Improved accuracy and precision of thermodilution cardiac output measurement using a dual thermistor catheter system.

OBJECTIVES: To assess whether thermodilution cardiac output determination based on measurement of injectate temperature in vivo leads to more accurate and precise estimates and to study the influence of chilled injectate on test performance. BACKGROUND: Cardiac output measurement via right heart catheterization is used extensively for hemodynamic evaluation in a variety of diagnostic, perioperative and critical care settings. Maximizing accuracy is essential for optimal patient care. METHODS: This prospective study of 960 thermodilution cardiac output measurements was conducted using conventional and dual thermistor techniques. Specialized dual thermistor right heart catheters were constructed using a second thermistor positioned to measure injectate temperature in vivo just prior to entry into the right atrium. To eliminate interinjection variability, a custom set-up was developed that permitted output measurement using both techniques simultaneously. Both ambient temperature injections and cooled injections were investigated. RESULTS: The dual thermistor technique demonstrated significantly less measurement variability than the conventional technique for both ambient temperature (precision = 0.41 vs. 0.55 L/min, p < 0.001) and cooled (precision = 0.35 vs. 0.43 L/min, p = 0.01) injections. Similarly, the average range of cardiac output values obtained during five sequential injections in each patient was less using the dual thermistor approach (1.05 vs. 1.55 L/min, p < 0.001). The use of cooled injectate reduced the mean error of the dual thermistor technique but actually increased the mean error of the conventional technique. Even with ambient temperature injections, injectate warming during catheter transit varied considerably and unpredictably from injection to injection (2 SD range = -0.22 to 5.74 degrees C). Conventional ambient temperature and cooled measurements significantly overestimated Fick cardiac output measurements by 0.32 and 0.50 L/min, respectively (p < 0.001). In contrast, dual thermistor measurements were statistically similar (-0.08 and -0.08 L/min, p = 0.34) to Fick measurements. CONCLUSIONS: This new dual thermistor approach results in a significant improvement in both precision and accuracy of thermodilution cardiac output measurement.

Effect of thrombolysis on acute mitral regurgitation during evolving myocardial infarction. Experience from the Thrombolysis in Myocardial Infarction (TIMI) Trial.

OBJECTIVES: This study was undertaken to determine whether early successful thrombolysis can reverse infarct-associated mitral valve dysfunction. BACKGROUND: Mitral regurgitation is a common complication of acute myocardial infarction and has been shown to adversely affect both short- and long-term prognosis. Although anecdotal reports have suggested that reperfusion of the infarct-related artery may restore normal function to the mitral valve, this theory has not been subjected to formal investigation. METHODS: Patients with total or partial obstruction of the infarct-related artery received intravenous thrombolytic therapy with either streptokinase or recombinant tissue-type plasminogen activator within 7 h of symptom onset (mean 4.8 h) as part of the Thrombolysis in Myocardial Infarction (TIMI) Phase I trial. Repeat coronary angiography assessed arterial patency at 90 min and 10 days after attempted reperfusion. The presence and severity of mitral regurgitation were determined by contrast ventriculography both before thrombolysis and before hospital discharge. RESULTS: Overall, 21 (16%) of the 132 study patients exhibited mitral regurgitation on either their initial or their predischarge ventriculogram. The proportion of infarct-related arteries found to be patent (TIMI flow grade 2 or 3) was statistically similar in patients with and without mitral regurgitation during each angiographic evaluation period (initial, 90 min and 10 days). Although coronary artery perfusion increased overall during sequential measurement (mean TIMI grade was 0.4 +/- 0.6 initially, 1.5 +/- 1.3 at 90 min and 2.2 +/- 1.0 at 10 days), the pattern of reperfusion observed could not predict an increase or decrease in regurgitant severity (p = NS). Early mitral regurgitation resolved in 57% of patients by 10 days, but this resolution appeared independent of the presence or absence of improved coronary perfusion (60% vs. 50%). The development of new regurgitation during the recovery period (6%) was also unrelated to improved perfusion (7% vs. 4%). CONCLUSIONS: Acute mitral regurgitation developing during myocardial infarction shows frequent changes in its presence or severity during the 1st 10 days, appears independent of coronary artery patency both early and late after thrombolysis and cannot be reliably treated by improving arterial perfusion with thrombolytic agents.

