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OBJECTIVES: The study compared procedural outcomes and long-term survival for patients undergoing percutaneous coronary intervention (PCI) of a chronic total coronary artery occlusion (CTO) with a matched non-CTO cohort to determine whether successful PCI of a CTO is associated with improved survival. BACKGROUND: Percutaneous coronary intervention of a CTO is a common occurrence, and the long-term survival for patients with successful PCI of a CTO has not been clearly defined. METHODS: Between June 1980 and December 1999, a total of 2,007 consecutive patients underwent PCI for a CTO. Utilizing propensity scoring methods, a matched non-CTO cohort of 2,007 patients was identified and compared to the CTO group. The cohorts were stratified into successful and failed procedures. RESULTS: The in-hospital major adverse cardiac event (MACE) rate was 3.8% in the CTO cohort. Technical success has improved over the last 10 years (overall 74.4%, slope 1.0%/yr, p = 0.02, R2 = 49.9%) as did procedural success (overall 69.9%, slope 1.2%/yr, p = 0.02, R2 = 51.5%) without a concomitant increase in in-hospital MACE rates (slope 0.1%/yr, p = 0.7). There was a distinct 10-year survival advantage for successful CTO treatment compared with failed CTO treatment (73.5% vs. 65.1%, p = 0.001). The CTO versus non-CTO 10-year survival was the same (71.2% vs. 71.4%, p = 0.9). Diabetics in the CTO cohort had a lower 10-year survival compared with nondiabetics (58.3% vs. 74.3%, p < 0.0001). CONCLUSIONS: These data represent follow-up of the largest reported series of patients undergoing PCI for a CTO. The 10-year survival rates for matched non-CTO and the CTO cohorts were similar. Success rates have continued to improve without an accompanying increase in MACE rates. A successfully revascularized CTO confers a significant 10-year survival advantage compared with failed revascularization.

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OBJECTIVE: To assess optimal control of blood anticoagulation to maximize antithrombotic protection after mechanical cardiac valve replacement. DESIGN: A population-based study of 96 patients with a mean follow-up of 7.7 years (range, 1 month to 23 years) was performed in Olmsted County, Minnesota, and 10,301 prothrombin time (PT) ratios were determined after mechanical heart valve replacement. MATERIAL AND METHODS: PT ratios were analyzed in a new time-dependent Cox proportional-hazards model by defining an algorithm for comparing variability in PT ratios at each month of follow-up and relating these to thromboembolic events. The new method was compared with several conventional time-independent definitions. RESULTS: During 740 person-years of follow-up, 19 of 96 patients (20%) had 27 thromboembolic events. Of these 19 patients, 8 (42%) had events within 3 months after valve replacement. Freedom from any thromboembolic event was 72% at 15 years. The event rate was high (7.5% per year) during high variability and low (0.9% per year) during low variability in the PT ratio. This relationship was lost when time dependence was removed. More PT ratios were less than 1.5 during high (27%) than during low (19%) variability. Several conventional definitions of adequacy of anticoagulation that averaged PT ratios before a thromboembolic event or throughout follow-up or that compared the proportion of PT ratios above or below a fixed ratio did not define or only partially defined different thromboembolic risks. CONCLUSION: Periods of high and low variability of PT ratios define high and low risk of thromboembolism, respectively.

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Direct percutaneous transluminal coronary angioplasty (PTCA) has emerged as effective reperfusion therapy for acute myocardial infarction; however, few data exist on its use in octogenarians. Thrombolytic therapy in this age group has reduced early mortality from approximately 30% to 20%, but is associated with an increased risk of stroke and major hemorrhage. We analyzed the acute and long-term results of direct PTCA performed on patients aged > or = 80 years at our institution between 1980 and 1993. The study group consisted of 55 patients (mean patient age 83.3 +/- 2.3 years). Infarcts were anterior in 27 patients (49%). Cardiogenic shock was present in 6 patients (11%). The mean time to reperfusion was 4.3 +/- 2.8 hours. Direct PTCA was successful in 53 patients (96%). There were no emergent bypass operations. In-hospital death occurred in 9 patients (16%), including 4 of 6 (67%) presenting in cardiogenic shock and 5 of 49 (10%) who were hemodynamically stable on presentation. Repeat PTCA for recurrent ischemia was performed in 6 patients (11%). There were no strokes during hospitalization. Bleeding complications requiring blood transfusion were present in 4 patients (7%). Thirty-day mortality was 16% and 1-year actuarial survival was 67%. Direct PTCA in patients aged > or = 80 years can be performed safely with a high procedural success rate. The clinical outcome with PTCA in this high risk subset of patients compares favorably with that reported previously for both thrombolytic and medical therapy.

