It has been observed that during exercise electrocardiography, variable depression of the ST-segment may progress to ST-segment changes diagnostic of ischemia at peak exercise [1]. However, the authors have not given any representative electrocardiogram. Details of exercise electrocardiography finding of such cases are also not mentioned. Further, they have not mentioned that in some cases, transient ST-segment depression during exercise may be followed by diagnostic ST-segment changes only during recovery and not at peak exercise. Also there is no mention about the upward slope of ST-segment and downward slope of the Pq-segment in such cases. We have observed eight cases where transient ST-segment depression during exercise were followed by ST-segment changes diagnostic of myocardial ischemia at peak exercise or only during recovery. Detailed electrocardiographic findings and their significance are discussed. Possible pathogenetic mechanisms and clinical relevance of such changes are also discussed.

Case 1

A 62 years female presented for treadmill test. Her resting supine heart rate was 68 beats per minute. Resting supine blood pressure was 140/86 mm Hg. Resting supine electrocardiogram was normal except mild inversion of T waves in leads III, aVF and V₄. There were no new changes during standing and hyperventilation (Figure 1, mild inversion of T waves are marked as). She could exercise for 8:31 minutes (9.7 METs). Peak heart rate was 150 beats per minute (95% of age predicted maximal heart rate). Peak blood pressure was 200/90 mm Hg. Heart rate recovery was normal (52 beats in initial three minutes of recovery) A Review of the raw electrocardiogram during peak exercise ( exercise duration 8:30 minutes and heart rate 150 beats per minute ) revealed transient horizontal ST-segment depression in leads III, V₄, V₅ and V₆ . (Figure 2, marked as ). There was intermittent ST-segment elevation in lead aVR (Figure 2 marked as ). Pq- segment of the beats showing horizontal ST-segment depression was isoelectric (Figure 2, marked as ). There was cyclic variation in the amplitude of the QRS complex. Beats showing horizontal ST-segment depression had small QRS. (Figure 2, marked as ). There was no significant shift in base line and there were no artefacts. Averaged beats showed upsloping ST-segment in leads II, III, aVF, V₄, V₅ and V₆ (Figure 3, marked as). During fifth minute of recovery patient developed diagnostic ST-segment depression in leads II, III, aVF, V₃, V₄, V₅ and V₆ (Figure 4 marked as) and ST-segment elevation in lead aVR (Figure 4, marked as).

Figure 1: Pre-exercise electrocardiogram (averaged beats) of  first case recorded after standing and hyperventilation showing mild inversion of the T waves in leads III aVF and V₄ (Marked as ).

Figure 2: Raw electrocardiogram of case number 1 recorded at peak exercise showing transient horizontal ST-segment depression in leads III, V₄, V₅, V₆ (marked as ) intermittent ST-segment elevation in lead aVR (marked as ), isoelectric Pq segment of beats showing depression of ST-segment (marked as ), cyclic variation in amplitude of QRS complexes and low amplitude of the QRS complex in the beats showing ST-segment depression (marked as ).

Figure 3: Averaged beats of the electrocardiogram recorded at peak exercise from case number 1 showing upsloping ST-segment in leads II, III, aVF, V₄, V₅ and V₆ (marked as ).

Figure 4: Averaged beats recorded during fifth minute of recovery from case number 1 showing diagnostic ST-segment depressions in leads II, III, aVF V₄ , V₅ and V₆ (marked as ) and ST-segment elevation in lead aVR (marked as ).

