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Background: The accuracy of quantitative gated single photon emission computed tomography (SPECT) (QGS) and the potential limitations for estimation of left ventricular ejection fraction (LVEF) have been extensively evaluated. However, few studies have focused on the serial variability of QGS. This study was conducted to assess the serial variability of QGS for determination of LVEF between 2 sequential technetium 99m sestamibi- gated SPECT acquisitions at rest in both healthy and unhealthy subjects. Methods and Results: The study population consisted of 2 groups: group I included 21 volunteers with a low likelihood of CAD, and group II included 22 consecutive patients with documented CAD. Both groups underwent serial SPECT imaging. The overall correlation between sequential images was high (r = 0.94, SEE = 5.3%), and the mean serial variability of LVEF was 5.15% ± 3.51%. Serial variability was lower for images with high counts (3.45% ± 3.23%) than for images with low counts (6.85% ± 3.77%). The mean serial variability was not different between normal and abnormal high- dose images (3.0% ± 1.56% vs 3.9% ± 2.77%). However, mean serial variability for images derived from abnormal low- dose images was significantly greater than that derived from normal low- dose images (9.6% ± 2.22% vs 3.1% ± 2.12%, P < .05). Conclusions: Although QGS is an efficacious method to approximate LVEF values and is extremely valuable for incremental risk stratification of patients with coronary artery disease, it has significant variability in the estimation of LVEF on serial images. This should be taken into account when used for serial evaluation of LVEF.

OBJECTIVES

The purpose of this study was to evaluate the alterations of ventricular wall movement in patients with acute posteroinferior myocardial infarction with extension to right cavities with multiplane transesophageal echocardiography (TEE), as well as the utility of dobutamine with this technique to analyze myocardial viability. Nine men with a mean age of 51 years fulfilled the inclusion criteria. Myocardial TEE was performed in all the men 72 hours after the acute event with long‐ and short‐axis transgastric images of both ventricles under basal conditions and with dobutamine infusions of 5 and 10 μg/kg per minute. Results were compared with myocardial perfusion findings obtained with Tc‐99m Sestamibi SPECT. Left ventricular myocardial viability was demonstrated in 28 of 45 altered segments with dobutamine stress myocardial TEE and Tc‐99m Sestamibi SPECT. Right ventricular myocardial viability was identified in 27 of 30 altered segments with dobutamine stress myocardial TEE in transgastric short and long axes, and with Tc‐99m Sestamibi SPECT in 23 of 25 segments only in short‐axis images. Multiplane TEE provided excellent image resolution and better definition of endocardial and epicardial borders, which facilitated detailed evaluation of ventricular segmental wall movement. Infusion of low doses of dobutamine made it possible to identify viable tissue in both ventricles, and results were comparable to those of nuclear medicine.

Twenty persons living at an altitude of 2,240 meters were studied in order to examine the relative roles of passive and active factors in the genesis of pulmonary arterial hypertension in obesity (overweight, 75 ± 39 percent). Pulmonary arterial hypertension was present in 80 percent (16) of the patients (mean pulmonary arterial systolic pressure, 45 ± 17 mm Hg). In 95 percent (19) of the 20 patients, resistance to pulmonary flow at the end of diastole was increased (estimated mean pulmonary arteriolar resistance, 210 ± 144 dynes•sec•cm−5; mean pulmonary arterial diastolic-pulmonary wedge pressure gradient 7.86 ± 1.40 mm Hg). The mean arterial oxygen pressure was 50 ± 9 mm Hg, the arterial carbon dioxide tension was 37 ± 6 mm Hg and the arterial pH was 7.42 ± 0.08. Since the pulmonary arterial systolic pressure has been reasonably predicted (r = 0.91; P < 0.001), it would appear that the compliance of the elastic pulmonary arteries in obese patients follows a normal pattern. The behavior of the right ventricular end-diastolic pressure at rest (mean change, 4.6 nun Hg; P < 0.001) and of the pulmonary wedge pressure (mean change, 4.7 mm Hg; P < 0.001) during passive lifting of the legs was indirect evidence of the increase in pulmonary blood volume. The presence of an abnormal resistance to pulmonary blood flow at the end of diastole is suggestive of a decrease in the distention of the pulmonary microcirculation. The pulmonary arterial diastolic-pulmonary wedge pressure gradient and the pulmonary arterial diastolic pressure were related to arterial oxygen unsaturation (r = 0.70; P < 0.05) but not to the concentration of hydrogen ions; thus hypercapnic acidemia appears as a secondary factor in the genesis of pulmonary arterial hypertension at high altitudes. The explanation could be the relative hyperventilation of high altitudes, with a compensatory metabolic alkalosis. The increased pulmonary blood volume and the alveolar hypoxia are the main causes in the pathogenesis of pulmonary arterial hypertension in the grossly obese patient at this altitude.

