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Background The CPORT-E trial showed the noninferiority of nonprimary percutaneous coronary intervention (PCI) at hospitals without cardiac surgery on-site (SoS) compared with hospitals with SoS for 6-week mortality and 9-month major adverse cardiac events (MACE). However, target vessel revascularization (TVR) was increased at non-SoS hospitals. Therefore, we aimed to determine the consistency of the CPORT-E trial findings across the spectrum of enrolled patients. Methods Post hoc subgroup analyses of 6-week mortality and 9-month MACE, defined as the composite of death, Q-wave myocardial infarction, or TVR, were performed. Patients with and without 9-month TVR and rates of related outcomes were compared. Results There was no interaction between SoS status and clinically relevant subgroups for 6-week mortality or 9-month MACE (P for any interaction = .421 and .062, respectively). In addition to increased 9-month rates of TVR and diagnostic catheterization at hospitals without SoS, non-TVR was also increased (2.7% vs 1.9%, P = .002); there was no difference in myocardial infarction–driven TVR, non-TVR, or diagnostic catheterization. Predictors of 9-month TVR included intra-aortic balloon pump use, any index PCI complication, and 3-vessel PCI, whereas predictors of freedom from TVR included SoS, discharge on a P2Y12 inhibitor, and stent implantation. Conclusions The noninferiority of nonprimary PCI at non-SoS hospitals was consistent across clinically relevant subgroups. Elective PCI at an SoS hospital conferred a TVR benefit which may be related to a lower rate of referral for diagnostic catheterization for reasons other than myocardial infarction.

Primary percutaneous coronary intervention (PPCI) yields superior mortality outcomes compared with thrombolysis in ST-elevation acute myocardial infarction (STEMI) but takes longer to administer. Previous meta-regressions have estimated that a procedure-related delay of 60 minutes would nullify the benefits of PPCI on mortality. Using a combined database from randomized clinical trials and registries (n = 2,781) and an independently developed model of mortality risk in STEMI, we developed logistic regression models predicting 30-day mortality for PPCI and thrombolysis by examining the influence of baseline risk on the treatment effect of PPCI and on the hazard of treatment delay. We used these models to solve mathematically for "time interval to mortality equivalence," defined as the PPCI-related delay that would nullify its expected mortality benefit over thrombolysis, and to explore the influence of baseline risk on this value. As baseline risk increases, the relative benefit of PPCI compared with thrombolytic therapy significantly increases (p = 0.002); patients with STEMI at relatively low risk of mortality accrue little or no incremental mortality benefit from PPCI, but high-risk patients benefit greatly. However, as baseline risk increases, the hazard associated with longer treatment-related delay also increases (p = 0.007). These 2 effects are compensatory and yield a roughly uniform time interval to mortality equivalence of approximately 100 minutes in patients who have at least a moderate degree of mortality risk (> approximately 4%). In conclusion, the mortality benefits of PPCI and the hazard of PPCI-related delay depend on baseline risk. Previous meta-regressions appear to have underestimated the PPCI-related delay that would nullify the incremental benefits of PPCI.

Background This study was done to determine whether cardiovascular reactivity to mental stress is associated with exercise-induced occult ischemia in an asymptomatic population at high risk for premature coronary heart disease (CHD). Methods and Results One hundred fifty-two siblings of persons with premature CHD underwent mental stress testing. Exercise thallium tomography and 24-hour Holter monitoring were also performed. Hemodynamic changes were monitored during both stressors. Siblings positive for exercise-induced ischemia were offered cardiac catheterization. During mental stress, siblings with an abnormal exercise ECG and/or thallium scan (n=15) had greater maximal increases in systolic blood pressure (SBP, P =.0004) and diastolic blood pressure (DBP, P =.05) and had greater heart rate variability in the normalized low frequency domain of an analysis of Holter monitor recordings, compared with siblings without exercise-induced ischemia. Coronary arteriography confirmed coronary atherosclerosis in 85% of siblings with exercise-induced ischemia. Regression analyses showed that occult ischemia during exercise was a strong independent predictor of maximal change in SBP and DBP during mental stress. A multivariate logistic model demonstrated that siblings with exercise-induced occult ischemia were 21 times more likely to be “hot” responders (top quartile of change in SBP and DBP) during mental stress. Conclusions An exaggerated cardiovascular response to mental stress is associated with exercise-induced myocardial ischemia in persons with preclinical coronary heart disease.