Case 2

A 42 years male was referred for treadmill exercise electrocardiography test. Resting supine heart rate was 100 beats per minute. Resting supine blood pressure was 130/90 mm Hg. Resting supine electrocardiogram was normal. There were no new changes during standing and hyperventilation (Figure 5). He could exercise for 10:01 minutes (11.3 METs). Peak heart rate was 191 beats per minute (107% of the age predicted maximal heart rate). Peak blood pressure was 170/90 mm Hg. Heart rate recovery was normal (56 beats in initial three minutes). A review of the raw electrocardiogram recorded during second stage (exercise duration 6:00 minutes, heart rate 165 beats per minute) revealed transient ST-segment depression in leads I, II, aVF, V₃, V₄, V₅ and V₆ (Figure 6 marked as). Identical beat showed ST-segment elevation in lead aVR (Figure 6 marked as). Pq segment of the beats showing horizontal ST-segment depression was isoelectric (Figure 6, marked as). There was cyclic variation in the amplitude of the QRS complexes. Beats showing horizontal ST-segment depression had relatively small amplitude of the QRS complexes in leads V₄, V₅ and V₆ (Figure 6 marked ). There was no significant shift in baseline and there were no artifacts. Averaged beats (Figure 7) showed upsloping ST-segment (Figure 7 marked as) which were associated with significantly downsloping Pq segment (Figure 7 marked as). At peak exercise the patient developed diagnostic horizontal ST-segment depression in leads V₂, V₃, V₄, V₅ and V₆. (Figure 8, marked as) and ST-segment elevation in lead aVR (Figure 8, marked as). Pq segment was significantly downsloping (Figure 8 marked as). ST-segment changes gradually normalized during recovery.

                                   Figure 5: Preexercise electrocardiogram (averaged beats) from case number 2 recorded after standing and hyperventilation.

Figure 6: Raw electrocardiogram recorded during second stage of  exercise from case number 2 showing honsient ST-segment depression in leads I, II, aVF, V₃, V₄ , V₅ and V₆ (marked as  ), ST-segment elevation in lead aVR (marked as  ), isoelectric PQ segment of the beats showing ST-segment depression (marked as ), cyclic variation in the amplitudes of the QRS complexes and relatively small amplitude of the QRS complex in beats showing ST-segment depression in leads V₄ , V₅ and V₆ (marked as ).

Figure 7: Averaged beats of the electrocardiogram recorded during stage 2 of exercise from case number two showing upsloping ST-segment (marked as ) with significantly downsloping Pq segment (marked as ).

Figure 8: Averaged beats of electrocardiogram recorded at peak exercise from case number two showing diagnostic horizontal ST-segment depression in leads V₂, V₃, V₄ , V₅ and V₆ (marked as ), ST-segment elevation in lead aVR (marked as ) and significantly downsloping Pq segment (marked as ).

Case 3

A 55 years male was referred for treadmill exercise electrocardiography test. Resting supine heart rate was 72 beats per minute. Resting supine blood pressure was 120/80 mm Hg. Resting supine electrocardiogram was normal. There were not changes during standing and subsequent hyperventilation (Figure 9) Patient could exercise for 9:31 minutes (10.8 METs). Peak heart rate was 161 beats per minute (98% of the age predicted maximal heart rate). Peak blood pressure was 180/80 mm Hg. Heart rate recovery was normal ( 54 beats in initial three minutes of recovery). A review of the raw electrocardiogram recorded during third stage of exercise (exercise duration 9:00 minutes, heart rate 157/minute) revealed intermittent ST-segment depression in leads II, aVF and V₄ (Figure 10, marked as ). ST-segment was elevated in the corresponding beats in lead aVR (Figure 10 marked as ). There was cyclic variation in the amplitude of the QRS complexes. ST-segment changes were prominent in beats having relatively low amplitude of the QRS complexes (Figure 10, marked as ). Pq - segment of these beats was markedly downsloping (Figure 10, marked as ). There was no significant shift in the base line and there were no significant artifacts. Averaged beats of the electrocardiogram recorded during stage 3 showed upsloping ST-segment (Figure 11 marked as ) with markedly downsloping Pq- segment (Figure 11 marked as ). During fifth minute of recovery patient developed downsloping ST-segment in leads II, III, aVF, V₄, V₅ and V₆ (Figure 12, marked as). Pq- segment was isoelectric (Figure 12, marked as).

Figure 9: Averaged beats of pre-exercise electrocardiogram of case number three recorded after standing and hyperventilation.

