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Modern coronary revascularization therapies, coronary artery bypass graft (CABG) surgery and percutaneous coronary intervention (PCI), continue to evolve and are widely applied. However, for patients with mild stable angina, or those who are asymptomatic with angiographically documented coronary artery disease (CAD), no survival benefit or reduction in the incidence of myocardial infarction has been demonstrated with CABG or PCI, except in the case of subgroups with angiographically determined high risk due to extensive multivessel disease with depressed LV function or left main CAD. At the same time, medical therapy continues to advance, with demonstrable benefit in both primary and secondary prevention of atherosclerotic coronary disease events. Patients with type 2 diabetes mellitus, at increased risk for adverse cardiac events, have been shown to benefit from these approaches as well. However, in asymptomatic or mildly symptomatic patients with documented ischemia and angiographically significant CAD, the incremental benefit-or hazard-associated with early revascularization superimposed on aggressive medical and risk factor modification therapies is unknown. We discuss the background and rationale for investigating the impact of early revascularization in patients with diabetes and CAD.

The influence of diabetic treatment status on long-term outcome after percutaneous coronary intervention (PCI) is unclear. Previous reports have suggested that patients who receive insulin treatment have worse long-term outcome compared with patients who do not need insulin. To determine the influence of diabetes treatment status on outcome after PCI, patients with diabetes mellitus who underwent successful PCI from January 1, 1996, to June 30, 2001, were divided into 2 groups based on whether or not they required insulin; patients with shock or recent (< or =7 days) myocardial infarction were excluded. Cox proportional hazards models were utilized to estimate the association between diabetes treatment status and long-term survival. One thousand one hundred four eligible diabetic patients were identified and divided into those treated with insulin (418 patients; median follow-up 35.5 months) and those treated with either an oral agent or diet alone (686 patients; median follow-up 27.9 months). Insulin-treated patients were less likely to be men, and had more previous coronary revascularizations, prior myocardial infarctions, and congestive heart failure on presentation. Angiographic and procedural characteristics were comparable. Unadjusted survival curves were constructed, demonstrating that insulin treatment was associated with worse survival than noninsulin treatment (p = 0.001). After adjusting for differences in baseline characteristics, insulin treatment did not adversely effect survival (odds ratio 1.10, 95% confidence intervals 0.77 to 1.58). Thus, among diabetic patients who underwent successful PCI, patients treated with insulin had worse survival. After adjusting for differences in baseline characteristics, insulin treatment was not independently associated with worse survival.

Use of catheter-based and surgical coronary revascularization has steadily increased in North America. Introduction of catheter-based "new devices," including intracoronary stents, has expanded the range of patients who can be treated with percutaneous approaches. We sought to address trends in the practice of catheter-based and surgical coronary revascularization during 1989 to 1997. The 17 North American institutions participating in the NHLBI Bypass Angioplasty Revascularization Investigation (BARI) periodically completed a 5-working day survey of all surgical and catheter-based coronary revascularizations. Data collected included patient demographics, vessel disease, prior interventions, and use of new devices or minimally invasive surgical techniques. The proportion of all procedures that were catheter based (vs surgical) increased from 52.1% in 1989/1990 to 62.0% in 1997 (p0.001). Among surgically treated patients, prevalence of prior bypass surgery decreased from 13.4% in 1989/1990 to 7.5% in 1997 (p0.001). In 1997, 3% of surgical procedures used minimal incisions or were performed without cardiopulmonary bypass. Among patients undergoing catheter-based intervention, prevalence of left main disease increased from 2.2% to 5.7% (p0.001), myocardial infarction within 24 hours increased from 2.4% to 9.7% (p0.001), and prior bypass surgery increased from 16.2% to 20.8% (p = 0.056). Use of new devices increased from 11.6% of catheter-based procedures in 1990 to 67.0% in 1997 (p0.001). Compared with the early 1990s, catheter-based revascularization is currently more commonly used for patients with acute myocardial infarction, prior bypass surgery, or severe left main narrowing. These trends are likely due to the proliferation of new devices, especially intracoronary stents, since the mid 1990s.