Objectives. This study sought to analyze the outcomes of revascularization procedures in the treatment of allograft coronary disease. Background. Allograft vasculopathy is the main factor limiting survival of heart transplant recipients. Because no medical therapy prevents allograft atherosclerosis, and retransplantation is associated with suboptimal allograft survival, palliative coronary revascularization has been attempted. Methods. Thirteen medical centers retrospectively analyzed their complete experience with percutaneous transluminal coronary angioplasty, directional coronary atherectomy and coronary bypass graft surgery in allograft coronary disease. Results. Sixty-six patients underwent coronary angioplasty. Angiographic success (≤ 50% residual stenosis) occurred in 153 (94%) of 162 lesions. Forty patients (61%) are alive without retransplantation at 19 ± 14 (mean ± SD) months after angioplasty. The consequences of failed revascularization were severe. Two patients sustained periprocedural myocardial infarction and died. Angiographic restenosis occurred in 42 (55%) of 76 lesions at 8 ± 5 months after angioplasty. Angiographic distal arteriopathy adversely affected allograft survival. Eleven patients underwent directional coronary atherectomy. Angiographic success occurred in 9 (82%) of 11 lesions. Two periprocedural deaths occurred. Nine patients are alive without transplantation at 7 ± 4 months after atherectomy. Bypass graft surgery was performed in 12 patients. Four patients died perioperatively. Seven patients are alive without retransplantation at 9 ± 7 months after operation. Conclusions. Coronary revascularization may be an effective palliative therapy in suitable cardiac transplant recipients. Angioplasty has an acceptable survival in patients without angiographic distal arteriopathy. Because few patients underwent atherectomy and coronary bypass surgery, assessment of these procedures is limited. Angiographic distal arteriopathy is associated with decreased allograft survival in patients requiring revascularization.

A prospective study of 53 patients employed in the 6-month period before coronary angioplasty was performed to determine the direct and indirect costs of lag time in work resumption. The total direct costs calculated were $273,480; indirect costs for this sample were $150,944. When these costs are generalized to all patients in the US undergoing uncomplicated percutaneous transluminal coronary angioplasty, the costs are more than $1.2 billion. This study demonstrated that even in patients with a high a priori probability of work return, delay in work resumption results in a greater cost to the individual and society through absence from the labor force.

The ischemic pain associated with balloon inflation during coronary angioplasty remains a significant source of procedural discomfort and sets a limit on the duration of percutaneous transluminal intravascular interventions. The present study examined whether intracoronary lidocaine reduced the pain of coronary angioplasty. Sixteen patients undergoing elective coronary angioplasty underwent three 90 sec balloon inflations: the first with administration of no intracoronary agent, and the second and third with administration of one or the other of placebo or an equal volume of lidocaine (10-16 mg). Placebo or lidocaine were randomized in administration sequence and were given just before balloon inflation. During the occlusions, pain was scored on an ordinal scale (0 = no pain; 10 = most severe pain). Lidocaine delayed the onset of pain (23 +/- 4 vs. 48 +/- 7 sec, P < 0.005) and reduced its magnitude (at end-inflation: 7.8 +/- 1.3 vs. 3.2 +/- 1.3, P < 0.01). There were no significant hemodynamic or electrophysiologic effects in this group of patients, although atrioventricular conduction was delayed when lidocaine was administered into the epicardial coronary which had the atrioventricular node artery as a branch. Intracoronary analgesia with lidocaine is safe and effective in a select group of patients with normal ventricular function undergoing elective coronary angioplasty.

A lethal complication associated with acute heart failure syndrome (AHFS) is out-of-hospital cardiac arrest due to a sudden ventricular arrhythmia, either ventricular fibrillation (VF) or ventricular tachycardia (VT) deteriorating into VF (1, 2, 3, 4, 5, 6). However, the unique morbidity of AHFS makes management more of a challenge. One potential intervention that should be considered is evolving technology for automated external defibrillation, the main focus of this chapter.