Maintenance of hemostasis after invasive cardiac procedures: implications for outpatient catheterization.

OBJECTIVES: This study investigated the efficacy of four different methods of arterial puncture site management during recovery from invasive cardiac procedures. The primary goals were less patient discomfort and improved clinical outcome. BACKGROUND: The increasing use of outpatient catheterization, large interventional devices and potent periprocedural anticoagulation regimens has made the reduction of groin complications a high priority. Despite these trends, there are no randomized trials comparing commonly used techniques in treating the catheter entry site for the first few hours after the procedure. METHODS: Four-hundred consecutive patients undergoing catheterization laboratory procedures were randomly assigned to one of four dressing techniques applied after achieving hemostasis: a sandbag placed over the site; a pressure dressing constructed from surgical gauze and elastic tape; a commercially available compression device; and no use of compressive dressing. Of these 400 patients, 171 would have been eligible for outpatient procedures in the absence of geographic constraints. The dressings were removed, and ambulation was encouraged 5 h after sheath removal. Uniform initial compression times, patient instructions, nursing follow-up and a structured interview and physical examination at 24 h were used. RESULTS: The level of patient discomfort before and after dressing removal, as well as site tenderness at 24-h follow-up, was statistically similar in all four groups. Hematomas (typically small) and areas of ecchymosis were observed in 58 and 122 patients, respectively, but both their frequency and size were equally represented in each group. Important adverse events were confined to bleeding, rated as mild in 5.8%, moderate in 0.8% and severe in 0.6% of patients. Again, all four groups were statistically similar. Comparable findings were observed in the subgroup of patients eligible for outpatient procedures. CONCLUSIONS: Despite an increase in inconvenience and expense, none of the three compression techniques that were investigated improved patient satisfaction or outcome. Therefore, the routine use of compression dressings after invasive cardiac procedures cannot be recommended.

Cardiovascular abnormalities accompanying acute spinal cord injury in humans: incidence, time course and severity.

The frequency of cardiovascular abnormalities was evaluated in 71 consecutive patients with acute injury to the spinal cord. Persistent bradycardia was universal in all 31 patients with severe cervical cord injury and less common in milder cervical injury (6 of 17) or thoracolumbar injury (3 of 23) (p less than 0.00001). Marked sinus slowing (71 versus 12 versus 4%, respectively, p less than 0.00001), hypotension (68 versus 0 versus 0%, p less than 0.00001), supraventricular arrhythmias (19 versus 6 versus 0%, p = 0.05) and primary cardiac arrest (16 versus 0 versus 0%, p less than 0.05) were significantly more frequent in the severe cervical injury group. The frequency of bradyarrhythmias peaked on day 4 after injury and gradually declined thereafter. All observed abnormalities resolved spontaneously within 2 to 6 weeks. The primary mechanism underlying these observations appears to involve the acute autonomic imbalance created by the disruption of sympathetic pathways located in the cervical cord. Acute severe injury to the cervical spinal cord is regularly accompanied by arrhythmias and hemodynamic abnormalities not found with thoracolumbar cord trauma. These abnormalities are limited to the first 14 days after injury, a period in which life-threatening disturbances must be anticipated.

Right atrial-esophageal fistula and hydropneumopericardium after esophageal dilation.

Esophagoatrial fistula formation is a rare and heretofore fatal event. A patient presented with esophageal reflux and stricture that later developed into a right atrial-esophageal fistula during biweekly esophageal dilation. Clinical recognition and surgical therapy led to a successful outcome. There were several unique features of this case, including fistulous connection to the right rather than the left atrium, concomitant hydropneumopericardium and esophagoatrial fistula, occurrence during esophageal dilation and surgical cure.

Non-Q-wave myocardial infarction following thrombolytic therapy: a comparison of outcomes in patients randomized to invasive or conservative post-infarct assessment strategies in the Veterans Affairs non-Q-wave Infarction Strategies In-Hospital (VANQWISH) Trial.

