Does low individual operator coronary interventional procedural volume correlate with worse institutional procedural outcome?

OBJECTIVES: To assess the relation between individual operator coronary interventional volume and incidence of complications, the in-hospital outcome at a single, moderate volume urban academic center was prospectively collected over a 3-year period. BACKGROUND: A minimum of 75 coronary interventions/operator per year may be required in the future to obtain formal certification. However, few data exist regarding individual operator volumes and procedural outcome. METHODS: Between January 1993 and December 1995, 1,389 consecutive procedures were performed or supervised by nine geographic full-time operators: 171 (12.3%) utilized various devices, and 350 (25.2%) involved multivessel coronary intervention. Left ventricular ejection fraction was 59 +/- 15% (mean +/- SD), and there were 1.7 +/- 0.7 vessels diseased (with > or = 70% stenosis). Clinical indications included stable angina in 22.5% of cases, unstable angina in 31.9%, acute myocardial infarction (MI) in 2.9%, post MI in 20.6%, shock or acute heart failure in 3.0% and restenosis in 19.1%. In the last consecutive 857 lesions in 655 cases, 20.7% type A, 55.5% type B and 23.8% type C lesions were categorized before coronary intervention. RESULTS: Average yearly operator volume ranged from 26 to 83 cases (mean 51 +/- 26). Each operator has performed a total of 590 +/- 268 coronary interventions, with 10.0 +/- 4.3 years of coronary interventional experience. The mean angioplasty volume rating for the nine operators was 180 +/- 37 (> 170 considered adequate). The in-hospital major complication rate was 1.4% (95% confidence interval 0.7% to 1.893%) for all coronary interventions, including death in 3 patients, bypass surgery in 13, arrhythmia in 3 and Q wave MI in 2. To ascertain how these outcomes compared with standard measures of coronary interventional outcome, four previously published registries were reanalyzed in a similar manner. The rate of complications in the present study was found to be significantly lower than that of the 1992-1993 Society for Cardiac Angiography and Intervention registry (1.9%, n = 19,594, p < 0.05 [excludes ventricular arrhythmias]), the 1994 American College of Cardiology database (3.9%, n = 38,963, p = 0.001), the Mid-America Heart Institute outcome in 1988 (2.3%, n = 5,413, p = 0.02) and the 1985-1986 National Heart, Lung, and Blood Institute Registry (7.2%, n = 1,801, p = 0.001). Odds ratios and 95% confidence intervals showed the outcome in the current study to be at least comparable to the standard registries. CONCLUSIONS: Despite individual operator volumes below those currently being considered for credentialing, the overall institutional outcome was excellent in a diverse and complex patient population.

Distribution of blood viscosity values and biochemical correlates in healthy adults.

Increases in the viscosity of blood and plasma predict clinical manifestations of atherothrombotic vascular disease. The clinical utility of viscosity measurements in cardiovascular risk factor analysis requires reference values established from a healthy disease-free population. A cohort of 126 (71 men, 55 women) healthy nonsmoking adults had fasting blood analysis after a 12-14-h fast. Viscosity measurements were made on samples of whole blood, plasma, and serum at 37 degrees C with a coaxial cylinder microviscometer. The mean blood viscosity at shear rates of 100, 50, and 1 s-1 were 3.26 +/- 0.43, 4.37 +/- 0.60, and 5.46 +/- 0.84 mPa.s, respectively. Men had significantly higher blood viscosity values than women at each shear rate. The differences in blood viscosity did not remain significant after blood viscosity values were normalized to a hematocrit of 45%, except at 100 s-1. For the entire group, normalized blood viscosity values at each measured rate correlated inversely with HDL cholesterol and positively with fibrinogen. The mean plasma viscosity was 1.39 +/- 0.08 mPa.s and the mean serum viscosity was 1.27 +/- 0.06 mPa.s. Plasma viscosity correlated with fibrinogen (r = 0.51, P < 0.0001), total serum protein (r = 0.33, P < 0.0001), and triglyceride concentrations (r = 0.33, P < 0.0015). Serum viscosity correlated with total serum protein (r = 0.50, P < 0.0001) and LDL cholesterol (r = 0.24, P = 0.0065). This study provides reference values for the viscosity of blood, plasma, and serum that may assist in evaluating hemorheological profiles.

