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M L Stadius

Publications and source records attributed to M L Stadius.

32 records · Page 2Linked to original sources
PubMed1991

Determinants of normal coronary artery dimensions in humans.

BACKGROUND: Studies of normal human coronary dimensions have been performed primarily in postmortem hearts. We evaluated the influence of age, body habitus, and regional myocardial mass on coronary dimensions in living patients with normal coronary vessels. METHODS AND RESULTS: Arteriographically normal coronary angiograms were analyzed from the following groups of subjects: group 1 (age, 15-34 years) consisted of 30 post-cardiac transplant patients with donor hearts from male subjects aged 15-34 years, group 2 (age, 35-54 years) consisted of 12 post-cardiac transplant patients with donor hearts from male subjects aged 35-54 years and 26 male subjects investigated for atypical chest pain, and group 3 (age, 55-74 years) consisted of 26 male subjects investigated for atypical chest pain. All angiograms were performed after sublingual nitroglycerin. Measurements of the dimensions of the left main, proximal left anterior descending, proximal left circumflex, and proximal right coronary arteries were made using a computer-assisted edge-detection algorithm. The regional myocardial mass supplied by each vessel was derived from echocardiographically derived total left ventricular mass and a semiquantitative angiographic territory scoring system based primarily on the number and length of its terminal nutrient branches. CONCLUSIONS: Linear regression analysis showed that coronary vessel cross-sectional area and total coronary cross-sectional area increase with regional myocardial mass and decrease linearly with age. Multivariate regression analysis revealed that regional myocardial mass and age were independent predictors of cross-sectional area for each vessel and for the total coronary cross-sectional area. We speculate that age-related decline in physical activity, in part, may be responsible.

Adolescent↗
PubMed1990

Evaluation of catheters and metallic catheter markers as calibration standard for measurement of coronary dimension.

Measurement of coronary dimension requires an accurate and reproducible dimensional reference. Angiographic catheters are frequently used for this purpose. We measured the angiographic diameters of a broad range of diagnostic and angioplasty guiding catheters by using two commonly used edge-detection algorithms. Angiographic diameters are significantly less than true catheter outer diameter. Therefore the use of contrast-filled catheters as a dimensional reference may lead to considerable error in vessel measurement with overestimation of absolute dimension. Tables of reference values for multiple catheter as calibration standard, tested under a variety of angiographic conditions. The metallic-tipped marker was found to have a better degree of reproducibility than catheters. These findings have implications for studies employing serial measurements of coronary artery dimension and for the clinical practice of estimating vessel diameter for choice of balloon size during angioplasty.

Calibration↗
PubMed1990

After thrombolytic therapy: angiography, angioplasty, or surgery?

Thrombolytic therapy has been found to improve the prognosis of selected patients with acute myocardial infarction. Many investigators advocate that combined emergency coronary angiography and percutaneous transluminal coronary angioplasty be performed immediately after thrombolytic therapy. Emergency angiography documents the anatomic extent of coronary artery disease, shows whether reperfusion has occurred, and indicates whether emergency angioplasty is necessary. In this setting, emergency catheterization without angioplasty is associated with relatively little additional risk. However, a number of prospective trials have compared emergency angioplasty to more conservative treatment strategies, and emergency angioplasty has been not found to offer any advantage in terms of improved prognosis or preservation of left ventricular function. Therefore, it is probable that most patients with evolving Q-wave myocardial infarction are best treated with conservative strategies after initial thrombolytic therapy, although there may still be a role for emergency angioplasty in a relatively small subset who present with evolving myocardial infarction and severely depressed left ventricular function. Emergency coronary artery bypass surgery also appears to have a limited role in patients treated with thrombolytic therapy. Nevertheless, in occasional patients with a poor prognosis at hospital presentation, in whom thrombolytic therapy and emergency angioplasty have failed or are contraindicated, prompt emergency coronary artery bypass grafting may salvage the ischemic myocardium and improve the prognosis.