OBJECTIVES: We wished to determine the effect of post-infarct management strategy on event rates (death or recurrent nonfatal myocardial infarction [MI]) in patients who evolved non-Q-wave MI (NQMI) following thrombolytic therapy. BACKGROUND: Patients who evolve NQMI following thrombolytic therapy are often considered to be at high risk and are frequently managed with routine early invasive testing despite a lack of data supporting improved outcome. METHODS: The Veterans Affairs Non-Q-Wave Infarction Strategies In-Hospital (VANQWISH) study included 115 patients who evolved NQMI following thrombolytic therapy. We compared the event rates in patients randomized to routine early coronary angiography with those in patients randomized to a conservative strategy of noninvasive functional assessment, with angiography reserved for patients with spontaneous or induced ischemia. RESULTS: During an average follow-up of 23 months, 19 of 58 patients (33%) randomized to the invasive management strategy died or suffered recurrent nonfatal MI, compared with 11 of 57 patients (19%) randomized to the conservative strategy (p = 0.152). Equivalent numbers of patients were subjected to revascularization (percutaneous transluminal coronary angioplasty or coronary artery bypass graft). There were more deaths in the invasive management group than in the conservative management group (11 vs. 2). Excess deaths could not be attributed to periprocedural mortality. CONCLUSIONS: Overall event rates (death or recurrent nonfatal MI) are comparable with conservative and invasive strategies in patients who evolve NQMI following thrombolytic therapy. Mortality rate in patients managed conservatively is low (3.5%), and routine invasive management may be associated with an increased risk of death.

Vascular remodeling and the local delivery of cytochalasin B after coronary angioplasty in humans.

OBJECTIVES: This study sought to determine the safety, feasibility and outcome of local delivery of cytochalasin B at the site of coronary angioplasty. BACKGROUND: Previous failures in the pharmacologic prevention of restenosis may have been related to inadequate dosing at the angioplasty site as a result of systemic drug administration. Alternatively, although previous experimental protocols have typically targeted control of excess tissue growth (intimal hyperplasia), it now appears that overall arterial constriction (vascular remodeling) is the major contributor to late lumen loss. Cytochalasin B inhibits the polymerization of actin and has proved to be a potent inhibitor of vascular remodeling in animal models. METHODS: In this phase I, multicenter, randomized, controlled trial, cytochalasin B (or matching placebo) was administered to the site of a successful balloon angioplasty using a microporous local delivery infusion balloon. RESULTS: The rate of drug delivery at a constant infusion pressure varied significantly from patient to patient (range 1.7 to 20.2 ml/min), perhaps related to a variable constricting effect of the atherosclerotic plaque on the infusion balloon. The minimal stenosis diameter after the procedure was slightly better in the active drug group (1.86 +/- 0.44 vs. 1.49 +/- 0.63 mm, p < 0.03), but this difference was not seen at four to six weeks. Although the study was not powered for clinical outcomes (n = 43), the combined end point (death, nonfatal infarction or repeat revascularization) was encountered in 20% of the patients receiving cytochalasin B and in 38% of the patients receiving placebo. Clinical restenosis occurred in 18% of the treatment group and 22% of the placebo group. There were no significant differences between groups in biochemical or electrocardiographic variables. CONCLUSIONS: Cytochalasin B can be safely administered by local delivery after successful coronary angioplasty and warrants further study of its efficacy in reducing restenosis.

Repeat interventions as a long-term treatment strategy in the management of progressive coronary artery disease.