The hypothesis that rheological properties of the coronary perfusate account for the curvilinearity and high zero-flow pressure (Pf = 0) of the diastolic coronary-pressure flow relationship (DCPFR) was tested by measuring these relationships using coronary perfusates of varying rheological character. In 16 open-chest, heart-blocked dogs the left circumflex coronary artery was cannulated and perfused using an extra-corporeal circuit, and autoregulation was abolished with intracoronary adenosine. DCPFRs were constructed from data obtained at multiple steady-state levels of coronary pressure during long diastoles while left ventricular diastolic pressure was held constant. Although isovolumic hemodilution reduced hematocrit from 46 +/- 3% to 32 +/- 3% and increased coronary conductance, it neither abolished the curvilinearity nor changed Pf = 0, which remained significantly higher than left ventricular diastolic pressure. In 10 additional animals, DCPFRs obtained during blood perfusion were compared with those obtained using crystalloid perfusate. Crystalloid perfusion increased coronary conductance and failed to abolish curvilinearity. However, with crystalloid perfusate, Pf = 0 was reduced to a value essentially equal to left ventricular diastolic pressure. We conclude that while the rheological properties of coronary perfusates do not fully account for the curvilinearity of the DCPFR, they do importantly influence coronary conductance and Pf = 0.

Primary percutaneous coronary intervention (PCI) yields better outcomes than thrombolytic therapy in the treatment of patients with ST-segment elevation myocardial infarctions (STEMIs). Emergency medical service systems are potentially important partners in efforts to expand the use of PCI. This study was conducted to explore the probable impact on patient mortality and hospital volumes of competing strategies for the emergency transport of patients with STEMIs. Emergency transport was simulated for 2,000 patients with STEMIs from the Atlantic Cardiovascular Patient Outcomes Research Team (C-PORT) trial in a geospatial model of Dallas County, Texas. Patient mortality estimates were obtained from a recently developed predictive model comparing PCI and thrombolytic therapy. A strategy of transporting patients to the closest hospital and treating with PCI if available and thrombolytic therapy if not yielded a 5.2% 30-day mortality rate (95% confidence interval [CI] 4.2% to 6.3%). A strategy of universal PCI, in which patients were transported only to PCI-capable hospitals, yielded 4.4% (95% CI 3.6% to 5.4%) mortality and an increase in patient volume at 2 full-time PCI hospitals of >1,000%. A strategy of targeted PCI, in which high-benefit patients were transported or transferred to PCI-capable hospitals, yielded 4.5% (95% CI 3.8% to 5.5%) mortality if transfers were decided in the emergency department and 4.2% (95% CI 3.4% to 5.1%) if transport was decided in the emergency vehicle. Targeted PCI strategies increased patient volumes at full-time PCI hospitals by about 700%. In conclusion, the selection of high-benefit patients for transport or transfer to PCI-capable hospitals can reduce mortality while minimizing major shifts in hospital patient volumes.

UNLABELLED It has been speculated but never proven that tachycardia-induced ischemia per se may lead to myocardial infarction. In 17 anesthetized dogs, the proximal left anterior descending (LAD) artery was cannulated and perfused via bypass from the left subclavian artery. Distal LAD pressure was reduced by a screw clamp to cause > or =20% decrease in wall thickening during pacing tachycardia but no decrease in resting heart rate (approximately 90 bpm). Dogs were randomly assigned to three groups: 1) control (n = 6) maintained at resting heart rate (approximately 90 bpm) and mean coronary pressure of 49+/-5 mm Hg for 4 h; 2) 4-h ischemia (n = 6), paced at 150 bpm and mean coronary pressure maintained at 59+/-6 mm Hg for 4 h; and 3) 1-h ischemia (n = 5), paced at 150 bpm and mean coronary pressure of 54+/-8 mm Hg for 1 h. Myocardial blood flow and infarct area were measured by radiolabeled microspheres and triphenyl-tetrazolium chloride staining, respectively. Despite the higher coronary pressure in the 4-h ischemia group (P = 0.02), patchy subendocardial necrosis occurred in all these dogs and in two of the 1-h ischemia dogs, and one control dog had minimal papillary muscle necrosis. Infarct area was largest in the 4-h ischemic group (15.5%+/-9.1%) compared with control and 1-h ischemia groups (0.09%+/-0.2% and 1.6%+/-2.1%, respectively) (P < 0.002). Relative (risk/ nonrisk areas) subendocardial flow was lower at the end of ischemia in the 4- and 1-h ischemia groups compared with the control group (0.3+/-0.1 and 0.4+/-0.1 vs 0.9+/-0.2; P = 0.008 and 0.01, respectively). Prolonged tachycardia-induced ischemia, in the face of fixed coronary stenosis causing no ischemia at the resting heart rate, leads to patchy subendocardial necrosis, despite anticoagulation and antiplatelet treatment. IMPLICATIONS Prolonged tachycardia-induced ischemia, in the face of fixed coronary stenosis causing no ischemia at the resting heart rate, leads to subendocardial infarction in dogs. These findings suggest a possible mechanism for postoperative myocardial infarction.

