Prodromal Unstable Angina in Acute Myocardial Infarction
Background: An estimated 50% of patients with myocardial infarction have prodromal unstable angina. There is controversy over whether prodromal unstable angina identifies a group of patients at lower risk of short- and long-term death and the clinical importance of recording this event.
Methods: Of 207 patients enrolled at a single Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) site, 196 survived the 24 hours after presentation, achieved peak creatine kinase MB concentrations, and were classified as having either abrupt symptom onset or prodromal unstable angina in the 2 weeks before myocardial infarction. Creatine kinase MB peak was used to categorize infarct size as aborted myocardial infarction, minor myocardial damage, or extensive myocardial injury. Follow-up was performed at 24 hours, 30 days, 1 year, and 5 years. Multiple variables, including prodromal unstable angina, time to treatment, age, sex, previous infarction and infarct location, were analyzed for predicting infarct size. Also, these variables plus peak creatine kinase MB level and a combined variable of prodromal unstable angina and peak creatine kinase MB level were examined for predicting survival.
Results: Mortality rate was 2.5% within 24 hours, 9.0% at 30 days, 13.5% at 1 year, and 27.1% at 5 years. Patients categorized as either aborted infarction or minor myocardial damage were significantly more likely to have prodromal unstable symptoms (81.3% vs 51.2%, P < .001) and better survival at each follow-up period. Prodromal presentation was the most significant predictor of infarct size category (P = .001). Five-year survival was predicted by age (P < .0001), peak creatine kinase MB level (P = .007), infarct location (P = .009), the combined variables (P = .029), and prodromal unstable angina (P = .017). Prodromal unstable angina had the highest odds ratio for 5-year survival at 3.83 (95% confidence interval 1.27-11.47).
Conclusions: Prodromal unstable angina is a strong predictor of infarct size and survival. Recognizing prodromal unstable angina is important for clinically assessing prognosis.
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Prodromal unstable angina represents a continuum of acute ischemic episodes that have also been called preinfarction angina, premonitory angina, intermittent angina, winking and blinking angina, and stuttering angina. Prodromal unstable angina occurring shortly before acute myocardial infarction (AMI) is distinct from "previous angina" because this latter term encompasses symptoms that may have occurred long before the index event. Prodromal unstable angina likely represents the clinical constellation of the cyclic coronary flow phenomenon in which the affected artery undergoes episodic ischemia, shown on the electrocardiogram as oscillation in the ST-segment elevation.
Prodromal unstable angina occurs in an estimated 50% of patients according to a recent editorial by Braunwald. Although there is no unanimity that benefit is conferred by prodromal unstable angina, its presence has been linked to improved short-term, 1-year, and 5-year outcomes. Several physiologic mechanisms may contribute to improved outcome. One mechanism is the opening of thin-walled vascular channels that connect coronary arteries, termed coronary collaterals, caused by the increased pressure resulting from subtotal occlusion. Another possible mechanism is ischemic preconditioning of myocardium, a protective process involving brief episodes of ischemia before a sustained occlusion. Ischemic preconditioning is believed to have an energy-sparing protective effect on myocardium by stimulating A1-adenosine receptors, which serves to reduce the cellular influx of calcium. A third possible mechanism involves the formation of thrombi that are less resistant to fibrinolysis when preceded by prodromal unstable angina. Andreotti et al suggested that distinct patterns of chest pain represent 2 types of thrombus growth: recurrent transient growth causing prodromal angina and persistent growth resulting in abrupt symptoms onset. Thus cyclic coronary flow, which occurs in 30% to 50% of patients with AMI, may be the alternative to sustained coronary thrombosis and myocardial necrosis.
Regardless of the mechanism(s) responsible, AMI preceded by prodromal unstable angina may be associated with a more favorable outcome. The purpose of this study was to examine this issue and whether prodromal unstable angina independently contributes to the ability of time to treatment and other variables for predicting infarct size and survival at 30 days, 1 year, and 5 years.