Figure 10: Raw electrocardiogram of case number 3 recorded during third stage of exercise showing intermittent depression of the ST-segment in leads II, aVF and V₄ (marked as  ), elevation of the ST-segment in lead aVR (marked as ), cyclic variation in the amplitude of the QRS complexes, relatively low amplitude of the QRS complex in beats showing depression of the ST-segment (marked as ) and markedly downsloping Pq segment (marked as ).

Figure 11: Averaged beats of the electrocardiogram recorded during stage 3 (case number 3) showing upsloping ST-segment (marked as ) and markedly downsloping Pq-segment (marked as ).

Figure 12: Averaged beats of the electrocardiogram recorded during the fifth minute of recovery of case number three showing downsloping ST-segment in leads II, III, aVF, V₃, V₄ , V₅ and V₆ (marked as ). Pq-segment in isoelectric (marked as ). ST-segment is elevated in lead aVR (marked as ).

Case 4

A 60 years male was reffered for treadmill exercise electrocardiography test. Resting supine heart rate was 69 beats per minute. Resting supine blood pressure was 120/80 mm Hg. Resting supine electrocardiogram was normal. There were no changes during standing and subsequent hyperventilation (Figure 13). Patient could exercise for 12:00 minutes (13.5 METs). Peak heart rate was 168 beats per minute (105% of the age predicted maximal heart rate). Peak blood pressure was 190/80 mm Hg. Heart rate recovery was normal (65 beats in the initial three minutes of recovery). A review of the raw electrocardiogram recorded at peak exercise (exercise duration 11:59 minutes, heart rate 168 beats per minute) revealed intermittent horizontal ST-segment depression in leads III, aVF and V₅ (Figure 14, marked as). Corresponding beats showed ST-segment elevation in lead aVR (Figure 14 marked as). There was cyclic variation in the amplitude of the QRS complexes. ST-segment depression were prominent in beats having relatively low amplitude of QRS (Figure 14, marked as ). Pq-segment of these beats was markedly downsloping (Figure 14 marked as). Averaged beats of the electrocardiogram recorded at peak exercise showed minimal up sloping ST-segment depression (Figure 15 marked as) with markedly down sloping Pq-segment (Figure 15, marked as) in leads II, III, aVF, V₄, V₅ and V₆. Patient developed down sloping ST-segment depression in leads II, III, aVF, V₄, V₅ and V₆ during seventh minute of recovery (Figure 16, marked as). At this time the Pq-segment were isoelectric (Figure 16, marked).

Figure 13: Preexercise electrocardiogram (averaged beats) from case number four recorded after standing and hyperventilation.

Figure 14: Raw electrocardiogram recorded at peak exercise from case number four. It shows intermittent ST-segment depression in leads III, aVF and V₅ (marked as ). Corresponding beats in lead aVR show ST-segment elevation (marked as ). Beats showing ST-segment depression had low amplitude of the QRS complex (marked as ). Pq-segment of these beats is markedly downsloping (marked as  ).

Figure 15: Electrocardiogram (averaged beats) recorded at peak exercise from case number four. It shows minimal upsloping ST-segment (marked as  ) with markedly downsloping Pq-segment (marked as ) in leads II, III, aVF, V₄, V₅ and V₆.

Figure 16: Electrocardiogram of case number four recorded  during seventh minute of recovery. It shows downsloping ST-segment depression in leads II, III, aVF, V₄, V₅ and V₆ (marked as ). Pq segment (marked as ) is isoelectric.

