First-pass evaluation of myocardial output during dipyridamole stress using turbo-FLASH magnetic resonance imaging.

RATIONALE AND OBJECTIVES: This study evaluated the value of dynamically enhanced fast low-angle shot (FLASH) magnetic resonance (MR) imaging in measuring cardiac output with and without dipyridamole pharmacological stress. METHODS: Ten subjects underwent rest and stress MR imaging. Rest images were acquired using electrocardiogram gated MR (turbo-FLASH: repetition time = 6 mseconds; echo time = 12 mseconds; flip angle = 12 degrees, inversion time = 100) 10 to 45 seconds after intravenous bolus of 0.04 mmol/kg gadolinium (Gd)-DTPA using a Siemens 1.0-tesla Magnetom SP. Stress was induced within the MR imaging scanner with 0.56 mg/kg dipyridamole over 4 minutes with stress MR images obtained after a second bolus of Gd-DTPA in exactly the same position and time intervals. Cardiac output was calculated with a least squares error analysis before and after dipyridamole stress for the left and right ventricles in all 10 patients, and comparison was made with cardiac output by Fick dilution technique during cardiac catheterization in seven patients. RESULTS: This MR analysis methodology shows reasonable correlation (r = 0.953) between left ventricular and right ventricular cardiac output with no effect on cardiac output during immediate dipyridamole stress. Fick dilution studies demonstrated a correlation of 0.96. CONCLUSIONS: Turbo-FLASH MR can demonstrate time-activity curves and cardiac output calculations consistent with theoretical predictions.

Detection of myocardial ischemia: value of combined myocardial perfusion and cineangiographic MR imaging.

OBJECTIVE: Established noninvasive methods for assessing myocardial ischemia have limitations that might be overcome by MR imaging. We investigated MR myocardial perfusion imaging and MR ventriculography, before and after dipyridamole-induced stress, to determine whether the superior spatial and temporal resolution of MR imaging has advantages for the evaluation of myocardial ischemia. SUBJECTS AND METHODS: Eighteen patients with symptoms suggestive of myocardial ischemia were examined by use of MR perfusion imaging and MR cineangiography before and during dipyridamole-induced stress. Multiplanar gradient-echo MR cineangiography and cardiac gated fast low-angle shot (turbo-FLASH) MR imaging during injection of gadopentetate dimeglumine were used. Results were compared with findings from perfusion scintigraphy and coronary arteriography. RESULTS: The accuracy of the combination MR technique for detecting myocardial ischemia was similar to that of scintigraphy. No significant difference was found between the MR technique and scintigraphy for detecting segments of myocardium supplied by stenosed coronary arteries (> 70% reduction in diameter, as determined by coronary arteriography). The sensitivity of the combination MR technique for angiographically detecting significant coronary artery narrowing was 92%, and the specificity was 100%. For scintigraphy, the sensitivity was also 92% and the specificity was 100%. CONCLUSION: Initial results indicate that a combination of stress MR myocardial perfusion imaging and MR ventriculography is feasible and that this technique can detect myocardial ischemia with an accuracy similar to that of scintigraphy. This technique may make more complete noninvasive assessment of myocardial ischemia possible.

The diagnosis of a pulmonary artery thrombus by transesophageal echocardiography.

We describe a patient with an acute inferior wall myocardial infarction who underwent percutaneous coronary angioplasty. He subsequently had a cardiac arrest and developed progressive severe hypoxia. Although findings from pulmonary angiography were nondiagnostic, transesophageal echocardiography demonstrated a nonocclusive, right pulmonary artery thrombus. Therapy was changed, and the patient recovered. Transesophageal echocardiography was also used to monitor anticoagulation therapy.

Post-ischemic cardiac chamber stiffness and coronary vasomotion: the role of edema and effects of dextran.

Contributions of edema to left ventricular (LV) chamber stiffness and coronary resistance after ischemia were studied in isolated buffer-perfused rabbit hearts, with constant LV chamber volume, subjected to 30 min global ischemia and 60 min reperfusion. During reperfusion hearts were perfused with standard buffer or with 3% dextran to increase oncotic pressure and decrease water content. LV chamber volume was adjusted to an initial diastolic pressure (LVEDP) of 10 mmHg. In nonischemic hearts (n = 6) LVEDP was 11 +/- 0.3 mmHg and water content was 5.0 +/- 0.1 ml/g dry weight after 90 min of perfusion. In untreated ischemic hearts (n = 8) LVEDP was 51 +/- 4 mmHg and water content was 6.0 +/- 0.1 ml/g dry weight after 60 min reperfusion (P less than 0.001 v. nonischemic). In dextran-treated ischemic hearts (n = 8) LVEDP was 38 +/- 3 mmHg (P less than 0.05 v. untreated ischemic) and water content was 5.2 +/- 0.1 ml/g dry weight (P less than 0.001 v. untreated ischemic). Coronary resistance in untreated ischemic hearts increased by 26% from 2.0 +/- 0.06 to 2.6 +/- 0.06 mmHg/ml/min after 60 min reperfusion. In treated hearts coronary resistance increased by 16% from 1.9 +/- 0.09 to 2.2 +/- 0.09 mm/Hg/ml/min (P less than 0.01 v. untreated ischemic). To determine whether the decrease in coronary resistance with dextran could be ascribed to active vasodilation, dilator responses to 2 min hypoxia or 10(-4)M adenosine were tested in nonischemic and reperfused ischemic hearts. Dilator responses were stable in nonischemic hearts or hearts reperfused after 15 min ischemia but after 30 min ischemia the dilator response to hypoxia was reduced by 72% (P less than 0.025) and the dilator response to adenosine was eliminated (P less than 0.02). Thus the response to dextran was unlike that of a direct vasodilator. These data suggest that myocardial edema plays a significant role in maintaining increased ventricular chamber stiffness and coronary resistance during reperfusion after ischemia.

Acid and isoproterenol cause serotonin release by acting on opposite surfaces of duodenal mucosa.

Although most bodily serotonin (5-HT) is stored in intestinal enterochromaffin (EC) cells, the mechanism of its release is only now being elucidated. It has previously been reported that such stimuli as luminal acidification or exposure of both sides of a rabbit duodenal mucosal sheet to certain autonomic agonists stimulate release from the mucosal surface in the Ussing chamber model. The hypothesis in the present study is that acid acts only on the mucosal surface, whereas neural receptor agonists and antagonists act specifically on the serosal surface, as would be predicted by the location of acid in the gut lumen and nerve terminals at the bases of the EC cells. 5-HT release was measured by radioimmunoassay from the mucosal surface bathing solution. Duodenal mucosal sheets were exposed separately on the mucosal or serosal surfaces to acid (citric phosphate buffer, pH 5) or to isoproterenol (10(-5) M). The effect of atropine (10(-6) M) and propranolol (10(-6) M) on acid-stimulated mucosal release was studied by combining luminal acid stimulation with one of these antagonists, on either the mucosal or serosal surface. The results demonstrate significant (P less than 0.01) mucosal serotonin release (56 +/- 9 ng cm-2 hr-1) only with mucosal acidification. On the other hand, isoproterenol causes significant (P less than 0.05) serotonin release (12.4 +/- 3 ng cm-2 hr-1) only when introduced onto the serosal surface. Finally, the antagonists, atropine and propranolol, blocked acid-stimulated serotonin release only when added to the serosal surface. Since acid-induced serotonin release has been shown to be partially mediated by cholinergic and beta-adrenergic mechanisms, these findings suggest interconnection of mucosal acid receptors with submucosal neurons which mediate serotonin release by acting on the basal surface of the enterochromaffin cell.