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Sumario Vol. 43 - Nº 1 Enero - Marzo 2014

Risk factors associated with increased QTc dispersion
during acute myocardial infarction

Elibet Chávez-González (1), Fernando Rodríguez-González (2),
Wilfredo J Machín-Cabreras (3), Vielka González Ferrer (4)

Hospital “Celestino Hernández Robau". Villa Clara, Cuba.
(1) Cardiocentro Ernesto Che Guevara. Villa Clara, Cuba. (2) Centro diagnóstico Hospital Arnaldo Milián Castro. Villa Clara, Cuba. (3) Hospital Manuel Fajardo.
Villa Clara, Cuba. (4) Cardiocentro Ernesto Che Guevara. Villa Clara, Cuba.
E mail

Recibido 30-NOV-13 – ACEPTADO después de revisión el 15-ENERO-2014.

The authors declare not having a conflict of interest.

Rev Fed Arg Cardiol. 2013; 43(1): 25-31


Print version Imprimir sólo la columna central

 

 

SUMMARY

Introduction: Electrocardiogram remains a valuable tool in prognostic evaluation of acute coronary syndrome. The QT interval dispersion is an electrocardiographic parameter of interest for prognostic assessment in ischemic heart disease. There are risk factors associated with a prolonged QT interval prior to an acute coronary syndrome. QT interval and its dispersion can increase even more during acute coronary syndrome.
Objective: To determine the risk factors associated with increased QT dispersion corrected during acute myocardial infarction after symptom onset.
Method: A descriptive, retrospective study in 194 patients admitted with acute coronary syndrome diagnosis,who underwent QT interval measurement and estimation of their dispersion in the first electrocardiogram.
Results: there wasa prevalence ofmales with normal (53.5%) and prolonged dispersion (65.6%). Among the risk factors associated to prolonged corrected QT interval were: hypertension (30.4%), diabetes mellitus (28.6%) and chronic ischemic heart disease (17.5%).
Conclusions: Theseresults can illustrate that the risk factors most associated to the increased dispersion of repolarization in the first ECG were arterial hypertension, diabetes and coronary artery disease. Therefore we need to control risk factors to avoid ischemic heart disease and the complications that can arise from a prolonged QT interval during an acute coronary syndrome.

Key words: Risk factors. Coronary artery diseases. QT interval dispersion.

 

 

INTRODUCTION
Cardiovascular diseases are the main cause of mortality both in men and in women in developed countries [1].

One of the most valuable contributions to electrocardiography has been the diagnosis of acute coronary syndrome (ACS). It is an easily available technique and simple to interpret; it is usually the first diagnostic procedure performed before the suspicion of acute coronary event. At the onset of ACS, the electrocardiogram (ECG) allows for an approximate diagnosis in 60% of the cases; in 25% of the cases is non-diagnostic but abnormal and normal in around 15%. Sensibility varies depending on the extension and location of necrosis. The characteristic changes are present in 90% of the patients with anterior descending artery occlusion, in 70 to 80% of the cases the coronary obstruction involves the right coronary artery, and only 50% of the cases the circumflex artery is culprit for the event [2,3].

Signs, as QT interval (QTI) and its dispersion, may relate to the extension of necrosis and thus, with a prognosis in the short and long term [4].

Different papers have manifested consistently, the negative prognostic implications in the short and long term of the presence of ST changes in the ECG made at the time of admittance. However, we know that 34 to 54% of the patients with non-ST segment elevation ACS, at times do not show ECG alterations at admittance, and the subsequent course is very heterogeneous. From there the interest of the study on other electrocardiographic variables that may contribute additional and supplementary information to ST segment, as corrected QT interval dispersion (cQTI), the usefulness of which was manifest in some series, most with patients from a single center and not very wide [5,6,7].

It has been shown that acute myocardial ischemia modifies QTI duration, increases the heterogeneity of repolarization (expressed by QTI dispersion increase) and prolongs maximal QTI duration.

Several mechanisms have been proposed that could be involved in QTI prolongation secondary to acute myocardial ischemia: myocardial response alteration to catecholamines or cholinergic stimulation, Calcium (Ca) or potassium (K) ion current disturbance, or induction of changes in intracellular concentration of hydrogen (H) [5].

Nowinski et al [8], showed that myocardial ischemia produced during the periods of balloon insufflation in percutaneous coronary interventionism caused immediate alterations in ventricular repolarization, included significant QTI prolongation, which persisted minutes and even hours. These findings originated the possibility of implementing using the QTI as an early marker of acute and transient myocardial ischemia.

Knowing the relation between cardiovascular risk factors, ischemic heart disease and increased values of QTI dispersion in a scenario of ACS, we set out to determine the risk factors associated to a greater corrected QT interval dispersion over the course of acute myocardial infarction after the onset of symptoms.

 

MATERIAL AND METHODS
A descriptive, retrospective study related to the behavior of QTI dispersion in 237 patients admitted in the Intensive Care Unit (ICU) of the Celestino Hernández Robau Hospital with the diagnosis of ACS during the term between January 2010 and June 2011.

The (non-intentional) sample was made up by 194 cases, after having analyzed inclusion and exclusion criteria.

Inclusion criteria:

  • Patients that were admitted into the ICU with the diagnosis of ACS.

Exclusion criteria:

  • Patients admitted into the ICU with another diagnosis and that during their stay presented ACS.
  • K serum concentration ≤3.5 mEq/ml.
  • Treatment with antiarrhythmic drugs that modify QTI.
  • Rhythm or conduction disorders as Wolff-Parkinson-White syndrome, complete atrioventricular blocks, pacemaker rhythm, atrial fibrillation, atrial flutter and frequent PVC or PAC prior to ACS.
  • Previous channelopathies.
  • Alterations proper of ECG: less than 7 useful leads for measurement, deficient tracing definition.
  • Mortality of non-cardiovascular etiology.

