Clinical significance of terminal QRS abnormalities in the setting of inferior myocardial infarction.

To ascertain the clinical relevance of terminal electrocardiographic (ECG) QRS prolongation in the setting of inferior myocardial infarction, 32 patients were studied by radionuclide ventriculography to evaluate regional left ventricular contractility. Of the 32 patients, 16 had evidence of terminal QRS prolongation and notching associated with inferior myocardial infarction, and 16 had isolated ECG evidence of inferior myocardial infarction without terminal QRS prolongation. The regional ejection fraction in the posterolateral and inferoapical regions of patients with terminal conduction delay was lower than those without this conduction delay. This group also demonstrated a lower global ejection fraction than those patients with ECG evidence of inferior myocardial infarction without terminal QRS changes. Terminal QRS abnormalities are important qualitative predictors of left ventricular dysfunction in the setting of inferior myocardial infarction.

Intracoronary adenosine administration during reperfusion following 3 hours of ischemia: effects on infarct size, ventricular function, and regional myocardial blood flow.

Previous studies have demonstrated that adenosine significantly enhances myocardial salvage after 90 minutes of regional ischemia. To determine its effect after prolonged ischemia, closed-chest dogs underwent 3 hours of left anterior descending artery occlusion followed by 72 hours of reperfusion. Intracoronary adenosine (3.75 mg/min; at 1.5 ml/min:total volume = 90 ml; n = 10) or an equivalent volume of saline (1.5 ml/min: total volume = 90 ml; n = 9) was infused into the left main coronary artery during the first 60 minutes of reperfusion. Regional myocardial blood flow was assessed serially with microspheres and regional ventricular function was assessed by contrast ventriculography. Infarct size was determined histologically. Light and electron microscopy were utilized to assess neutrophil infiltration and microvascular injury. Adenosine failed to reduce infarct size expressed as a percentage of the area at risk (38.0 +/- 4.9% versus 34.8 +/- 4.6%; p = NS) or to improve regional ventricular function as measured by the radial shortening method (3.2 +/- 1.8% versus 2.2 +/- 3.1%; p = NS) at 72 hours after reperfusion. Vasodilatory effects were not observed in the endo- and midmyocardial regions of the ischemic zone during adenosine administration. This was associated with a similar extent of capillary endothelial changes and neutrophil infiltration in both adenosine-treated and saline control groups. These results suggest that severe functional abnormalities are present in the vasculature after 3 hours of ischemia and that adenosine therapy is ineffective in enhancing myocardial salvage.

Prevention of neutrophil-mediated injury to endothelial cells by perfluorochemical.

Myocardial salvage after reperfusion may be limited by neutrophil-mediated microvascular damage. The effect of the perfluorochemical, Fluosol-DA, and its various components on neutrophil adherence, cytotoxicity, and proteolytic enzyme release was examined on sheep large and small vessel endothelial cells in vitro. Cells were studied under normoxic (N) and anoxic conditions (A). Various concentrations of Fluosol (10%, 25%, and 50%) significantly reduced neutrophil adherence under both experimental conditions [mean 22 +/- 3.25% versus 7 +/- 0.8% (N) and 20 +/- 3.2% versus 7.5 +/- 0.9% (A); P less than 0.01]. The perfluorocarbons, perfluorodecalin (PFD), and perfluoro-tripropylamine (PFTP) in a 50 volume/percent concentration exhibited profound effects on adherence, particularly on cells subjected to anoxia (51% and 69% reduction in adherence, respectively; P less than 0.01). No effect on adherence was observed with other components, including the detergent, pluronic F68. A 25% reduction (P less than 0.02) in endothelial cytotoxicity was noted when neutrophils were preincubated with Fluosol. However, pretreatment of endothelial cells with Fluosol did not inhibit neutrophil adherence. Neutrophils stimulated with cytochalasin B and FMLP showed a significant reduction in lysozyme release after incubation with Fluosol (28 +/- 5% versus 17 +/- 4%; P less than 0.01). This study demonstrates that Fluosol significantly attenuates neutrophil adherence, cytotoxicity, and enzyme release in an in vitro model of microvascular injury. It also suggests that prevention of neutrophil-mediated microvascular damage may be an important mechanism whereby Fluosol enhances myocardial salvage after ischemia and reperfusion.

Intracoronary adenosine administered after reperfusion limits vascular injury after prolonged ischemia in the canine model.

