Faculty Bibliography

BACKGROUND: It is not clearly understood why concentric left ventricular hypertrophy (increased left ventricular mass and relative wall thickness) is associated with higher cardiovascular risk than eccentric hypertrophy (increased left ventricular mass but normal relative wall thickness). Possible reasons include lower myocardial efficiency or perfusion reserve in concentric than in eccentric hypertrophy. We compared myocardial perfusion reserve and efficiency in normotensive controls and in hypertensive patients with concentric and with eccentric hypertrophy. METHODS: Study subjects comprised 16 patients with hypertension-induced left ventricular hypertrophy and 10 normotensive controls. We measured myocardial perfusion reserve and oxygen consumption by positron emission tomography. We calculated myocardial efficiency by dividing left ventricular minute work by myocardial oxygen consumption. RESULTS: There was no significant difference in myocardial perfusion reserve between patients with concentric (n = 9) as compared to eccentric (n = 7) hypertrophy. However, myocardial perfusion reserve in both patient groups were lower than in controls. Although myocardial efficiency in patients with eccentric hypertrophy and in controls were not different, both values were higher than measurements in patients with concentric hypertrophy (18% +/- 6% v 16% +/- 3% v 13% +/- 4%, eccentric hypertrophy versus controls versus concentric hypertrophy, respectively, P =.04 for both eccentric versus concentric hypertrophy and for controls versus concentric hypertrophy). CONCLUSIONS: Myocardial efficiency but not perfusion reserve is lower in hearts with concentric compared with eccentric left ventricular hypertrophy. This might be an explanation for the higher cardiovascular morbidity and mortality associated with concentric left ventricular hypertrophy.

BACKGROUND: Calculation differences between various gated blood pool (GBP) single photon emission computed tomography (SPECT) (GBPS) algorithms may arise as a result of different modeling assumptions. Little information has been available thus far regarding differences for right ventricular (RV) function calculations, for which GBPS may be uniquely well suited. METHODS AND RESULTS: Measurements of QBS (Cedars-Sinai Medical Center, Los Angeles, Calif) and BP-SPECT (Columbia University, New York, NY) algorithms were evaluated. QBS and BP-SPECT left ventricular (LV) ejection fraction (EF) correlated strongly with conventional planar-GBP LVEF for 422 patients (r = 0.81 vs r = 0.83). QBS correlated significantly more strongly with BP-SPECT for LVEF than for RVEF (r = 0.80 vs r = 0.41). Both algorithms demonstrated significant gender differences for 31 normal subjects. BP-SPECT normal LVEF (67% +/- 9%) was significantly closer to values in the magnetic resonance imaging (MRI) literature (68% +/- 5%) than QBS (58% +/- 9%), but both algorithms underestimated normal RVEF (52% +/- 7% and 50% +/- 9%) compared with the MRI literature (64% +/- 9%). For 21 patients, QBS correlated similarly to MRI as BP-SPECT for LVEF (r = 0.80 vs r = 0.85) but RVEF correlation was significantly weaker (r = 0.47 vs r = 0.81). For 16 dynamic phantom simulations, QBS LVEF correlated similarly to BP-SPECT (r = 0.81 vs r = 0.91) but QBS RVEF correlation was significantly weaker (r = 0.62 vs r = 0.82). Volumes were lower by QBS than BP-SPECT for all data types. CONCLUSIONS: Both algorithms produced LV parameters that correlated strongly with all forms of image data, but all QBS RV relationships were significantly different from BP-SPECT RV relationships. Differences between the two algorithms were attributed to differences in their underlying ventricular modeling assumptions.

