Sympathetic nerve alterations assessed with 123I-MIBG in the failing human heart.
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Norepinephrine (NE) reuptake function is impaired in heart failure and this may participate in myocyte hyperstimulation by the neurotransmitter. This alteration can be assessed by 123I-metaiodobenzylguanidine (MIBG) scintigraphy. METHODS: To determine whether the impairment of neuronal NE reuptake was reversible after metoprolol therapy, we studied 18 patients (43+/-7 y) with idiopathic dilated cardiomyopathy who were stabilized at least for 3 mo with captopril and diuretics. Patients underwent, before and after 6 mo of therapy with metoprolol, measurements of radionuclide left ventricular ejection fraction (LVEF), maximal oxygen consumption and plasma NE concentration. The cardiac adrenergic innervation function was scintigraphically assessed with MIBG uptake and release measurements on the planar images obtained 20 min and 4 h after tracer injection. To evaluate whether metoprolol had a direct interaction with cardiac MIBG uptake and release, six normal subjects were studied before and after a 1-mo metoprolol intake. RESULTS: In controls, neither cardiac MIBG uptake and release nor circulating NE concentration changed after the 1-mo metoprolol intake. Conversely, after a 6-mo therapy with metoprolol, patients showed increased cardiac MIBG uptake (129%+/-10% versus 138%+/-17%; P = 0.009), unchanged cardiac MIBG release and decreased plasma NE concentration (0.930+/-412 versus 0.721+/-0.370 ng/mL; P = 0.02). In parallel, patients showed improved New York Heart Association class (2.44+/-0.51 versus 2.05+/-0.23; P = 0.004) and increased LVEF (20%+/-8% versus 27%+/-8%; P = 0.0005), whereas maximal oxygen uptake remained unchanged. CONCLUSION: Thus, a parallel improvement of myocardial NE reuptake and of hemodynamics was observed after a 6-mo metoprolol therapy, suggesting that such agents may be beneficial in heart failure by directly protecting the myocardium against excessive NE stimulation. (+info)
Using vascular structure for CT-SPECT registration in the pelvis.
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The authors outline a method for three-dimensional registration of pelvic CT and 111In-labeled monoclonal antibody capromab pendetide (111In MoAb 7E11.C5) images using 99mTc-labeled red blood cell SPECT data. METHODS: This method of CT-SPECT registration relies on the identification of major blood vessels in the CT and 99mTc SPECT images. The vessels are segmented from the image datasets by outlining them on transverse planar slices using a mouse-based drawing tool. Stacking the transverse outlines provides a three-dimensional representation of the vascular structures. Registration is performed by matching the surfaces of the segmented volumes. Dual isotope acquisition of 111In and 99mTc activities provides precise SPECT-SPECT registration so that registration in three dimensions of the 111In MoAb and CT images is achieved by applying the same transformation obtained from the 99mTc SPECT-CT registration. RESULTS: This method provided accurate registration of pelvic structures and significantly improved interpretation of 111In MoAb 7E11.C5 exams. Furthermore, sites of involvement by prostate cancer suggested by the 111In MoAb examination could be interpreted with the bony and soft tissue (nodal) anatomy seen on CT. CONCLUSION: This method is a general clinical tool for the registration of pelvic CT and SPECT imaging data. There are immediate applications in conformal radiation therapy treatment planning for certain prostate cancer patients. (+info)
Thallium-gated SPECT in patients with major myocardial infarction: effect of filtering and zooming in comparison with equilibrium radionuclide imaging and left ventriculography.
