Evaluation of restenosis and extent of coronary artery disease in patients with previous percutaneous coronary interventions by dobutamine stress real-time myocardial contrast perfusion imaging.

OBJECTIVES: To assess the accuracy of real-time myocardial contrast perfusion imaging (MCPI) for the diagnosis of restenosis and extent of coronary artery disease (CAD) in patients with previous percutaneous coronary intervention (PCI). METHODS: 56 patients were studied 1.9 (SD 1.4) years after PCI. They underwent MCPI with commercially available ultrasound contrast agents (Optison or Definity) at rest and at peak dobutamine-atropine stress. Coronary angiography was performed within one month. Significant CAD was defined as >or= 50% stenosis in >or= 1 major epicardial coronary artery. Significant restenosis was defined as >or= 50% stenosis in a coronary segment with previous intervention. RESULTS: Reversible perfusion abnormalities were detected in 40 of 43 patients with significant CAD and in 4 of 13 patients without (overall sensitivity 93%, 95% CI 85% to 99%; specificity 69%, 95% CI 44% to 94%; and accuracy 88%, 95% CI 79% to 96%). Significant restenosis in >or= 1 coronary artery with previous PCI was detected in 38 (68%) patients. Reversible perfusion abnormalities were present in 35 of them (sensitivity 92%, 95% CI 84% to 99%). Reversible perfusion abnormalities were detected in >or= 2 vascular distributions in 20 of 28 patients with multivessel CAD and in 3 of 28 patients without (sensitivity 71%, 95% CI 55% to 88%; specificity 89%, 95% CI 78% to 99%; and accuracy 80%, 95% CI 70% to 91%). Restenosis was detected in 41 coronary arteries. Sensitivity of MCPI for regional diagnosis of restenosis was 73% (95% CI 60% to 87%), specificity was 75% (95% CI 60% to 90%), and accuracy was 74% (95% CI 64% to 84%). CONCLUSION: Dobutamine stress MCPI is a useful technique for the evaluation of restenosis and extent of CAD after PCI.

Real-time assessment of myocardial perfusion and wall motion during bicycle and treadmill exercise echocardiography: comparison with single photon emission computed tomography.

OBJECTIVES: We sought to determine the feasibility and accuracy of real-time imaging of myocardial contrast echocardiography (MCE) in detecting myocardial perfusion defects during exercise echocardiography compared with radionuclide tomography. BACKGROUND: Ultrasound imaging at a low mechanical index and frame rate (10 to 20 Hz) after intravenous injections of perfluorocarbon containing microbubbles has the potential to evaluate myocardial perfusion and wall motion (WVM) simultaneously and in real time. METHODS: One hundred consecutive patients with intermediate-to-high probability of coronary artery disease underwent treadmill (n = 50) or supine bicycle (n = 50) exercise echocardiography. Segmental perfusion with MCE and WM w ere assessed in real time before and at peak exercise using low mechanical index (0.3) and frame rates of 10 to 20 Hz after 0.3 ml bolus injections of intravenous Optison (Mallinckrodt Inc., San Diego, California). All patients had a dual isotope (rest thallium-201, stress sestamibi) study performed during the same exercise session, and 44 patients had subsequent quantitative coronary angiography. RESULTS: In the 100 patients, agreement between MCE and single photon emission computed tomography (SPECT) was 76%, while it was 88% between MCE and WM assessment. Compared with quantitative angiography, sensitivity of MCE, SPECT and WM was comparable (75%), with a specificity ranging from 81% to 100%. The combination of MCE and WM had the best balance between sensitivity and specificity (86% and 88%,respectively) with the highest accuracy (86%). CONCLUSIONS: The real-time assessment of myocardial perfusion during exercise stress echocardiography can be achieved with imaging at low mechanical index and frame rates. The combination of WM and MCE correlates well with SPECT and is a promising important addition to conventional stress echocardiography.

Adenosine infusion during early reperfusion failed to limit myocardial infarct size in a collateral deficient species.