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Balloon angioplasty (PTCA) of left main (LM) stenoses is limited by frequent clinical restenosis. Directional coronary atherectomy (DCA) may be an effective alternative to PTCA due to its ability to achieve a greater postprocedural luminal diameter when treating bulky, eccentric plaques and aorto-ostial lesions. We analyzed the acute and long-term results following 24 DCA procedures in 22 patients with "protected" LM lesions. Acute success (residual stenosis < or = 40%, no major ischemic complications) was 88% overall, 100% in 13 planned procedures, and 73% in 11 adjunctive DCA procedures that followed suboptimal PTCA. Mean LM stenosis was reduced from 86% to 13% (P < 0.01). There were no procedural complications directly attributed to DCA. At a mean of 24 +/- 3 months, the clinical restenosis rate was 16%, survival was 100%, and event-free survival (freedom from death, MI, or repeat lesion-related interventions) was 89%. We conclude that DCA in protected LM lesions (1) can achieved excellent angiographic results with low procedural complication rates, (2) may succeed where PTCA yields suboptimal results, and (3) may provide late clinical outcomes superior to those of balloon angioplasty.

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To assess the effectiveness of angiotensin converting enzyme inhibition in a proliferative porcine coronary restenosis model, 35 animals received orally administered trandolapril (10 mg) or captopril (200 mg) or no drug (control group) for 6 days before and 28 days after injury by oversized metallic coils in one or more coronary arteries. Twenty arterial lesions in the trandolapril group, 17 in the captopril group, and 18 in the control group were evaluated. There was no significant difference in neointimal thickness or percentage luminal area stenosis for the groups as a whole. However, in quantitative comparisons in which vessel injury score was used as a covariate, the fractional increase in mean neointimal thickness per unit of injury was significantly less for the trandolapril group (p = 0.019) but not for the captopril group when compared with control animals. In this model, neointimal proliferation from arterial injury was inhibited by angiotensin converting enzyme inhibition with trandolapril but only modestly. Such an effect may not be clinically significant.

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Coronary restenosis, a major unresolved problem for percutaneous coronary revascularization procedures, has thus far been resistant to all therapeutic strategies. In part, ineffective treatment or prevention of coronary restenosis may be due to reliance on a conceptualization of the restenosis process that incompletely reflects the pathophysiologic factors associated with neointimal formation after arterial injury. In a porcine coronary restenosis model, three stages of neointimal growth after arterial injury have been identified: an early thrombotic stage, with platelets, fibrin, and erythrocytes; a cellular recruitment stage, with endothelialization and an infiltration by lymphocytes and monocytes; and a proliferative stage, in which smooth muscle cells migrate into and proliferate within the fibrin-rich degenerating thrombus. Evaluation of basic mechanisms responsible for neointimal formation has been possible with this model. In particular, a direct relationship exists between the depth of arterial injury and subsequent neointimal thickness. This relationship can be used for investigating the efficacy of new therapies. Treatment strategies for restenosis should be directed toward interference with the cellular or humoral events that lead to neointimal formation, with the specific goal of decreasing the neointimal volume. These strategies may include delivery of drugs to the site of arterial injury to limit the amount of early mural thrombus or decreasing subsequent cellular recruitment and proliferation as well as synthesis of extracellular matrix.

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Restenosis is a reparative response to arterial injury occurring with percutaneous coronary revascularization. However, the quantitative characteristics of the relation between vessel injury and the magnitude of restenotic response remain unknown. This study was thus performed to determine the relation between severity of vessel wall injury and the thickness of resulting neointimal proliferation in a porcine model of coronary restenosis. Twenty-six porcine coronary artery segments in 24 pigs were subjected to deep arterial injury with use of overexpanded, percutaneously delivered tantalum wire coils. The vessels were studied microscopically 4 weeks after coil implantation to measure the relation between the extent of injury and the resulting neointimal thickness. For each wire site, a histopathologic score proportional to injury depth and the neointimal thicknesses at that site were determined. Mean injury scores were compared with both mean neointimal thickness and planimetry-derived area percent lumen stenosis. The severity of vessel injury strongly correlated with neointimal thickness and percent diameter stenosis (p less than 0.001). Neointimal proliferation resulting from a given wire was related to injury severity in adjacent wires, suggesting an interaction among effects at injured sites. If the results in this model apply to human coronary arteries, restenosis may depend on the degree of vessel injury sustained during angioplasty.