Analysis of high frequency (150–250 Hz) in the signal-averaged electrocardiogram (SAECG) is one of the emerging methods for detecting vessel patency in acute myocardial infarction following thrombolytic therapy and angioplasty. Root-mean-square voltage (RMSV) of the filtered QRS has been used in earlier studies to detect reperfusion; however, previous analysis indicated that RMSV is sensitive to residual noise in the SAECG and errors in QRS delineation (onset/offset). A new measurement is proposed, high-frequency energy (HFQE), and the robustness of the RMSV and HFQE was evaluated for simulated errors in QRS delineation. In this study, two measures (RMSV and HFQE) were tested on 24 control subjects and 21 patients undergoing thrombolytic therapy. Results indicate that unfiltered QRS duration is more stable than filtered QRS duration for the control subjects and patients and that HFQE had less fluctuation than RMSV in thrombolytic therapy patients. In the control group, HFQE was sensitive to the amplitude variation of the filtered SAECG. Therefore, another new measurement is proposed high-frequency integral of absolute value (HFAV), for reducing the sensitivity to amplitude changes in the filtered SAECG. This new feature was tested on control subjects and was found to be more stable than HFQE. In the thrombolytic therapy group, HFAV provided similar information as HFQE. These three measurements—RMSV, HFQE, and HFAV—provide a comprehensive analysis of the high-frequency SAECG for detecting vessel patency and reocclusion. Relative merits of these measures need to be evaluated on a larger database of patients undergoing thrombolysis and angioplasty for acute myocardial infarction.

The hypothesis that an increase in the amplitude (root-mean-square voltage) of the high frequency (150-250 Hz) components of the QRS complex occurs with successful reperfusion following thrombolytic therapy in acute myocardial infarction (AMI) and fails to occur when thrombolysis fails was tested. Clinical markers for successful or failed reperfusion following thrombolytic therapy for AMI are notoriously insensitive. The amplitude of the high-frequency components of the QRS complex decreases during ischemia and returns to normal with resolution of ischemia, but neither the variability in measurement of these potentials nor their patterns of change during the course of AMI have been described. In 32 control subjects, the average coefficient of variation for the amplitude of the highfrequency QRS complex was 10% or 0.3 uV. Based on these data, for the acute infarction population a significant change in this measurement was therefore defined as a change in amplitude > 20% or 0.6 uV on two consecutive recordings. In 30 patients with AMI treated with a thrombolytic agent, either cardiac catheterization, serial serum myoglobin, or complete resolution of ST-segment elevation were used to define successful or failed reperfusion. High-frequency QRS electrocardiograms were obtained at the start of treatment with a thrombolytic agent and for 3 h thereafter using a signal-averaging technique and digital filtering. Standard 12-lead electrocardiograms were obtained at the same time. In patients who reperfused successfully, the high-frequency QRS amplitude increased significantly (1.2 ± 0.9 uV above its nadir at 83 ± 36 min after initiation of thrombolytic therapy) in 23 of 25 patients. In contrast, the highfrequency QRS amplitude did not change or declined in all five patients who failed to reperfuse (-0.4 ± 0.4 uV, p < 0.05 compared with successful reperfusion). Traditional clinical markers such as resolution of chest pain and ST-segment elevation failed to distinguish successful and failed reperfusion. High-frequency QRS electrocardiography is a rapid, reliable bedside technique for discriminating between successful and failed reperfusion in patients treated with thrombolytic agents for AMI.

