Measurement of coronary artery stenosis is an invaluable tool in the study of coronary artery disease. Clinical trials and even day-to-day decision making should ideally be based on accurate and reproducible quantitative methods. Quantitative coronary angiography (QCA) using digital angiographic techniques has been shown to fulfill these requirements. Yet many laboratories have abandoned visual analysis in favor of the intermediate quantitative approach involving hand-held calipers. Thus, the purpose of this study was to determine the relation between QCA and the commonly used caliper measurements. Percent stenosis was assessed in 155 lesions using 3 techniques: QCA, caliper measures from a 35-mm cine viewer (cine) and caliper measures from a video display (CRT). Good overall correlation was noted among the 3 different techniques (r greater than or equal to 0.72). Both of the caliper methods underestimated QCA for stenosis greater than or equal to 75% (p less than or equal to 0.001) and overestimated stenosis less than 75% (p less than 0.05). Reproducibility assessed in 52 lesions by independent observers showed QCA to be superior (r = 0.95) to either of the caliper measurements (cine: r = 0.63; CRT: r = 0.73). Therefore, the commonly used caliper method is not an adequate substitute for QCA because overestimation of noncritical stenoses and underestimation of severe stenoses may occur and the measurements have poor reproducibility. These factors definitely preclude its use in rigorous clinical trials. Moreover, since they do not appear to overcome known deficiencies of visual analysis, caliper measurements for day-to-day clinical use must also be seriously questioned.

Cineangiography↗

PubMed1990

Acute intervention during myocardial infarction in patients with prior coronary bypass surgery.

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Adult↗

PubMed1990

Effects of video frame averaging, smoothing and edge enhancement on the accuracy and precision of quantitative coronary arteriography.

Digital analysis of cine film provides numerous options for altering images by frame averaging or filtering algorithms that either smooth or enhance edges. While these may subjectively enhance image quality, there is no uniformity in their use among laboratories and effects on quantitative coronary analysis may not be ideal. To determine which processing algorithms might help or hinder quantitative coronary arteriography, cine film images of precision drilled stenotic cylinders (0.83 to 1.83 nm diameter) implanted in dog coronary arteries were analyzed with and without such algorithms. Video frame averaging of 1 to 49 frames had no effect on measures of accuracy (mean differences) but precision (standard deviation of mean differences) was improved from 0.23 to 0.17 mm (p less than 0.05) with video averaging of greater than or equal to 25 frames. Edge enhancement filtering algorithms resulted in slight deterioration of accuracy and precision and smoothing filtering algorithms caused modest improvements in these parameters; however, these changes were not significantly different from unprocessed images. Using edge enhancement filtering algorithms, accuracy was significantly worse (-0.27 mm) compared to a smoothing filter enhancement algorithm (-0.08 mm, p less than 0.001). The combination of video averaging and smoothing algorithms had no additional beneficial effects. Thus, precision of quantitative coronary analysis of cine film can be optimized by appropriate video averaging. Edge enhancement filtering algorithms should be avoided whereas smoothing filter enhancement algorithms may improve accuracy.

Algorithms↗

PubMed1990

The effects of propranolol on regional cardiac metabolism during ischemia and reperfusion assessed by magnetic resonance spectroscopy.

Sixteen anesthetized New Zealand white rabbits were subjected to thoracotomy, and a reversible snare occluder was attached around a large branch of the left circumflex coronary artery. A 1.3 cm. diameter nuclear magnetic resonance (NMR) surface coil was placed adjacent to the myocardium perfused by this vessel. The animals were divided into two groups of eight animals each, treatment and control. The rabbits were studied using a 2.0 T magnetic resonance (MR) spectrometer, and baseline spectra were acquired. The treatment animals then received intravenous propranolol (1.5 mg/kg) and the control animals received an equal volume of saline. Spectra were then acquired during a 20-minute occlusion period and during subsequent reperfusion. Animals in both groups showed expected decreases in phosphocreatine and adenosine triphosphate and an increase in inorganic phosphate during occlusion; these changes reverted toward baseline values with reperfusion. There were no significant differences between the two groups. The myocardium became acidotic during occlusion in both groups, but significantly more so in the control animals: during the first 10 minutes of occlusion pH was 7.30 +/- 0.41 in the treatment group versus 6.55 +/- 0.24 for controls (p = 0.0005). During the second 10 minutes of occlusion pH was 7.05 +/- 0.65 in the treatment group versus 6.24 +/- 0.25 in controls (p = 0.0053). We conclude that attenuation of intracellular acidosis by propranolol during myocardial ischemia was evident by MR spectroscopy in this animal model.

