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J Am Coll Cardiol, 1998; 32:876-881
© 1998 by the American College of Cardiology Foundation
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CLINICAL STUDIES

Effects of thrombolytic therapy in acute inferior myocardial infarction with or without right ventricular involvement

Uwe Zeymer, MD*, Karl-Ludwig Neuhaus, MD*, Karl Wegscheider, PhDa, Ulrich Tebbe, MD{dagger}, Peter Molhoek, MD{ddagger}, Rolf Schröder, MD, FACCa for the HIT-4 Trial Group1

a Coordinating Centers of the HIT-4 Trial, Kassel and Berlin, Germany
* Städtische Kliniken, Kassel, Germany
{dagger} Klinikum Lippe-Detmold, Detmold, Germany
{ddagger} Medisch Spectrum Twente, Enschede, The Netherlands

Manuscript received January 20, 1998; revised manuscript received May 11, 1998, accepted June 17, 1998.

Address for correspondence: Dr. Rolf Schröder, Universitätsklinikum Benjamin Franklin, Free University Berlin, Hindenburgdamm 30, D-12200 Berlin, Germany


   Abstract
Top
 Abstract
Methods
 Results
 Discussion
 References
 
Objectives. This study assessed the prognostic impact of right ventricular involvement (RVI) in streptokinase-treated patients with inferior acute myocardial infarction (AMI) stratified for small or large AMI.

Background. Only scant data exist from small studies about the impact of reperfusion therapy on survival in patients with RVI during inferior AMI.

Methods. Right ventricular involvement was assessed by ST-segment elevation ≥0.1 mV in lead V4R and infarct size by the extent of ST-segment deviation on the baseline electrocardiogram: small AMI = sum ST-segment elevation ≤0.8 mV and no precordial ST-segment depression (small ST); large AMI = presence of precordial ST-segment depression or sum ST-segment elevation >0.8 mV (large ST) in 522 inferior AMI patients of the Hirudin for Improvement of Thrombolysis (HIT-4) Trial. In 187 patients, 90-min coronary angiography was performed.

Results. Right ventricular involvement was present in 169 patients (32%). Higher 30-day cardiac mortality rates with RVI (5.9% vs. 2.5%) were related to larger infarct size rather than to RVI. For large ST, a proximal right coronary artery lesion was observed in 52% with and in 23% without RVI. Patency rates at 90 min were similar (54% vs. 52%). In the 28% of patients who had small ST, cardiac mortality was less than 1% irrespective of the presence of RVI. Coronary artery lesions were mostly located distally. Patency rates were 27% with and 80% without RVI.

Conclusions. ST-segment elevation of ≥0.1 mV in V4R in inferior AMI patients is associated with larger infarct size and higher 30-day mortality rates. Right ventricular involvement is not an independent predictor of survival. In patients with small ST, cardiac mortality is low, even if ST V4R is ≥0.1 mV.

Abbreviations and Acronyms
  AMI = acute myocardial infarction
  CK = creatine kinase
  ECG = electrocardiogram
  HIT = Hirudin for Improvement of Thrombolysis
  large ST = Presence of precordial ST-segment depression or ST-segment elevation >0.8 mV
  small ST = ST-segment elevation ≤0.8 mV and no precordial ST-segment depression
  RVI = right ventricular involvement

The risk-to-benefit ratio of thrombolytic therapy in patients with inferior acute myocardial infarction (AMI) continues to be controversial (1–5). It has been suggested that patients with inferior AMI only benefit from thrombolytic therapy when presenting with larger ST-segment deviations (5) or when right ventricular involvement (RVI) is present (3). Right ventricular involvement has been shown to occur in at least one third of patients suffering an inferior AMI (6). Without thrombolytic therapy in these patients, a significantly increased risk of major complications and in-hospital death has been reported (6–9). Data on the benefits of thrombolytic therapy or primary coronary angioplasty are limited and partly controversial (3,9,10–15). All studies are limited by very small sample sizes.

