Faculty Bibliography

Beta-blockers were documented to reduce reinfarction rate more than 3 decades ago and subsequently touted as being cardioprotective for a broad spectrum of cardiovascular indications such as hypertension, diabetes, angina, atrial fibrillation as well as perioperatively in patients undergoing surgery. However, despite lowering blood pressure, beta-blockers have never shown to reduce morbidity and mortality in uncomplicated hypertension. Also, beta-blockers do not prevent heart failure in hypertension any better than any other antihypertensive drug class. Beta-blockers have been shown to increase the risk on new onset diabetes. When compared with nondiuretic antihypertensive drugs, beta-blockers increase all-cause mortality by 8% and stroke by 30% in patients with new onset diabetes. Beta-blockers are useful for rate control in patients with chronic atrial fibrillation but do not help restore sinus rhythm or have antifibrillatory effects in the atria. Beta-blockers provide symptomatic relief in patients with chronic stable angina but do not reduce the risk of myocardial infarction. Adverse effects of beta-blockers are common including fatigue, dizziness, depression and sexual dysfunction. However, beta-blockers remain a cornerstone in the management of patients having suffered a myocardial infarction and for patients with heart failure. Thus, recent evidence argues against universal cardioprotective properties of beta-blockers but attest to their usefulness for specific cardiovascular indications

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

The utilization of stress echocardiography has undergone considerable expansion and evolution over the past three decades. Although stress echocardiography was first conceived as a noninvasive diagnostic tool for determining the presence or absence of coronary artery disease (CAD), its prognostic value is now well established. Thus, identification of patients at risk for future cardiac events has become a primary objective in the noninvasive evaluation of patients with chest pain syndromes and among patients with 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 patient management decisions. 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 review addresses the current role and summarizes current literature with respect to the use of stress echocardiography in determining patient risk for cardiac events and the cost-effective integration of such information into patient management decisions

AIMS: A transthoracic echocardiographic (TTE) parameter that would stratify atrial fibrillation (AF) risk would be useful. Tissue Doppler imaging can quantify left atrial appendage contraction velocity (LAA A(M)). METHODS AND RESULTS: We studied 141 patients referred for transoesophageal echocardiogram (TEE); 48 were in AF. We obtained TEE and TTE LAA A(M) velocities from the LAA apex on the parasternal short-axis and apical two-chamber views. Adequate traces were obtained in 118 patients (84%). In these patients, we measured 5382 LAA A(M) velocity tracings. There was a strong correlation between LAA A(M) on TEE and TTE parasternal short-axis (r = 0.741; P < 0.0001) and apical two-chamber views (r = 0.729; P < 0.0001). Patients in AF had lower LAA A(M) than those with sinus rhythm on parasternal short-axis (12 +/- 5 vs. 23 +/- 7 cm/s, P < 0.0001) and apical two-chamber (14 +/- 5 vs. 23 +/- 8 cm/s, P < 0.0001) views. On parasternal short axis, LAA A(M) velocities were lower in patients with spontaneous echo contrast, 11 +/- 4 vs. 22 +/- 8 cm/s (P < 0.0001), and in those with thrombus, 8 +/- 2 cm/s (P < 0.0001). On apical two-chamber, LAA A(M) velocities were also lower with spontaneous echo contrast, 12 +/- 4 vs. 22 +/- 7 cm/s (P < 0.0001), and with thrombus, 10 +/- 4 cm/s (P < 0.0001). In patients with AF and TTE LAA A(M) < or =11 cm/s, we found that nearly one-third had LAA thrombus. In patients with AF and a history of stroke or transient ischaemic attack (TIA), LAA A(M) velocities were lower compared with those without history of stroke or TIA in the parasternal short-axis (9 +/- 3 vs. 13 +/- 5 cm/s, P = 0.02) and apical two-chamber views (11 +/- 3 vs. 15 +/- 6 cm/s, P = 0.008). CONCLUSION: Acquiring and quantifying LAA A(M) contraction velocity is feasible on TTE in a high percentage of patients and correlates with TEE. LAA A(M) was lower in AF compared with sinus rhythm, with spontaneous echo contrast compared to without spontaneous echo contrast, and in AF patients with a history of stroke or TIA. Those with LAA thrombus had the lowest LAA A(M) velocities. LAA A(M) is a novel functional parameter that may prove useful for risk stratification of AF

BACKGROUND: The use of calcium channel blockers (CCBs) in patients with coronary artery disease remains controversial, with reports of increased risk of myocardial infarction and all-cause mortality. Short-acting CCBs have an unfavorable hemodynamic profile. The role of long-acting CCBs in patients with coronary artery disease is unknown. METHODS: MEDLINE/CENTRAL/EMBASE database were searched from 1966 to August 2008 for randomized controlled trials of long-acting CCBs in patients with coronary artery disease with follow-up for at least 1 year. We extracted from the studies the baseline characteristics and 6 outcomes: all-cause mortality, cardiovascular mortality, nonfatal myocardial infarction, stroke, angina pectoris, and heart failure. RESULTS: Of the 100 randomized controlled trials of CCBs in patients with coronary artery disease, 15 studies evaluating 47,694 patients fulfilled our inclusion criteria. When compared with the comparison group (including placebo), CCBs were not associated with an increased risk of all-cause mortality (relative risk [RR] 0.99; 95% confidence interval [CI], 0.94-1.05), cardiovascular mortality (RR 1.03; 95% CI, 0.95-1.11), nonfatal myocardial infarction (RR 0.96; 95% CI, 0.87-1.06), or heart failure (RR 0.86; 95% CI, 0.71-1.05), and with a 21% reduction in the risk of stroke (95% CI, 0.70-0.89) and 18% reduction in the risk of angina pectoris (95% CI, 0.72-0.94). When compared with placebo, CCBs resulted in a 28% reduction in the risk of heart failure (95% CI, 0.73-0.92). The results were similar for both dihydropyridines and nondihydropyridine CCBs. CONCLUSIONS: In patients with coronary artery disease, long-acting CCBs (either dihydropyridines or nondihydropyridines), were associated with a reduction in the risk of stroke, angina pectoris, and heart failure, with similar outcomes for other cardiovascular events as the comparison group