles were compared. Correlations between dyssynchrony indexes and HR were also performed. Student’s t test was used for continuous variables and Pearson chi-square test for categorical variables. Data are presented as mean ± SD for continuous variables and as percentage for categorical variables. Spearman correlation coefficient was used to evaluate bivariate relations. All p values were 2-tailed with a p value <0.05 set a priori and used as the level of statistical significance. All statistical analyses were performed using SPSS 11.5 for Windows (SPSS, Inc., Chicago, Illinois).

This study was approved by the institutional review board at the University of Alabama at Birmingham.

Results

Baseline characteristics are presented in Table 1 . There were 140 patients in the ESRD group and 133 patients in the control group. Patients with ESRD were younger, more likely to be African-Americans, and to have diabetes mellitus. Most patients had hypertension and 2% had previous myocardial infarction, although the perfusion pattern was normal. Mean LVEFs were 62 ± 8% versus 69 ± 9% in the ESRD and control groups with normal EF (p <0.001) and 41 ± 8% versus 43 ± 7% in patients with abnormal EF, respectively (p = NS). LV volumes, mass, and dyssynchrony indexes are presented in Table 2 . HR at rest was 75 ± 13 beats/min (range 48 to 113) for all patients. Patients with abnormal LVEF had higher phase SD (30 ± 13° vs 22 ± 11° and 28 ± 16° vs 15 ± 6° for the ESRD and control groups, respectively, p <0.001 each) and greater histographic bandwidth (88 ± 44° vs 62 ± 33° and 80 ± 49° vs 43 ± 14° for ESRD and control groups, p <0.001 each). Patients with ESRD and normal LVEF had higher SD and bandwidth than control patients with normal EF (22 ± 11° vs 15 ± 6° and 62 ± 33° vs 43 ± 14°, respectively, p <0.001 for the 2 comparisons).

Table 2

Quantitative analysis of gated single-photon emission computed tomogram based on tertiles of heart rate

	ESRD, EF ≥50%			ESRD, EF <50%			Control, EF ≥50%			Control, EF <50%
	(n = 69)			(n = 71)			(n = 68)			(n = 65)
	All	T1	T3	All	T1	T3	All	T1	T3	All	T1	T3
End-diastolic volume (ml)	152 ± 56 † §	130 ± 49	155 ± 67	222 ± 73 † ‡	222 ± 67	220 ± 72	108 ± 44 † §	112 ± 46 ∥	88 ± 29 ∥	185 ± 67 † ‡	171 ± 57	194 ± 69
End-systolic volume (ml)	51 ± 30	33 ± 21	58 ± 35	114 ± 46 † ‡	113 ± 45	108 ± 51	25 ± 17 † §	27 ± 13 ∥	19 ± 10 ∥	90 ± 49 † ‡	79 ± 39	96 ± 54
Left ventricular mass (g)	163 ± 36	146 ± 33 ∥	170 ± 40 ∥	208 ± 41 † ‡	209 ± 37	203 ± 38	137 ± 30 † §	139 ± 13 ∥	123 ± 22 ∥	187 ± 42 † ‡	187 ± 34	185 ± 47
Left ventricular ejection fraction (%)	62 ± 8	69 ± 6 ¶	59 ± 10 ¶	41 ± 8 †	41 ± 8	42 ± 7	69 ± 9 † §	69 ± 7	69 ± 12	43 ± 7 †	44 ± 8	43 ± 7
Heart rate	74 ± 10	63 ± 6 ¶	84 ± 6 ¶	78 ± 15 ⁎	64 ± 4 ¶	94 ± 10 ¶	70 ± 13 † ‡	58 ± 4 ¶	85 ± 10 ¶	79 ± 14 †	65 ± 4 ¶	95 ± 8 ¶
(beats/min)	(48–100)			(54–113)			(48–109)			(57–113)
QRS duration (ms)	90 ± 12 ⁎	88 ± 11	93 ± 14	95 ± 13 ⁎	98 ± 11	92 ± 14	94 ± 23	94 ± 13	91 ± 23	97 ± 21	93 ± 16	97 ± 21

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