Tumor necrosis factor alpha and interleukin 1beta are responsible for in vitro myocardial cell depression induced by human septic shock serum.

Previous studies have demonstrated the presence of myocardial depression in clinical and experimental septic shock. This depression is associated with the presence of a circulating myocardial depressant substance with physical characteristics consistent with cytokines. The present study utilized an in vitro myocardial cell assay to examine the role of various human recombinant cytokines, including tumor necrosis factor (TNF)alpha and interleukin (IL)1beta, in depression of cardiac myocyte contractile function induced by serum from humans with septic shock. The extent and velocity of electrically paced rat cardiac myocytes in tissue culture was quantified by a closed loop video tracking system. Individually, TNF-alpha and IL-1beta each caused significant concentration-dependent depression of maximum extent and peak velocity of myocyte shortening in vitro. In combination, TNF-alpha and IL-1beta induced depression of myocardial cell contractility at substantially lower concentrations consistent with a synergistic effect. Using immunoabsorption, removal of both TNF-alpha and IL-1beta (but not either alone) from the serum of five patients with acute septic shock and marked reversible myocardial depression resulted in elimination of serum myocardial depressant activity. IL-2, -4, -6, -8, -10, and interferon gamma failed to cause significant cardiac myocyte depression over a wide range of concentrations. These data demonstrate that TNF-alpha and IL-1beta cause depression of myocardial cell contraction in vitro and suggest that these two cytokines act synergistically to cause sepsis-associated myocardial depression in humans.

Cost and appropriateness of radionuclide exercise stress testing by cardiologists and non-cardiologists.

The hypothesis that a diagnostic evaluation performed by a generalist is less expensive than that performed by a specialist is untested. We retrospectively evaluated the indications and financial ramifications of radionuclide exercise stress testing by cardiologists and noncardiologists in 1,902 consecutive adults with normal resting electrocardiograms. Subjects completed radionuclide exercise tests for the diagnosis or management of coronary artery disease during a 14-month period. Tests were considered "indicated" or "not indicated" based on criteria determined from published reports and established practice guidelines. Savings in costs and charges were determined for a strategy of referral to a cardiologist before ordering tests. Non-cardiologists ordered more tests that were not indicated than cardiologists (69.6% vs 36.2%, chi-square = 209.07, p < 0.00001). Non-cardiologists also ordered tests that were not indicated in patients with (chi-square = 110.02, p < 0.00001) and without (chi-square = 110.02, p < 0.00001) and without (chi-square = 45.44, p < 0.00001) chest pain. Tests that were not indicated resulted in excess costs of $591,384 and excess charges of $1,082,400. Referral to a cardiologist before ordering tests could have saved $63,257 in costs and $169,800 in charges. Both cardiologists and non-cardiologists overutilized radionuclide exercise stress test; however, non-cardiologists were more likely to order tests that were not indicated. A strategy of referral to a cardiologist before ordering tests may be cost-effective in this population.

Utility of various clinical, noninvasive, and invasive procedures for determining the causes of recurrence of myocardial ischemia or infarction > or = 1 year after percutaneous transluminal coronary angioplasty.

In patients with recurrent symptoms > or = 1 year after successful percutaneous transluminal coronary angioplasty (PTCA), the decision of whether to proceed directly with coronary angiography or to evaluate the patient noninvasively can be difficult. To determine which demographic, historical, clinical, and laboratory factors are useful in helping to make this decision, 76 consecutive patients who presented > 1 year (768 +/- 309 days) after successful PTCA with resolution of symptoms were studied. The initial PTCA successfully treated all stenoses (except chronically occluded vessels) in all major vessels and segments. The patient group was predominantly men (68%), with a mean age of 64 +/- 10 years. A prior myocardial infarction was present in 39 patients (51%), and there was a mean of 2.8 risk factors per patient. In patients who presented with recurrent symptoms, the Canadian Cardiovascular Society functional class was 2.0 +/- 0.9; 2 patients presented with acute infarctions, 57 were admitted to the hospital with unstable angina, and 17 had stable angina. New electrocardiographic changes at rest were found in 19 of 74 patients (26%) with recurrent angina. A thallium stress test was performed in 40 patients (53%), with a sensitivity of 77% and a specificity of 36% for the presence of a significant stenosis. No nonangiographic variable was predictive of angiographic findings. At angiography, the number of coronary arteries with > or = 50% diameter narrowing was 1.4 +/- 1.0. Forty-two patients had stenosis at a new site, 7 had restenosis, and 27 had no new stenoses.(ABSTRACT TRUNCATED AT 250 WORDS)