The experience derived from the administration of isoproterenol in six patients with pulmonary hypertension of unknown etiology (PAH-UE) is presented. The diagnosis was made after exclusion of other known diseases capable of producing hypertension in the pulmonary circuit. Catheterization was performed, and basal cardiopulmonary parameters, mean pulmonary artery pressure (PAP), pulmonary arteriolar resistance (PAR), cardiac index (CI), alveolar-arterial oxygen tension difference P(A-a)O2, and PaO2were investigated. The effect of infusing 3 µg/min of isoproterenol into the pulmonary artery was studied in five cases. Isoproterenol was given sublingually to one patient who had previously received it intravenously; in another case it was given only sublingually. Significant P values (P < .05) as a group were obtained, in relation to heart rate, CI, PAR, and mean PAP after isoproterenol. A favorable effect on the heart and lungs was seen in two cases, maintained for three years with sublingual isoproterenol with a favorable cardiorespiratory effect. Use of isoproterenol in PAH-UE is justified at present in those cases with a favorable cardiopulmonary response while no specific therapy is available.

The experience we describe derives from the short-term administration of isoproterenol in 15 patients with ventricular septal defect (VSD) and severe pulmonary artery hypertension (PAH). For the whole study group, mean pulmonary artery pressure (PAP) was 68.5 ± 2.6 mm Hg, pulmonary vascular resistance (Rp) was 11.6 ± 0.9 U/m2, pulmonary vascular resistance/systemic vascular resistance ratio (Rp/Rs) was 0.9 ± 0.03, and the pulmonary vascular gradient (PAd-PWP) was 45 ± 3.5 mm Hg. Infusions of isoproterenol decreased PAP, Rp, Rp/Rs ratio, and PAd-PWP an average of 10.2 mm Hg, 2.88 U/m2, 0.13, and 6.6 mm Hg, respectively, for the whole group (P < 0.001). On the basis of isoproterenol response, the patients could be divided into two groups: A (n=4) and B (n=11). In group A, the PAP decreased from 61.7 ± 1 to 45 ±4 mm Hg, the Rp from 8.9 ± 0.3 to 4.62 ± 0.5 U/m2, the Rp/Rs from 0.84 ±0.02 to 0.55 ±.05, and the PAd-PWP from 34.5 ± 0.9 to 24 ± 2 mm Hg (mean ± 1 SE). In group B a less significant change in these measurements was observed. Group A patients underwent VSD repair, and the mean average postoperative decrease in PAP was 31 mm Hg (P < 0.001). Our findings suggest that in patients with VSD and severe PAH, in whom surgical treatment is controversial, a trial with isoproterenol should be routinely attempted. If the preceding hemodynamic parameters improve significantly, the VSD repair should be performed.

A case of a 57‐year‐old patient with regional pulmonary edema secondary to obstruction of the right lower pulmonary vein by a left atrial myxoma is described. Diagnosis was established by transesophageal echocardiography.