PURPOSE/OBJECTIVE:The purpose of this investigation was to determine whether left ventricular mass (LVM) assessed from myocardial perfusion gated SPECT (GSPECT) data corresponds with echocardiographic estimates, and whether mass accuracy decreases as relative myocardial wall thickness increases. MATERIALS AND METHODS/METHODS:Myocardial perfusion tomograms were selected retrospectively for 37 patients, of whom 18 had Tl-201 and 19 had Tc-99m sestamibi GSPECT poststress data collections, which were subsequently processed using quantitative gated SPECT software (Cedars Sinai Medical Center, Los Angeles, CA). These patients also had clinically indicated echocardiograms for assessment of wall thickness and possible valvular involvement. In addition, LV internal diameter and posterior wall thickness were measured at end-diastole by two-dimensional guided M-mode echocardiography to assess relative myocardial wall thickness, and LVM was measured by three-dimensional echocardiography using an acoustic spatial locator device. RESULTS:LVM values were not significantly different between GSPECT and three-dimensional echocardiography (153 +/- 39 g versus 146 +/- 35 g, respectively; P = NS). GSPECT correlated significantly (r = 0.63, P < 0.0001) with three-dimensional echocardiography, with a mean difference of 7 +/- 32 g but a substantial root mean squared error of 31 g. Results were similar for similar mass ranges when subgrouped by isotope and by the presence of significant myocardial perfusion defects. Results were independent of relative myocardial wall thickness determined by two-dimensional echocardiography. The two methods yielded similar results in the highest mass range of 400 to 500 g. CONCLUSIONS:GSPECT and three-dimensional echo LVM correlated significantly, but given the large spread of statistical errors, these two techniques should not be considered interchangeable. Because gamma camera resolution is limited, GSPECT LVM should be viewed as an approximation.

BACKGROUND: The aim of this study was to identify the best correlate of myocardial oxygen demand (MVO(2)) in patients with hypertension induced left ventricular hypertrophy (LVH), and to examine whether relationships between these surrogates and MVO(2) differed between patients with LVH and control subjects. METHODS: We measured MVO(2) by positron emission tomography using carbon-11 acetate in 20 patients and 10 normotensive control subjects, and compared the relationships between commonly used surrogates and MVO(2). RESULTS: With the exception of diastolic blood pressure, the same variables correlated with resting MVO(2) in the patients and control subjects. CONCLUSIONS: The best correlate of resting MVO(2) in the patients with hypertension induced LVH was the stress-mass-heart rate product.

BACKGROUND: This study examines the relationship between functional capacity, left ventricular diastolic function, and myocardial perfusion reserve (MPR) in patients with left ventricular hypertrophy (LVH). METHODS: We studied 16 patients with LVH and 10 controls. Functional capacity was assessed by cardiopulmonary exercise, MPR by positron emission tomography, and left ventricular diastolic function by echo-Doppler. RESULTS: Functional capacity and MPR were significantly lower in the patients. Functional capacity correlated positively with MPR and left ventricular diastolic function. CONCLUSIONS: Diminished functional capacity in patients with hypertension-induced LVH is related to the impairment in MPR and left ventricular diastolic function.

OBJECTIVES: The goal of this study was to compare myocardial perfusion reserve (MPR) before and after long-term treatment with lisinopril and losartan in patients with hypertension and left ventricular hypertrophy (LVH). BACKGROUND: Studies have suggested that treatment with angiotensin-converting enzyme inhibitors (ACEIs) improves MPR in patients with hypertension by potentiating endogenous bradykinins. Because angiotensin receptor blockers (ARBs) lack a direct effect on bradykinins, we hypothesized that they may not improve MPR. METHODS: We measured pre- and post-treatment myocardial blood flow (MBF) by positron emission tomography in 17 patients (lisinopril: 9 patients, losartan: 8 patients) with hypertension and LVH at baseline and after coronary vasodilation with intravenous dipyridamole. In addition, we measured rest and hyperemic blood flow in eight normotensive controls. RESULTS: Post-treatment maximal coronary blood flow and MPR in the lisinopril group increased significantly compared with pretreatment values (3.5 +/- 1.2 vs. 2.6 +/- 1.1 ml/min/g, p = 0.02; 3.7 +/- 1.1 vs. 2.4 +/- 1 ml/min/g, respectively, p = 0.002, respectively). Post-treatment hyperemic flow in the patients treated with lisinopril was not significantly different from corresponding measurements in controls (3.5 +/- 1.2 vs. 3.9 +/- 1 ml/min/g, respectively, p = NS). In the patients treated with losartan, there was no difference between pre- and post-treatment MBF values and MPR. CONCLUSIONS: Myocardial perfusion reserve and maximal coronary flow improved in asymptomatic patients with hypertension-induced LVH after long-term treatment with lisinopril but not with losartan. Thus, ACEIs, but not ARBs, might be effective in repairing the coronary microangiopathy associated with hypertension-induced LVH.