Right ventricular involvement during inferior AMI can be diagnosed with predictive accuracy well above 80% by the presence of ST-segment elevation of ≥0.1 mV in the right chest lead V4R (8,16,17). During the first 12 h of inferior AMI, combined electrocardiographic criteria were not better diagnostically or prognostically than ST-segment elevation in V4R alone (18). In the Hirudin for Improvement of Thrombolysis (HIT)-4 Study (19), along with the baseline 12-lead electrocardiogram (ECG) the right chest lead V4R was recorded to compare prospectively the outcome in inferior AMI patients with or without RVI. In addition, from the HIT-4 angiographic substudy (20), location and patency status of the infarct-related coronary artery lesion 90 min after start of thrombolytic therapy could be compared in patients with or without RVI.


   Methods
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 Abstract
 Methods
Results
 Discussion
 References
 
The HIT-4 Study was a multicenter, double-blind randomized trial which compared r-hirudin and heparin as adjuncts to streptokinase in patients within 6 h of onset of AMI (19). The primary objective was to demonstrate higher 90-min infarct-related coronary artery patency rates with r-hirudin in a subset of 400 patients in whom early angiography had been performed (20). Patients above 18 years were eligible for randomization if they had no contraindication to thrombolytic therapy and had ST-segment elevation ≥0.1 mV in at least two limb leads or ≥0.2 mV in two contiguous chest leads or presence of bundle branch block.

Study patients.   Of all 1,208 patients recruited for the HIT-4 study, 522 patients with inferior AMI were considered for analysis. They did show the required amount of ST-segment elevation, had no bundle branch block and had received streptokinase.

Electrocardiographic analysis.   A 12-lead ECG and the right chest lead V4R were recorded before randomization. ST-segment elevation was measured with lens-intensified caliper to the nearest of 0.025 mV 20 ms after the end of the QRS complex from leads II, III, aVF, V5 and V6. Reference baseline for the ST amplitude measurement is the PR segment immediately preceding QRS onset. Reciprocal ST-segment deviations in leads with ≥0.1 mV depression were measured from leads V1 to V4. The intensity of the initial epicardial injury was quantified by the sum of ST-segment elevation from the aforementioned leads by excluding V4R. The number of leads with ST-segment elevation ≥0.1 mV were also counted. Evaluation was performed centrally independent of and blinded to the other study data or results.

According to a study about the prognostic impact of initial ST-segment changes for thrombolytic treatment in first inferior AMI (5), subgroup analyses were performed with either small (small ST) or large (large ST) initial ST-segment deviations. Small ST was defined as {sum} ST-segment elevation ≤0.8 mV and no precordial ST-segment depression, that is, ≥0.1 mV ST-segment depression in at most one of leads V1 to V4. Large ST was defined as presence of ST-segment depression of ≥0.1 mV in at least two of leads V1 to V4 or {sum} ST-segment elevation >0.8 mV.

Enzyme analysis.   Peak creatine kinase (CK) isoenzyme serum activity was measured in the participating hospitals and is expressed as fraction of the upper normal limit of the different method used. Enzyme data are available from 515 patients (99%).

Quantitative angiographic analysis.   In the angiographic substudy, coronary angiography was performed 90 min after start of streptokinase infusion. Cinefilms were sent to a core lab and evaluated independent of and blinded to the other study data or results. In 187 patients with inferior AMI, the infarct-related artery could be identified and the Thrombolysis In Myocardial Infarction flow grade assessed. Vessel disease is defined as >50% stenosis in a major epicardial artery. Proximal coronary artery lesion is defined as proximal to the origin of any right ventricular branches.

Statistical analysis.   For univariate analyses only nonparametric methods were applied. For comparisons of two dependent/independent samples, Wilcoxon signed rank test/Mann–Whitney U tests or Fisher’s exact test were applied. For comparisons of three or more independent samples we used Kruskal–Wallis tests.