OBJECTIVES: This study investigates whether repeat coronary interventions, applied over an extended time period, can successfully curtail the progression of ischemic symptoms and angiographic lumen narrowing. BACKGROUND: Coronary artery disease is a chronic and generally progressive disorder, and potential treatment strategies should be examined and compared with this chronicity in mind. Percutaneous interventional revascularization procedures could theoretically be useful in controlling progression of the disease through repeated use as new coronary lesions arise. However, the outcome of this long-term management concept has not previously been subjected to detailed investigation. METHODS: From a consecutive series of 4,357 interventional cardiac procedures, 544 patients were identified who received two or more interventions during the 13-year study period. These patients were categorized into one of three groups: restenosis (repeat interventions limited to the same target segment, n = 261), new stenosis (all repeat interventions directed to stenoses not previously treated, n = 155) or both (repeat interventions directed both to the same and to different target lesions, n = 128). RESULTS: Two to five procedures were performed per patient; the time period (mean +/- SD) separating each procedure was significantly less (p < 0.0001) for the restenosis group (4.2 +/- 2.3 months) than for the new stenosis (24.2 +/- 23.5 months) or the "both" groups (11.4 +/- 11.0 months). Despite the need for repeat procedures, the severity of angina (mean New York Heart Association functional class 1.6 +/- 0.9) after 6.2 +/- 2.3 years of follow-up was substantially better than before the initial procedure (mean functional class 3.2 +/- 0.8), with a similar magnitude of change found in all three groups. This long-term functional improvement was mirrored by a corresponding anatomic improvement, with the mean number of diseased vessels remaining constant at the time of each procedure (1.5 +/- 0.7, 1.5 +/- 0.7 and 1.6 +/- 0.7, respectively, for the first, second and third procedures, p = NS). The restenosis and the new stenosis groups also demonstrated statistically similar annual rates of mortality (1.9% vs. 1.8%) and coronary surgery (2.3% vs. 2.6%), although the restenosis group had a lower rate of infarction (1.4% vs. 3.2%, p = 0.002). CONCLUSIONS: Repeat interventional treatment of newly acquired stenoses provides a rational approach for the long-term management of chronic coronary artery disease. In addition to yielding a favorable late outcome, the use of this strategy can result in sustained functional improvement and can check the progression of clinically significant stenoses.

Structural constriction of the artery wall contributes to stenosis severity in unstable angina.

Eight consecutive patients with unstable angina underwent intravascular ultrasound imaging of the culprit artery with measurements recorded at the stenosis and at an adjacent reference site. In all patients, total artery cross-sectional area was smaller at the stenosis site than at the reference site, indicating that a structural change in the artery wall due to a constrictive process appears to contribute to the worsening of stenosis severity associated with unstable angina.

Reduction of ventricular arrhythmias by atropine during coronary arteriography.

Sustained ventricular arrhythmia is a well-recognized complication of cardiac catheterization, often occurring after selective coronary artery injection of contrast medium. The role of autonomic reflexes in the pathogenesis of this phenomenon is unclear. Although the muscarinic antagonist atropine is often administered prophylactically before coronary angiography to reduce the likelihood of sinus bradycardia and vasovagal reactions, its influence on ventricular arrhythmias in this setting has not been established. This case-control trial studied 648 patients undergoing coronary arteriography to investigate this issue. Eleven case subjects (those with ventricular tachyarrhythmia) were identified. Control subjects (those without ventricular tachyarrhythmia) were matched for baseline heart rate (+/- 6 beats/min), age (+/- 10 years), sex and calendar year of procedure using a 1:3 sampling ratio. All 26 potential clinical, anatomic and hemodynamic covariates were statistically similar between groups. Ventricular tachyarrhythmias were more likely to occur after selective right coronary injection (odds ratio 15.1, p = 0.0008) but not after multiple contrast injections (odds ratio 0.918, difference not significant). Most importantly, atropine sulfate was administered prophylactically to 18 of 33 control subjects (55 +/- 9%) but only 1 of 11 cases (9 +/- 9%), generating a significant odds ratio of 12.0 (p = 0.02). Thus, the odds of experiencing sustained ventricular tachyarrhythmias during coronary arteriography may potentially be reduced 12-fold by prior administration of atropine, even in patients with normal baseline heart rates.

Comparative accuracy of three automated techniques in the noninvasive estimation of central blood pressure in men.