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Previous studies have shown that tomographic perfusion imaging with technetium-99m sestamibi (RP-30A) can accurately measure the myocardium at risk during acute myocardial infarction. The ability of coronary angiography to predict the wide variability in myocardium at risk was studied in 21 patients with their first acute myocardial infarction. In blinded fashion, two experienced angiographers provided an overall "best estimate" of the percent of left ventricular myocardium at risk considering multiple angiographic variables--infarct-related artery, location of stenosis (proximal or nonproximal), vessel diameter, length, territory and the number and size of proximal branches and collateral vessels. Many of these individual variables showed a significant association with myocardium at risk. The most important angiographic variable was the mean best estimate of the two angiographers (r = 0.89, p less than 0.0001). However, the SEE was large (8.6% of the left ventricle) and angiography significantly (p less than 0.002) overestimated myocardium at risk. When patients with an anterior or an inferior infarct were considered separately, the angiographic best estimate had a weaker correlation with myocardium at risk measured by technetium-99m sestamibi in patients in both groups (anterior infarction r = 0.65, p = 0.04; inferior infarction r = 0.65, p = 0.04. Seven patients with an inferior infarct and myocardium at risk ranging from 7% to 32% of the left ventricle had identical angiographic best estimates. Although angiographic estimates correlate closely with measurements of myocardium at risk in groups of patients, their ability to predict the myocardium at risk in individual patients is limited.

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The risk of perioperative myocardial infarction and death was evaluated in 50 patients (mean age, 68 years) with severe coronary artery disease who underwent a noncardiac operation after revascularization had been achieved by successful percutaneous transluminal coronary angioplasty. Before angioplasty, all patients were thought to be at high risk for perioperative complications on the basis of assessment of clinical variables and findings on specialized diagnostic tests. Of the 50 patients, 31 had Canadian Heart Association class III or IV angina or unstable angina. All patients who underwent functional testing had positive results. At catheterization, 38 patients (76%) had multivessel disease. The 50 patients underwent 54 noncardiac operations at a median of 9 days after angioplasty. The overall frequency of perioperative myocardial infarction was 5.6%, and the mortality was 1.9%. Two nonfatal non-Q-wave infarctions and one fatal Q-wave infarction occurred. In patients who have undergone successful angioplasty for severe coronary artery disease, the risk of major cardiac complications associated with a noncardiac surgical procedure is low.

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OBJECTIVE: To assess the ability of the 12-lead electrocardiogram to estimate infarction size after reperfusion therapy for acute myocardial infarction. DESIGN: The presence or absence of Q waves and the Selvester QRS score obtained before and after hospital discharge were compared with radionuclide estimates of infarction size and ejection fraction at discharge and 6 weeks later, regional wall motion at discharge and 6 weeks later, and myocardial perfusion defect size quantitated with Tc-99m-sestamibi at discharge. SETTING: A tertiary referral center. PATIENTS: A consecutive series of 43 patients with acute myocardial infarction who received acute reperfusion therapy and were assessed using 12-lead electrocardiography, radionuclide angiography, and Tc-99m-sestamibi tomographic imaging before discharge. INTERVENTIONS: All 43 patients received acute reperfusion therapy: 21 patients received intravenous tissue plasminogen activator, and 22 patients underwent primary percutaneous transluminal coronary angioplasty. MAIN OUTCOME MEASURE: The correlation of QRS score and Q waves with three radionuclide estimates of infarction size. RESULTS: A significant correlation was found between myocardial perfusion defect size at discharge and both left ventricular ejection fraction and regional wall motion at discharge and 6 weeks later (r = -0.71 to -0.81; all comparisons, P less than 0.001). Little correlation was found between electrocardiographic findings and radionuclide measurements of left ventricular function and perfusion. Presence or absence of Q waves at discharge was not associated with any difference in ejection fraction, regional wall motion, or perfusion defect at discharge. No correlation was found between QRS score and ejection fraction or myocardial perfusion defect size at discharge. The QRS score at discharge correlated only weakly with regional wall motion at discharge and 6 weeks later. This lack of correlation was unchanged when electrocardiograms obtained after hospital discharge were analyzed. CONCLUSION: Although inexpensive and readily available, the 12-lead electrocardiogram does not appear to provide a reliable estimate of infarction size after reperfusion therapy for acute myocardial infarction.

