READERS’ COMMENTS

Segment Changes Detected by Ambulatory Electrocardiography After Acute Myocardial Infarction

Quintana et al’ report on the usefulness of ambulatory moni- toring for detection of ST-seg- ment shift in predicting subse- quent mortality and reinfarction in patients after acute myocardial in- farction. While these observations are not new, there is a convincing demonstration that detection of ST shift should be made in rela- tion to a 24-hour ST level median. There are also a number of tech- nical and clinical aspects of this study that may limit its general- izability .

It is not clear why bipolar lead V, , as opposed to a more conven- tionaI inferior lead, was chosen in addition to Vs. ST depression on ambulatory monitoring in lead V, is rare and it would be of interest to know whether most ST depres- sion was detected in lead V5 and most of ST elevation in lead V, .

ST elevation was detected at J + 0 to 5 ms, which has not been studied before. The authors sug- gest that this measurement is, for some reason, more specific for ischemia than the measurement of ST elevation at J + 60 or J + 80 ms. Their rationale is unfounded. Furthermore, since every episode of ischemic ST shift detected by computer-based algorithm should be visually verified by an experi- enced observer, 2,3 their concern of nonspecificity of J + 60/80 ms measurement in cases of tachycar- dia is unfounded. Were all ische- mic ST elevation and ST depres- sion episodes visually verified in this study? If so, was there any real difference between the speci- ficityofJ+Oto5msandJ+60/ 80 ms measurements?

ST elevation was not found to be predictive of poor outcome, and given that its use during am-

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bulatory monitoring with respect to risk stratification is uncertain, the authors should provide a rea- son for their conclusion that ST depression and ST elevation com- pared with ST depression alone is the best predictor of prognosis in this group of patients. Because most of the prognostic significance in the group with either ST depres- sion or ST elevation is related to the prognostic importance of ST de- pression, the addition of ST eleva- tion and its presumed importance as an indicator of recurrent ischemia remains unproven and should be clarified by the authors.

The most significant concern arising from this study relates to patient selection. It is not clear how 203 patients with acute myo- cardial infarction were arrived at: Were they presenting with chest pain to the emergency room? Was there any electrocardiographic re- quirement (e.g., ST elevation or ST depression)? Were these con- secutive patients? The mortality in the study group of 74 patients is dramatic and appears to occur mostly within the first year (Fig- ure 3 ) . Thus, there is a cumulative mortality of approximately 208 within the first month and approx- imately 30% by the end of the first year. Given the general character- istics of this patient population (Table I), it is unclear why such high mortality is observed in this small sample of patients, making the author’s observations less gen- eralizable. Did these patients un- dergo invasive or noninvasive risk stratification, and if so, what were the results and why were these pa- tients not intervened upon given the extremely poor outcome ob- served?

Anatdy langer, MD Toronto, Ontario, Canada

17 August 1995

1. Quintana M, Lindvall K, Brolund F. Assessment and significance of ST-segment changes detected by ambulatory electrocardiography after acute myocar- dial infarction. Am J Car&l 1995;76:6- 13. 2. Langer A, Minkowitz J, Dorian P, Casella L, Harris L, Morgan CD, Armstrong PW. Pathophy- sioloev and oroenostic siwificance of Holter-de- tected ST segment depression after myocardial in- farction. J Am Cd Car&l 1992;20: I3 13- 13 17.

3. Langer A, Kmcoff MW, Klootwijk P, Veldkamp R. Simoons ML, Granger C, Califf RM, Armstrong PW. Noninvasive assessment of speed and stability of infarct-related artery reperfusion: results of the GUSTO ST segment monitoring study. .I Am Cdl Cortliol 1995;25: 1552- 1557.

REPLY: Langer has raised some questions regarding the prognostic value of ST-segment changes de- tected by ambulatory monitoring after acute myocardial infarction (AMI) reported by us.’ We wish to thank Langer for the valuable com- ments on our manuscript, but we also want to clarify some inconsis- tencies in the criticism.