Case 5

A 70 years male was referred for treadmill exercise electrocardiography test. Resting supine heart rate was 67 beats per minute. Resting supine blood pressure was 130/80 mm Hg. Resting supine electrocardiogram was normal. There were no changes during standing and subsequent hyperventilation (Figure 17). Patient could exercise for 9:30 minutes (10.8 METs). Peak heart rate was 173 beats per minute (123% of the age predicted maximal heart rate). Peak blood pressure was 180/80 mm Hg. Heart rate recovery was normal (75 beats in the first three minutes of recovery). Review of raw electrocardiogram recorded during third stage of exercise (exercise duration 9:00 heart rate 167 beats per minute) showed transient ST-segment depression in leads V₃ to V₆ (Figure 18, marked as ). There was cyclic variation in the amplitude of QRS complexes. In leads V₃ and V₄, ST-segment depression was prominent in beats with large QRS. However, in leads V₅ and V₆, ST-segment depression had no correlation with the amplitude of the QRS complex. Pq-segment of these beats was isoelectric (Figure 18 marked as). There was no significant shift in the base line and there were no significant artefacts. Limb leads could not be analysed because of significant vibrations. Averaged beats of the electrocardiogram recorded during third stage of the exercise showed upsloping depression of the ST-segment in leads V₄, V₅ and V₆ (Figure 19, marked as). In the averaged beats, the Pq segment was significantly downsloping (Figure 19, marked as). During seventh minute of recovery , patient developed horizontal ST-segment in leads II, III, aVF (Figure 20, marked as) and shallow inversion of T waves in leads aVL, V₄, V₅ and V₆ (Figure 20, marked as ). At this time the Pq-segment were isoelectric (Figure 20, marked).

Figure 17: Pre-exercise electrocardiogram (averaged beats) from case number five, recorded after standing and hyperventilation.

Figure 18: Raw electrocardiogram recorded during the third stage of exercise from case number five. It shows transient ST-segment depression in leads V₃, V₄, V₅ and V₆ (marked as ). Pq-segment is isoelectric (marked as ).

Figure 19: Electrocardiogram (averaged beats) recorded during third stage of exercise from case number five. It shows upsloping ST-segment in leads V₄, V₅ and V₆ (marked as ). Pq segment is significantly downsloping (marked as ).

Figure 20: Electrocardiogram from case number five recorded during seventh minute of recovery. It shows horizontal ST-segment in leads II, III, aVF (marked as ) and shallow T wave inversion in leads V₄, V₅ and V₆ (marked as ). Pq segments are isoelectric (marked as  ).

Case 6

A 62 years male was referred for treadmill exercise electrocardiography test. He was a known case of systemic hypertension and diabetes mellitus. Echocardiography showed mild concentric hypertrophy and impaired relaxation of the left ventricle. Resting supine heart rate was 85 beats per minute. Resting supine blood pressure was 130/90 mm Hg. Resting supine electrocardiogram was normal. There were no changes during standing and subsequent hyperventilation (Figure 21). Patient could exercise for 7:21 minutes (5.2 METs). Peak heart rate was 157 beats per minute (99% of the age predicted maximal heart rate). Peak blood pressure was 190/90 mm Hg. Heart rate recovery was normal (59 beats in initial three minute of recovery). A review of the raw electrocardiogram recorded at peak exercise (exercise duration 7:30 minutes, heart rate 152 beats per minute) revealed transient ST-segment depression in leads V₃, V₄ and V₆ (Figure 22, marked as). The Pq-segment of these beats could not be analysed because of downwards shift of the base line from the preceding beat (second beat). There was no shift in baseline as compared to subsequent beats (4^th to 7^th beats). There were no significant artefacts. Limb leads and lead V₅ could not be analysed due to significant drift in base line. During third minute of recovery, patient developed horizontal depression of the ST-segment in leads V₂, V₃ and V₄ (Figure 23, marked as).

Figure 21: Preexercise electrocardiogram (averaged beats) from case number six, recorded after standing and hyperventilation.

Figure 22: Raw electrocardiogram recorded at peak exercise from case number six. It shows transient ST-segment depression in leads V₃, V₄ and V₆ (marked as ).

Figure 23: Electrocardiogram recorded during third minute of recovery from case number six. It shows horizontal depression of ST-segment in leads V₂, V₃ and V₄.

