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Cardiovascular Research 2001 50(2):379-385; doi:10.1016/S0008-6363(00)00290-X
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Copyright © 2001, European Society of Cardiology

Increased QT dispersion in patients with Prinzmetal's variant angina and cardiac arrest

Nikhil Parchure, Velislav Batchvarov, Marek Malik, A John Camm and Juan Carlos Kaski*

Coronary Artery Disease Research Unit, Department of Cardiological Sciences, St George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK

* Corresponding author. Tel.: +44-181-725-5901; fax: +44-181-725-3328 jkaski{at}sghms.ac.uk

Received 13 September 2000; accepted 7 November 2000


   Abstract
Top
 Abstract
1 Introduction
 2 Methods
 3 Results
 4 Discussion
 5 Conclusions
 6 Condensed abstract
 References
 
Objectives: We sought to compare QT dispersion in patients presenting with Prinzmetal's variant angina complicated by cardiac arrest or syncope and patients with uncomplicated variant angina. Background: Despite the usually benign course of treated Prinzmetal's variant angina, a proportion of vasospastic angina patients develop ventricular arrhythmias and sudden death in association with coronary spasm. Increased QT dispersion has been suggested to increase susceptibility to ventricular arrhythmias in patients with coronary artery spasm. Methods: We studied 25 consecutive patients (mean age 58 years; 14 men) with classical Prinzmetal's variant angina and documented coronary artery spasm. None of the patients had coronary artery stenoses ≤40%. Five patients had suffered a documented cardiac arrest, two had recurrent syncope and 18 had no arrhythmic events or syncopal episodes. In all patients QT dispersion (QT maximum–QT minimum in every ECG lead) was measured on the baseline 12-lead electrocardiogram at study entry using a digitising board. Results: Mean (±S.D.) QT dispersion of study patients was 62.3±19.5 ms. QT dispersion in patients with cardiac arrest and syncope (79.4±17.3 ms) was significantly higher compared to patients with no such events (56.3±16.9 ms), (95% CI 7.5–38.8, P = 0.005). No significant clinical, biochemical or angiographic differences were found between patients with and those without cardiac arrest or syncope. Conclusion: QT dispersion is increased in patients with Prinzmetal's variant angina complicated by cardiac arrest and syncope compared to patients without such events. Increased QT dispersion may be both a substrate for sudden cardiac death and a marker of risk in patients with Prinzmetal's variant angina.

KEYWORDS Coronary disease; QT dispersion; Sudden death; Ventricular arrhythmias


   1 Introduction
Top
 Abstract
 1 Introduction
2 Methods
 3 Results
 4 Discussion
 5 Conclusions
 6 Condensed abstract
 References
 
Treated patients with Prinzmetal's variant angina usually have good long-term prognosis [1–3]. However, myocardial infarction, sudden cardiac death and syncope have been shown to occur in a sizeable proportion of patients with variant angina [4–6]. Life threatening ventricular arrhythmias have been documented during spontaneous coronary spasm in 5–15% of patients with Prinzmetal's variant angina [1,4–10]. The factors responsible for increased risk of malignant ventricular arrhythmias and/or sudden death in patients with coronary artery spasm remain to be elucidated. Studies have suggested that these patients have abnormalities of ventricular repolarization, even during asymptomatic phases of their disease [7]. It has also been suggested that in the presence of a reduced threshold, or a substrate for ventricular arrhythmias, coronary artery spasm may be a triggering mechanism for life-threatening rhythm disturbances in some victims of cardiac arrest [11–13]. Lengthening of the QT interval may represent such a substrate.

Prolongation of the QT interval is recognised as a marker of increased risk of malignant ventricular arrhythmias and/or sudden cardiac death in a variety of clinical conditions [14–16]. Moreover, QT interval has been shown to exhibit a certain degree of interlead spatial variability (dispersion) which may be considered to represent an approximate measure of ventricular repolarization abnormalities [17,18]. Based on the evidence that abnormalities of ventricular repolarization provide a substrate for malignant ventricular arrhythmias, the variation in QT interval duration has been advocated as a marker of arrhythmogenicity [19]. Interestingly, a recent study showed that variant angina patients with increased QT dispersion have an increased susceptibility to ventricular arrhythmias during acetylcholine induced coronary artery spasm [7]. However, the relationship between cardiac death, QT dispersion and spontaneous coronary spasm in variant angina patients has not been assessed systematically.

In the present study, we investigated the association among coronary artery spasm, increased QT dispersion and cardiac arrest or syncope in patients with Prinzmetal's variant angina pectoris.