The hypothesis that the ATP-sensitive potassium channel provides the link between change in coronary blood flow and myocardial oxygen demand was tested in 9 dogs instrumented to measure coronary flow and regional wall thickening in the basal state and at a high level of myocardial oxygen consumption produced by systemic infusion of phenylephrine and simultaneous atrial pacing at an elevated heart rate. Measurements were recorded before and after blockade of ATP-sensitive potassium channels with intracoronary glibenclamide (2 mumol/min). While glibenclamide reduced the absolute level of coronary flow in the basal state, the increase in flow due to increased metabolic demand was unchanged compared with control. Thus, activity of the ATP-sensitive potassium channel determines the set point from which adjustments of coronary flow in response to metabolic stimuli occur, but does not provide a link between changes in oxygen demand and changes in coronary flow.

The factors which determine coronary blood flow in myocardium subjected to ischemia and reperfusion are numerous, complex, and interrelated. They can be conveniently, if arbitrarily, divided into three broad categories. First, cellular and protein elements of the coronary perfustate, such as the leukocyte and fibrinogen, may affect coronary blood flow through effects on the microvasculature and on blood rheological properties, respectively. Second, the coronary conduit itself, the blood vessel, can also be affected by ischemia and reperfusion, particularly in its endothelial component and the associated vascular responses. Finally, the environment in which the coronary vessel finds itself, determined by characteristics of the myocyte and the interstitial space, can affect coronary flow by itself being profoundly changed after ischemia and reperfusion. While ischemia and reperfusion affects all three of these major determinants of coronary blood flow, whether or not coronary blood flow responses following reperfusion have a role in producing myonecrosis is unclear at this time.

Restenosis following coronary angioplasty can usually be treated effectively and safely by repeated angioplasty. However, the presence of a complex lesion morphology may bias the clinician away from angioplasty toward either recommending bypass surgery or continuing medical therapy alone in spite of recurrence of the symptoms which were sufficient indication for the initial angioplasty. One type of complex morphology at the site of the restenosis is due to the presence of a focal, eccentric aneurysmal dilatation similar in appearance to a saccular aneurysm. In two previously reported cases in the literature both were referred to bypass surgery. We report eight additional cases including the use of repeat successful angioplasty in six of the cases in spite of the potential problems posed by the complexity of the restenosed lesion. In addition, this case review suggests that this type of complex lesion morphology with restenosis may be more common when the initial angioplasty was associated with deep arterial injury, as in patients whose initial angloplasty was done in an infarct-related vessel or was associatedwith evidence of a large dissection.

Percutaneous aortic valvuloplasty using a single dilating balloon has been associated with significant but modest reduction in transvalvular pressure gradient and increase in valve area. The balloon diameter is usually 20 mm or smaller to avoid disruption of aortic root structure and to permit forward blood flow during inflation. To evaluate the safety and efficacy of valvuloplasty using a combination of balloons with larger maximum inflated diameters, we compared results of aortic valvuloplasty in 21 patients using either the single or double balloon technique. Mean maximum inflated balloon diameter was 19.4 mm +/- 1.4 for the single balloon technique, while the mean sum of diameters for the simultaneous double balloon technique was 36.3 mm +/- 3.9. The mean age, aortic annulus diameter, and predilatation aortic valve area were not different among groups. Mean aortic transvalvular gradient reduction and mean aortic valve area increase were greater for the double balloon technique. The procedure was well tolerated with no major complications. No change in the degree of aortic regurgitation was noted. The double balloon technique for aortic valvuloplasty is safe and more effective at improving aortic valve area and transvalvular gradient than the conventional single balloon technique.

