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Historically, percutaneous coronary intervention (PCI) was relegated to hospitals with colocated cardiac surgery because of the potential need for emergent surgical treatment of PCI-related complications. In the current issue of Circulation , Lee and colleagues1 compare outcomes of PCI at hospitals with and without on-site cardiac surgery and show that emergency cardiac surgery is, in fact, rarely needed ( 1 million patients and demonstrates that the incidence of other PCI-related complications, including myocardial infarction, stroke, cardiogenic shock, aortic dissection, and tamponade, as well as early (within 30 days) and late (after 30 days) all-cause mortality, is not different at hospitals with and without colocated cardiac surgery.1 Article see p 388 Because of inconsistencies among the studies, other outcomes indicators of quality, including the need for target vessel revascularization, could not be evaluated in detail. However, when results from the 2 randomized, controlled trials reporting target vessel revascularization (Cardiovascular Patient Outcomes Research Team Trial [CPORT-E]2 and Percutaneous Coronary Intervention [PCI] Outcomes in Community Versus Tertiary Settings [MASS COMM]3) were combined, rates of target vessel revascularization were similar at hospitals with and without on-site cardiac surgery. This important contribution confirms and puts on a more solid evidence-based foundation current guideline recommendations that allow the performance of primary and nonprimary PCI at hospitals without on-site surgery.4 Like all important studies, this report raises a number of questions. Although PCI at hospitals without on-site cardiac surgery is safe and effective, what is the motivation for extending nonprimary PCI at these facilities? What are the consequences of extending PCI to more hospitals? How should the extensive research knowledge base summarized by Lee and colleagues be applied to the development of PCI programs at hospitals without on-site cardiac surgery? The cynical view is that …

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.

Background In the EPIC trial, c7E3 Fab, an antiplatelet IIb/IIIa receptor antibody, reduced 30-day ischemic end points after high-risk coronary angioplasty by 35% and 6-month ischemic events by 23% but increased in-hospital bleeding episodes. Methods and Results Of the 2099 patients randomized in EPIC, data were collected on 2038 (97%) for prospective hospital cost and major resources. Physician fees were estimated from the Medicare Fee Schedule. Regression analysis was used to examine the economic tradeoff between reduced ischemic events and increased major bleeding during the initial hospitalization. A potential cost savings of $622 per patient during the initial hospitalization from reduced acute ischemic events with c7E3 Fab was offset by an equivalent rise ($521) in costs as the result of an increase in bleeding episodes. Baseline medical costs for the bolus and infusion c7E3 Fab arm averaged $13 577 (exclusive of drug cost) compared with $13 434 for placebo ( P =.42). During the 6-month follow-up, c7E3 Fab decreased repeat hospitalization rates by 23% ( P =.004) and repeat revascularization by 22% ( P =.04), producing a mean $1270 savings per patient (exclusive of drug cost) ( P =.018). With a cost of $1407 for the bolus and infusion c7E3 Fab regimen, the cumulative net 6-month cost to switch from standard care to routine c7E3 Fab averaged $293 per patient. Conclusions In high-risk coronary angioplasty, aggressive platelet inhibition with c7E3 Fab, by significantly reducing ischemic events and repeat revascularization, recoups most of the cost of therapy and has the potential to pay for itself.

For coronary artery disease (CAD), female gender is ’protective’, so that women typically present with clinically apparent CAD a decade later than men. We examined the extent to which traditional cardiovascular risk factor influence the age at presentation with STEMI in men and women. The Cardiovascular Patient Outcomes Research Team (C-PORT) primary PCI registry includes 7197 patients (5070 males and 2109 females) who presented with STEMI at 33 participating hospitals. The table below depicts the average age at presentation with STEMI in males and females with and without diabetes, hypercholesterolemia, hypertension, a family history of coronary artery disease and smoking history (current or former). The effect of smoking, family history and hypertension on age at presentation remained significant in multivariate analysis in both men and women. In both males and females, a family history of CAD and a positive smoking history are associated with presentation with STEMI at a younger age. Both have a greater effect in females. This is particularly true of smoking with lowers the age of presentation by 9 years in women, compared with 3.8 years in men. Male and female patients with a history of hypertension are older at presentation with STEMI, perhaps because the anti-ischemic effects of anti-hypertensive medications. We conclude that while the effect of most traditional risk factors for CAD on age at presentation with STEMI are similar in men and women, smoking lowers the age at presentation to a much greater degree in women. In women who do not smoke, STEMI is delayed for a decade or more compared to men; for women who do, the protective effect of female gender is nearly obliterated.