   2 Methods
Top
 Abstract
 1 Introduction
 2 Methods
3 Results
 4 Discussion
 5 Conclusions
 6 Condensed abstract
 References
 
2.1 Patients
We studied 25 consecutive patients (14 men and 11 women; mean age 58 years, range 39–82 years) referred to our unit for the assessment and management of coronary artery spasm from 1992 to 1998. All patients had a history classical of Prinzmetal's variant angina with ST-segment elevation associated with typical anginal chest pain at rest, usually occurring in the early morning hours or at night time. All patients had a preserved exercise capacity and normal exercise stress test responses. In nine patients who underwent ergonovine provocative testing of coronary artery spasm, the typical symptoms and ECG changes of variant angina were reproduced with the administration of intravenous or intracoronary ergonovine. In the remainder, spontaneous coronary artery spasm occurred during coronary angiography (six patients) or transient ST segment elevation developed at rest in the presence of completely normal coronary arteries.

Of the 25 patients, seven had a history of cardiac arrest or syncope (Tables 1 and 2Go) [Group I: mean age 55 years (range 44–71; 4 men)]. The remaining 18 patients (Tables 1 and 3Go) [Group II: mean age 59 years (range 39–82; 10 men)] had no history of syncope or cardiac arrest.


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  		Table 1 Clinical characteristics and coronary artery disease risk factors in 25 patients with Prinzmetal's variant angina

 

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  		Table 2 Angiographic characteristics of patients in Group I [variant angina patients with cardiac arrest (n = 5) and syncope (n = 2)]

 

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  		Table 3 Angiographic characteristics of patients in group II (variant angina patients without arrhythmic complications)

 
Patients in Group I met the criteria described by Myerburg et al. [4]: (1) cardiac arrest with documented ventricular fibrillation or sustained rapid ventricular tachycardia; (2) the absence of previous history of angina pectoris or acute myocardial infarction; (3) normal angiographic left ventricular ejection fraction and no wall motion abnormalities; (4) the absence of significant coronary artery narrowing (50%) or any structural cardiac abnormalities; (5) the absence of identifiable or correctable causes of ventricular arrhythmia, such as pre-excitation syndrome, long QT interval, metabolic or electrolyte disturbances or drug toxicity. At the time of the study, patients in both groups were receiving treatment with calcium antagonists, usually diltiazem (360–540 mg daily) and isosorbide mononitrate (40–80 mg daily). Clinical characteristics and biochemical variables in the two patient groups are presented in Table 1.

2.2 Measurement of QT dispersion
Manual electrocardiographic measurement was performed independently by two experienced observers blinded to the clinical and angiographic profile of the patients. Measurement was performed on standard paper-based 12-lead ECGs recorded 3 months after the index event at a paper speed of 25 mm/s and standard gain of 1 mV/cm. All 12 leads were acquired simultaneously. The recordings were composed of four triplets of simultaneously acquired ECG leads (i.e. leads I, II, III, leads aVR, aVL, aVF, leads V1, V2, V3, and leads V4, V5, V6). A high resolution (±50 mm in both horizontal and vertical directions) digitising board (Cherry, Harpender, UK) driven by a purpose-built in-house interactive software was used for measurement. In each lead of each electrocardiographic tracing, the RR, QRS and QT interval was measured in at least two consecutive cardiac cycles of sinus rhythm and the results were subsequently averaged.

Before the actual measurement of each ECG, the observer was required by the software programme to classify the repolarisation pattern in each lead into one of seven categories, as described in previous studies from this department [37]. The main distinction was the T wave of very low amplitude, T–U pattern consisting of distinct T and U wave separated by an isoelectric segment, partial fusion of the T and U wave with clearly visible transition between both waves (nadir or sudden change in the slope of the T wave), and complete fusion of the T and U wave. In case of partial T–U fusion the T wave end was determined to the nadir between the T wave and the U wave [20]. In case of complete fusion of the T and U wave no determination of the T wave end was attempted and the corresponding lead was excluded from measurement. As suggested in other studies [21,22], leads in which the T wave amplitude was very low (i.e. <0.05 mV (<0.05 mm)) were excluded from measurement. T wave inversion did not interfere in QT dispersion measurements. QT dispersion was defined as the difference between the maximum and minimum QT interval in all measured leads.

2.3 Statistical analysis
Data are expressed as the mean value±S.D., mean difference±S.D., and 95% confidence interval of mean difference as appropriate. The unpaired Student's t-test was used to compare QT dispersion in Group I and Group II. Differences in the clinical and angiographic characteristics of patients in Group I and II were compared using either a chi-square test or unpaired Student's t-test as appropriate. A probability (P) value<0.05 was considered statistically significant. The variability of measurement of QT dispersion by the two observers was assessed by relative errors calculated according to the formula ((A–B)/((A+B)/2))x100 [%], where A and B were the values of QT dispersion measured by the two observers, respectively [23].