Journal Article↗
PubMed1988

Coronary artery vasoconstriction routinely occurs after percutaneous transluminal coronary angioplasty. A quantitative arteriographic analysis.

To determine whether percutaneous transluminal coronary angioplasty (PTCA) increases coronary artery luminal dimensions by stretching and injuring ("paralyzing") the smooth muscle of the arterial wall, we prospectively analyzed spontaneous changes and then intracoronary nitroglycerin-induced changes in segmental coronary artery diameters during the first 30 minutes after uncomplicated single-vessel PTCA in 10 patients. Five additional patients received intravenous nitroglycerin throughout the procedure to determine whether nitroglycerin could prevent vasoconstriction after PTCA. All of the patients were maintained on oral doses of diltiazem and aspirin at the time of the study. Coronary arteriography was performed at 2, 5, 15, and 30 minutes after PTCA and then 3 minutes after 300 micrograms i.c. nitroglycerin. Quantitative measurements (computerized edge-detection) were performed at each time, in coronary segments centered in the dilated segment, distal to the dilated segment, and in a control vessel not manipulated with the balloon catheter or guidewire. Progressive vasoconstriction (defined as a loss of diameter that was reversed by intracoronary nitroglycerin) was observed after PTCA in the dilated and distal segments (10 of 10 patients) but not in the control segment. The vasoconstriction in the dilated segment at 30 minutes (mean, 30 +/- 4%) was highly statistically significant compared with vasoconstriction at 2 and 5 minutes after PTCA (p less than 0.001) and compared with the control segment at 30 minutes (p less than 0.005). There was no significant loss of diameter after PTCA in the dilated segment in the five patients who received intravenous nitroglycerin. In conclusion, 1) spontaneous coronary artery vasoconstriction after PTCA occurs routinely at and distal to the site of balloon dilatation despite pretreatment with aspirin and calcium channel blockers; 2) coronary artery vasoconstriction after PTCA is rapidly reversed by intracoronary nitroglycerin and can be prevented by the continuous administration of intravenous nitroglycerin during and after the procedure; 3) these results are incompatible with the hypothesis that PTCA improves coronary luminal dimensions by arterial "paralysis"; and 4) these findings have implications concerning the etiology and prophylaxis of abrupt vessel closure after PTCA.

Aged↗
PubMed1986

Risk stratification for 1 year survival based on characteristics identified in the early hours of acute myocardial infarction. The Western Washington Intracoronary Streptokinase Trial.

We evaluated the relationship between baseline factors defined at 4.6 +/- 2.1 hr after onset of acute myocardial infarction and 1 year survival in 245 patients entered in the Western Washington Intracoronary Streptokinase Trial. Univariate statistics identified a significant relationship between 10 of these factors and survival. Multivariate analysis identified three factors as being most closely related to survival: (1) left ventricular ejection fraction (LVEF) (p less than .0001), (2) treatment with streptokinase (p = .03), and (3) location of infarction (p = .04). Mathematic models based on this analysis and applied to our patients identified high- and low-risk subgroups for 1 year mortality. Patients receiving standard, not interventional, therapy with anterior infarction and an LVEF of 50% or less and those with inferior infarction and an LVEF of 39% or less comprised the high-risk group. For patients receiving standard therapy, 1 year mortality was 41% in the high-risk group and 4% in the low-risk group. The models illustrated the magnitude of benefit of streptokinase treatment and achievement of complete reperfusion for those at low and high risk. We conclude that LVEF determined in the first hours of acute myocardial infarction is the most important of all baseline factors for prediction of 1 year survival. Mathematic models based on left ventricular function measured as ejection fraction are useful for risk stratification in this setting.

Adult↗
PubMed1986

Effects of thrombolytic therapy on evolution of left ventricular function in acute myocardial infarction.