Animals↗

PubMed1989

Effects of diltiazem on phosphate metabolism in ischemic and reperfused myocardium using phosphorus31 nuclear magnetic resonance spectroscopy in vivo.

Diltiazem may provide a protective effect to ischemic and reperfused myocardium through preservation of high-energy phosphate metabolism. To test this hypothesis, rabbits had a 1.3 cm solenoidal coil placed over the myocardium to be rendered ischemic. Data were acquired with a 22 cm bore nuclear magnetic resonance spectrometer at 2.0 T. Animals were treated with diltiazem (200 micrograms/kg intravenous bolus of drug followed by a 15 micrograms/kg/min continuous intravenous infusion, n = 10) or by an equal volume of saline (n = 6). The left circumflex artery was occluded and reperfused using a reversible snare while electrocardiogram-gated spectra were accumulated. Levels of phosphocreatine were decreased during occlusion in both groups; however, this decrease was attenuated in the diltiazem treated animals compared to control (in relative percent area: 7.8 +/- 1.0 to 2.5 +/- 0.5, p less than 0.01). Levels of phosphocreatine promptly returned to baseline following reperfusion and there was no difference between the two groups. The inorganic phosphate metabolites of high-energy phosphate consumption increased with occlusion, though more so in the control group compared with the diltiazem-treated rabbits (in relative percent area: 72.5 +/- 0.9 to 55.4 +/- 1.3, p less than 0.01). With reperfusion, levels of inorganic phosphates returned toward baseline in both groups; however, the diltiazem group had a more complete recovery relative to control (in relative percent area: 38.8 +/- 2.1 to 47.6 +/- 2.7, p less than 0.05). Levels of adenosine triphosphate decreased in both groups relative to baseline; however, the amount of decrease was similar in the two groups. With reperfusion there was a definite though incomplete recovery of levels of adenosine triphosphate in the diltiazem-treated group (in relative percent area: 10.7 +/- 1.0 at occlusion, 12.3 +/- 0.4 during reperfusion, p less than 0.05), but in the control group levels of adenosine triphosphate remained depressed (in relative percent area: 9.8 +/- 0.6 at occlusion, 9.8 +/- 0.8 during reperfusion, p = NS). During ischemia there was a trend toward attenuation of intracellular acidosis in the diltiazem group; however, this trend did not reach statistical significance. These data indicate that diltiazem provides a protective effect on myocardial high-energy phosphate metabolism during regional ischemia and reperfusion in the intact animal.

Adenosine Triphosphate↗

PubMed1989

Regional metabolism during coronary occlusion, reperfusion, and reocclusion using phosphorus31 nuclear magnetic resonance spectroscopy in the intact rabbit.

Few studies have examined metabolic consequences of coronary occlusion and reperfusion using phosphorus31 nuclear magnetic resonance (31P-NMR) in an intact animal model. Accordingly, we developed a model to study serial changes in myocardial metabolism in the intact open-chest rabbit. Ten animals underwent 20 +/- 2 minutes of regional coronary occlusion and 60 +/- 10 minutes of reperfusion followed by reocclusion. Cardiac-gated 31P-NMR spectra were obtained with a regional surface coil over the ischemic area during baseline, occlusion, reperfusion, and reocclusion conditions. Phosphocreatine fell with both the initial and second ischemic insults to 65% +/- 5% of baseline for the first occlusion (p less than 0.01) and tended to decrease to 89% +/- 8% of baseline for the second occlusion (p = 0.07), with normal levels reattained in the intervening period of reperfusion (99% +/- 5% of baseline, p = NS). Concordant inverse changes were seen with inorganic phosphates. At occlusion levels of inorganic phosphates were 135% +/- 10% of baseline (p less than 0.05) and 139% +/- 10% of baseline at reocclusion (p less than 0.05). Levels of adenosine triphosphate decreased during occlusion to 78% +/- 9% of baseline and were significantly lower than baseline during the second occlusion (75% +/- 5% of baseline, p less than 0.01). The ratio of phosphocreatine to inorganic phosphates, when compared with values at baseline, decreased at occlusion (49.6% +/- 4.7% of baseline, p less than 0.01) and at reocclusion (64.7% +/- 4.9% of baseline, p less than 0.01), with a normal ratio reattained in the intervening period of reperfusion (93.3% +/- 3.1% of baseline, p = NS). We conclude that reperfusion restores levels of phosphocreatine and adenosine triphosphate while returning levels of inorganic phosphates to baseline. Deleterious changes in high-energy phosphate metabolism are not potentiated by reocclusion in this model. 31P-NMR spectroscopy holds promise as a technique to noninvasively monitor intracellular biochemical processes serially during various interventions in the intact animal model.