Developers of systems to improve access to primary percutaneous intervention (PCI) must recognize that most ST-elevation myocardial infarction (STEMI) patients present to hospitals that do not have PCI capability. Indeed, only ≈25% of US hospitals are currently capable of delivering this intervention.1 These non-PCI-capable institutions are often located in rural areas and face real challenges related to distance from PCI centers. In addition, these institutions face significant financial challenges2 in pursuing any of the 3 potential strategies to increase timely access to primary PCI. These 3 strategies include the following3: (1) hospitals currently without PCI capability can develop primary PCI services without cardiac surgery on-site (SOS); (2) non-PCI-capable facilities can rapidly diagnose and transfer STEMI patients to primary PCI-capable hospitals and thereby serve as STEMI referral hospitals; or (3) communities can develop systems that bypass non-PCI-capable hospitals. Each of these strategies is addressed in this article. For each, we review the current status, the ideal system, gaps in and barriers to development of the ideal system, and recommendations. ### Current Status Early observational studies from single institutions demonstrated potential efficacy and safety of primary PCI without SOS. In the Myocardial Infarction, Triage and Intervention (MITI) trial, 233 of 441 primary PCIs were performed at hospitals without SOS. Emergency cardiac surgery was rare (1.4% of patients), and its presence or absence did not affect survival after myocardial infarction.4 In another observational study, among 334 patients undergoing primary PCI at a hospital without SOS, there were no deaths, and no patient required emergency coronary artery bypass grafting (CABG).5 In a nonrandomized comparison of patients undergoing primary PCI at hospitals without SOS with those undergoing primary PCI after transfer to a tertiary hospital, there was no difference in 30-day or 1-year mortality, although time to reperfusion was significantly shorter, and …

Although augmentation of flow does not improve the performance of normal myocardium, the hyperemic response after brief coronary occlusion is associated with transient hyperfunction in the previously ischemic region. In this study we assessed the effect of vasodilator-enhanced coronary blood flow on the systolic function of postischemic stunned myocardium. In 18 open-chest, anesthetized dogs the anterior descending artery was occluded for 5 min, followed by a 10 min period of reflow, repeated 12 times with a final 90 min recovery period. After the recovery period, either 0.06 mg/min dipyridamole (n = 6), 1 mg/min papaverine (n = 6), or 1.5 micrograms/kg/min nitroglycerin (n = 6) was infused intravenously for 15 min. Regional myocardial blood flow, which had returned to normal before administration of vasodilator, was increased 150% above baseline by dipyridamole and 80% by papaverine, but was unchanged by nitroglycerin. Segmental shortening decreased after repeated occlusions: from 17.5% to 0.9% in the group later treated with dipyridamole, from 18.6% to 6.7% in the papaverine group, and from 19.2% to-1.9% in the nitroglycerin group (p less than .005 for all groups). Segmental shortening increased to 8.8% after dipyridamole, 13.6% after papaverine, and 5.1% after nitroglycerin (p less than .05 for all groups), although the load-independent end-systolic pressure-length relationship (ESPLR) showed a significant shift to the left, reflecting enhanced performance, only after dipyridamole and papaverine. For all dogs combined, the percent improvement in ESPLR was correlated with the percent increase in flow (R = -.73, p less than .001). Performance was unchanged in the control region despite similar augmentation of flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Dimension change measures of regional ventricular function, such as absolute or percent wall thickening (delta T or % delta T) or segmental shortening (delta L or % delta L), are highly load dependent. In 16 anesthetized mongrel dogs we assessed use of the end-systolic pressure-thickness and end-systolic pressure-length relationships (ESPTR, ESPLR) as more load-independent measures of regional function. We found that the ESPTR and ESPLR could be measured without detectable baroreceptor-mediated reflex changes in cardiac contractile state. Systemic administration of dobutamine shifted the ESPTR to the right and the ESPLR to the left of control, mainly due to a change in the slope (Ees) of the relationships. Both delta T, % delta T and delta L, % delta L failed to detect the positive inotropic effect of dobutamine because of an associated reduction in preload. With systemic administration of propranolol, ESPTR, ESPLR, delta T, % delta T, and delta L, % delta L detected the negative inotropic effect. Thus systemic propranolol shifted the ESPTR to the left and the ESPLR to the right of control, mainly due to a change in Ees. Regional administration of dobutamine shifted the ESPTR and the ESPLR in the direction of positive contractility in the region receiving the drug, whereas simple dimension change measures of regional function failed to detect the inotropic effect because preload fell and the timing of regional end-systole was altered. With regional propranolol both the ESPTR, ESPLR and simple dimension change measures detected the negative inotropic effect. Thus the ESPTR, ESPLR is a reliable measure of regional ventricular function and may be better than simple dimension change measures of regional function, particularly when loading conditions or the timing of regional systole is altered by an intervention.