Left atrial (LA) abnormality, an easily quantifiable parameter of left ventricular (LV) diastolic dysfunction, has been associated with cardiovascular risk. Because during myocardial perfusion study (MPS), the abnormal LV activation pattern in patients with left bundle branch block (LBBB) frequently induces perfusion defects, a clinical correlate of early myocardial ischemia such as LA enlargement could alleviate some of these inherent challenges. We prospectively studied 144 consecutive patients with LBBB who underwent MPS after screening for electrocardiographic and echocardiographic LA enlargement over a 6-month period. Of those, 114 had a positive MPS result. We found that LA size (p <0.0001) and P-wave duration (p = 0.001) were significantly increased in patients as the severity of the defects increased on MPS, whereas LV ejection fraction was decrementally reduced (p = 0.001). Importantly, LA size (≥43.5 mm; sensitivity 70%, specificity 89%) and P-wave duration (≥135 milliseconds; sensitivity 63%, specificity 90%) were greatest when the MPS defect was severe. In conclusion, the presence of LA enlargement appears significantly correlated with myocardial ischemia among patients with LBBB and could therefore assist during MPS interpretation among patients in whom MPS interpretation could be challenging.
Left atrial (LA) enlargement is associated with significant cardiovascular morbidity and mortality. It has been shown to function as a barometer of left ventricular (LV) diastolic burden and portends significant cardiovascular outcomes such as atrial fibrillation, stroke, heart failure, myocardial ischemia, and cardiovascular death. During myocardial perfusion study using single-photon emission computed tomography (MPS), the abnormal LV activation pattern in patients with left bundle branch block (LBBB) frequently induces perfusion defects, particularly erroneous anteroseptal and septal perfusion abnormalities, and thus a clinical correlate of early myocardial ischemia such as LA enlargement may perhaps help alleviate some of these inherent clinical interpretational challenges. We therefore studied the correlation of this cardiovascular marker with myocardial ischemia during MPS among a subset of patients with LBBB.
Methods
We prospectively identified all consecutively hospitalized patients from Saint Vincent Hospital, Worcester, Massachusetts, over a 6-month period with previously identified LBBB on the electrocardiogram (ECG) who underwent MPS. Patients were subsequently screened for 2-dimensional transthoracic echocardiogram reports performed within 14 days (range 6.2 to 22.0 months; mean 13.4 months) of MPS assessment. Because coronary artery disease and hypertension have proved to be highly prevalent correlates of LA electrocardiographic as well as echocardiographic abnormality, both otherwise unselected groups were matched for these comorbidities. MPS reports were then assessed for reported reversible perfusion abnormalities that were consistent with myocardial ischemia. Reports with nonreversible defects suggesting the presence of myocardial scar were excluded from this investigation. All patients had been referred by either cardiologists or primary care physicians who were directly involved in their care for evaluation of myocardial ischemia. We also appraised common medical comorbidities that had been documented in patients’ records by physicians involved directly in their care and were consistent with current classifications and guidelines for disease definition as well as diagnosis outlined by American College of Cardiology/American College of Physicians-American Society of Internal Medicine Task Force on Practice Guidelines.
Resting 12-lead ECGs had been recorded in the supine position from a Marquette 2000 electrocardiograph (Marquette Electronics Incorporated, Milwaukee, Wisconsin) standardized at 25 mm/s and 10 mm/mV. ECGs were evaluated for previously diagnosed LBBB using the following criteria: (1) QRS complex widening >120 milliseconds, (2) tall, upright (monophasic) QRS complexes without Q waves in leads I, aVL, and V6, and (3) a predominantly negative QRS complex in lead V1, with or without an initial small r wave (i.e., occurring either as a QS or rS complex). All ECGs with such LBBB had to have been diagnosed >6 months with 12-lead ECG documentation (range 6.2 to 22.0 months; mean 13.4 months) to be considered for this study.
Two-dimensional transthoracic echocardiograms had been performed on each study participant in the left lateral recumbent position for parasternal long and short axes and apical 4- and 2-chamber views as well as in the supine position for subcostal views using an ATI HDL 5000W imaging system with a P4-2 scan head and 2.6-MHz transducer (Phillips Medical Systems Company, Bothell, Washington). LA enlargement was considered when anteroposterior measurement from leading edge to leading edge during systolic frames exceeded 40 mm in male and 38 mm in female patients. Systolic frames were defined as the frame depicting the cardiac systolic event just before separation of the mitral valve tips. All echocardiograms were recorded and analyzed by experienced, board-certified echocardiographers who were blinded to both clinical presentation and ECG findings.
