1979Acta Medica ScandinavicaRequires access

The variability of ST segment in the early phase of acute myocardial infarction

Kristian Thygesen, Mogens Hørder, Bent Nielsen, Per Hyltoft Petersen

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Abstract

Abstract The ST segment elevation was measured hourly, via a single surface unipolar lead for 48 hours after admission, in 30 patients with acute myocardial infarction (AMI), admitted, on average, 2 hours after the onset of symptoms. In 14 patients with anterior AMI, the recordings were made through the precordial lead that initially showed the maximum ST elevation. In 16 patients with inferior AMI, the aV F lead was used. Twenty‐five control patients without AMI had the ST deviation measured hourly for 24 hours; 15 of them had the recording made via the Vs, aV F being used with the others. Our data for the reliability of the method showed that the variations in ST deviations in the control group were of the same magnitude as those observed with the measuring error of the method itself. The investigation showed that the spontaneous course of the hourly measured ST elevations in the early phase of AMI was marked by pronounced variability, and that this applied to both anterior and inferior infarctions. The intra‐individual patient variation of the ST elevation was significantly greater than in the control group of patients. The inter‐individual patient variation of the ST elevation with AMI was also significant. The ST elevation was correlated to heart rate, mean arterial blood pressure, heart rate multiplied by systolic blood pressure, and respiratory rate and it could be shown partly that there was a significant dispersion of the correlation coefficients within the separate correlation groups, and partly that the correlation coefficients were variable between the groups. It was also shown that nasal oxygen therapy and cardiac pain had no bearing on ST elevation. The variability of ST elevation was thus most often inexplicable and only rarely accounted for by alterations in the clinical status. It is generally accepted that ST segment elevation in the ECG is one of the characteistic features of acute myocardial infarction (AMI), but the electrophysiological basis of changes in the ST segment in myocardial ischaemia has not been completely clarified (1). In recent years, several investigations have been carried out where ST elevation has been used as a quantitative indicator of myocardial ischaemia. With multiple leads and epicardial and precordial mapping techniques, the sum of ST elevations has been used as an estimate of the extent of ischaemic injury after coronary occlusion in animals and after AMI in man (7, 8, 9, 12, 13). However, from the theoretical and experimental bases of ST segment deviation, it has been suggested that ST segment mapping is not a reliable measure of myocardial ischaemia (4, 5). Other investigators have pointed out the limitations of this method when used for the bedside estimate of ischaemic injury (11, 15). These studies suggest that there is a considerable variability of the ST deviation after AMI. Therefore, in an attempt to elucidate this problem, we have studied the ST elevation from hour to hour in a single surface lead for the first 2 days after admission of patients with AMI and have related the ST elevation to ST deviations measured hourly in patients without AMI. In addition, the ST elevations in patients with AMI have been related to heart rate, blood pressure, respiratory rate, retrosternal pain and oxygen treatment; clinical factors that can be associated with, or can influence, myocardial ischaemia.

