An improved model for the measurement of myocardial perfusion in human beings using N-13 ammonia.

BACKGROUND: Oxygen 15 water and nitrogen 13 ammonia are widely used for the quantitative measurement of myocardial perfusion with positron emission tomography. However, blood flow obtained with N-13 ammonia by use of the conventional 2-compartment model frequently underestimates flow by 30% to 50% compared with O-15 water. We hypothesized that this discrepancy is a result of the model configuration of N-13 ammonia and investigated changes to the mathematical model to determine whether more accurate measurements of perfusion could be obtained. METHODS AND RESULTS: Twelve healthy volunteers were sequentially studied with O-15 water and N-13 ammonia at rest and during maximal coronary vasodilation with adenosine. Perfusion measurements obtained with the conventional and modified models were compared with values obtained with O-15 water. The conventional N-13 ammonia model underestimated flow by 37% +/- 16% at rest and by 20% +/- 24% with stress when compared with flows obtained with O-15 water. The modified model yielded flow values closer to the line of identity than the conventional model (y = 1.07x + 0.04 vs y = 0.69x + 0.08; respectively; P < .01). CONCLUSIONS: Model changes made N-13 ammonia myocardial blood flow estimates more comparable to those obtained with O-15 and may allow for better comparison of flows obtained with these two tracers in the future. Further efforts are warranted to evaluate the accuracy of flow models in human subjects.

Assessment of cardiac wall motion and ejection fraction with gated PET using N-13 ammonia.

BACKGROUND: Cardiac gating is not routinely used in cardiac positron emission tomography (PET). The aim of this study was to determine the feasibility of assessing regional wall motion, ejection fraction (EF), cardiac volumes, and mass with nitrogen-13 ammonia (N-13 ammonia) at the time of PET myocardial perfusion imaging. METHODS: We studied 12 healthy volunteers (mean age, 28 +/- 8 years) and 53 patients with documented coronary artery disease (CAD) (mean age, 59 +/- 11 years). All subjects received a single administration of approximately 600 MBq (16 mCi) of N-13 ammonia intravenously. A 6-minute dynamic scan was performed for quantitative assessment of myocardial perfusion at rest, followed by a separate, 13-minute static scan acquired in the gated mode (8 equal bins). Gated data was imported into the Emory Toolbox. Wall motion was evaluated by dividing the myocardium into 9 anatomic regions graded semiquantitatively. RESULTS: Healthy volunteers had a normal EF (61 +/- 6), end systolic volume (ESV) (37 +/- 15 mL), end diastolic volume (EDV) (89 +/- 25 mL), and cardiac mass (116 +/- 18 g). In contrast, patients with CAD showed reduced EF (32 +/- 13%) and increased ESV (129 +/- 56 mL), EDV (188 +/- 68 mL), and cardiac mass (173 +/- 45 g) (P < 0.001 for each). In patients with CAD, EF measured by gated PET correlated significantly to independent measurements of EF (P < 0.001). CONCLUSIONS: Gating of cardiac perfusion images obtained after administration of N-13 ammonia is feasible and appears to be an accurate means of evaluating regional and global cardiac function. Gating can provide important additional diagnostic and prognostic information.

Myocardial blood flow and efficiency in concentric and eccentric left ventricular hypertrophy.

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.

Correlates of myocardial oxygen demand measured by positron emission tomography in the hypertrophied left ventricle.

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.

Positron emission tomography, echo-doppler, and exercise studies of functional capacity in hypertensive heart disease.

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.

Augmentation of myocardial blood flow in hypertensive heart disease by angiotensin antagonists: a comparison of lisinopril and losartan.

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.