Automated devices have regularly replaced manual sphygmomanometry for the determination of blood pressure not only in homes and clinics, but also in emergency and critical care settings. Few studies exist that correctly assess the accuracy of these devices, and even fewer that specifically compare commercially available units that rely on different physiologic events for measurement. Six hundred pressure measurements were obtained from 120 subjects using 1 of 3 randomly selected blood pressure monitors. In addition, central arterial pressure measurements were obtained simultaneously and directly from the ascending aorta of each subject. Overall, these devices tended to overestimate diastolic (+2.5 mm Hg, p < 0.0001) and mean (+3.8 mm Hg, p < 0.0001) pressures, but not systolic (+0.7 mm Hg, p = NS) pressure. Compared with the other 2 devices, device I, relying on oscillometric detection, demonstrated a significantly smaller mean absolute error for diastolic pressure (4.9 +/- 3.0 vs 7.0 +/- 4.8 and 6.2 +/- 5.3 mm Hg, p < 0.0001) and mean pressure (4.0 +/- 3.2 vs 7.8 +/- 5.9 and 8.6 +/- 7.5 mm Hg, p < 0.0001), and a trend toward smaller error with systolic pressure (6.8 +/- 6.5 vs 7.3 +/- 6.8 and 8.0 +/-5.6 mm Hg, p = 0.19). Clinically significant (+/-10 mm Hg) errors were common with each device (24.8% overall), but serious (+/-20 mm Hg) errors were unusual (3.2%) and did not occur at all with device I during diastolic and mean pressure measurement. All of the devices tested could be expected to perform satisfactorily in most clinical settings provided that an average error of 4.0 to 8.6 mm Hg is tolerable. This level of accuracy typically extended throughout the range of pressures anticipated in most noncritical clinical situations. As implemented in the devices tested, noninvasive measurement by oscillometry with stepped deflation is more accurate than automated auscultation.

Prevalence of catheter-induced valvular regurgitation as determined by Doppler echocardiography.

It has been suggested that cardiac catheters traversing competent heart valves may induce valvular regurgitation. To evaluate this possibility, continuous-wave and pulsed Doppler echocardiographic studies were performed immediately before, during and immediately after removal of various catheters in a total of 47 adult patients without clinical evidence of valvular regurgitation. With the tip of a 7Fr balloon flotation catheter positioned in the pulmonary artery, 9 of 36 patients (25%) had pulmonary regurgitation documented by continuous-wave Doppler. Evidence for regurgitation by pulsed Doppler examination was noted in 4 of these 9, with the regurgitant signal extending a mean of 1.8 cm into the right ventricular outflow tract. Similarly, a tricuspid regurgitant signal was present in 10 of 37 patients (27%) by continuous-wave Doppler and in 6 of these 10 by pulsed Doppler, with a mean regurgitant signal depth of 2.3 cm. Doppler examination also was performed in 7 patients (2 with aortic regurgitation) with a 7Fr pigtail catheter across the aortic valve, and in 4 patients (1 with tricuspid regurgitation) with a 6Fr bipolar pacing catheter across the tricuspid valve. Catheter removal resulted in no change in either the presence or absence of a regurgitant signal, or in the regurgitant signal depth in any of the patients studied. It is concluded that standard cardiac catheters neither induce Doppler-detected valvular regurgitation, nor do they affect the retrograde distance to which an existing regurgitant signal can be mapped.

Altered ventricular repolarization in central sympathetic dysfunction associated with spinal cord injury.

Complete injury to the cervical spinal cord results in total disruption of central sympathetic outflow. Although ventricular repolarization can be significantly influenced by disorders of autonomic function, the effects of cervical sympathectomy are unknown. Therefore, 40 subjects with complete chronic spinal cord injury were prospectively divided into 2 groups, half with total disruption of central sympathetic outflow (level of injury C5 to C8) known as the high level injury group, and half with nearly intact sympathetic innervation (T10 to L1) serving as controls. The completeness of autonomic dysfunction was verified by the cold pressor response. ST-segment analysis of the resting surface electrocardiogram revealed multilead ST elevation in the high level injury group, with maximum ST height significantly higher than the control group (131 +/- 21 [standard error] vs 47 +/- 8 microV; p = 0.0005). Unlike the control subjects, maximal arm ergometry exercise in the high level injury subjects failed to decrease ST-segment height (delta ST = -3 +/- 6 vs -43 +/- 14 microV in controls; p = 0.02). This difference persisted even after matching for exercise capacity. However, during exogenous stimulation with the sympathomimetic amine isoproterenol, ST-segment height in the high level injury group markedly decreased (mean delta ST = -84 +/- 26 vs -17 +/- 18 microV in controls; p = 0.04). Thus, central sympathetic dysfunction regularly results in multilead ST-segment elevation that decreases to or below isoelectric baseline during low dose isoproterenol infusion. Unlike normal subjects and individuals with normal variant ST-segment elevation, ST height is not altered by exercise. These findings document that ST-segment height in man is greatly influenced by central sympathetic nervous activity both at baseline and during physiologic and pharmacologic stress.