Objectives.This study attempted to determine whether neutrophil sequestration in reperfused myocardium can be inhibited and infarct size reduced by treatment with a chimeric, monoclonal IgG4 antibody (CLB54) directed against CD18 in a primate model of acute myocardial ischemia and reperfusion.Background.Reperfusion injury, in part mediated by neutrophils, may limit the potential benefit of reestablishing infarctrelated artery patency in patients with acute myocardial infarction.Methods.Nineteen closed-chest baboons (10 control, 9 treated with CLB54) had the left anterior descending coronary artery occluded for 90 min, followed by 4 h of reflow. CLB54 (mean [±SD] 11 ± 2 mg/kg body weight) or saline solution was administered intravenously 20 min before reflow. Coronary flow was determined using radiolabeled microspheres, infarct size by triphenyltetrazolium chloride staining, global and regional ventricular function by contrast ventriculography and neutrophil accumulation by a myeloperoxidase assay.Results.Risk region size was the same in both groups. CLB54 treatment reduced infarct size expressed as a percent of the risk region from 41 ± 20% in the saline-treated group to 19 ± 17% in the CLB54-treated group (p < 0.02). This was associated with diminished myeloperoxidase activity and greater postreperfusion coronary flow in the risk region in CLB54-treated than in control baboons. Ejection fraction declined to the same extent in both groups, whereas anterior wall regional cord shortening was better preserved in CLB54-treated baboons.Conclusions.Inhibition of neutrophil sequestration with CLB54 administered before reperfusion reduces infarct size, preserves ischemic zone microvascular perfusion and minimizes the decline of regional wall motion.

Stunned myocardium can be produced by repeated short episodes of ischemia. Histochemical and ultrastructural abnormalities such as sarcomere lengthening and myofiber thinning have been noted in myocardium soon after the onset of ischemia and have been attributed to the mechanical stretching that occurs during ventricular systole. To test whether mechanical forces alone could produce the residual dysfunction seen in stunned myocardium, regional dyskinesia was produced in open chest dogs by six repeated intracoronary infusions of either potassium chloride, 0.2 mEq/min for 2.5 minutes, or lidocaine, a 10 mg bolus followed by 1 to 3 mg/min for 5 minutes. These dogs were matched with dogs that had six repeated coronary occlusions of 2.5 and 5 minutes' duration, respectively. Regional function was analyzed using fractional systolic shortening and the load-independent end-systolic pressure-length relation. Both potassium chloride and lidocaine produced regional dyskinesia that was similar to the dyskinesia produced by coronary occlusion. Although regional ventricular function after repeated coronary occlusions remained significantly reduced, function returned completely to normal within 5 minutes after the last druginduced dyskinesia. In conclusion, regional dysfunction produced by potassium chloride and lidocaine does not produce residual dysfunction despite mechanical forces during systole similar to those seen during coronary occlusion.

The influence of afterload resistance on the end-systolic pressure-thickness relationship (ESPTR) was assessed in six isolated canine left ventricles made to eject into a simulated arterial system. An increase of simulated peripheral resistance from 1.5 to 6.0 mmHg.s.ml-1 resulted in a modest but significant shift of the ESPTR upward and to the right, indicating augmented contractile performance. A relationship between the extent of systolic wall thickening and end-systolic performance was also observed: increased wall thickening impairing and decreased wall thickening enhancing end-systolic performance. The dependence of end-systolic performance on wall thickening history in this setting is consistent with shortening deactivation. This phenomenon appears to account at least in part for the observed shift in the ESPTR with altered afterload resistance.

To study the influence of ischemic zone size on function in nonischemic regions, wall thickening and the end-systolic pressure-thickness (ESPTR) relationship were measured before and during a 90-s coronary occlusion, which produced either a small or large (24 or 35% of left ventricular mass) area of ischemia. With both size ischemic areas, nonischemic zone isovolumic and ejection phase wall thickening increased during occlusion, primarily because of increased preload and, to a lesser extent, a reduced pressure component of afterload. The nonischemic region ESPTR was unchanged from preocclusion control with small ischemic mass. With larger ischemic mass, the nonischemic region ESPTR was shifted downward and to the left, indicating reduced end-systolic performance. The decline in the nonischemic zone ESPTR with large ischemic zone size was not due to reduced blood flow, shortening deactivation, reflex effects, or "tethering" but rather to the associated decline in coronary perfusion pressure. Thus the increase of nonischemic region wall thickening during acute ischemia is due to a change in ventricular loading conditions and not augmentation of contractile performance. Larger ischemic zone size can impair function in nonischemic myocardium by reducing the erectile component of end-systolic performance.