The multivariate analysis consisted of a stepwise logistic regression for outcome at 30 days. In addition to presence of ST-segment elevation ≥0.1 mV in lead V4R, nine variables were offered as covariates: 1) age (taken as a continuous variable, unit 10 years); 2) gender; 3) previous AMI; 4) diabetes mellitus; 5) history of angina pectoris; 6) ex-smoker or nonsmoker; 7) Killip class >1; 8) large ST; 9) treatment with r-hirudin. In a second analysis peak CK >12 times fraction of the upper normal limit was added as potential covariate. To eliminate bias caused by missing data, two patients, who died from cardiac failure before the maximum CK value could be obtained, were assigned to peak CK >12.

Logistic regression was performed using the procedure "LOGISTIC REGRESSION" of SPSS for Windows, version 6.1.3, choosing the forward-stepping selection method with ML estimates and the defaults criteria offered by SPSS. The odds ratios, confidence intervals and p values of the final model (i.e., adjusted for all other significant covariates) are reported.


   Results
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 Abstract
 Methods
 Results
Discussion
 References
 
Clinical characteristics of the 522 study patients are displayed in Table 1. ST-segment elevation of ≥0.1 mV in lead V4R at baseline was present in 169 patients (32%). Compared with patients without ST-segment elevation in the right chest lead, no differences were observed between groups in the clinical and demographic characteristics except for a higher proportion of females with RVI. Intensity of ischemia as measured by the sum of ST-segment elevation at baseline was more severe in patients with RVI both in all patients and in those with large ST at baseline. Total ST-segment deviation was only slightly larger with RVI probably because RVI attenuates precordial ST-segment depression in inferior AMI. The extent of ischemia as assessed by the number of leads with ST-segment elevation ≥0.1 mV (V4R not included) was not different between groups. The peak level of CK was higher with RVI both in all patients and in the subgroup with large ST; this was statistically significant only in the total group of all patients.


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  		Table 1 Clinical Characteristics of 522 Patients With Inferior AMI According to Presence or Absence of ST-Segment Elevation of ≥0.1 mV in Lead V4R

 
Clinical course.   More patients with RVI suffered a complicated in-hospital course (Table 2). However, a significant difference was only observed for the incidence of malignant tachyarrhythmia. A higher reinfarction rate reached marginal significance. High degree atrioventricular block and severe bradycardia are not included in Table 2 because these variables were not prospectively collected in the HIT-4 study.


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  		Table 2 Clinical Event Rate According to Presence or Absence of ST-Segment Elevation of ≥0.1 mV in Lead V4R

 
Mortality.   Total 30-day mortality was not significantly different between groups, but cardiac mortality was significantly higher with RVI (Table 3). A higher cardiac mortality was restricted to patients with large ST. In 147 patients with small ST, only 1 died from cardiac cause while 4 suffered a noncardiac death (1 stroke, 1 lethal bleeding complication, 1 fulminant pulmonary embolism after angiography, and 1 worsening leukemia).


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  		Table 3 Thirty-Day Mortality According to Presence or Absence of ST-Segment Elevation of ≥0.1 mV in Lead V4R

 
Independent determinants of 30-day cardiac mortality were assessed by multiple logistic regression analysis (Table 4). The first analysis, in addition to other prognostic factors available at the time of admission, includes large ST-segment elevation on the baseline ECG. In a second analysis (B in Table 4) peak CK >12 times of the upper normal limit was also incorporated. Age, history of angina pectoris, large ST-segment elevation on the baseline ECG and peak CK >12 were selected as independent predictors of mortality. Right ventricular involvement was not an independent determinant of 30-day cardiac mortality.