Usefulness of exercise-induced ST-segment depression in the inferior leads during exercise testing as a marker for coronary artery disease.

Multiple lead systems are shown to have a higher sensitivity than that of single leads for detecting coronary artery disease (CAD) during exercise testing, but the value of ST-segment depression isolated to the inferior leads is questionable. To ascertain the diagnostic accuracy of inferior limb lead II compared with that of precordial lead V5, a retrospective analysis of 173 men was performed (108 in a training population and 65 in a validation cohort). All patients had a standard exercise test and underwent diagnostic coronary angiography within 15 days of the exercise test (range 1 to 65). Sixty-three patients had greater than or equal to 1 coronary stenoses greater than or equal to 70%, or left main lesion greater than or equal to 50%, whereas 45 patients in the training population did not. Exclusion criteria were female sex, left ventricular hypertrophy, left bundle branch block or resting ST-segment depression on the baseline electrocardiogram, previous myocardial infarction or revascularization procedures, and any significant valvular or congenital heart disease. Lead V5 had a better combination of sensitivity (65%) and specificity (84%) (chi-square = 24.11; p less than 0.001) than that of lead II (sensitivity 71%, specificity 44%) (chi-square = 2.25; p = 0.13) at a single cut point, and this improved specificity was substantial (95% confidence interval for observed difference 22 to 58%). Receiver-operating characteristic curve analysis also revealed that lead V5 (area = 0.759) was markedly superior to lead II (area = 0.582) over multiple cut points (z = 3.032; 2p = 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Mitral valve E point-septal separation as an index of left ventricular function with valvular heart disease.

Echocardiographic mitral valve E point-septal separation (EPSS) has been found to be a useful hemodynamic index. Prior studies have shown a high negative correlation between EPSS and left ventricular ejection fraction (EF) in selected patients, but the utility of this index with valvular heart disease has not been examined in detail. Cardiac catheterization and M-mode echocardiographic data were retrospectively analyzed from 30 patients with aortic stenosis, 18 patients with chronic aortic regurgitation, and 25 patients with chronic mitral regurgitation. For aortic stenosis patients (including those with coronary artery disease), an excellent correlation (r = -0.89, p less than 0.001) was observed between EPSS and angiographic EF. More modest correlations were noted for patients with aortic regurgitation (r = -0.58, p less than 0.01) and mitral regurgitation (r = -0.63, p less than 0.001). For patients with aortic regurgitation, correlation improved to r = -0.83 by excluding subjects with marked (greater than 4 mm) fluttering of the anterior mitral valve leaflet. For patients with mitral regurgitation, the EPSS-EF correlation improved to r = -0.72 after excluding patients with atrial fibrillation. Compared with other echocardiographic indices of left ventricular function (percent shortening of the minor diameter or echo-derived EF), the EPSS demonstrated an equivalent or superior correlation with angiographic EF for each valvular lesion studied. We conclude that EPSS is a highly reliable index of left ventricular function with aortic stenosis, but its utility in unselected patients with chronic mitral or aortic regurgitation is limited.

Restenosis rate after percutaneous transluminal coronary angioplasty: a literature overview.

In order to elucidate factors affecting the rate of angioplasty restenosis, we reviewed 212 published reports on restenosis after percutaneous transluminal coronary angioplasty. We used five specific methodologic standards to select the 31 reports most likely to produce unbiased results. Sixty one factors judged to be related to restenosis rate were investigated. Only shorter duration of data collection (p=0.0003) was related to higher restenosis rate. This factor may be related to inexperience in choosing subjects or performing procedures. Other factors whose association with restenosis rate did not reach our predetermined level of statistical significance (p less than .01) were angioplasties of the left circumflex artery (p=.02), angioplasty of total occlusions (p=.02) and advanced age (p=.05). The association of shorter data collection with higher restenosis rates suggests that improved outcome may result from consolidation to a few centers specializing in this technique.