Morphological and quantitative angiographic analyses of progression of coronary stenoses. A comparison of Q-wave and non-Q-wave myocardial infarction.

BACKGROUND: The purpose of this study was to determine differences in coronary stenosis severity and morphology and time course of progression between Q-wave and non-Q-wave myocardial infarction (MI). METHODS AND RESULTS: We studied 32 patients with new Q-wave MI and 38 patients with new non-Q-wave MI who underwent coronary angiography both before and after MI without interval revascularization procedures. Quantitative coronary angiographic analysis was performed by the caliper method, and morphological analysis of coronary angiograms was obtained before and soon after acute MI. Before infarction, the stenosis severity at the site of future MI was worse in Q-wave (44 +/- 25%) versus non-Q-wave (23 +/- 35%) MI patients (P < .01). Eccentric and irregular plaques were more common in Q-wave MI patients (18 of 32, 56%, versus 5 of 38, 13%; P < .001). Non-Q-wave MI patients were more frequently found to have significant collaterals after MI compared with Q-wave MI patients (18 of 38, 47%, versus 1 of 32, 3%; P < .001) despite no difference in post-MI stenosis severity. Analysis according to time interval after pre-MI angiography showed that 9 of 11 patients (82%) with Q-wave MI < 18 months later had a stenosis of > or = 50% versus 7 of 21 (33%) with an interval > 18 months (P < .05). By comparison, non-Q-wave MI patients tended to fall into two categories regardless of time of progression: Either minimal or no stenosis (< 20%) or else a severe stenosis (> 70%) was typically present. CONCLUSIONS: The atheromatous plaque substrate is different in Q-wave and non-Q-wave MI. Non-Q-wave MI occurs typically at a site shown by pre-MI angiography to involve either minimal luminal narrowing or a severe stenosis before MI, which is usually nonulcerated. By comparison, Q-wave MI follows a moderate stenosis in which the plaque is eccentric and ulcerated. Such differences culminate in differences in thrombus lability and collateral development and consequently in different clinical profiles.

Permanent pacemaker placement in chronic atrial fibrillation associated with intermittent AV block and cerebral symptoms.

We examined the hypothesis that a greater than or equal to 2 second pause detected on 24-hour Holter monitoring in patients with persistent atrial fibrillation and complaints of syncope or dizziness lacked sufficient specificity to warrant implantation of a permanent pacemaker. We retrospectively reviewed cases from our 24-hour electrocardiographic (Holter) monitoring data base. A total of 411 consecutive Holter monitoring records demonstrating persistent atrial fibrillation obtained during a 5-year period (1982 to 1987) were examined. One hundred and five (26%) patients had cerebral symptoms (dizziness or syncope) as a primary indication for monitoring 80 (76%) patients were identified with documented ventricular pauses of greater than or equal to 2 seconds. Three hundred and six patients (74%) underwent 24-hour monitoring without cerebral symptoms as an indication and 209 (68%) patients had greater than or equal to 2-second pauses. Clinical information was available in 164 (50 symptomatic and 114 asymptomatic) patients. There were no significant differences in the clinical or Holter findings between the two groups. Of the 50 symptomatic patients, 15 (30%) underwent permanent pacemaker placement and the remaining 35 (70%) were managed conservatively during a mean follow-up of 23 +/- 5 months. Eleven of 15 paced (73%) and 31 of 35 (89%) nonpaced patients experienced resolution of their cerebral symptoms (NS). The sensitivity of Holter monitoring in detecting pauses of greater than or equal to 2 seconds in patients with cerebral symptoms was high (76%), but the specificity (32%) and positive predictive values (28%) were low.(ABSTRACT TRUNCATED AT 250 WORDS)

Significance of the clinical presentation in ventricular tachycardia/fibrillation.