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  		Table 4 Multivariate Analysis for Prediction of 30-Day Cardiac Mortality on the Basis of Presence of RVI ≥0.1 mV and 9 Other Variables (A) and After Offering Peak CK >12 Fraction of the Upper Normal Limit as Additional Variable (B)

 
Angiographic data.   In 187 patients coronary angiography was performed 90 min after the start of thrombolytic therapy. The infarct artery was the right coronary artery in 139 patients, and in 48 patients (26%) it was the circumflex coronary artery. Right ventricular involvement was present in 69 patients (37%); in only 2 patients (3%) the circumflex coronary artery was the infarct vessel. The angiographic data of the 139 patients, in whom the right coronary artery was the infarct vessel, are presented in Table 5. Right ventricular involvement was present in 67 patients (48%). The coronary lesion was located proximally to the origin of any right ventricular branches in 48% with presence, and in 26% with absence of RVI. The right coronary artery was the dominant vessel more often in patients without RVI while multivessel disease was present in about two thirds of all patients. The 90-min postthrombolytic therapy patency rate was slightly lower in patients with RVI. This disparity, however, was entirely caused by an occluded vessel (mostly located distally) in 11 of 15 patients with RVI who had small ST on the baseline ECG. With large ST the patency rates were not different.


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  		Table 5 Angiographic Right Coronary Artery Data According to Presence or Absence of ST-Segment Elevation of ≥0.1 mV in Lead V4R

 

   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
References
 
Right ventricular involvement as assessed by various diagnostic criteria has been shown to occur in 30% to 50% of patients suffering an inferior AMI (6,8,9,17,21). A most accurate and readily available electrocardiographic sign of RVI is ST-segment elevation of ≥0.1 mV in the right precordial chest lead V4R (6,8,16,17). In our study, which is the largest prospective study on RVI, 32% of all inferior AMI patients had 0.1 mV or more ST-segment elevation in lead V4R. There are conflicting data concerning pathologic anatomy, clinical significance and prognostic implication of RVI in inferior AMI. Most studies suffer from small sample sizes in selected groups of patients.

Pathologic anatomy.   The infarct vessel in patients suffering inferior AMI complicated by RVI is the right coronary artery. Right ventricular involvement only occasionally develops after occlusion of the circumflex artery, as in our angiographic substudy in 2 of 48 patients. It is generally believed that it is a proximal occlusion of the right coronary artery that results in infarction of the anterolateral wall of the right ventricle, which is mainly perfused by right ventricular branches (6,11,12,21). However, pathologic analyses consistently have shown that it is the posterior right ventricular wall that is most frequently involved in right ventricular infarction in association with left ventricular posterior and posteroseptal infarction (6,17,22,23). Acute vessel lesions were distributed throughout the right coronary artery tree with a somewhat higher incidence of proximal location (22,23). Proximal right coronary artery occlusion caused larger right ventricular infarction than distal occlusion (23). There was no difference between the two groups in severity of coronary arterial atherosclerosis (22). Our angiographic data (Table 5) are in concordance with these pathologic findings. The incidence of multivessel disease was similar in both groups. Although patients with RVI more often had a proximal coronary artery lesion than patients without RVI, in 52% of patients the coronary artery lesion was located distally of the origin of the right ventricular branch. Of all patients with proximal lesions, 63% developed RVI. Patients with a small infarction as assessed by small ST mostly had a distally located infarct-related coronary artery lesion. In patients who had large ST-segment elevations, the 90-min postthrombolytic therapy patency rate was similar in those with or without RVI, while patients with small ST and RVI mostly had an occluded and without RVI mostly had a patent infarct vessel (Table 5).

Clinical significance of RVI.   In most patients with inferior AMI RVI is not recognized clinically. About one half of patients with RVI have no clinical abnormalities (6,21). Serious adverse events that occur are particularly high degree atrioventricular block, severe bradycardia and malignant ventricular tachyarrhythmias (3,6–9,21). In some studies a high incidence of cardiogenic shock is reported (7–9). In our study the incidence of cardiac adverse events in patients with RVI (Table 2) is similar to that observed in patients with inferior AMI presenting with large ST (5).

Right ventricular dysfunction in the setting of inferior AMI is predominantly due to ischemia and probably stunned myocardium (6,21). Right ventricular wall motion abnormalities and right ventricular ejection fraction substantially improve in the majority of patients over a few days to several weeks (10–13,17,23–26). Pharmacologic reperfusion therapy (10,12,15,26) or angioplasty (14) may or may not (11,13) enhance spontaneous recovery of right ventricular dysfunction. ST-segment elevation in right chest leads indicates right ventricular ischemia rather than necrosis. The relative infrequency of subsequent right ventricular infarction is believed to be due to a more favorable oxygen supply–demand relation of the right ventricle as compared to the left ventricle (6,21).