Correlation between resting ST segment depression, exercise testing, coronary angiography, and long-term prognosis.

Resting ST segment depression has been identified as a marker for adverse cardiac events in patients with and without known coronary artery disease. To correlate this with exercise testing, coronary angiography, and how it impacts on long-term prognosis, a retrospective study was performed on 476 patients, of whom 223 had no clinical or electrocardiographic evidence of prior myocardial infarction while 253 were survivors of an infarction. All patients performed a standard exercise test and underwent diagnostic coronary angiography within an average of 32 days of their exercise test (range 0 to 90 days). Exclusions were women, those with left bundle branch block, left ventricular hypertrophy, use of digoxin, previous revascularization procedures, or significant valvular or congenital heart disease. Long-term follow-up was carried out for an average of 45 months (+/- 17). Of the patients without prior infarction, 23 (10%) had persistent resting ST segment depression, and of those with a prior history of infarction, 37 (15%) also had resting ST segment depression. Patients with resting ST segment depression and no prior myocardial infarction had a higher prevalence of severe coronary disease (three-vessel and/or left main) (30%) than those without resting ST segment depression (16%) (95% confidence interval [CI] for observed difference -5.0% to 33.9%, p = 0.12). The criterion of greater than or equal to 2 mm of additional exercise-induced ST segment depression was a particularly useful marker in these patients for the diagnosis of any coronary disease (likelihood ratio 3.35, 95% CI 0.56 to 19.93, p = 0.06). Patients with resting ST segment depression and a prior myocardial infarction had a 2.5 times higher prevalence of severe coronary artery disease compared with patients without resting ST segment depression (43% versus 17% prevalence, respectively, 95% CI for observed difference 9.38% to 42.8%, p less than 0.001) and also had larger left ventricles postinfarction (left ventricular end-diastolic volume index 102 ml/m2 compared with 96 ml/m2, p less than 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)

Contributions of frequency distribution analysis to the understanding of coronary restenosis. A reappraisal of the gaussian curve.

BACKGROUND: Clinical restenosis after balloon angioplasty can be categorized by use of dichotomous terms based on the presence or absence of recurrent myocardial ischemia. In contrast, recent investigations have concluded that late luminal renarrowing, documented through angiographic imaging, occurs to a variable extent in nearly all stenoses. This process has been characterized by a gaussian or normal frequency distribution, with restenosis simply representing an extreme form of this delayed remodeling. In the current study, frequency distribution analysis was used to examine the process of coronary restenosis in a large cohort of patients at risk. METHODS AND RESULTS: Quantitative coronary angiographic analysis was applied to 9279 cineangiograms obtained in 3093 patients before and immediately after angioplasty and after 6-month follow-up. Late loss, defined as the change in minimum lumen diameter of the target stenosis from postdilation to follow-up, did not statistically conform to a normal distribution (P<.0001 by both chi2 statistic and Kolmogorov-Smirnov test), even after the exclusion of the 236 stenoses that displayed total occlusions at follow-up angiography. Examination of deviation from a normal curve revealed an excessively high frequency of stenoses that experienced either little change (0.0+/-0.3 mm) or marked change (1.0 to 2.0 mm) in late loss, with a low frequency of stenoses with intermediate values (0.3 to 1.0 mm). Similarly, although the distribution of percent diameter stenosis of the target lesion was statistically normal immediately after dilation, this gaussian distribution disappeared during the follow-up period. Other angiographic indexes of restenosis also failed to approximate a normal curve. In an attempt to improve the goodness of fit, a probabilistic model of late loss was created on the basis of deconvolution of the observed data distribution. Two theoretical, discrete populations of stenoses were identified, one with and one without overall late luminal narrowing. Unlike the gaussian distribution, this model provided a good representation of the observed data (P=NS for lack of fit). CONCLUSIONS: The frequency distributions of angiographic indexes of restenosis often superficially resemble a gaussian curve, an appearance that is artifactually enhanced by the measurement imprecision of current quantitative techniques. Nevertheless, standard indexes of coronary restenosis fail to conform statistically to a normal distribution. The pattern of deviations observed supports the possible existence of discrete subpopulations of lesions, each with a different propensity toward the development of restenosis after coronary intervention.