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What this paper is about

Abstract The ST segment elevation was measured hourly, via a single surface unipolar lead for 48 hours after admission, in 30 patients with acute myocardial infarction (AMI), admitted, on average, 2 hours after the onset of symptoms. In 14 patients with anterior AMI, the recordings were made through the precordial lead that initially showed the maximum ST elevation. In 16 patients with inferior AMI, the aV F lead was used. Twenty‐five control patients without AMI had the ST deviation measured hourly for 24 hours; 15 of them had the recording made via the Vs, aV F being used with the others. Our data for the reliability of the method showed that the variations in ST deviations in the control group were of the same magnitude as those observed with the measuring error of the method itself. The investigation showed that the spontaneous course of the hourly measured ST elevations in the early phase of AMI was marked by pronounced variability, and that this applied to both anterior and inferior infarctions. The intra‐individual patient variation of the ST elevation was significantly greater than in the control group of patients. The inter‐individual patient variation of the ST elevation with AMI was also significant. The ST elevation was correlated to heart rate, mean arterial blood pressure, heart rate multiplied by systolic blood pressure, and respiratory rate and it could be shown partly that there was a significant dispersion of the correlation coefficients within the separate correlation groups, and partly that the correlation coefficients were variable between the groups. It was also shown that nasal oxygen therapy and cardiac pain had no bearing on ST elevation. The variability of ST elevation was thus most often inexplicable and only rarely accounted for by alterations in the clinical status. It is generally accepted that ST segment elevation in the ECG is one of the characteistic features of acute myocardial infarction (AMI), but the electrophysiological basis of changes in the ST segment in myocardial ischaemia has not been completely clarified (1). In recent years, several investigations have been carried out where ST elevation has been used as a quantitative indicator of myocardial ischaemia. With multiple leads and epicardial and precordial mapping techniques, the sum of ST elevations has been used as an estimate of the extent of ischaemic injury after coronary occlusion in animals and after AMI in man (7, 8, 9, 12, 13). However, from the theoretical and experimental bases of ST segment deviation, it has been suggested that ST segment mapping is not a reliable measure of myocardial ischaemia (4, 5). Other investigators have pointed out the limitations of this method when used for the bedside estimate of ischaemic injury (11, 15). These studies suggest that there is a considerable variability of the ST deviation after AMI. Therefore, in an attempt to elucidate this problem, we have studied the ST elevation from hour to hour in a single surface lead for the first 2 days after admission of patients with AMI and have related the ST elevation to ST deviations measured hourly in patients without AMI. In addition, the ST elevations in patients with AMI have been related to heart rate, blood pressure, respiratory rate, retrosternal pain and oxygen treatment; clinical factors that can be associated with, or can influence, myocardial ischaemia.

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Available abstract

Abstract The ST segment elevation was measured hourly, via a single surface unipolar lead for 48 hours after admission, in 30 patients with acute myocardial infarction (AMI), admitted, on average, 2 hours after the onset of symptoms. In 14 patients with anterior AMI, the recordings were made through the precordial lead that initially showed the maximum ST elevation. In 16 patients with inferior AMI, the aV F lead was used. Twenty‐five control patients without AMI had the ST deviation measured hourly for 24 hours; 15 of them had the recording made via the Vs, aV F being used with the others. Our data for the reliability of the method showed that the variations in ST deviations in the control group were of the same magnitude as those observed with the measuring error of the method itself. The investigation showed that the spontaneous course of the hourly measured ST elevations in the early phase of AMI was marked by pronounced variability, and that this applied to both anterior and inferior infarctions. The intra‐individual patient variation of the ST elevation was significantly greater than in the control group of patients. The inter‐individual patient variation of the ST elevation with AMI was also significant. The ST elevation was correlated to heart rate, mean arterial blood pressure, heart rate multiplied by systolic blood pressure, and respiratory rate and it could be shown partly that there was a significant dispersion of the correlation coefficients within the separate correlation groups, and partly that the correlation coefficients were variable between the groups. It was also shown that nasal oxygen therapy and cardiac pain had no bearing on ST elevation. The variability of ST elevation was thus most often inexplicable and only rarely accounted for by alterations in the clinical status. It is generally accepted that ST segment elevation in the ECG is one of the characteistic features of acute myocardial infarction (AMI), but the electrophysiological basis of changes in the ST segment in myocardial ischaemia has not been completely clarified (1). In recent years, several investigations have been carried out where ST elevation has been used as a quantitative indicator of myocardial ischaemia. With multiple leads and epicardial and precordial mapping techniques, the sum of ST elevations has been used as an estimate of the extent of ischaemic injury after coronary occlusion in animals and after AMI in man (7, 8, 9, 12, 13). However, from the theoretical and experimental bases of ST segment deviation, it has been suggested that ST segment mapping is not a reliable measure of myocardial ischaemia (4, 5). Other investigators have pointed out the limitations of this method when used for the bedside estimate of ischaemic injury (11, 15). These studies suggest that there is a considerable variability of the ST deviation after AMI. Therefore, in an attempt to elucidate this problem, we have studied the ST elevation from hour to hour in a single surface lead for the first 2 days after admission of patients with AMI and have related the ST elevation to ST deviations measured hourly in patients without AMI. In addition, the ST elevations in patients with AMI have been related to heart rate, blood pressure, respiratory rate, retrosternal pain and oxygen treatment; clinical factors that can be associated with, or can influence, myocardial ischaemia.

Key concepts: Medicine, Cardiology, Myocardial infarction, ST elevation, Internal medicine, Blood pressure, Heart rate, ST segment

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