This report describes the baseline angiographic findings in the Bypass Angioplasty Revascularization Investigation (BARI) 2 Diabetes (BARI 2D) trial, a randomized study that was initiated after the original BARI trial (BARI 1). Unlike BARI 1, which compared coronary artery bypass graft surgery with coronary angioplasty (percutaneous coronary intervention) in patients with and without diabetes, BARI 2D is investigating early versus deferred revascularization as needed in selected patients with type 2 diabetes mellitus and significant stable coronary artery disease (CAD). This analysis included 1,773 patients without previous procedures. The intended mode of revascularization, percutaneous coronary intervention or coronary artery bypass graft surgery, was specified before randomization. Angiographic findings in those randomized to revascularization versus medical treatment were similar. Overall, the mean number of lesions >or=20% diameter stenosis was 4.6 +/- 2.3, and the myocardial jeopardy index was 46 +/- 24%. Patients selected for the coronary artery bypass graft stratum had a higher mean number of lesions >or=20% diameter stenosis (5.7 vs 4.0, p

The Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) is a National Institutes of Health (NIH)-sponsored randomized clinical trial that evaluates treatment efficacy for patients with type 2 diabetes mellitus and angiographically documented stable coronary artery disease. Using a 2 x 2 factorial design, BARI 2D compares revascularization combined with aggressive medical treatment versus aggressive medical treatment alone; simultaneously, BARI 2D compares 2 glycemic control strategies, insulin sensitization versus insulin provision. All patients have goals of glycosylated hemoglobin values

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Between 1960 and 1973, a total of 104 patients at the Mayo Clinic had a diagnosis of idiopathic dilated cardiomyopathy on the basis of clinical and angiographic criteria; these patients were followed up for 6 to 20 years. Twenty-one percent of the patients had a history of excessive consumption of alcohol, 20 percent had had a severe influenza-like syndrome within 60 days before the appearance of cardiac manifestations and 8 percent had had rheumatic fever without involvement of cardiac valves several years before; thus, possible etiologic risk factors of infectious-immunologic type may be important. Eighty patients (77 percent) had an accelerated course to death, with two thirds of the deaths occurring within the first 2 years. Twenty-four patients (23 percent) survived, and 18 of them had clinical improvement and a normal or reduced heart size. Univariate analysis at the time of diagnosis revealed three factors that were highly predictive (p less than 0.01) of the clinical course: age, cardiothoracic ratio on chest roentgenography and cardiac index. Systemic emboli occurred in 18 percent of the patients who did not receive anticoagulant therapy and in none of those who did; thus, anticoagulant agents should probably be prescribed unless their use is contraindicated.

Serial serum glutamic oxaloacetic transaminase (SGOT) determinations and electrocardiograms were obtained from 40 patients after myocardial revascularization procedures for treatment of severe coronary artery disease. SGOT was measured in units (U), with 1 U equalling 1 micromole of oxaloacetic acid formed per minute at 37C. Twenty-three patients had initial SGOT levels lower than 100 U/liter (mean, 50 U/liter) on the first postoperative day, followed by a gradual decrease by postoperative day 7 (mean, 25 U/liter). The electrocardiographic changes in this group were confined to repolarization abnormalities. Seventeen patients had initial SGOT levels higher than 100 U/liter or a secondary increase greater than 50 percent of the preceding value. Seven of these 17 patients had electrocardiographic evidence of a postoperative myocardial infarction, only 3 of which were clinically recognized. In 4 additional patients the diagnosis of myocardial infarction was suspected on the basis of an abnormal enzyme pattern and temporally related symptoms suggesting myocardial ischemia, although the electrocardiographic changes were nonspecific. Five patients had unexplained increases in the level of SGOT. The incidence of postoperative myocardial infarction was greater in the present series than is usually emphasized. This finding must be considered in selecting individual patients for operation and in evaluating the postoperative clinical result.

Regional wall dynamics of the left ventricle before and after sublingual administration of 0.6 mg of nitroglycerin were determined from left ventricular angiograms in 27 patients undergoing coronary arteriography. Regional wall dynamics were quantitatively measured from 60/sec determinations of wall thickness and derived peak rate of systolic wall thickening (peak dTw/dt) in selected sites of the left ventricle. A total of 70 regions were studied. Analysis of the same segment before and after administration of nitroglycerin revealed that the mean change in peak dTw/dt was +1.97 cm/sec in segments with an initial peak dTw/dt of less than 5 cm/sec, in contrast to a change of +0.66 cm/sec in segments with an initial control value of 5 cm/sec or greater. Akinetic or dyskinetic areas did not show improvements after nitroglycerin. In 11 left ventriculograms, an area that was initially hypokinetic manifested an increase in rate of wall thickening after nitroglycerin. The mean increase in peak dTw/dt in anterior segments with electrocardiographic evidence of myocardial infarction was 0.18 cm/sec (P less than 0.05) after nitroglycerin, compared with a mean change of 1.33 cm/sec in anterior segments without such evidence. This study presents evidence for a regional myocardial response to nitroglycerin with differing responses within the same ventricle apparently depending upon the functional state of the underlying myocardium.