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Technetium-99m-hexakis-2-methoxy-2-isobutyl-isonitrile (technetium-99m isonitrile) is a new radiopharmaceutical compound that reflects myocardial perfusion. Its kinetics, especially its lack of redistribution after intravenous administration, permits the assessment of changes in myocardial perfusion without delay of therapy. Tomographic images at rest were obtained immediately and 6 to 10 days later in 17 consecutive patients undergoing successful primary angioplasty during their first transmural myocardial infarction. Thirteen patients had anterior infarction. The initial (acute) defect size before angioplasty of 48 +/- 17% of the left ventricle decreased significantly (p less than 0.0001) to 29 +/- 19% on the late scans. There was no correlation between the time to therapy and the reduction in defect size. Twelve of the 17 patients, including 7 of the 11 patients treated after 4 h, demonstrated a definite reduction in the initial defect size. Eight patients with angiographically proved persistent coronary occlusion underwent a similar imaging sequence. The initial defect size in this group remained unchanged on the late scans (24 +/- 16% versus 26 +/- 18%, p = NS). Primary angioplasty is an effective approach toward salvaging myocardium; comparison with thrombolytic drug therapy must await the results of controlled clinical trials.

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Quantitation of perfusion defect size using tomographic imaging with technetium-99m-hexakis-2-methoxy isobutyl isonitrile was performed at the time of hospital discharge in 32 patients with a first myocardial infarction who underwent successful coronary reperfusion within 8 h of the onset of chest pain. Reperfusion was accomplished with thrombolysis or primary coronary angioplasty. Radionuclide angiography was performed at discharge and 6 weeks later. There was a close correlation between perfusion defect size and values for ejection fraction and regional wall motion both at discharge (r = -0.80 and -0.75, respectively) and 6 weeks later (r = -0.81 and -0.81, respectively). There was no overall group difference in ejection fraction between the value at discharge and at 6 weeks; however, five patients had a significant increase (greater than or equal to 0.08) and six had a significant decrease (greater than or equal to 0.08) in ejection fraction. In patients with a significant increase at 6 weeks, ejection fraction was significantly lower at discharge than the value predicted from perfusion defect size (0.37 +/- 0.09 measured versus 0.47 +/- 0.13 predicted, p less than 0.05) and it improved at 6 weeks to near predicted values (0.51 +/- 0.07). In patients with a significant decrease at 6 weeks, ejection fraction was significantly higher at discharge than the value predicted from perfusion defect size (0.60 +/- 0.10 measured versus 0.50 +/- 0.10 predicted, p less than 0.05) and it decreased at 6 weeks to near predicted levels (0.51 +/- 0.09). Left ventricular ejection fraction at the time of hospital discharge is a potentially misleading index of the efficacy of reperfusion therapy for myocardial infarction. In a significant minority (34%) of patients this index does not accurately reflect perfusion defect size, apparently because of the effects of myocardial stunning and compensatory hyperkinesia.

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A patient with symptoms of acute myocardial infarction but ST-segment depression rather than elevation constitutes a clinical dilemma for which few guidelines exist. Herein we describe such a patient, in whom serial tomographic imaging with a new radiopharmaceutical agent, technetium-99m sestamibi, was useful in demonstrating a large area of myocardium at risk and subsequent substantial benefit from acute reperfusion therapy. Because this perfusion agent washes out slowly from the myocardium, imaging can be delayed for several hours; thus, acute reperfusion therapy can be performed without delay. Subsequent imaging, however, will reflect myocardial perfusion at the time of administration of the radionuclide. Additional studies with this agent may be valuable in identifying those patients with ST-segment depression who will benefit from acute reperfusion therapy.

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T-cell subsets were measured in the peripheral blood of 33 patients with heart failure from idiopathic dilated cardiomyopathy, 22 patients with heart failure from other causes, and 33 normal controls. Mean T-suppressor cell percentage was 30% in normals, 21% in patients with idiopathic dilated cardiomyopathy whose duration of symptoms was less than 1 year (P = 0.0005), and 26% in those with symptoms for greater than 1 year (P = 0.05). Similarly, percentage of T-suppressor cells in the group with heart failure from causes other than idiopathic dilated cardiomyopathy was significantly lower (23%; P = 0.005) in those with short duration of symptoms. When both heart failure groups were combined those with symptoms for less than 1 year had significantly lower T-suppressor frequencies (22%) than those with symptoms for more than 1 year (P = 0.015). Multivariate analysis identified duration of symptoms and age as the only independent predictors of T-suppressor cell frequencies. Decreased percentage of T-suppressor cells in patients with idiopathic dilated cardiomyopathy may be an epiphenomenon related to duration of heart failure. This should be taken into account in assigning an etiologic mechanism for T-suppressor cells in idiopathic dilated cardiomyopathy.

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