BACKGROUND: Previous studies have shown that the risk of major cardiovascular events at 1 year is less than 1% in patients with normal myocardial stress perfusion study results. However, the racial distribution of patients enrolled in these studies is not known. Hence, the prognostic value of normal stress perfusion study results in black patients is not well established. Our objective was to determine the incidence of major cardiovascular events in black patients with normal stress perfusion study results over a 12-month period. METHODS AND RESULTS: We searched the nuclear cardiology database at our institution for all black patients who had normal stress perfusion study results between January 1990 and December 1996. We excluded patients with a history of coronary revascularization, valvular heart disease, cardiomyopathy, congenital heart disease, left bundle branch block, or pre-excitation syndrome. Patients were followed up for at least 12 months from the time of inclusion. A total of 592 patients were enrolled and were followed up for 18 +/- 6 months (mean +/- SD). Of these, 388 underwent treadmill exercise testing, 155 underwent dipyridamole stress testing, and the remainder underwent dobutamine stress testing. Perfusion studies were performed in all patients with thallium 201 single photon emission computed tomography imaging. During the follow-up period, 11 cardiac deaths and 7 myocardial infarctions (MIs) occurred. The incidence of cardiac deaths was 1.2% per year, and that of nonfatal MIs was 0.8% per year. The total incidence of major cardiovascular events was 2% per year. In patients who underwent treadmill exercise testing, the incidence of major cardiovascular events was 1% per year. Performance of a pharmacologic stress test and a prior MI were significantly associated with death or nonfatal MI (P <.05). CONCLUSIONS: The overall incidence of major cardiovascular events in black patients after normal exercise perfusion study results were obtained was low (1%). However, black patients who had normal perfusion study results but underwent pharmacologic stress testing or had a history of MI were at intermediate risk. These patients require close surveillance for major cardiovascular events.

OBJECTIVE: The study was done to determine whether coronary steal (defined as an absolute decrease in perfusion from resting blood flow) is induced by intravenous (IV) dipyridamole in patients with severe coronary artery disease (CAD). BACKGROUND: Myocardial ischemia during coronary vasodilation is usually attributed to coronary steal. However, there is limited data on the absolute magnitude of coronary steal in humans. METHODS: Eighteen patients with multivessel CAD underwent dynamic positron emission tomography (PET) imaging with 13NH3 at rest and after infusion of IV dipyridamole. Eight myocardial sectors were analyzed per short axis slice and myocardial blood flow calculated with a two-compartment model in absolute terms. RESULTS: Coronary steal occurred in 8 of the 18 patients. In the 8 patients with coronary steal, myocardial blood flow decreased from 90 +/- 18 ml/100 g/min at rest to 68 +/- 27 ml/100 g/min following dipyridamole in the segments with steal, and increased from 87 +/- 19 to 138 +/- 16 ml/100 g/min following dipyridamole in the segments without steal. Significant clinical correlates of coronary steal were either ST elevation or the combination of ST depression and angina. CONCLUSIONS: Coronary vasodilation with IV dipyridamole is associated with significant reductions in blood flow to collateral-dependent myocardium consistent with coronary steal in about 45% of patients with severe CAD.