Aortocoronary saphenous vein grafts from 40 patients (total 62 grafts) were studied at autopsy. The earliest change seen was the insudation of blood constituents into the vein intima. Occluding thrombi were seen in six grafts from short-term survivors, and one organized thrombus was seen in a graft from a long-term survivor (28 months). Various degrees of intimai thickening were seen in grafts from all patients surviving for more than a month; this had progressed to diffuse occlusion in three cases. Gross and microscopic findings correlated well with postmortem angiographic findings in the long-term survivors. Electron microscopic examination showed smooth muscle cells, collagen fibers and ground substance in the thickened intima. Fibroblasts were not a feature of this thickening. Increased permeability of the graft endothelium, due to injury or hemodynamic factors, may result in exposure of medial smooth muscle cells to certain plasma factors and thus promote smooth muscle cell hyperplasia as has been produced in certain experimental models.

Serial preoperative and postoperative electrocardiograms and vectorcardiograms were obtained in 500 patients undergoing saphenous vein aortocoronary artery bypass graft surgery. Evidence of transmural myocardial infarction was found early postoperatively in 67 patients (13 percent). Age and sex distributions, number of vessels diseased or vessels grafted, and preoperative and postoperative New York Heart Association functional classification (mean follow-up, 26 months) did not differ in the groups with and without infarction. Increased duration of cardiopulmonary bypass time (more than 120 minutes) was slightly greater in the group with infarction (P smaller than 0.05). Multivariate analysis revealed that 60 percent of patients in the group with infarction were identified by a 1st day serum glutamic oxaloacetic transaminase value greater than 100 U/liter; however, for each such patient identified, there was approximately one false positive result. Use of other values (creatine phosphokinase, cardiopulmonary bypass time and total anoxic rest time) did not improve discrimination. Twenty-five percent of all transmural infarctions occurred within the zone of myocardium supplied by a diseased ungrafted artery. In 32 patients with early evidence of transmural mycardial infarction in a zone of myocardium supplied by a grafted artery, postoperative angiography showed as many with patent as with occluded grafts. Of 154 patients in the group without infarction who had early postoperative graft angiograms, 30 (19 percent) had one graft occluded and yet no evidence of transmural infarction by our criteria. Therefore, early postoperative evidence of transmural myocardial infarction as defined in this study is an unreliable indicator of the status of the graft supplying the zone of infarction.

Verapamil has a negative inotropic action in isolated cardiac muscle. Its effects on left ventricular function were tested in 25 patients with suspected coronary artery disease. A double-blind, randomized, placebo-controlled study design was used. Verapamil (0.2 mg/kg over 10 minutes) significantly lowered mean arterial pressure (from 105 to 89 mm Hg) while increasing the cardiac index (from 2.8 to 3.1 liters/min/m 2 ). No statistically significant effect was seen on heart rate, left ventricular end-diastolic pressure or end-systolic volume index, ejection fraction, peak rates of systolic wall thickening or diastolic wall thinning, or percentage of hemiaxial shortening. However, there was a small increase in the left ventricular end-diastolic volume index (from 94 to 102 ml/m 2 ). Important findings were a reduction in systemic vascular resistance (from 39 to 30 U·m 2 ), an increase in left ventricular end-diastolic volume index consistent with a negative inotropic effect, and no evidence of improved regional wall dynamics in portions of the left ventricular wall considered hypokinetic because of myocardial ischemia.

At cardiac catheterization, 16 patients with coronary artery disease (14 men and 2 women) were allocated by a random, double-blind method to intervention with placebo (saline solution) or verapamil (0.2 mg/kg total by bolus and by 10-minute infusion). In all patients, resting and exercise (3 minutes with a bicycle at 150 kg-m/min) hemodynamic values were obtained during a control period and after intervention. Subsequent left ventriculography and coronary arteriography revealed a mean ejection fraction of 52 and 53% and the mean number of diseased vessels (3-vessel scale) of 2.1 and 1.5 in the placebo and verapamil groups, respectively. In both groups of patients, exercise induced significant increased heart rate, mean arterial pressure, left ventricular end-diastolic pressure and cardiac index. Verapamil increased the heart rate and decreased the mean arterial pressure at rest and the arterial pressure during exercise. It did not affect exercise-induced increases in left ventricular enddiastolic pressure or cardiac index. These results support a role for peripheral mechanisms mediating the antianginal effects of verapamil.