Each patient received an intravenous infusion of dipyridamole (0.56 mg/kg over 4 minutes) while they underwent continuous ECG monitoring under the supervision of board-certified cardiologist and qualified technicians per institutional protocols. Weight-based calculated doses of 99mTc-tetrofosmin were then administered intravenously at 4.5 minutes after completion of the dipyridamole infusion. Stress images were acquired 30 to 45 minutes after the administration of the radiopharmaceutical and immediately after such acquisition, another weight-based calculated dose of 99mTc-tetrofosmin was administered for each patient. Rest images were then obtained 15 to 30 minutes later. Single-photon emission computed tomography or images were acquired using an Elscint SP4 scintillation gamma camera with an all-purpose, high-resolution collimator by use of a step-and-shoot approach every 3° over a 180° clockwise circular orbit beginning at a 30° right anterior oblique projection and ending at 45° left posterior projection. Images were reconstructed using standard back projection algorithms (Butterworth filter, order 5, section frequency 0.4). Quantitative gating was also performed. Stress and rest images from the short-axis, horizontal long-axis, and vertical long-axis slices were obtained according to the American Society of Nuclear Cardiology guidelines and were viewed by experienced board-certified cardiologists. Perfusion defect that were noted in the short-axis slices were confirmed in the other 2 planes. The myocardial radiopharmaceutical uptake was assessed by consensus for reversible perfusion abnormality as normal, mild defect, moderate defect, or severe defect in relation to the background uptake and quantified by size (large, medium, or small) when perfusion abnormalities were noted.
Data are expressed as mean ± SD for continuous variables and frequencies for categorical variables. Differences between groups were assessed using chi-square statistics for categorical variables and analysis of variance for continuous variables. A p value <0.05 was considered significant. Logistic multivariate regression analysis using significant variables was also performed. Statistical analyses were performed using SPSS Version 13.0 statistical software (SPSS Inc., Chicago, Illinois).
Results
One hundred forty-four patients, aged 47 to 95 years (mean ± SD = 69.4 ± 11), qualified for our analysis. Baseline characteristics were similar, with no significant association with age or gender. Approximately 2/3 of the patients had LA enlargement. One hundred eleven patients were reported to have a positive MPS result for myocardial ischemia ( Table 1 ). Increasing left atrial size and P-wave duration as well as decreasing LV ejection fraction acquired via MPS appeared proportionately associated with the increasing severity of the MPS defect. Left atrial size (p <0.0001) and P-wave duration (p = 0.001) were significantly increased in patients with increasing severity of defects on MPS, whereas LV ejection fraction was decrementally reduced (p = 0.001). Importantly, LA size (≥43.5 mm; sensitivity 70%, specificity 89%; Table 2 ) and P-wave duration (≥135 milliseconds; sensitivity 63%, specificity 90%; Table 3 ) were greatest when the MPS defect was severe ( Figures 1 and 2 ).
| Variable | Myocardial Perfusion Study Defects | p for Trend | |||
|---|---|---|---|---|---|
| None (n = 33) | Mild (n = 33) | Moderate (n = 32) | Severe (n = 46) | ||
| Age (mean ± SD) | 71.0 ± 11 | 70.2 ± 11 | 67.1 ± 10 | 69.2 ± 12 | 0.522 |
| Female | 20 (61%) | 11 (33%) | 16 (50%) | 23 (50%) | 0.169 |
| Male | 13 (39%) | 22 (67%) | 16 (50%) | 23 (50%) | 0.169 |
| Diabetes mellitus | 9 (27%) | 10 (30%) | 7 (22%) | 12 (26%) | 0.894 |
| Hyperlipidemia (LDL >160 mg/dl) | 16 (49%) | 21 (64%) | 16 (50%) | 25 (54%) | 0.605 |
| Atrial flutter | 0 | 0 | 0 | 2 (4%) | 0.229 |
| Atrial fibrillation | 6 (18%) | 6 (18%) | 6 (19%) | 6 (13.0%) | 0.886 |
| Valvular heart disease | 6 (18%) | 8 (24%) | 5 (16%) | 15 (33%) | 0.291 |
| Chronic obstructive pulmonary disease | 9 (27%) | 7 (21%) | 10 (31%) | 13 (28%) | 0.828 |
| Dilated cardiomyopathy | 15 (46%) | 15 (46%) | 14 (44%) | 17 (37%) | 0.841 |
| Beta-adrenergic blocker use | 20 (61%) | 14 (42%) | 15 (47%) | 19 (41%) | 0.344 |
| Angiotensinogen converting enzyme inhibitor use | 8 (24%) | 6 (18%) | 7 (23%) | 3 (7%) | 0.134 |
| Angiotensin receptor blocker use | 4 (12%) | 5 (15%) | 3 (9%) | 9 (20%) | 0.619 |
| Statin | 15 (46%) | 20 (61%) | 16 (50%) | 25 (54%) | 0.644 |
| LA size (mm) | 34.8 ± 6 | 38.4 ± 5 | 41.2 ± 8 | 48.8 ± 9 | <0.0001 |
| LV end systolic volume (ml) | 43.4 ± 7 | 43.6 ± 8 | 45.9 ± 9 | 43.2 ± 7 | 0.446 |
| LV end diastolic volume (ml) | 108.3 ± 17 | 111.7 ± 10 | 112.1 ± 17 | 111.6 ± 16 | 0.724 |
| Intraventricular septum (mm) | 11.1 ± 2 | 11.7 ± 2 | 11.4 ± 2 | 11.9 ± 2 | 0.369 |
| LV ejection fraction (echocardiogram; %) | 49.5 ± 9 | 43.6 ± 10 | 45.1 ± 10 | 46.6 ± 9 | 0.079 |
| LV ejection fraction (MPS; %) | 49.7 ± 11 | 44.1 ± 9 | 44.3 ± 10 | 40.8 ± 7 | 0.001 |
| P-wave duration (ms) | 123.6 ± 14 | 119.7 ± 8 | 124.4 ± 13 | 132.2 ± 17 | 0.001 |
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