Case 7

A 52 years male presented for treadmill exercise electrocardiography. Resting supine heart rate was 78 beats per minute. Resting supine blood pressure was 120/80 mm Hg. Resting supine electrocardiogram was normal. There were no changes during standing and subsequent hyperventilation (Figure 24). Patient could exercise for 9:03 minutes (10.2 METs). Peak heart rate was 167 beats per minute (99% of the age predicted maximal heart rate). Peak blood pressure was 160/80 mm Hg. Heart rate recovery was normal (58 beats in initial three minutes of recovery). Review of the raw electrocardiogram recorded during third stage of exercise (exercise time 9:00 minutes, heart rate167 beats per minutes) revealed transient depression of the ST-segment in leads II, III, aVF, V₄, V₅ and V₆ (Figure 25, marked as ). Corresponding beat showed elevation of the ST-segment in lead aVR (Figurte 25, marked as ). There was cyclic variation in the amplitude of the QRS complexes in leads II, III, aVF, V₄, V₅ and V₆. ST-segment depression was present in beats with large amplitude of the QRS (Figure 25, marked as ). In lead V₂, ST-depression was present in the beat with low amplitude of QRS (Figure 25 marked as). The Pq-segment of these beats was markedly downsloping (Figure 25 marked as ). Averaged beats from stage three showed rapid upsloping ST-segment (Figure 26, marked as ) and significantly down sloping of Pq segments (Figure 26, marked as ). Averaged beats recorded at peak exercise (9:02 minutes) showed similar changes. During fifth minute of recovery, electrocardiogram showed horizontal ST-segment depression in leads II, III, aVF, V₄, V₅ and V₆ (Figure 27, marked as ). At this time Pq-segment was isoelectric (Figure 27, marked as ).

Figure 24: Preexercise electrocardiogram (averaged beats) from case number seven, recorded after standing and hyperventilation.

Figure 25: Raw electrocardiogram recorded during third stage of exercise from case number seven. It shows transient depression of the ST-segment in leads II, III, aVF, V₂, V4, V₅ and V₆ (marked as ). Corresponding beats shows elevation of the ST-segment in lead aVR (marked as  ), QRS amplitude of the beats showing depression of the ST-segment are marked as and. Pq segments are markedly downsloping (marked as ).

Figure 26: Averaged beats from stage 3 of exercise from case 7 showing rapid upsloping ST-segments (marked as  ) and significantly downsloping Pq segment (marked as ).

Figure 27: Averaged beats recorded during fifth minute of recovery from case number seven. It shows horizontal depression of the ST-segment in leads II, III, aVF, V₄, V₅ and V₆ (marked as ). Pq-segments are isoelectric (marked as ).

Case 8

A 70 years male was referred for treadmill exercise electrocardiography. He was a known diabetic. Resting supine heart rate was 62 beats per minute. Resting supine blood pressure was 130/80 mm Hg. Resting supine electrocardiogram was normal. There were no changes during standing and subsequent hyperventilation (Figure 28). Patient could exercise for 8:00 minutes (10.0 METs). Peak heart was 150 beats per minute (100% of the age predicted maximal heart rate). Peak blood pressure was 170/80 mm Hg. Heart rate recovery was normal. (59 beats within initial three minute of recovery). Review of raw electrocardiogram recorded during stage 2 of exercise (exercise duration 6:00 minutes, HR 134/minute) showed transient depression of the ST-segment in leads V₂, V3 and V₄ (Figure 29 marked as ). The Pq-segment of these beats was sharply downsloping (Figure 29, marked as ). Averaged beats of the electrocardiogram recorded at peak exercise revealed horizontal ST-segment depression in leads I, II, aVF, V₂, V₃, V₄, V₅ and V₆ (Figure 30 marked as ). The Pq-segment of these leads was sharply downsloping (Figure 30, marked as ). ST-segment was elevated in lead aVR (Figure 30, marked as ). During fifth minute of recovery, patient developed downsloping ST-segment depression in leads II, III, aVF, V₂, V₃, V₄, V₅ and V₆ (Figure 31 marked as ). At this time, the Pq-segments were isoelectric.