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The effect of filtering and zooming on 201TI-gated SPECT was evaluated in patients with major myocardial infarction. METHODS: Rest thallium (TI)-gated SPECT was performed with a 90 degrees dual-head camera, 4 h after injection of 185 MBq 201TI in 32 patients (mean age 61 +/- 11 y) with large myocardial infarction (33% +/- 17% defect on bull's eye). End diastolic volume (EDV), end systolic volume (ESV) and left ventricular ejection fraction (LVEF) were calculated using a commercially available semiautomatic validated software. First, images were reconstructed using a 2.5 zoom, a Butterworth filter (order = 5) and six Nyquist cutoff frequencies: 0.13 (B5.13), 0.15 (B5.15), 0.20 (B5.20), 0.25 (B5.25), 0.30 (B5.30) and 0.35 (B5.35). Second, images were reconstructed using a zoom of 1 and a Butterworth filter (order = 5) (cutoff frequency 0.20 [B5.20Z1]) (total = 32 x 7 = 224 reconstructions). LVEF was calculated in all patients using equilibrium radionuclide angiocardiography (ERNA). EDV, ESV and LVEF were measured with contrast left ventriculography (LVG). RESULTS: LVEF was 39% +/- 2% (mean +/- SEM) for ERNA and 40% +/- 13% for LVG (P = 0.51). Gated SPECT with B5.20Z2.5 simultaneously offered a mean LVEF value (39% +/- 2%) similar to ERNA (39% +/- 2%) and LVG (40% +/- 3%), optimal correlations with both ERNA (r = 0.83) and LVG (r = 0.70) and minimal differences with both ERNA (-0.9% +/- 7.5% [mean +/- SD]) and LVG (1.1% +/- 10.5%). As a function of filter and zoom choice, correlation coefficients between ERNA or LVG LVEF, and gated SPECT ranged from 0.26 to 0.88; and correlation coefficients between LVG and gated SPECT volumes ranged from 0.87 to 0.94. There was a significant effect of filtering and zooming on EDV, ESV and LVEF (P < 0.0001). Low cutoff frequency (B5.13) overestimated LVEF (P < 0.0001 versus ERNA and LVG). Gated SPECT with 2.5 zoom and high cutoff frequencies (B5.15, B5.20, B5.25, B5.30 and B5.35) overestimated EDV and ESV (P < 0.04) compared with LVG. This volume overestimation with TI-gated SPECT in patients with large myocardial infarction was correlated to the infarct size. A zoom of 1 underestimated EDV, ESV and LVEF compared with a 2.5 zoom (P < 0.02). CONCLUSION: Accurate LVEF measurement is possible with TI-gated SPECT in patients with major myocardial infarction. However, filtering and zooming greatly influence EDV, ESV and LVEF measurements, and TI-gated SPECT overestimates left ventricular volumes, particularly when the infarct size increases. (+info)
Echocardiographic assessment of ejection fraction in left ventricular hypertrophy.
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OBJECTIVE: To investigate the value of Simpson's rule, Teichholz's formula, and recording of mitral ring motion in assessing left ventricular ejection fraction (EF) in patients with left ventricular hypertrophy. DESIGN: Left ventricular ejection fraction calculated by Simpson's rule and by Techholz's formula and estimated by mitral ring motion was compared with values obtained by radionuclide angiography. SETTING: Secondary referral centre. PATIENTS: 16 patients with left ventricular hypertrophy and a clinical diagnosis of hypertrophic cardiomyopathy or hypertension. RESULTS: Calculation by Teichholz's formula overestimated left ventricular ejection fraction by 10% (p = 0.002) and estimation based on mitral ring motion-that is, long axis measurements-underestimated ejection fraction by 19% (p = 0.002), without significant correlation between ring motion and ejection fraction. There was no significant difference between mean values of ejection fraction calculated by Simpson's rule and measured by the reference method, but a considerable scatter about the regression line with a standard error of the estimate of 9.3 EF%. CONCLUSIONS: In patients with left ventricular hypertrophy the ejection fraction, calculated by Teichholz's formula or Simpson's rule, is a poor measure of left ventricular function. When mitral ring motion is used for the assessment in these patients the function should be expressed in ways other than by the ejection fraction. (+info)
Influence of arrhythmias on gated SPECT myocardial perfusion and function quantification.