We agree with Langer in that the addition of an inferior lead to a Vg- like lead would increase the sensi- tivity of ambulatory monitoring to detect ST-segment depression. The V,-like lead was primarily chosen to detect arrhythmias (one of the purposes of the present study).

ST-segment elevation (STE) is a common finding in several path- ologic conditions (pericarditis, car pulmonale, cerebrovascular accidents, left ventricular hyper- trophy, left bundle branch block, hypothermia, hyperpotasemia, thoracic malformations), and in normal hearts (STE induced by postural changes and by the so- called “early repolarization” phe- nomenon) .2 Transmural myocar- dial ischemia, as occurring during Prinzmetal’s angina or during the early phase of AM1 (“injury cur- rent”) also cause STE. The mor- phology of STE in the first men- tioned conditions, compared with that caused by transmural myocar- dial ischemia are, however, differ- ent. Whereas in the first case, STE is discrete and mainly explained by a steeping in the ascending branch of the T wave, transmural ischemia and “injury current” oc- curs abruptly and is mainly ex- plained by an elevation of the J point. Assessing STE by measur- ing the J point (or as we did, J + 0 or J + 5 ms) may help to differ- entiate episodes of true ischemia from those caused by the above- mentioned conditions. In fact, Currie and Saitissi,’ evaluating patients early and late after AMI,

READERS’ COMMENTS 1027

showed that STE (measured 80 ms after the J point) was more com- mon during early evaluation, and that 60% of the episodes were as- sociated with periods of increased heart rate (arbitrarily defined as an increase in 10 beats/min above the adjacent base line). They found that the mortality rate tended to be higher in patients with STE, but STE was too infrequent to be a valuable prognostic indicator. More recently, Mickley et aL4 in a long-term follow-up study of post-AM1 patients, reported an an association between episodes of STE and (1) cardiac deaths, and (2) cardiac death and nonfatal reinfarction. STE did, however, not correlate with different indi- cators of myocardial ischemia. Cinca et al5 showed, in an animal model, that acute ischemia adja- cent to a chronic infarction in- duces STE at the surface of the scar. The magnitude of STE is, however, lower than that induced by myocardial ischemia not adja- cent to a necrosis.

As we clearly stated ( “study limitations” paragraph), ’ we could not confirm the hypothesis that STE represented myocardial ischemia. The achievement of this issue dur- ing ambulatory monitoring is al- most impossible. What we clearly demonstrated, was a statistical as- sociation between the presence of STE (measured from the J point and using the “24-hour” median as ref- erence line) and mortality. STE oc- curred in 4 of 18 (22%) versus 3 of 56 (5%) patients dying/surviving, p = 0.03. This association was stronger when either ST-segment deptession or STE was present: 14 of 18 (78%) versus 16 of 56 (29%) pa- tients dying/surviving, p = 0.0002.

In our study, leads showing pathologic Q waves or rS com- plexes were excluded from the anal- ysis, indicating that the VI-like lead (usually characterized by an rS complex) was excluded for evalu- ation of STE. STE was therefore di- agnosed in a Vs-like lead. All pa- tients, but 2, presented with ST-segment depression in a Vs-like lead (in those patients, the QRS complex showed an R wave >25% of S wave). STE was, in addition, analyzed according to the com-

monly used criteria (shifts ~0.1 mV measured 80 ms after the J point from the reference baseline). No association was found between cardiac events and its presence (un- published data).

Langer also expresses concern with respect to the studied popula- tion. Ambulatory monitoring was performed 4 + 2 days after hospital arrival. All patients met intemation- ally accepted criteria for diagnosing AM1 (chest pain during >30 minutes accompanied by electro- cardiographic changes and/or en- zyme alterations). Additional de- tails of the studied group are published elsewhere.6

Langer has absolutely misin- terpreted the survival curves (Fig- ure 3) of our report.’ The mortal- ity rates reported at 1 month, 1 year, and at the end of follow-up period were as follows: 8% (6 of 74), 12% (9 of 74), and 24% (18 of 74), respectively. These fig- ures, although somewhat higher than those reported by the GISSI and GUSTO megatrials,‘p8 are in accordance with those shown by the TRACE trial.g In that study, the l-year mortality in the entire screened group was 23%. The l-year mortality reported in the GUSTO and GISSI trials’~* only represented the mortality of randomized patients. What Langer surely means is that the l-month and 1 -year mortality rates in the group of patients showing ST- segment depression/STE were ap- proximately 20% and 30%. This is correct and stresses the necessity to investigate more invasively patients showing these characteristics.