Mitral regurgitation was found in 6 percent (46 patients) of all patients with a secundum atrial septal defect who were operated on during a 13 year period at the Mayo Clinic. The presence of two separate systolic murmurs, expiratory splitting of the second heart sound and evidence of overactivity of both the right and the left ventricles were the most reliable clues to the diagnosis. Nineteen of 39 patients (49 percent) had increased pulmonary arterial pressure, but only 3 patients had obstructive pulmonary vascular disease. Electrocardlographic findings rarely helped differentiate the patient who had a secundum atrial septal defect and associated mitral regurgitation from the one who had an isolated septal defect. The causes for the mitral regurgitation varied. Six patients had rheumatic valvulitis, 8 had redundant mitral valve tissue with prolapsing leaflets, 9 patients had two or more causes, and in 18, no cause for the regurgitation could be found.

Twenty-six patients with tetralogy of Fallot and Potts anastomosis were evaluated 6 to 18 years after creation of the anastomosis. Thirteen of the 26 patients had evidence of moderate to severe pulmonary vascular obstructive disease, as indicated by a high ratio of pulmonary to systemic vascular resistance. Evidence of isolated right ventricular hypertrophy on the electrocardiogram in the presence of severe pulmonary hypertension and the absence of a continuous murmur indicated severe pulmonary vascular obstructive disease. In patients with low pulmonary arterial pressure, the prognosis of complete repair was excellent. In patients with severe pulmonary hypertension, however, the operative results were poor and directly related to the degree of elevation of pulmonary resistance. For the proper estimation of pulmonary vascular resistance, catheterization of both the left and right pulmonary arteries is essential. The calculated pulmonary flow is almost always overestimated when the pulmonary arterial oxygen saturation is obtained only from the pulmonary artery on the side of the Potts anastomosis. Our experience indicates that a pulmonary to systemic resistance ratio of 0.6 or greater is always associated with severe pulmonary vascular disease. The data suggest that the risk of severe pulmonary vascular disease developing after Potts anastomosis is high, especially in the patient in whom the diameter of the anastomosis is large. There is also evidence that the diameter of the anastomosis tends to increase with time.

Twenty cases of partial anomalous pulmonary venous connection without an associated atrial septal defect have been reviewed in regard to clinical findings, hemodynamic and angiographic observations and surgical therapy. Of particular interest was the finding of a correlation between the QRS configuration in lead V 1 and the site of drainage of the anomalous pulmonary venous connection. The presence of an rsR′ QRS pattern in this lead was most frequently associated with drainage of the anomalous pulmonary veins into the superior vena cava or right atrium, whereas a terminal S wave in this lead was found only in those patients with an anomalous connection of the pulmonary veins to the inferior vena cava. Large left to right shunts with pulmonary-systemic flow ratios of greater than 2.0 were noted in 7 patients, all of whom had a complete anomalous connection of one lung.

Ventricular aneurysms developed in 3 of 25 patients with idiopathic hypertrophic subaortic stenosis who underwent resection of hypertrophic muscle from the left ventricular outflow tract through a combined aortic and left ventricular approach. Two large aneurysms developed rapidly and were possibly attributable to interruption of coronary blood supply. A third smaller aneurysm was located intramurally; it has not produced complications over a 5 year period.