Myocardial salvage after reperfusion may be limited by deleterious vascular changes in the previously ischemic microcirculatory bed. This could result in a progressive decrease in blood flow in the capillary bed to potentially viable myocytes (no-reflow phenomenon). The effect of intracoronary adenosine on these changes was assessed in 15 closed-chest dogs subjected to 2 hours of proximal left anterior descending artery (LAD) occlusion followed by 3 hours of reperfusion. Animals randomly received adenosine (n = 8) 3.75 mg/min into the proximal LAD or an equivalent volume of saline (control) (n = 7) for 1 hour after reperfusion. Endothelial-dependent and independent coronary vasodilator reserve was determined using a chronically implanted volume-flowmeter on the mid-LAD at baseline and 1 and 3 hours after reperfusion with acetylcholine and papaverine infusions, respectively, into the proximal vessel. Regional myocardial blood flow was measured serially with radioactive microspheres and regional contractile function with contrast ventriculography. Both agonists produced a significant increase in LAD flow before occlusion. Endothelial-dependent and independent vasodilatory reserve was significantly reduced (p less than 0.05) at 1 and 3 hours after reperfusion in control animals compared with adenosine treatment. A progressive decrease in mid-LAD flow and increase in coronary vascular resistance after reperfusion was observed in control animals (p less than 0.05). The treated group manifested improved regional myocardial blood flow in endocardial regions from the central (0.73 +/- 0.15 versus 0.24 +/- 0.11 ml/g/min; p less than 0.02) and lateral ischemic zones (0.80 +/- 0.15 versus 0.34 +/- 0.12 ml/g/min; p less than 0.05) 3 hours after reperfusion. A significant reduction (p less than 0.05) in endocardial and midmyocardial flow compared with baseline was seen in control animals at 3 hours. Intravascular and interstitial neutrophil infiltration was reduced in adenosine animals and this was associated with relative ultrastructural preservation of endothelial cells. Regional ventricular function in the ischemic zone was improved in the adenosine group 3 hours after reperfusion (13.4 +/- 3.9% versus -5.3 +/- 1.6%; p less than 0.001). This study demonstrates that selective administration of adenosine after reperfusion significantly attenuates functional and structural abnormalities in the microvasculature after prolonged (2 hours) regional ischemia in the canine model. Prevention of microvascular injury and the non-reflow phenomenon by adenosine may preserve reversibly injured myocytes following restoration of blood flow to previously ischemic myocardium.

Intracoronary verapamil for reversal of refractory coronary vasospasm during percutaneous transluminal coronary angioplasty.

Coronary artery spasm unresponsive to intracoronary nitroglycerin was observed in eight patients undergoing percutaneous transluminal coronary angioplasty for unstable ischemic symptoms (unstable angina or recent nontransmural infarction, or both). All patients manifested eccentric lesions angiographically with the right coronary artery involved in four, circumflex artery in two and left anterior descending in two. Severe coronary spasm was documented angiographically in all patients after angioplasty and resulted in symptomatic and electrocardiographic evidence of ischemia. Multiple sites of spasm were present in the dilated vessel in three patients. Coronary artery spasm persisted despite the infusion of large doses of intracoronary nitroglycerin (200 to 2,000 micrograms, mean 850 micrograms) over 10 min. Administration of intracoronary verapamil (1 to 1.5 mg over 10 min) resulted in complete relief of spasm with restoration of brisk anterograde flow in all patients. These findings suggest that intracoronary verapamil may be a useful agent for the relief of coronary spasm occurring in the setting of coronary angioplasty.

Explicit Plancherel theorem for ground state representation of the Heisenberg chain.

In its ground state representation, the infinite spin 1/2 Heisenberg chain provides a model for spin wave scattering that entails many features of the quantum mechanical N-body problem. Here, we give a complete eigenfunction expansion for the Hamiltonian of the chain in this representation, for all numbers of spin waves. Our results resolve the questions of completeness and orthogonality of the eigenfunctions given by Bethe for finite chains, in the infinite volume limit.

Factors influencing the yield of satellite DNA in extractions from Drosophila virilis and Drosophila melanogaster adults and embryos.

The application of different DNA extraction methods to identical batches of Drosophila virilis and Drosophila melanogaster flies or embryos has revealed that the ionic strength of a homogenization medium is of critical importance if chloroform extractions are performed. The low yield of satellite DNA after homogenization in low salt buffers is less severe if EDTA is included in the buffer. Phenol extraction procedures result in no such differential behavior of satellite and main band DNA, but under certain circumstances a particular satellite fraction of Drosophila virilis DNA may be lost.