We examined the hypothesis that clinical presentation in patients with sustained ventricular tachycardia/fibrillation (VT/VF) predicts clinical, electrophysiologic (EP) findings and long-term outcome. We included in the study 121 consecutive patients seen in our EP laboratory with documented and inducible sustained VT/VF. Patients were categorized into three groups according to their clinical presentation: (1) cardiac arrest (CA)-53 patients; (2) syncope (S)-20 patients; (3) palpitations/dizziness (P)-48 patients. There were no significant differences in age, sex, or prevalence of underlying heart disease between groups. The left ventricular ejection fraction (LVEF) was significantly lower for patients with CA (mean +/- S.D.; 31 +/- 14%) or S (30 +/- 11%) when compared with P (39 +/- 15%) (p less than 0.05). Induction of VT/VF required a more aggressive stimulation protocol (three extrastimuli) in patients with CA (53%) when compared with patients with S (30%) or P (29%) (p less than 0.05). The cycle length of the induced VT was shorter for CA (239 +/- 64 msec) patients as compared with the S (294 +/- 67 msec) or the P (319 +/- 94 msec) patients (p less than 0.01). Polymorphic VT or VF was induced in 28% of CA patients, in 9% of S patients, and in 12% of P patients (p less than 0.05). There were significantly more sudden deaths observed during the 4-year follow-up interval in patients presenting with CA compared to the P group (p less than 0.05). The 4-year survival was 67 +/- 8% for P, 45 +/- 15% for S, and 45 +/- 10% for CA patients (N.S.).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical predictors of electrophysiologic findings in patients with syncope of unknown origin.

Unexplained syncope is a common medical problem. Intracardiac electrophysiologic studies (EPS) have been used to uncover the underlying arrhythmic mechanisms. Electrophysiologic studies are especially helpful in the management of patients with inducible tachyarrhythmias, but is of limited usefulness in those with normal EPS findings. We investigated whether clinical and noninvasive laboratory variables can predict the results of EPS in 89 patients with unexplained syncope. The prevalence of inducible ventricular tachycardia (VT) was 15%; supraventricular tachycardia, 15%; bradyarrhythmias, 41%; and normal EPS, 29%. We used multivariate discriminant function analysis to predict the results of EPS. The variables selected for identification of patients with inducible VT by this analysis include New York Heart Association (NYHA) functional class, gender, digitalis use, nonsustained VT, and atrial fibrillation. Based on our statistical model, performing EPS on 45% of the patients with unexplained syncope would result in a 90% sensitivity in detecting patients with inducible VT. The variables selected for identification of patients with normal EPS findings include: New York Heart Association functional class, heart disease, digitalis use, and intraventricular conduction. Based on this model, it would require that all but 12% of patients with unexplained syncope be studied to achieve a 90% predictive accuracy for identification of patients with normal EPS. During follow-up, recurrence rates for the different EPS categories did not differ significantly. The five-year cumulative survival among the EPS groups were as follows: VT, 37% +/- 28%; SVT, 90% +/- 9%; bradyarrhythmias, 71% +/- 10%; and normal EPS, 96% +/- 4%. Survival of the VT group differed significantly from that of the normal group. In patients with unexplained syncope, EPS findings can be predicted from clinical and noninvasive laboratory data. Mortality during follow-up relates to EPS findings.

Findings on routine right heart catheterization in patients with suspected coronary artery disease.