Use of thrombolytic therapy in the early hours of acute myocardial infarction (AMI) has gained widespread acceptance. One potential benefit of early reperfusion could be improved left ventricular (LV) function. Experimental animal studies have demonstrated that duration of coronary occlusion determines ultimate infarct size and have also raised the issue of reperfusion injury. The evolution of LV function after AMI in man where there is no attempt at early reperfusion is discussed. Studies of LV function following thrombolytic therapy in man have illustrated the following points. Time to successful reperfusion appears to be a critical determinant for potential for LV functional recovery. If reperfusion is achieved within 2.5 hours after onset of symptoms, consistent recovery of function within the infarct zone appears to be possible. With reperfusion from 2.5 to six hours after onset of symptoms, there is no predictable, substantial improvement in either global or regional LV function. Within the framework of this general conclusion, there are three potential exceptions: Successful reperfusion up to six hours after onset of symptoms may prevent infarct expansion. Patients with subtotal occlusion of the infarct vessel prior to therapy in this time period may have more potential for recovery of LV function than those with initial total occlusion. A tight residual stenosis following thrombolytic therapy may mask potential for functional recovery in the infarct zone. Earlier diagnosis and treatment of AMI is one obvious solution for the overall lack of beneficial results on evolution of LV function seen in most studies to date.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1985

The western Washington randomized trial of intracoronary streptokinase in acute myocardial infarction. A 12-month follow-up report.

After cardiac catheterization and coronary arteriography, 134 patients who had had an acute myocardial infarction were randomly assigned to treatment with intracoronary streptokinase (4000 U per minute, begun approximately 4 1/2 hours after the onset of symptoms, for a total of 286,000 +/- 77,800 U over 72 +/- 24 minutes); 116 control patients received standard care after they returned to the coronary care unit, immediately after angiography. Preliminary results of this trial have been published in the Journal (1983; 309:1477-81). During the first 30 days, 5 deaths occurred in the streptokinase group and 13 occurred in the control group (3.7 vs 11.2 per cent, P = 0.02); during the first year, the corresponding figures were 11 and 17 deaths (8.2 vs. 14.7 per cent, P = 0.10). However, when a minor imbalance in the ejection fraction and infarct location between the two groups was adjusted by logistic regression, the difference in one-year mortality became significant (P = 0.03). In the streptokinase group, 2 of the 80 patients in whom perfusion was reestablished (2.5 per cent) had died by one year, whereas 3 of the 13 with partial reperfusion (23.1 per cent) and 6 of the 41 with no reperfusion (14.6 per cent) had died (P = 0.008). Mortality among patients with partial reperfusion was not significantly different from that among those without reperfusion (P greater than 0.90). No base-line clinical, angiographic, or hemodynamic variable was predictive of successful reperfusion, according to univariate and multivariate analyses. We conclude that intracoronary streptokinase reduces one-year mortality among patients with acute myocardial infarction, but this improvement occurs only among those in whom thrombolysis results in coronary artery reperfusion.

Coronary Angiography↗
PubMed1985

Left ventricular volume determination using single-photon emission computed tomography.

A new method for measuring left ventricular (LV) volume based on gated single-photon emission computed tomography (SPECT) is described. Preliminary phantom studies showed an excellent correlation between SPECT and observed volumes (r = 0.99, standard error of the estimate [SEE] = 4.9 ml). SPECT was performed 24 hours after biplane contrast LV angiography in 36 patients. Transaxial blood pool tomograms were reconstructed by filtered back projection and reoriented to views orthogonal to the cardiac axes. Volume was calculated from serial short-axis tomograms by determining the base, apex and lateral borders of the LV blood pool, ascertaining the number of pixels in this volume and multiplying by the known volume of a pixel. Gated SPECT volumes were compared with contrast angiographic volumes. At end-systole, r = 0.96 and SEE = 12 ml; at end-diastole, r = 0.81 and SEE = 27 ml. For ejection fraction, r = 0.85 and SEE = 0.06. To test interobserver variation in processing, count data from 5 patients were processed twice (r = 0.98, SEE = 8.3 ml). There is an excellent correlation between SPECT and contrast angiographic volumes at end-systole; at end-diastole the relation is good. SPECT requires no arbitrary background correction, allows systematic isolation of the left ventricle from other overlapping cardiac chambers and requires no geometric assumptions for volume determination. It has promise as a direct method for measuring LV volume in a minimally invasive manner.