   3 Results
Top
 Abstract
 1 Introduction
 2 Methods
 3 Results
4 Discussion
 5 Conclusions
 6 Condensed abstract
 References
 
The clinical characteristics and coronary artery disease risk factors of the patients included in the study are presented in Table 1. Except for the higher systolic blood pressure in Group I there were no differences in clinical, biochemical, hemodynamic and angiographic variables between the two groups.

All patients had a normal physical examination and no previous history of cardiac disease. Six patients had an abnormal baseline ECG i.e. one patient had right bundle branch block and five had T wave inversion (two in inferior and three in anterior leads). Two patients in Group I and five in Group II were found to be hypertensive.

Seven of the 25 patients (three in group I and four in group II) had angiographically demonstrable coronary artery stenoses ≤40% luminal diameter (Tables 2 and 3Go). Five patients (in group II) had previous history of myocardial infarction and their average left ventricular ejection fraction was 68%±1.57 (range 66%–70%).

All patients had normal resting 2-dimensional echocardiograms. No patient was receiving antiarrhythmic agents or other therapy that could affect the QT interval but all patients were treated with calcium antagonists (diltiazem) and nitrates (isosorbide mononitrate).

3.1 QT dispersion on surface ECG
Table 4 summarises the ECG variables assessed in patients with Prinzmetal's variant angina. The QTmax in Group I was significantly higher (P = <0.001) than Group II but there was no difference in QTmin between the two groups. The mean QT dispersion in Prinzmetal's variant angina patients with cardiac arrest and/or syncope (Group I) was 79.43±17.32 (range 52.70–105.03) as compared to 56.28±16.87 (range 26.17–82.31) in patients without these events (Group II) (Fig. 1). The difference was statistically significant (95% CI: 7.5–38.8, combined standard error 7.56; P = 0.005).


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  		Table 4 QT measurements in patients with prinzmetal's variant angina

 

Figure 1
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  		Fig. 1 QT dispersion was significantly higher in patients with cardiac arrest (group 1) compared to those without events (group 2).

 
QT Dispersion Measurement were reproducible and the Bland—Altman plot [24] of the differences between the measurements of the two observers was 0.17±0.37%.


   4 Discussion
Top
 Abstract
 1 Introduction
 2 Methods
 3 Results
 4 Discussion
5 Conclusions
 6 Condensed abstract
 References
 
Our study showed for the first time that QT dispersion is significantly higher in patients with Prinzmetal's variant angina complicated by cardiac arrest and syncope than in patients without such events. This finding suggests that patients with variant angina complicated by cardiac arrest may have abnormalities of ventricular repolarization, that may increase the risk of malignant ventricular arrhythmias. Our results also indicate that evaluation of QT dispersion on the surface ECG may provide useful information about the susceptibility of certain variant angina patients to suffer cardiac arrest.

4.1 Ventricular arrhythmias in variant angina
The occurrence of ventricular arrhythmias in patients with variant angina is well established. Prinzmetal's original description of vasospastic angina included one patient who had runs of ventricular tachycardia during episodes of pain [25]. Since then, several studies have shown that serious ventricular arrhythmias may occur in this syndrome [5,7,9,10,6] and sudden cardiac death has also been documented [5,6] often in association with ventricular arrhythmias. Studies have reported that myocardial infarction and sudden cardiac death occur in 10–20% of patients with variant angina over several years of follow-up [26–28]. Whether silent or symptomatic, transient myocardial ischemia may be the triggering mechanism for fatal ventricular arrhythmias in victims of cardiac arrest [11–13].

Previous studies of survivors of arrhythmic cardiac arrest due to isolated coronary artery spasm have been scarce and limited in size. Kerin et al. [10] demonstrated that most of their study patients had high-grade obstructive lesions (significant coronary artery disease >50% stenosis) and that the angiographic site of spasm correlated well with electrocardiographic findings. Furthermore, arrhythmias in this study were more common in the group with coronary obstructive disease. Conversely, Nakamura et al. [29] demonstrated that the risk of serious arrhythmias or sudden death did not depend on the presence of severe fixed stenoses. This is consistent with our findings in the present study and with data reported by Maseri et al. [30], who found no correlation between the development of fatal arrhythmia and the patients' coronary anatomy. In our study most of the patients had completely normal coronary arteriograms and the seven patients with coronary stenoses (≤40% diameter reduction) were evenly distributed between the two groups.