Whether catheterization of the right heart should be performed routinely in all patients undergoing coronary angiography for assessment of coronary artery disease is controversial. To objectively assess the utility of routine right heart catheterization, hemodynamic data from 2,178 patients studied for angina having no signs, symptoms, or history of congestive heart failure were analyzed retrospectively. The salient results are as follows: 0.9% patients had unsuspected mitral valve gradients greater than or equal to 5 mm Hg; 0.4% had occult left-to-right shunts; 1% had pulmonary hypertension (pulmonary artery systolic pressure greater than or equal to 40 mm Hg) not attributable to an elevated mean pulmonary capillary wedge pressure (PCWP); 4.8% had PCWP greater than or equal to 18 mm Hg; 6% had cardiac indexes less than or equal to 2.0 L/min/m2, suggesting subclinical left ventricular failure. Overall, 14.5% of patients had at least one abnormal right-sided hemodynamic variable revealed by right heart catheterization. The frequency of abnormalities increased with increasing Canadian Cardiovascular Society grade of angina. Ten percent of grade 1, 14% of grade 2, 15% of grade 3, and 19% of patient 4 patients had at least one abnormality (phi 2 test, p less than or equal to 0.005). It is concluded that the right heart catheterization adds an important dimension to the diagnosis and treatment of patients undergoing coronary angiography for assessment of coronary artery disease and might significantly influence subsequent patient management.

Prevalence of late potentials in patients undergoing Holter monitoring.

UNLABELLED: High-frequency, low-amplitude signals detected in the terminal portion of the surface QRS, called late potentials (LP), have been shown to correlate with inducible sustained ventricular tachycardia and to be absent in normal subjects. We studied LP in 152 patients without a history of sustained ventricular tachycardia who underwent 24-hour Holter monitoring for varying clinical indications (chest pain 21%, syncope 17%, palpitations 32%, dizziness 20%, other 10%). Twenty-one patients (14%) had a positive test. Of the 152 patients, 84 (55%) had complex ventricular arrhythmias and 68 (45%) had simple or no ventricular arrhythmias. Complex ventricular arrhythmias were present in 71% of patients with and in 52% of those without LP. IN CONCLUSION: patients without history of sustained ventricular tachycardia who demonstrate complex nonsustained ventricular arrhythmias on Holter monitoring have a low prevalence of LP; the presence of LP on signal-averaged ECG indicates an electrical property of the heart, which is distinct from complex ventricular arrhythmias detected on Holter monitoring.

Determinants of arrhythmogenic ventricular activity detected on the body surface QRS in patients with coronary artery disease.

The prevalence of arrhythmogenic ventricular activity (AVA) was investigated in 166 patients with coronary artery disease. Thirty patients had documented ventricular tachycardia (VT)/ventricular fibrillation (VF). Bipolar X, Y, Z leads were signal-averaged and filtered with a 40-Hz, bidirectional, high-pass digital filter. The filtered QRS signals were analyzed for the amplitude of the last 40 and 50 ms; duration of low-amplitude potentials (less than 40 microV) in the terminal portion; and duration of the filtered QRS. A positive AVA test result was defined as the presence of 2 or more abnormal indexes. Of the 30 patients with VT/VF, 66% had positive AVA test results (AVA-positive patients). Of the 136 patients without VT/VF, 25% had positive AVA test results. The following univariate variables showed significant correlation with an AVA-positive test: age, previous myocardial infarction, previous VT/VF, left ventricular wall motion abnormalities and left ventricular ejection fraction. Multivariate stepwise discriminant function analysis revealed that the presence of previous myocardial infarction and history of sustained VT/VF were the only independent determinants of AVA. During electrophysiologic studies, sustained VT/VF could be induced in 77% of the AVA-positive patients (24 of 31) and in 30% of the AVA-negative patients (3 of 10). The survival probabilities for 6, 12 and 18 months of follow-up were 92%, 85% and 85% for the AVA-positive and 97%, 92% and 90% for the AVA-negative patients. Our findings support the concept that a positive AVA test result reflects areas of delayed ventricular activation. The areas of delayed ventricular activation are associated with previous myocardial injury and scar tissue and serve as an anatomic basis for reentry.(ABSTRACT TRUNCATED AT 250 WORDS)

Relation of ventricular premature beats to underlying heart disease.