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Despite the importance of R-wave gating myocardial perfusion tomography for ventricular function assessment, neither prevalence of gating errors nor their influence on quantified cardiac parameters has been studied. METHODS: Arrhythmia-induced anomalies in curves of counts versus projection angle for each R-wave segment were detected visually and algorithmically. Arrhythmia prevalence was tabulated for 379 patients (group 1) with prospective coronary artery disease (mean age 63+/-13 y, 47% male). Myocardial counts were analyzed from all reconstructed cinematic midventricular slices to assess arrhythmia effects on percentage of systolic count increase, generally assumed to equal percentage of wall thickening. In a separate retrospective analysis of 41 patients (group 2), with coronary artery disease (mean age 64+/-12 y, 68% male) having no significant arrhythmias, 36 of whom also underwent equilibrium radionuclide angiography, original projection data were altered to simulate arrhythmia-induced aberrant count patterns to evaluate effects on ventricular function and perfusion measurements. RESULTS: Group 1 patients consisted of 26% without gating errors, 32% with count losses only in the last R-wave interval due to inconsistent transient increase of heart rate, 24% with count decreases in several late intervals due to consistently variable rates, 8% with early interval count increases paired with late interval count decreases due to ectopic beats and 9% with erratic count changes due to atrial fibrillation. Observed count patterns were strongly associated (P < 10(-3)) with arrhythmias detected by electrocardiogram monitoring. In group 2 simulations, ventricular volumes changed by only 2%+/-9% and ejection fraction (EF) by only 1%+/-4% from control values and correlated linearly (r> or = 0.96) with control values for all simulated arrhythmias. SPECT and equilibrium radionuclide angiography EFs correlated similarly (r = 0.85-0.89) for control and all simulations. Percentage changes from control in perfusion defect extent and severity were larger than processing reproducibility limits, the largest change being for atrial fibrillation. Control wall thickening was 38%+/-17%, significantly lower (P < 10(-6)) than for simulated arrhythmias, reflecting similar observations for group 1 patients. CONCLUSION: Even though ventricular volumes and EFs were affected minimally by arrhythmias, both perfusion analysis and wall thickening were compromised. Consequently, quality assurance of gating may be critically important for obtaining accurate quantified parameters. (+info)
BMIPP imaging to improve the value of sestamibi scintigraphy for predicting functional outcome in severe chronic ischemic left ventricular dysfunction.
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Mismatching between beta-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) and perfusion accurately predicts functional outcome after acute myocardial infarction. The current investigation was aimed at evaluating the value of this method to predict the evolution of global function according to the applied treatment in patients with chronic ischemic heart disease. METHODS: Twenty patients with infarction and chronic left ventricular dysfunction were studied (median infarction age 12 wk, range 2 wk-15 y). Radionuclide angiography, two-dimensional echocardiography and BMIPP and gated sestamibi scintigraphy were performed with the patient at rest before and >6 mo after treatment (revascularization in 13 patients and conservative therapy in 7 patients). In 7 patients, radionuclide angiography was repeated after 1 y. RESULTS: On a patient basis, mismatching with BMIPP less than sestamibi was noted in 15 patients at baseline. Of these 15 patients, 11 had significant functional improvement at follow-up versus only 1 of the 5 patients with a matched decreased uptake. Hence, the combined sestamibi/BMIPP was 73% positive and 80% negative in predicting functional outcome, with a global accuracy of 75%. On a segmental basis, using an optimal threshold of uptake defined by receiver operating characteristic curve analysis, sestamibi was only 63% accurate in predicting regional outcome. Adding BMIPP improved the accuracy to 80% (P = 0.001). At follow-up, significant mismatching was still noted in 7 patients in the revascularized group and 1 in the medically treated group. The mismatch was associated with a further increase in ejection fraction at 1-y follow-up in only the revascularized group. CONCLUSION: In patients with chronic left ventricular dysfunction after infarction, a mismatching with BMIPP less than sestamibi reliably identifies jeopardized but viable myocardium and predicts functional recovery with an accuracy similar to that reported in the acute and subacute phases of the infarction. (+info)
Decreased no-reflow in patients with anterior myocardial infarction and pre-infarction angina.