In the present study,’ the pa- tients’ attending physicians were unaware of the results of ambula- tory monitoring. A noninvasive risk stratification was done by means of known clinical risk pre- dictors and by means of a predis- charge exercise test. These results are under publication elsewhere.” The patient approach during risk stratification was conservative ow- ing to limited technical resources. This was evidenced by the low rate of referrals to coronary angiog- raphy (39%). This fact does not make the results of the study less generalizable. On the contrary, they emphasize the prognostic value of

the ST-segment changes detected with the new criteria and encourage the attending physicians to investi- gate more aggressively and treat these patients in order to avoid poor prognoses.

MigUd QUinbnO, MD Stockholm, Sweden

20 October 1995

I. Quintana M, Lindvall K, Brolund F. Assessment and significance of ST-segment changes detected by ambulatory electrocardiography after acute myocar- dial infarction. Am J Cardiol 1995;76:6- 13. 2. Fisch C. Electrocardiography and vectorcardiog- raphy. In Braunwald E. ed. Heart Disease. A text- book of Cardiovascular Medicine. Philadelphia: WB Saunders, 1992:116- 160. 3. Currie P, Salt&i S. Significance of ST-segment elevation during ambulatory monitoring after acute myocardial infarction. Am Heart J 1993;125:41- 47. 4. Mickley H, Nielsen JR, Beming J, Junker A, Moller M. Characteristics and prognostic impor- tance of ST-segment elevation on Halter monitoring early after acute myocardial infarction. Am J Car- diol 1995;76:537-542. 5. Cinca J, Bardaji A, Carrerio A, Mont Ll, Bosch R, Soldevilla A, Tapias A, Soler-Soler J. ST seg- ment elevation at the surface of a healed transmural myocardial infarction in pigs. Conditions for pas- sive transmission from the ischemic p&infarction zone. Circu2arion 1995;91:1552- 1559. 6. Quintana M, Lindvall K, Carlens P, Bevegtid S, Brolund F. ST-segment depression on ambulatory electrocardiography in the early in-hospital period after acute myocardial infarction predicts early and late mortality: a short-term and a 3-year follow-up study. Clin Cardiol 1995;18:392-340. 7. Gruppo Italiano per lo Studio della Streptochinasi nell’Infsrt0 miocardico (GISSI). Long-tetm effects of intravenous thrombolysis in acute myocardial in- farction: final report of the GISSI study. Lancer 1987;2:872-874. 8. Califf RM, Top01 EJ, Van de Werf F, Lee KL, Woodlief L. One year follow-up from the GUSTO- I trial (abstr). Circulation 1994;90 (suppl I):I- 325. 9. Keber L, Torp-Pedersen C. On behalf of the TRACE study. Clinical characteristics and mortality in patients screened for entry into the trandalopril cardiac evaluation (TRACE) study. Am J Cardiol 1995:76:1-5. IO. Quintana M, Lindvall K, Brolund F, Eriksson SV, Ryddn L. Prognostic value of exercise stress test versus ambulatory electrocardiography after acute myocardial infarction: a three-year follow-up study. Coronary Artery Disease; in press.

Short-Coupled Variant of Torsades De Pointes With Normal QT Interval and Risk of Sudden Death

I read with interest the report by Eisenberg and associates’ of 15 patients with polymorphic ven- tricular tachycardia, normal QT interval, and sudden death. How- ever, this electrocardiographic en- tity is not new and has been de- scribed before by the French in- vestigators under a different name.’ Leenhardt and associates,’ in 1994, reported 14 patients with

1028 THE AMERICAN JOURNAL OF CARDIOLOGY” VOL. 77 MAY 1, 1996