Faculty Bibliography

Stroke is a major cause of morbidity and mortality worldwide. Hypertension is one of the most important risk factors for stroke - increasing the risk significantly. The presence and severity of coronary artery disease (CAD), which often coexists with hypertension, also predicts an increased risk of stroke. Lowering blood pressure (BP) to target in patients with hypertension can significantly reduce the incidence of fatal and non-fatal stroke. Effective BP control is even more important in CAD patients who are at greater risk of stroke. Data regarding the effects of antihypertensive therapy on stroke in patients with angina or CAD are limited and have been variable. To date, BP management strategies in patients with CAD have relied on small subsets of data based on high-risk hypertensive patients. Results with calcium channel blockers (CCBs) have been more positive than those with other classes of antihypertensive agents. Findings from the ACTION trial have provided a significant insight into the benefits of CCBs in patients with CAD and hypertension. Nifedipine gastrointestinal therapeutic system (GITS), in addition to best practice therapy for stable angina pectoris, contributes to a significant reduction in the risk of stroke in patients with CAD and hypertension who are at high risk and require effective BP control. Moreover, the incidence of stroke is significantly related to baseline BP, which may be an important factor to consider when deciding on treatment strategies in high-risk patients with CAD

BACKGROUND: The role of coronary artery collaterals in transient ischemic left ventricular (LV) dilatation (TID) during stress echocardiography is not well defined. HYPOTHESIS: Transient ischemic LV dilatation is a marker for extensive and severe coronary artery disease and represents patients without good collaterals. METHODS: We evaluated 212 consecutive patients (57 +/- 16 years, 70% male) who had coronary angiography and stress echocardiography within a 3-month period. This cohort of patients was divided into three groups based on type of collaterals: Group A: no collaterals; Group B: collaterals supplied by vessels without flow-limiting stenosis (good collaterals); Group C: collaterals supplied by vessels with flow-limiting stenosis (bad/jeopardized collaterals). In all patients, angiographic jeopardy score (AJS), ejection fraction (EF), and wall motion score index (WMSI) at rest and during stress were evaluated. Transient ischemic LV dilatation was defined as transient increase in the end-systolic dimensions from rest to peak stress. RESULTS: Transient ischemic LV dilatation was present in 42 (20%) patients. Patients with TID had a lower EF, higher AJS, greater number of ischemic segments, and higher peak WMSI. Patients with TID in Group A (no collaterals) and Group C (jeopardized collaterals) had a greater percentage of multivessel disease than those in Group B (good collaterals). Presence of Group A or Group C collaterals was a predictor of TID even after controlling for multivessel disease, rest and peak WMSI, and left anterior descending artery disease. CONCLUSIONS: Transient ischemic LV dilatation on stress echocardiography is a marker for extensive and severe coronary artery disease and represents patients with angiographically absent collaterals or those with jeopardized coronary collaterals

BACKGROUND: Patients with prior myocardial infarction (MI) are at increased risk of subsequent cardiac events (MI or cardiac death). The incremental prognostic value and warranty time of a normal stress echocardiogram in this high-risk population is not well defined. METHODS: We evaluated 251 consecutive patients (62 +/- 11 years; 64% males) with remote history of MI (>6 weeks) undergoing stress echocardiography (83% dobutamine). Ischemia was defined as a new reversible wall motion abnormality and/or biphasic response. Follow-up for up to 4 years (mean 2.9 +/- 1.0 years) for confirmed MI (n = 7) and cardiac death (n = 15) were obtained. RESULTS: Stress echocardiography effectively risk stratified patients into normal versus abnormal subgroups (Event rate 0.8% per year vs 4.2% per year; P = 0.01; RR = 5.6, 95% CI = 1.3-24.7). In patients with a normal stress echocardiogram, the event rate at the end of 6, 12, and 18 months were <1% per year. After 18 months the event rate in patients with a normal stress echocardiogram increased greatly (>1% per year). Stress echocardiography yields incremental prognostic value over clinical and stress electrocardiographic variables (Global chi-square increased from 12.4 to 25 to 31.1, P < 0.0001 both groups). CONCLUSIONS: Stress echocardiography yields appropriate risk stratification and prognosis and provides incremental prognostic value over clinical and stress electrocardiographic variables even in patients with prior MI. A normal stress echocardiogram portends a benign prognosis (<1% event rate/year) for up to 18 months