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Sally Greaves

Publications and source records attributed to Sally Greaves.

4 recordsLinked to original sources
PubMed2004

Angina pectoris prior to myocardial infarction protects against subsequent left ventricular remodeling.

OBJECTIVES: To investigate the hypothesis that prior angina pectoris confers protection from remodeling occurring after myocardial infarction (MI), we analyzed echocardiograms from the Healing and Early Afterload Reducing Therapy (HEART) trial. BACKGROUND: Ischemia occurring before MI has been shown to reduce infarct size in experimental models and to improve outcomes in patients. The extent to which ischemia occurring before MI influences subsequent changes in ventricular size and function is unclear. METHODS: We studied 283 patients enrolled in the HEART trial who had echocardiograms at days 1 and 90 after MI. Left ventricular (LV) dilation from days 1 to 90 was used as a measure of LV remodeling. We explored the relationship between symptomatic angina occurring before infarction and subsequent LV remodeling. RESULTS: In patients who reported angina (n = 111) during the three months preceding MI, LV volume change was -0.73 +/- 2.6 ml over the 90-day post-MI period, compared with 6.8 +/- 2.6 ml for patients (n = 172) without angina (p = 0.017). In contrast, there were no differences in changes in ejection fraction based on prior angina. Maximal creatine kinase was significantly lower in patients with prior angina (2,119 +/- 1,729 vs. 2,701 +/- 2,088, p = 0.016). In a multivariate model, prior angina remained protective for ventricular remodeling after adjusting for age, gender, baseline ejection fraction, Killip class, baseline end-diastolic volume, and drug treatment group (p = 0.042). However, the protective effect of pre-infarction angina appeared to be attenuated in diabetic patients. CONCLUSIONS: Ischemic symptoms occurring before MI may protect against LV remodeling. These protective effects may be secondary to recruitment of collaterals or ischemic preconditioning of the myocardium, and they appear to be attenuated in diabetic patients.

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PubMed2003

Value of the electrocardiogram in predicting left ventricular enlargement and dysfunction after myocardial infarction.

To identify electrocardiographic predictors of left ventricular enlargement or persistent dysfunction following a myocardial infarction. Baseline and predischarge 12-lead electrocardiograms (ECGs) from 272 patients with anterior myocardial infarction who were enrolled in the Healing and Early Afterload Reducing Therapy trial were evaluated and related to echocardiographic data obtained at baseline and day 90. ST-segment elevation, QRS score, and number of negative T waves were assessed at both time points. The majority of patients (87%; n = 237) received reperfusion therapy. Multivariate models were used to adjust for potential confounders, including maximal creatine kinase level and ejection fraction at baseline. None of the baseline electrocardiographic variables independently predicted ventricular enlargement or recovery of function. In contrast, the sum of ST- and maximum ST-segment elevation, and the number of leads with ST-segment elevation > or =1 mm in the predischarge ECG, were independent predictors of ventricular enlargement from baseline to day 90. Each lead with ST-segment elevation > or =1 mm was associated with 3.5 mL of ventricular enlargement (95% confidence interval [CI]: 1.6 to 5.5 mL; P <0.0001). Similarly, the sum of ST-segment elevation (odds ratio [OR] = 0.78; 95% CI: 0.69 to 0.89; P <0.0001), the maximum ST-segment elevation (OR = 0.25; 95% CI: 0.13 to 0.45; P <0.0001), and the number of leads with ST-segment elevation > or =1 mm (OR = 0.58; 95% CI: 0.45 to 0.74; P <0.0001) were independently associated with a lower likelihood of recovery of function at day 90. Predischarge ECG may be a useful tool for early identification of patients at risk of ventricular enlargement and persistent dysfunction following myocardial infarction.

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