Prognosis related to infarct size.   Some (8,9) but not all (13,24) studies reported that RVI in patients with inferior AMI is associated with a substantially increased mortality risk. Only scant data exist from small studies about the impact of reperfusion therapy on survival in patients with RVI during inferior AMI (3,10–15). Unfortunately, the influence of thrombolytic therapy was not examined in the placebo-controlled thrombolytic trials. In our study all patients had thrombolytic therapy. In univariate analysis patients with RVI had a significantly higher cardiac mortality than patients without. However, multivariate analysis made it likely that this increased mortality is due to larger infarct sizes rather than directly related to the presence of ST-segment elevation in right chest leads (Table 4). Likewise, as in our study, patients with RVI had larger maximum cardiac enzyme levels (7–9,27) and greater impairment of left ventricular function (26). We recognized, in addition, a larger epicardial injury as quantified by the sum of ST segment elevation on the baseline ECG in patients with RVI (Table 1). Several studies have shown that long-term prognosis was not adversely affected by RVI (7,13,24–27) but was related to concomitant significant left ventricular dysfunction (7,25). It is suggested that the higher mortality in patients with anterior as opposed to inferior AMI, despite adjustment for infarct size, may in part be due to coexistent RVI in patients with inferior AMI, resulting in less left ventricular impairment relative to the total cardiac enzyme release (7,28).

Clinical implications.   There is accumulating evidence that patients with small inferior AMI do not benefit from thrombolysis (4,5,21). Since mortality from cardiac causes is low, the risks inherent to thrombolytic treatment may lead to an adverse outcome. Patients in whom thrombolytic therapy may be contraproductive are those presenting with small ST, that is sum ST-segment elevation from leads II, III, aVF and V5, V6 ≤0.8 mV, and no precordial ST-segment depression (5). In contrast to patients presenting with large ST, left ventricular function is relatively well preserved also without thrombolysis, and improvement by thrombolytic therapy is small (5). It is believed that patients who had inferior AMI complicated by RVI may particularly benefit from thrombolytic therapy (3,6,14,15,21,26). Our study shows that patients with inferior AMI and small ST on admission have a very low cardiac mortality regardless of whether ST-segment elevation in lead V4R was present. Of 147 patients with small ST, only 1 suffered cardiac death, but 4 others died from noncardiac causes. In a placebo-controlled trial total mortality tended to be higher in patients with inferior AMI presenting with small ST who had been allocated to streptokinase therapy (5). Thus, it appears unlikely that patients with small ST and RVI will benefit from thrombolysis, the more so as reperfusion was mostly not achieved 90 min after the start of streptokinase infusion (Table 5). In the usual clinical setting in AMI patients, right ventricular chest leads are often not recorded. Our data suggest that for early clinical decision making to thrombolytic therapy a 12-lead ECG recording indeed is sufficient. In most cases patients who have small ST can easily be identified visually without exact measurements of ST-segment deviation. On the principle of doing no harm unless one can be reasonably sure of doing more good than harm (29), reperfusion therapy in inferior AMI patients presenting with small ST appears not to be indicated irrespective of presence of RVI unless advanced heart block or hemodynamic instability indicates larger infarcts (5,21).

Study limitations.   Although this was a prospective study, only patients eligible for thrombolytic therapy are included and all patients had thrombolytic therapy within 6 h from symptom onset. In inferior AMI patients who have large ST-segment deviation without thrombolytic therapy, the presence of RVI may be associated with a relatively more unfavorable outcome.


   Footnotes
 
1 A complete list of collaborators and participating centers appears in reference 19. Back


   References
Top
 Abstract
 Methods
 Results
 Discussion
 References
 

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