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AIMS: Pre-infarction angina is associated with better outcome after myocardial infarction. The aim of this study was to assess whether pre-infarction angina is associated with decreased no-reflow after coronary recanalization. METHODS AND RESULTS: Twenty-three patients underwent intracoronary myocardial contrast echocardiography during the acute phase of anterior myocardial infarction after successful recanalization, and before hospital discharge. Myocardial perfusion was graded semi-quantitatively in the area at risk (dyssynergic segments). Global left ventricular function was assessed by radionuclide angiography on days 8 and 42 and regional wall motion was assessed by 2D echocardiography on days 0 and 42. Fourteen patients had pre-infarction angina (angina less than 7 days before myocardial infarction) and nine did not. Baseline characteristics were similar in the two groups. The myocardial contrast echocardiography perfusion score in the area at risk after recanalization was higher in the patients with pre-infarction angina than in those without (0.72 +/- 0.19 vs 0.53 +/- 0.22, P=0.04), and the incidence of no-reflow (myocardial contrast echocardiography perfusion score < or =0.5) was lower (14% vs 56%, P=0.04). This difference persisted 8 +/- 2 days after myocardial infarction (0. 87 +/- 0.11 vs 0.69 +/- 0.26, P=0.04), and was associated with greater mid-term (day 42) improvement in left ventricular function in patients with pre-infarction angina than in those without, as assessed by changes in radionuclide left ventricular ejection fraction (+5.8 +/- 8.1% vs -3.3 +/- 4.6%, respectively;P=0.01) and by changes in regional wall motion score on 2D echocardiography (-0. 61 +/- 0.39 vs -0.24 +/- 0.17, respectively;P=0.04). CONCLUSION: Pre-infarction angina is associated with preservation of the microvasculature, reflected by reduced no-reflow. This may be a mechanism underlying greater recovery of left ventricular function in patients with pre-infarction angina. (+info)
Diastolic heart failure.
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Primary diastolic failure is typically seen in patients with hypertensive or valvular heart disease as well as in hypertrophic or restrictive cardiomyopathy but can also occur in a variety of clinical disorders, especially tachycardia and ischemia. Diastolic dysfunction has a particularly high prevalence in elderly patients and is generally associated, with low mortality but high morbidity. The pathophysiology of diastolic dysfunction includes delayed relaxation, impaired LV filling and/or increased stiffness. These conditions result typically in an upward displacement of the diastolic pressure-volume relationship with increased end-diastolic, left atrial and pulmo-capillary wedge pressure leading to symptoms of pulmonary congestion. Diagnosis of diastolic heart failure requires three conditions: (1) presence of signs or symptoms of heart failure; (2) presence of normal or slightly reduced LV ejection fraction (EF > 50%) and (3) presence of increased diastolic filling pressure. Assessment of diastolic function can be performed with several non-invasive (2D- and Doppler-echocardiography, color Doppler M-mode, Doppler tissue imaging, MR-myocardial tagging, radionuclide ventriculography) and invasive techniques (micromanometry, angiography, conductance method). Doppler-echocardiography is the most useful tool to routinely measure diastolic function. Different techniques can be used alone or in combination to assess LV diastolic function, but most of them are dependent on heart rate, pre- and afterload. The transmitral flow pattern remains the starting point, since it is easy to acquire and rapidly categorizes patients into normal (E > A), delayed relaxation (E < A), and restrictive (E >> A) filling patterns. Invasive assessment of diastolic function allows determination of the time constant of relaxation from the exponential pressure decay during isovolumic relaxation, and the evaluation of the passive elastic properties from the slope of the diastolic pressure-volume (= constant of chamber stiffness) and stress-strain relationship (= constant of myocardial stiffness). The prognosis of diastolic heart failure is usually better than for systolic dysfunction. Diastolic heart failure is associated with a lower annual mortality rate of approximately 8% as compared to annual mortality of 19% in heart failure with systolic dysfunction, however, morbidity rate can be substantial. Thus, diastolic heart failure is an important clinical disorder mainly seen in the elderly patients with hypertensive heart disease. Early recognition and appropriate therapy of diastolic dysfunction is advisable to prevent further progression to diastolic heart failure and death. There is no specific therapy to improve LV diastolic function directly. Medical therapy of diastolic dysfunction is often empirical and lacks clear-cut pathophysiologic concepts. Nevertheless, there is growing evidence that calcium channel blockers, beta-blockers, ACE-inhibitors and AT2-blockers as well as nitric oxide donors can be beneficial. Treatment of the underlying disease is currently the most important therapeutic approach. (+info)