AORTA-TO-CORONARY ARTERY SAPHENOUS VEIN BYPASS GRAFTS: COMPLETE VERSUS INCOMPLETE REVASCULARIZATION Jose L. Assad-Morell, MD; Robert L. Frye, MD, FACC; Daniel C. Connolly, MD, FACC; George D. Davis, MD; Robert B. Wallace, MD; Gordon K. Danielson, MD, FACC, Mayo Clinic and Mayo Foundation, Rochester, MN. A series of 159 patients (pts) with postop. graft angiograms (PGA) l-42 mo (median 11 mo) after coronary surgery were studied. To evaluate the completeness of myocardial revascularization, a vessel was considered left ungrafted (VLU) if (1) it had an obstruction >50% and was ungrafted or (2) the graft to the artery was occluded on the PGA. Four groups evolved: Gp I (44 pts), 0 VLU; Gp II (68 pts), 1 VLU; Gp III (35 pts), 2 VLU; and Gp IV (12 pts), 3 VLU. The clinical results in each group were correlated with the number of vessels diseased (VD). When revascularization was complete, of the 44 pts in G I, 36 pts (12, I-VD; 14, 2-VD; 10, 3-VD) were pain-free 3 82%). In 9 II, the 22 with 3-VD showed significant improvement, as 18 (77%) were pain-free (such pts had 2 normally functioning grafts); the 36 with 2-VD were equally divided in the pain-free, improved, and unimproved categories (all had 1 graft patent); of the 10 with l-VD (only graft occluded), only 2 were painfree. In Gp III, 7 (64%) of the 11 pts with 2-VD (all grafts occluded) were unimproved, while of the 24 pts with 3-VD, 12 had improved, and 4 (17%) were pain-free (these pts had only 1 patent graft). In *Iv (12 pts with 3-VD), 6 were unimproved, and only 1 was pain-free. Thus, by the evaluation of postop. symptoms at PGA, a high correlation existed between complete relief of angina and a complete revascularization. Such an approach allows a more precise analysis of whether the pt at symptom evaluation has remaining areas of myocardium with angiographic evidence of ischemia. FUNCTIONAL INSULATION OF THE RIGHT BUNDLE BRANCH John C. Bailey, MD; David A. Lathrop, MS; Charles Fisch, MD, FACC, Krannert Institute of Cardiology and Indiana University School of Medicine, Indianapolis, Indiana. Intracellular microelectrodes were used to assess electrotonic interaction between the intramyocardial segment of the canine right bundle branch (RBB) and the surrounding septal muscle (RVM) as a possible cause of RBB block aberrancy. A total of 15 in vitro experiments were performed. The RBB does not supply conducting fibers directly to the RVM in this segment, and by use of appropriate stimulus intensities, we stimulated the RBB without activating RVM and stimulated RVM without activating RBB. RBB and RVM were stimulated at similar constant rates, but independently. Stimulation of RVM was programmed to occur at numerous points before, during, and following the RBB action potential. There were no changes in RBB resting and action potential, V,, phase 0, RBB conduction time, or action potential duration of RBB measured at 95% repolarization, regardless of the temporal relationship between RVM and RBB activation. Moreover, using a single microelectrode for simultaneous intracellular stimulation and recording, there were no changes in RBB current threshold requirements for all-or-none depolarization (excitability). We conclude that, in this preparation, the proximal canine RBB is functionally insulated, and that the characteristics of conduction in the RBB are not influenced electrotonically by the electrical state of the RVM. MICROELECTRODE STUDY OF BLOCK MECHANISMS IN PURKINJE TISSUE SEGMEWlXi EXPOSED TO A SODIUM-FREE MILIEU Jack P. Bandura, PhD; James R. Wennemark, MD; Daniel A. Brody, MD, FACC, University of Tennessee, Memphis, Tenn. We employed an electrical blocking current in earlier microelectrode studies of block mechanisms. More recently a three chamber perfusion bath was devised in which a single Purkinje bundle can be exposed to three individual superfusates. Using this tri artite chamber, -? the middle chamber is perfused with Na tion (Na+ free Tyrode solureplaced with THAM), producing inactivation of the Purkinje tissue segment contained therein. Segments proximal and distal to the middle chamber are perfused with normal Tyrode, and are fully active. Fibers are electrically stimulated (0.5 2 pulses/set) in the proximal active segment and transmembrane recordings are taken from all three segments of the Purkinje bundle. In a total of ten preparations simple conduction delay, Wenckebach periodicity, 2:l block, and higher grades of block (3:l to complete) were observed. The results indicated that the degree of block obtained was inversely related to the slope of slow diastolic depolarization in the segment distal to the blocked region. Slow diastolic depolarization was a principal factor in sustaining periodic impulse conduction for two reasons: (1) it allowed a progressive rise of the resting membrane potential toward threshold at the distal block boundary; (2) there was augmentation of the transmitted electrotonic potential in accordance with voltage dependent changes in membrane resistance. This basically different method of producing block lends further support to the previously formulated hypothesis that conduction delay through a blocked segment of F'urkinje tissue is electrotonic, and that slow diastolic depolarization is of key significance in the maintenance of impulse transmission. DETERMINANTS OF REVERSIBLE ASYNERGY: THE NATIVE CORONARY CIRCULATION Vidya S. Banka, MD; Monty Bodenheimer, MD; Richard H. Helfant, MD. FACC, Presbyterian-University of Pennsylvania Medical Center, Philadelphia, Pennsylvania To determine the effect of native coronary circulation on reversibility of asynergy, ventriculograms before and after sublingual nitroglycerin were performed in 51 patients with coronary artery disease. Severity of stenotic lesions and caliber of the distal coronary vessels were determined by comparison with external catheter tip diameter corrected for magnification. Of 42 asynergic zones (AZ) associated with 190% proximal coronary occlusion (occl), 27 (64%) were akinetic or dyskinetic while 11 of 38 (29%) with 90% occl compared to only LO of 38 (26%) with 90% occl (p 9& proximal stenoses are associated with severe asynergy which is less likely to be reversible compared to asynergy with 90% occlusion, coronary collaterals significantly improve the chances of reversibility and thus appear to serve a protective function; however, caliber of the distal vessel per se does not affect reversibility. January 1975 The American Journal of CARDIOLOGY Volume 35 121