Figure 28: Preexercise electrocardiogram (averaged beats) from case number eight, recorded after standing and hyperventilation.

Figure 29: Raw electrocardiogram recorded during second stage of exercise from case number eight. It shows transient depression of the ST-segment in leads V₂, V₃ and V₄ (marked as ). Pq segment of these beats are rapidly downsloping (marked as ).

Figure 30: Averaged beats of the electrocardiogram of case number eight recorded at peak exercise. It shows horizontal depression of the ST-segment in leads I, II, III, aVF, V₂, V₃, V₄, V₅ and V₆ (marked as ). Pq segment of these leads is rapidly downsloping. ST-segment is elevated in lead aVR (marked as  ).

Figure 31: Averaged beats of the electrocardiogram of case number eight, recorded during fifth minute of recovery. It shows downsloping depression of the ST-segment in leads II, III, aVF, V₂, V₃, V₄, V₅ and V₆ (marked as  ). Pq-segments are isoelectric.

Intermittent ST-segment depression preceding diagnostic ST-segment changes have been attributed to variations in left ventricular filling and left ventricular enddiastolic pressure related to the phase of respiration [1]. It has been suggested that in individuals with coronary artery disease and impaired relaxation of the left ventricle, intermittent increase in left ventricular enddiastolic pressure could result in intermittent increase in left ventricular myocardial oxygen demand resulting in intermittent depression of the ST-segment. Previous workers observed that intermittent depression of the ST-segment was associated with increase in the amplitude of the QRS complex. In two of our cases (case 5 and 7), transient ST-segment depression was associated with increase in amplitude of the QRS complex. In two cases there was no appreciable difference in amplitude of the QRS complex. In remaining four cases (Cases no. 1, 2, 3 and 4), ST-segment depression was associated with decrease in amplitude of the R wave in the lateral precordial leads. Decrease in the total amplitude of the QRS complex in lateral precordial leads is likely to occur during inspiration due to covering of the lateral part of the anterior surface of heart by the distended left lung. Our observations, therefore, do not support the hypothesis intermittent ST-segment depression being due to intermittent increase in the end diastolic pressure of the left ventricle. Left ventricular end diastolic pressure increases in expiration due to increased filling of the left ventricle in expiration. We observed that depression of the ST-segment was transient i.e. localized to one to three beats only. This is unlikely to be due to macro or micro vascular spasm or some problem at the cellular level. Changes produced by these pathologies are likely to last longer than one to three beats only. These changes were not mechanical because there was no significant shift in the baseline and there were no artefacts. There was no simultaneous increase in the amplitude of the P wave. Therefore, these ST-segment depressions could not be attributed to prominent atrial repolarization wave (Ta wave) - causes of false positive ST-segment changes. These transient ST-segment depressions cannot be attributed to standing posture and/or hyperventilation as such changes were not observed on standing and during hyperventilation before start of exercise [2]. Any change in autonomic tone is unlikely to be so transient. These changes were observed during peak exercise or during the stage preceding peak exercise. ST-segment depression were present in the same beats in inferior as well as lateral precordial leads. Further, these depression of the ST-segment were associated with elevation of the ST-segments in lead aVR. ST-segment elevation of 1mm or more in lead aVR in association with ST-segment depression in other leads is highly suggestive of coronary artery disease [3,4]. These changes were seen at exercise duration of 6 to 9 minutes and at more than the target heart rate as calculated from the age predicted maximal heart rate. Therefore, these transient ST-segment depressions were most likely related to transient myocardial ischemia near peak exercise.

