Faculty Bibliography

The use of stress echocardiography has undergone considerable evolution in the past 3 decades. Although stress echocardiography was first introduced as a noninvasive diagnostic tool for determining the presence or absence of coronary artery disease (CAD), it later served a prognostic role as well. The importance of stress echocardiography in risk stratification and prognosis is substantially undervalued by clinicians. The identification of patients at risk for future cardiac events has become a primary objective in noninvasive evaluation of patients with suspected or known CAD. In particular, the ability of stress echocardiography to identify patients at low (< 1%), intermediate (1%-5%), or high (> 5%) risk for future cardiac events is essential to decision making in patient management. Moreover, previous studies have conclusively demonstrated the incremental prognostic value of stress echocardiography over clinical and treadmill exercise data in predicting future cardiac events. This article presents a primarily single-center experience of retrospective and observational studies that address the current role of stress echocardiography and summarize its use for risk stratification, prognosis, and determining clinical outcomes, as well as cost-effective integration of such information in patient management decision making

BACKGROUND: Stress echocardiography is an established technique for diagnosis, risk stratification, and prognosis in patients with known or suspected coronary artery disease. The ability of stress echocardiography to predict clinical outcomes, such as coronary angiography and revascularization, has not been reported previously. The purpose of this study was to evaluate the clinical outcomes of coronary angiography, revascularization, and cardiac events in patients undergoing stress echocardiography. METHODS: A total of 3121 patients (mean age, 60 + or - 13 years; 48% men) undergoing stress echocardiography (41% treadmill, 59% dobutamine) were assessed. Follow-up (mean, 2.8 + or - 1.1 years) for subsequent coronary angiography, revascularization (percutaneous coronary intervention [PCI] or coronary artery bypass grafting [CABG]), and confirmed hard events (nonfatal myocardial infarction or cardiac death) was obtained. RESULTS: Stress echocardiographic results were normal (peak wall motion score index [pWMSI], 1.0) in 66% and abnormal (pWMSI > 1.0) in 34% of patients. The pWMSI effectively risk-stratified patients into low-risk (pWMSI, 1.0; 0.8% per year), intermediate-risk (pWMSI, 1.1-1.7; 2.6% per year), and high-risk (pWMSI >1.7; 5.5% per year) groups for future cardiac events (P < .0001). Early coronary angiography (30 days following stress echocardiography) was performed in only 35 patients (1.7%) with normal stress echocardiographic results and 267 patients (25.5%) with abnormal stress echocardiographic results (P < .0001). Late coronary revascularization (2 years following stress echocardiography) occurred in 80 patients (PCI, 2.8%; CABG, 1.1%) with pWMSI values of 1.0, 123 patients (PCI, 13.5%; CABG, 7.3%) with pWMSI values of 1.1 to 1.7, and 102 patients (PCI, 12.7%; CABG, 9.6%) with pWMSI values > 1.7. Multivariate logistic regression analysis identified pWMSI as a predictor of coronary angiography (relative risk, 2.04; 95% confidence interval, 1.67-2.5), revascularization (relative risk, 1.91; 95% confidence interval, 1.68-2.17), and cardiac events (relative risk, 2.45; 95% confidence interval, 2.09-2.88) (all P values < .0001). Patients with markedly abnormal stress echocardiographic results (pWMSI > 1.7) had a significantly higher cardiac event rate in those who did not undergo coronary revascularization (9.6% per year vs 2.9% per year, P < .05). CONCLUSIONS: Stress echocardiography is an effective gatekeeper for coronary angiography and revascularization. Stress echocardiographic results influence clinical decision making in higher risk patients with significantly increased referral to coronary angiography and revascularization. Patients with markedly abnormal stress echocardiographic results (pWMSI > 1.7) were most likely to benefit from coronary revascularization

BACKGROUND: Aggressive blood pressure (BP) control has been advocated in patients with acute coronary syndrome, but few data exist in this population relative to cardiovascular outcomes. METHODS AND RESULTS: We evaluated 4162 patients enrolled in the PRavastatin Or atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction (PROVE IT-TIMI) 22 trial (acute coronary syndrome patients randomized to pravastatin 40 mg versus atorvastatin 80 mg). The average follow-up BP (systolic and diastolic) was categorized into 10-mm Hg increments. The primary outcome was a composite of death due to any cause, myocardial infarction, unstable angina requiring rehospitalization, revascularization after 30 days, and stroke. The secondary outcome was a composite of death due to coronary heart disease, nonfatal myocardial infarction, or revascularization. The relationship between BP (systolic or diastolic) followed a J- or U-shaped curve association with primary, secondary, and individual outcomes, with increased events rates at both low and high BP values, both unadjusted and after adjustment for baseline variables, baseline C-reactive protein, and on-treatment average levels of low-density lipoprotein cholesterol. A nonlinear Cox proportional hazards model showed a nadir of 136/85 mm Hg (range 130 to 140 mm Hg systolic and 80 to 90 mm Hg diastolic) at which the incidence of primary outcome was lowest. The curve was relatively flat for systolic pressures of 110 to 130 mm Hg and diastolic pressures of 70 to 90 mm Hg. CONCLUSIONS: After acute coronary syndrome, a J- or U-shaped curve association existed between BP and the risk of future cardiovascular events, with lowest event rates in the BP range of approximately 130 to 140 mm Hg systolic and 80 to 90 mm Hg diastolic and a relatively flat curve for systolic pressures of 110 to 130 mm Hg and diastolic pressures of 70 to 90 mm Hg, which suggests that too low of a pressure (especially <110/70 mm Hg) may be dangerous. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00382460