Background: An estimated 50% of patients with myocardial infarction have prodromal unstable angina. There is controversy over whether prodromal unstable angina identifies a group of patients at lower risk of short- and long-term death and the clinical importance of recording this event.
Methods: Of 207 patients enrolled at a single Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) site, 196 survived the 24 hours after presentation, achieved peak creatine kinase MB concentrations, and were classified as having either abrupt symptom onset or prodromal unstable angina in the 2 weeks before myocardial infarction. Creatine kinase MB peak was used to categorize infarct size as aborted myocardial infarction, minor myocardial damage, or extensive myocardial injury. Follow-up was performed at 24 hours, 30 days, 1 year, and 5 years. Multiple variables, including prodromal unstable angina, time to treatment, age, sex, previous infarction and infarct location, were analyzed for predicting infarct size. Also, these variables plus peak creatine kinase MB level and a combined variable of prodromal unstable angina and peak creatine kinase MB level were examined for predicting survival.
Results: Mortality rate was 2.5% within 24 hours, 9.0% at 30 days, 13.5% at 1 year, and 27.1% at 5 years. Patients categorized as either aborted infarction or minor myocardial damage were significantly more likely to have prodromal unstable symptoms (81.3% vs 51.2%, P < .001) and better survival at each follow-up period. Prodromal presentation was the most significant predictor of infarct size category (P = .001). Five-year survival was predicted by age (P < .0001), peak creatine kinase MB level (P = .007), infarct location (P = .009), the combined variables (P = .029), and prodromal unstable angina (P = .017). Prodromal unstable angina had the highest odds ratio for 5-year survival at 3.83 (95% confidence interval 1.27-11.47).
Conclusions: Prodromal unstable angina is a strong predictor of infarct size and survival. Recognizing prodromal unstable angina is important for clinically assessing prognosis.
>
Prodromal unstable angina represents a continuum of acute ischemic episodes that have also been called preinfarction angina, premonitory angina, intermittent angina, winking and blinking angina, and stuttering angina. Prodromal unstable angina occurring shortly before acute myocardial infarction (AMI) is distinct from "previous angina" because this latter term encompasses symptoms that may have occurred long before the index event. Prodromal unstable angina likely represents the clinical constellation of the cyclic coronary flow phenomenon in which the affected artery undergoes episodic ischemia, shown on the electrocardiogram as oscillation in the ST-segment elevation.
Prodromal unstable angina occurs in an estimated 50% of patients according to a recent editorial by Braunwald. Although there is no unanimity that benefit is conferred by prodromal unstable angina, its presence has been linked to improved short-term, 1-year, and 5-year outcomes. Several physiologic mechanisms may contribute to improved outcome. One mechanism is the opening of thin-walled vascular channels that connect coronary arteries, termed coronary collaterals, caused by the increased pressure resulting from subtotal occlusion. Another possible mechanism is ischemic preconditioning of myocardium, a protective process involving brief episodes of ischemia before a sustained occlusion. Ischemic preconditioning is believed to have an energy-sparing protective effect on myocardium by stimulating A1-adenosine receptors, which serves to reduce the cellular influx of calcium. A third possible mechanism involves the formation of thrombi that are less resistant to fibrinolysis when preceded by prodromal unstable angina. Andreotti et al suggested that distinct patterns of chest pain represent 2 types of thrombus growth: recurrent transient growth causing prodromal angina and persistent growth resulting in abrupt symptoms onset. Thus cyclic coronary flow, which occurs in 30% to 50% of patients with AMI, may be the alternative to sustained coronary thrombosis and myocardial necrosis.
Regardless of the mechanism(s) responsible, AMI preceded by prodromal unstable angina may be associated with a more favorable outcome. The purpose of this study was to examine this issue and whether prodromal unstable angina independently contributes to the ability of time to treatment and other variables for predicting infarct size and survival at 30 days, 1 year, and 5 years.
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