Some other possibilities can be considered to explain such transient depressions of the ST-segment at or before peak exercise. Low levels of carbon dioxide due to tachypnoea could be one possibility. Low carbon oxide concentration in the blood has been shown to increase coronary vascular tone [5,6]. Another contributing factor could be decreased filling of the left ventricle during inspiration. Inspiration is associated with decreased intrathoracic pressure and suction of blood from the venacavas into the right ventricle [7]. Increased right ventricular filling shifts the interventricular septum to the left (ventricular interaction). This results in reduced filling of the left ventricle. Reduced left ventricular filling causes transient reduction stroke volume and aortic systolic pressure. This could transiently reduce pressure dependent coronary flow in persons with coronary artery disease. One mm or greater of horizontal or downsloping ST-segment depression are considered suggestive of myocardial ischemia if such changes are seen in three consecutive beats [3]. In some of our cases, transient ST-segment depressions during exercise were mostly confined to one or two beats only. We feel that such changes should not be ignored because they were followed by diagnostic ST-segment changes at peak exercise or during recovery. ST-segment changes during recovery are as significant as changes at peak exercise [3]. Such transient ST-segment depression should be interpreted in the clinical context especially if the recovery electrocardiograms are not recorded for adequate period. Four of our cases (case no. 3, 4, 6, 7) had upsloping ST-segment at peak exercise. All these cases had markedly downsloping Pq-segment. Such upsloping ST-segment depressions are considered to have low specificity in diagnosing coronary artery disease [3,8]. All these cases had horizontal or downsloping ST-segment during recovery. Horizontal or downsloping ST-segment depression of 1mm or more during recovery are diagnostic of myocardial ischemia [9]. We, therefore, fell that upsloping ST-segment during exercise should not always be considered as false positive only because of their alignment with the slope of the preceding Pq- segment. Significance of such changes should be decided only after evaluating changes during recovery. An increase in R wave amplitude at peak exercise is considered suggestive of coronary artery disease [1]. We observed significant respiratory variation in amplitude of the R wave in inferior as well as lateral precordial leads. These changes were most appoint at peak exercise or in the stage preceding peak exercise. This is so because at these levels of exercise, patients have tachypnoea and the recorded electrocardiogram covers one or more respiratory cycles. R wave amplitude in averaged electrocardiogram significantly depends on the beats selected by the computer for averaging. We, therefore, feel that it is not justified to give undue significance to changes in the amplitude of the R wave in interpreting electrocardiogram recorded during exercise.

We have some additional impressions that are not directly related to the topic of this study. It is suggested that chronotropic incompetence predicts angiographic severity of coronary artery disease [10]. All of our cases attained more than 85% of the age predicted maximal heart rate using the formula of 220 -age. None of these had chronotrpopic incompetence which is defined as failure to attain at least 85% of the age predicted maximal heart rate during exercise. All these cases had electrocardiographic evidence of myocardial ischemia. Our observation, therefore, also suggest that absence of chronotropic incompetence cannot exclude significant myocardial ischemia. Similarly it has been suggested that delayed heart rate recovery after treadmill test correlates with mortality [11]. All of our cases had normal heart rate recovery (heart rate reduction of 50 beats per minute or more during initial three minutes of recovery). We, therefore, feel that normal heart rate recovery also cannot exclude myocardial ischemia during exercise electrocardiography. However, study of large number of cases in required to confirm these impressions.

Transient or intermittent depressions of the ST-segment may precede diagnostic ST-segment changes occurring at peak exercise or during recovery. Such changes usually occur at peak exercise or stage preceding peak exercise. Such changes should suggest underlying myocardial ischemia especially if the changes are seen in the same beats in more than one contiguous leads are associated with ST-segment elevation in the identical beat in lead aVR and there are diagnostic ST-segment changes during recovery. Shift in the base line and other artifacts should be excluded. Possibility of myocardial ischemia should not be excluded even if such ST-segment depression is seen only in one or two beats or is accompanied by rapidly down sloping Pq-segment. Recovery electrocardiograms should be recorded for at least eight minutes because in some cases diagnostic ST-segment changes may appear only after sixth minute of recovery. R wave amplitude shows significant, respiration dependent, change in inferior as well as lateral precordial chest leads. Such changes are also most prominent at or before peak exercise. Therefore, undue significance should not be given to changes in amplitude of the R wave in diagnosing myocardial ischemia. Diagnostic and prognostic significance of these observations needs study of larger number of patients, correlation with coronary angiography and long term follow up.

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