Bioabsorbable stents are an important advancement in stent technology providing a temporary scaffold and may be augmented with drugs to suppress neointimal hyperplasia.Though changes are being made to the design of the stents, to ensure similar rates of acute recoil, residual stenosis postintervention remains higher when compared to contemporary durable stents. In order to achieve similar clinical restenosis outcomes, bioabsorbable stents must first show similar MLD or percent diameter stenosis at follow-up to drug-eluting stents.While variable different acute gain and post-procedure MLD for bioabsorbable stents make late lumen loss a poor marker for restenosis probability by itself, late loss can be an informative metric for neointimal hyperplasia over time in these stents.Metrics which are independent of acute gain such as minimal luminal diameter and percentage diameter stenosis may make better surrogates for restenosis (Table 1). Moreover, remodelling over time requires measurement of the vessel and lumen diameters in later follow-up. Since the natural history of the vascular response to bioabsorbable stents is in its infancy of investigation, follow-up of these stents at least beyond the duration of polymer is prudent. Finally, given a disappearing frame of reference, both careful angiographic and intravascular ultrasound assessments are helpful to delineate the varying contributions of recoil, remodelling, and neointima formation.

BACKGROUND: The relationship between systolic blood pressure (BP) and the risk of cardiovascular events is complex. In patients with chronic coronary artery disease, a J-shaped relationship has been shown, such that there is an increased risk of events both at high and low BP. The current coronary artery disease risk prediction models, however, considers a linear relationship between presenting BP and outcomes in patients presenting with acute coronary syndromes. METHODS: We evaluated 139,194 patients with non-ST-segment elevation acute coronary syndromes in the Can Rapid risk stratification of Unstable anigina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines (CRUSADE) quality improvement initiative. The presenting systolic BP was summarized as 10-unit increments. Primary outcome was a composite of in-hospital events all-cause mortality, reinfarction, and stroke. Secondary outcomes were each of these outcomes considered separately. RESULTS: From the cohort of 139,194 patients, 9,566 (6.87%) patients had a primary outcome (death/reinfarction or stroke) of which 5,910 (4.25%) patients died, 3,724 (2.68%) patients had reinfarction, and 1,079 (0.78%) patients had a stroke during hospitalization. There was an inverse association between presenting systolic BP and the risk of primary outcome, all-cause mortality, and reinfarction such that there was an exponential increase in the risk with lower presenting systolic BP even after controlling for baseline variables. However, there was no clear relationship between stroke and lower presenting systolic BP. CONCLUSIONS: In contrast to longitudinal impacts, there is a BP paradox on acute outcomes such that a lower presenting BP is associated with increased risk of in-hospital cardiovascular events. These associations should be considered in acute coronary syndrome prognostic models

AIM: The purpose of this study was to assess the relationship between pulse pressure (PP) and cardiovascular outcomes in a large, elderly, coronary artery disease (CAD) population with hypertension, and compare the predictive power of PP with other blood pressure measures. METHODS AND RESULTS: In INternational VErapamil-trandolapril STudy, 22,576 CAD patients with hypertension (mean age 66 years) were randomized to verapamil-SR or atenolol-based strategies and followed for 2.7 years (mean). Primary outcome (PO) was time to first occurrence of death (all-cause), non-fatal myocardial infarction (MI), or non-fatal stroke. Mean follow-up PP was summarized by 5 mmHg subgroups for association with incidence of PO. Stepwise Cox proportional hazards models were used to estimate adjusted relative hazard ratios (HR) for the risk of PO with follow-up PP as a continuous variable, with linear and quadratic terms. Similar models were constructed for follow-up systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressures (MAP). A -2 log-likelihood statistic was used to assess the predictive power of PP compared with SBP, DBP, and MAP. For follow-up PP, the incidence and adjusted HR for the PO formed a J- or U-shaped curve. After adjusting for baseline covariates, both linear and quadratic terms for PP were significant (P < 0.0001 for both), with a nadir of 54 mmHg (bootstrapping 95% CI 42-60 mmHg). Similar quadratic relationships were found between PP and all-cause mortality or MI; the relationship between PP and stroke was linear. Pulse pressure was a predictor of PO even after including SBP (P = 0.007 linear term) or DBP (P < 0.0001 for both linear and quadratic terms) or MAP (P < 0.01 for both liner and quadratic terms) in the model. Using -2 log-likelihood differences, SBP (-2 log-likelihood difference 77.1 vs. 7.3 for PP), DBP (-2 log-likelihood difference 138.5 vs. 44.6 for PP), and MAP (-2 log-likelihood difference 125.0 vs. 13.4 for PP) were stronger predictors of PO than PP. CONCLUSION: In CAD patients with hypertension, PP (on anti-hypertensive treatment) is a weaker predictor of cardiovascular outcomes than SBP, DBP, or MAP