The relation between ventricular premature beats (VPBs) and physiologic disease was investigated in 305 patients who had 24-hour Holter monitoring tests, cardiac catheterization and angiography. Both frequency and Lown class of VPBs were measured. Analyses showed that occurrence of VPBs at an average frequency of more than 2 per hour or occurrence of complex VPBs (Lown class greater than 2) have the highest association with the presence and severity of cardiac disease. Using these criteria, VPB severity was then compared with extent of ventricular wall motion abnormality (right anterior oblique projection segments), ejection fraction, end-diastolic pressure, category of disease (normal, coronary artery disease [CAD], valvular heart disease, dilated cardiomyopathy), age and severity of CAD (major coronary arteries with greater than 75% diameter reduction). Severe VPBs defined either by complexity or frequency were significantly correlated with extent of wall motion abnormality, ejection fraction, category of disease and age. Severe VPBs were not significantly correlated with end-diastolic pressure or severity of CAD. Discriminant analysis then showed that in addition to wall motion abnormality and ejection fraction, category of disease and age are independently correlated with VPB severity.

Sleep and ventricular arrhythmias.

Sleep is usually associated with a reduction in the frequency of ventricular arrhythmias. We analyzed 1260 24-hour Holter recordings exhibiting ventricular ectopy and identified 50 patients who had significant increases in sleep-related ectopy. This study group was compared to an age, sex, and 24-hour ventricular ectopic frequency matched control group. There were 21 females and 29 males with a mean age of 64 years in each group. During sleep, the study patients had more frequency of ventricular ectopy per hour than did controls (mean +/- SEM; 143.2 +/- 30.7 vs 62.9 +/- 16.3; p less than 0.005). The study group had fewer daytime ventricular premature beats per hour than did the control patients (45.2 +/- 13.6 vs 67.7 +/- 13.8; p less than 0.05). The study patients also exhibited a significant sleep-related increase in complexity of ventricular arrhythmias (chi 2 = 22.1; p less than 0.001) and the control group a decrease (chi 2 = 19.1; p less 0.001). Nocturnal heart rates were slower than daytime rates in both the study (69.4 +/- 14.5 vs 79.2 +/- 12.2 bpm; p less than 0.005) and control groups (75.5 +/- 15.8 vs 82.6 +/- 16.4 bpm; p less than 0.005), without significant differences between the two groups. No significant differences in clinical and ECG characteristics of the study and control groups were found regarding presence or type of organic heart disease, pulmonary disease, hypertension, medication use, intraventricular conduction delay, abnormal Q waves, ventricular hypertrophy, or QT prolongation. Neurologic abnormalities (60% vs 28%; chi 2 = 9.38 p less than 0.005), in particular cerebrovascular disease (30% vs 14%; chi 2 = 7.56; p less than 0.01), were significantly more common in the study group. We have identified a subgroup of individuals with ventricular ectopy who increase the frequency and complexity of premature ventricular beats during sleep. The higher prevalence of neurologic disease in these individuals suggests a neurologic or neurohumoral mediation of these arrhythmias.

Quantitative analysis of the high-frequency components of the terminal portion of the body surface QRS in normal subjects and in patients with ventricular tachycardia.

Quantitative analysis of the high-frequency components of the terminal portion of the surface QRS was performed in 42 normal subjects (group 1, ages 18-67 years, mean +/- SEM 34.7 +/- 2.2 years) and in 12 patients with symptomatic, sustained ventricular tachycardia (VT) (group 2, ages 48-76 years, mean 59 +/- 2.3 years). Signal averaging and high-pass, bidirectional digital filtering were used for analysis. The total duration of the QRS, the duration of the low-amplitude signals (less than 40 microV) in the terminal portion of the QRS and the amplitude of the signals in the last 40 and 50 msec of the QRS were measured at filter settings of 25 and 40 Hz. Reproducibility of the measurements was tested in 15 normal subjects by comparing results obtained from two consecutive recordings. Significant differences were found between normal subjects and VT patients for all four indexes at both 25- and 40-Hz filters. Specific values for each of the indexes were identified at the 40-Hz filtering, which could separate normal subjects from VT patients (20 microV for the amplitude of last 40 msec; 30 microV for the amplitude of last 50 msec; 120 msec for the total duration; and 39 msec for the low-amplitude signal of the filtered QRS). Using these values for the four indexes, respectively, 90%, 98%, 100% and 90% of the normal subjects and 83%, 83%, 58% and 83% for the VT group were correctly classified. The results show that the high-frequency analysis of the signal-averaged body surface QRS is a reliable, reproducible, noninvasive method for distinguishing patients with VT from normal subjects.