Adenosine Triphosphate↗

PubMed1988

Effect of afterload alterations on the functional border zone measured with two-dimensional echocardiography during acute coronary occlusion.

In the setting of acute myocardial infarction, pharmacologic intervention resulting in afterload changes are common but the effect of these changes on regional left ventricular function, and specifically the functional border zone, has not been fully investigated. Accordingly, we studied the effects of afterload manipulation on circumferential flow-function relationships and the functional border zone in 16 open-chest, anesthetized dogs. During left circumflex coronary artery occlusion, eight animals were infused with phenylephrine to increase afterload; eight others received nitroprusside for afterload reduction. Following coronary artery occlusion, subendocardial blood flow and wall thickening decreased in the ischemic zone (p less than 0.001). The circumferential extent of hypoperfusion did not differ when coronary artery occlusion alone was compared to occlusion in combination with phenylephrine or nitroprusside, but in both groups the circumferential extent of the wall thickening abnormality was consistently greater than the extent of hypoperfusion. When blood pressure was decreased by 33%, the extent of the functional border zone did not change relative to that during coronary artery occlusion (22 +/- 11 degrees vs 36 +/- 16 degrees, p = ns). Similarly, when blood pressure was increased by 47%, the extent of the functional border zone did not change (32 +/- 10 degrees vs 37 +/- 10 degrees). Therefore circumferential flow-function relations and the spatial extent of the functional border zone are not altered by changing afterload during acute left circumflex coronary artery occlusion in this model.

Animals↗

PubMed1988

The effect of different mechanisms of myocardial ischemia on left ventricular function.

Myocardial ischemia may be produced by limitation of blood flow as in abrupt coronary occlusion, termed supply-type ischemia, or by increasing myocardial oxygen demand in the setting of restricted flow, termed demand-type ischemia. To examine the comparative extent and severity of the dysfunction related to both forms of ischemia, we studied anesthetized, open-chest dogs by means of two-dimensional echocardiography and tracer microspheres. Supply-type ischemia was produced by total occlusion of the LCx (n = 7); demand-type ischemia was induced by infusion of dobutamine after creation of a critical LCx stenosis (n = 6). At the time of the production of ischemia, the group with demand-type ischemia had significant increases in both heart rate (p less than 0.05) and mean arterial pressure (p less than 0.05), whereas the group with supply-type ischemia had a decrease in mean arterial pressure (p less than 0.05). Subendocardial blood flow in the LCx region was severely depressed in supply-type ischemia (0.09 +/- 0.04 ml/min/gm) compared to demand-type ischemia (1.04 +/- 0.07 ml/min/gm; p less than 0.01). Although both groups of animals had an abnormality of left ventricular function during ischemia, as determined by two-dimensional echocardiography, the extent of the dysfunction in the group with supply-type ischemia was greater (146 +/- 12 degrees) compared to the group with demand-type ischemia (99 +/- 9 degrees; p less than 0.01). Similarly, the degree of left ventricular dysfunction in the group with supply-type ischemia was greater than that for the group with demand-type ischemia (p less than 0.05). Thus these data suggest that supply-type ischemia produced by coronary occlusion results in a greater extent and degree of left ventricular functional abnormality than pharmacologically induced demand-type ischemia.

Animals↗

PubMedDate not supplied

Recognizing and helping older persons with vision impairments.

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Aged↗