Adult↗
PubMed1985

Late effects of intracoronary streptokinase on regional wall motion, ventricular aneurysm and left ventricular thrombus in myocardial infarction: results from the Western Washington Randomized Trial.

To determine whether intracoronary streptokinase improves late regional wall motion or reduces left ventricular aneurysm or thrombus formation in patients with acute myocardial infarction, two-dimensional echocardiography was performed at 8 +/- 3 weeks after infarction in 83 patients randomized to streptokinase (n = 45) or standard therapy (n = 38) in the Western Washington Intracoronary Streptokinase Trial. Among the patients treated with streptokinase, the average time to treatment was 4.7 +/- 2.5 hours after the onset of chest pain, and 67% had successful reperfusion. Regional wall motion was assessed in nine left ventricular segments on a scale of 1 to 4 (normal, hypokinetic, akinetic and dyskinetic). Left ventricular thrombus formation was interpreted as positive, equivocal or negative. All patients received anticoagulant therapy in the hospital and 52 received such therapy after hospital discharge. The mean (+/- SD) global (1.5 +/- 0.4 in both groups) and regional wall motion scores in the streptokinase-treated and control groups were not significantly different. The prevalence of aneurysm was 16% in both groups. Left ventricular thrombus was identified in only five patients (positive identification in four, and equivocal in one), all in the streptokinase-treated group (p = NS). There were also no differences between streptokinase and control treatment in any of the echocardiographic variables in subgroups of patients with anterior infarction, inferior infarction, no prior infarction or reperfusion with streptokinase. It is concluded that intracoronary streptokinase given relatively late in the course of acute myocardial infarction does not result in improved global or regional wall motion or a reduction in left ventricular thrombus or aneurysm formation in survivors studied 2 months after myocardial infarction.

Aged↗
PubMed1985

Coronary anatomy and left ventricular function in the first 12 hours of acute myocardial infarction: the Western Washington Randomized Intracoronary Streptokinase Trial.

The relationships among clinical variables, coronary anatomy, and left ventricular function during the early hours of acute myocardial infarction (AMI) were evaluated from data acquired in the Western Washington Intracoronary Streptokinase Trial. All patients had symptoms and electrocardiographic changes typical of AMI. All data were obtained before treatment with streptokinase. Mean time to catheterization was 4.1 hr after onset of symptoms. Coronary angiograms (n = 245) were analyzed for location of infarct-related occlusion and collateral flow to the infarct bed. Left ventricular ejection fraction and regional left ventricular function were quantitated in 227. Sixty-two percent of occlusions were in the most proximal segment of the involved coronary artery. Collateral circulation was seen in 42% overall, in 31% with left anterior descending artery (LAD) occlusion, and in 52% with right coronary artery (RCA) occlusion (p less than .005). Left ventricular ejection fraction was lowest and regional function was most abnormal in the group with proximal LAD occlusion. Hyperkinesis was present in 32%; in those with hyperkinesis, hyperkinetic segment length was longest in those with RCA or circumflex occlusion. Multivariate analysis identified proximal LAD occlusion as the factor most closely associated with left ventricular ejection fraction and with measures of left ventricular regional hypofunction. We conclude that (1) AMI is usually caused by occlusion or subtotal occlusion in the most proximal portion of the involved coronary artery, (2) collateral circulation is more frequent with RCA than with LAD occlusion, and (3) location of the infarct-related occlusion is the most important determinant of global and regional left ventricular function in the early hours of AMI.

Aged↗