Interestingly, Myerburg et al. [4] showed that even silent myocardial ischemia due to coronary artery spasm can initiate potentially fatal arrhythmias in patients without flow-limiting coronary artery lesions. Unfortunately however, the relationship between QT intervals and cardiac arrest was not assessed in Myerburg's study. It is conceivable that as suggested by our findings, Prinzmetal's variant angina patients with an arrhythmic substrate, of greater QT dispersion, may be more liable to develop potentially fatal arrhythmias in association with episodes of coronary spasm.

4.2 QT dispersion and variant angina
QT dispersion has been previously studied [7] in patients with Prinzmetal's variant angina and found to be higher compared to patients with atypical chest pain. However, the present investigation is the first study to compare QT dispersion in Prinzmetal's variant angina patients who presented with cardiac arrest versus those with an uncomplicated clinical course. The findings in the present study support previous reports [31–34] demonstrating that increased QT dispersion represents a marker of increased risk of sudden cardiac death in different patient subsets i.e. coronary artery disease, hypertrophic cardiomyopathy and heart failure. Although controversy exists as to what exactly QT dispersion represents in electrophysiological terms, a recent editorial article [35] has suggested that QT dispersion is an approximate expression of ventricular repolarization abnormalities.

Suzuki et al. [7] showed both that baseline QTc dispersion was significantly greater in patients with vasospastic angina than in patients with atypical chest pain and that QTc dispersion was significantly greater in patients who developed ventricular arrhythmias during provocation tests for spasm. However there were no patients with documented cardiac arrest in Suzuki's study. Contrary to the findings of Suzuki et al. [7], Ashikaga et al. [36] observed no significant differences in QT dispersion in 35 patients with vasospastic angina compared to 30 patients with atypical chest pain and normal coronary arteries (27±8 vs. 28±7 ms, P = NS). However, in the Ashikaga study [37] QT dispersion was significantly increased by dipyridamole administration in patients with vasospastic angina (53±14 ms, P<0.0001) compared to patients with atypical chest pain.

4.2.1 Clinical and angiographic features
These have been shown to be of limited value in recognising patients with variant angina who are at risk of developing life threatening ventricular arrhythmias. Therefore, our observations in the present study, that assessment of QT dispersion even when obtained in the asymptomatic state, may represent a useful, noninvasive predictive variable have important clinical implications.

4.3 Study limitations
Manual measurement of QT dispersion may have limitations, particularly low interobserver reproducibility as reported by other authors [37–39].

The reliability of manual measurement of the QT dispersion is influenced by many factors, such as the amplitude of the T wave, the noise level, and the number of measured leads. Moreover, it has been suggested that the use of a ruler instead of a calliper and even the respiratory phase of the patient during which the recording is made [40] may influence QT measurements.

To minimise these limitations we used a high resolution (±50 mm in both horizontal and vertical directions) digitising board (Cherry, Harpender, UK) driven by a purpose-built in-house interactive software which was demonstrated recently to provide accurate measurement of QT dispersion [41].

Another potential limitation of this study is the relatively small number of patients. However, Prinzmetal's variant angina is not a common condition and variant angina patients presenting with cardiac arrest are even more rare.


   5 Conclusions
Top
 Abstract
 1 Introduction
 2 Methods
 3 Results
 4 Discussion
 5 Conclusions
6 Condensed abstract
 References
 
QT dispersion is significantly higher in patients with Prinzmetal's variant angina complicated by cardiac arrest and/or syncope compared to uncomplicated patients. Increased QT dispersion may represent both a substrate for arrhythmic sudden cardiac death and a marker of increased mortality risk in variant angina patients.


   6 Condensed abstract
Top
 Abstract
 1 Introduction
 2 Methods
 3 Results
 4 Discussion
 5 Conclusions
 6 Condensed abstract
References
 
In this study we compared QT dispersion in patients with Prinzmetal's variant angina complicated by cardiac arrest or syncope and patients with uncomplicated variant angina. We observed that QT dispersion in patients with cardiac arrest and syncope (79.4±17.3 ms) was significantly higher compared to patients with no such events (56.3±16.9 ms), (95% CI 7.5–38.8, P = 0.005). No significant clinical, biochemical or angiographic differences were found between patients with, and those without cardiac arrest or syncope. Increased QT dispersion may represent both a substrate for arrhythmic sudden cardiac death/syncope and a marker of increased risk in variant angina pectoris.

Time for primary review 26 days.


   Acknowledgements
 
N. Parchure is a British Heart Foundation Junior Research Fellow.


   References
Top
 Abstract
 1 Introduction
 2 Methods
 3 Results
 4 Discussion
 5 Conclusions
 6 Condensed abstract
 References
 

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