STUDY OBJECTIVE: Intracoronary or intravenous adenosine during reperfusion in combination with lignocaine may attenuate "reperfusion injury" and limit myocardial infarct size in the canine heart. The aim of this study was to test whether intravenous adenosine also protects myocardium in the rabbit heart, which lacks xanthine oxidase and significant coronary collaterals in contrast to the canine heart. DESIGN: Five groups of rabbits underwent a 30 min occlusion of the circumflex coronary artery, followed by reperfusion. In adenosine treated groups, either a high dose of adenosine (0.37 mg.kg-1.min-1) with lignocaine treatment (5 mg intravenously 1 min before coronary occlusion and before reperfusion) or a low dose (0.15 mg.kg-1.min-1) of adenosine with or without lignocaine was infused for 60 min starting 5 min before the onset of reperfusion. Group 1 was untreated, while group 2 received a high dose of adenosine with lignocaine. These groups were reperfused for 3 h. Group 3 was untreated, group 4 received a low dose of adenosine, and group 5 a low dose of adenosine and lignocaine. These groups were reperfused for 72 h. EXPERIMENTAL MATERIAL: 60 anaesthetised open chest rabbits were used. Groups 1 and 2 were killed after 3 h coronary reperfusion. Groups 3, 4, and 5 recovered from surgery for 72 h and were then killed for further study. MEASUREMENTS AND MAIN RESULTS: The high dose of adenosine reduced mean blood pressure to 44% of baseline value and diminished reactive hyperaemia in the area at risk by "coronary steal". The low dose of adenosine did not significantly alter systemic blood pressure or heart rate. Infarct size did not differ between groups 1 and 2, at 39.7(SD 20.1)% of area at risk v 33.2(15.9)% (by tetrazolium staining), nor between groups 3, 4, and 5: 50.3(12.6)% v 52.7(15.6)% v 47.8(9.3)% (by histology). CONCLUSION: Neither a high dose nor a low dose of adenosine limited myocardial infarct size in the rabbit heart even when adenosine was combined with lignocaine treatment.

Changes in ambient temperature alter the blood pressure response to endotoxin and the effectiveness of naloxone.

At room temperature, naloxone, a competitive opiate antagonist, ameliorates the hypotensive effect of endotoxin, suggesting that endotoxin increases the secretion of endogenous opioids that have a cardiodepressor action. It was previously observed in our laboratory that reducing the ambient temperature from 24 degrees C to 19 degrees C blocked this protective effect of naloxone in dogs. This suggested that activation of peripheral cold receptors might also increase endogenous opioid activity and together with the opioid activity induced by endotoxin might be sufficient to override the competitive blockage by naloxone. In support of this, it was found in the present study that an increased dose of naloxone was effective at 19 degrees C. Studies done at 30 degrees C revealed that the hypotensive effect of endotoxin is inversely related to the ambient temperature, and naloxone is effective in low doses at the higher temperature. Core temperature was not altered significantly by the ambient temperatures used by naloxone, by endotoxin, or by any combination thereof. These findings suggest that, at least within moderate ranges, acute changes in ambient temperature induce inversely related changes in endogenous opioid activity, representing a specific thermal rather than a generalized stress response.

The effect of angiotensin and vasopressin blockade separately and in combination with cerebellectomy on recovery from hemorrhagic hypotention.

We demonstrated previously that cerebellectomy or ablation of the fastigial nuclei (FN) in the dog impairs markedly the restoration of blood pressure and increases the death rate after severe hypotension. Angiotensin (AII) and vasopressin (AVP) participate in the pressor response to hypotension, and plasma levels of both are increased by electrical stimulation of the FN. The present studies examined the importance of the FN in mediating the secretion of AII and AVP after hemorrhage to 50 mm Hg. Cerebellectomy reduced significantly both the rate of recovery and level of maintenance of blood pressure after hemorrhage. Blockade of conversion of AI of AII with captopril produced a similar deficit, and combination of both treatments produced a greater impairment than either alone. Treatment with an AVP antagonist decreased the level of maintenance of blood pressure but not be initial rate of recovery. The AVP antagonist in combination with cerebellectomy did not produce a greater deficit than cerebellectomy alone. This would suggest that although the cerebellum mediates some activation of the renin-angiotensin system during severe hypotension, it may mediate most of the AVP secretion under these conditions.