Obtaining the ECG and measurement of QTI:
Each patient in the study had a 12-lead ECG made at 25 mm/sec and standard gain, taken with a Cardiocid (ICID, Cuba) device. To fulfill the investigation, a QTI reading was made of the first ECG after the onset of the symptoms of acute coronary syndrome.

QTI was measured manually from the beginning of the QRS complex to the end of the T wave, defined as T wave returning point to the isoelectric line, or the nadir between the T and the U waves when the latter is present; to measure QT the guidelines published in JAMA 2003 were considered [9]. To obtain the value of corrected QTI, according to heart rate, the Bazzet’s formula was used [10]. In the practice, the dispersion of this interval could be defined as the difference between maximal corrected QTI and the minimal corrected QTI determined in a standard 12-lead ECG, although there are different methods to measure it and a normal value of up to 50 ms [9] was used, and as prolonged QTI dispersion ≥50 ms.

Risks factors related to ischemic heart disease were taken into account, including: known chronic ischemic heart disease, hypertension, diabetes mellitus, smoking, obesity, metabolic endocrine diseases, dyslipidemia, and history of cerebrovascular disease associated to atherosclerosis. All gathered from the clinical history of the patient.


Ethical aspects
The approval of the committee on ethics from our Hospital center was requested. The results were published in our cardiology services, extended to other diagnostic centers.


Statistical analysis
The results of these assessments were reflected in tables that enabled a careful reading and interpretation, and allowed providing inferential information. To prepare this study, a personal computer Pentium IV was used, with Windows XP environment, with the computer packages Microsoft Office. SPSS for Windows was used in its version 17 to perform the statistical process of the data.

The description of all the variables included in the study were made with absolute numbers and percentages. To determine the presence of association or not between variables, the Chi squared test was used; in the cases in which more than 20% of the expected frequencies were lower than five, Fisher’s exact test of significance was taken into account. When the significance associated to the statistical test used was less than 0.050, it was considered significant; when it was less than 0.010 it was considered highly significant.

After univariate analysis, a logistic regression analysis was made with interactions, with the aim of knowing the personal pathological history with greater influence on the cQTI dispersion variable; this had two categories: normal and prolonged, using the second as a reference category.

 

RESULTS
Table 1 reflects the distribution of the patients studied according to gender and age groups, both for the cases with normal and prolonged dispersion without statistical association (p=0.086 and p=0.195, respectively). The most represented age group in patients with normal cQTI dispersion was that older than 70 years, with 39 cases representing 38.6%, followed by that corresponding to the range from 61 to 70 years, with 24 patients representing 23.8%; a similar behavior was evident in those that presented prolonged dispersion with 43 (46.2%) and 24 (25.8%) cases, respectively. In the distribution according to gender, there was a predominance of the male gender, both for those that showed normal or prolonged dispersion, for 53.5% (54 cases) and 65.6% (61 patients) respectively; however, when observing the distribution of the oldest age groups in the cases without repolarization dispersion, there was a predominance of the female gender with 23 cases (22.8%) over a total of 39 (38.6%) in the group of more than 70 years; while in the range from 61 to 70 years there were 13 women (129%) and 11 men (10.9%). In the patients with increased repolarization dispersion there was also a female predominance in the range from 61 to 70 years, with 13 cases (14%) from all 24, representing 25.8%; however in the oldest range, the male gender reappeared as most prevalent, with 32 patients (34.4%) from all the 43 cases (46.2%).

cQTI dispersion

Age groups (years)

Gender

Totals

Male

Female

%

%

%

Normal
(p = 0.086)
X2 = 8.170

≤ 40

5

5.0

1

1.0

6

5.9

41 to 50

5

5.0

2

2.0

7

6.9

51 to 60

17

16.8

8

7.9

25

24.8

61 to 70

11

10.9

13

12.9

24

23.8

> 70

16

15.8

23

22.8

39

38.6

Totals

54

53.5

47

46.5

101

100

Prolonged
(p = 0.195)
X2 = 6.060

≤ 40

3

3.2

1

1.1

4

4.3

41 to 50

7

7.5

4

4.3

11

11.8

51 to 60

8

8.6

3

3.2

11

11.8

61 to 70

11

11.8

13

14.0

24

25.8

> 70

32

34.4

11

11.8

43

46.2

Totals

61

65.6

32

34.4

93

100

ACS: Acute coronary syndrome; cQTI: corrected QT interval

 
Table 1. Groups by age and gender of patients with acute coronary syndrome

Table 2 shows the personal pathological history significantly associated to cQTI dispersion. The patients with history of chronic ischemic heart disease had an odds ratio 2.69 times greater of presenting prolonged dispersion of repolarization, with a 95% confidence interval (CI) (1.23-5). Diabetic and hypertensive patients also had a greater risk of presenting increased cQTI dispersion, with an odds ratio (OR) of 2.21 (1.16-4.19) and 2.14 (1.15-4.0) respectively. The rest of the pathological history was not significantly associated to cQTI dispersion.

 

PPH

cQTI dispersion

OR:
CI 95%  (LL - UL)

p

Normal

Prolonged

Total

%

%

%

HTN

23

22.8

36

38.7

59

30.4

2.14:
(1.15 – 4.0)

0.016

Diabetes mellitus

21

21.0

34

37.0

55

28.6

2.21:
(1.16 - 4.19)

0.015

Smoking

17

16.8

25

26.9

42

21.6

1.82:
(0.91 - 3.64)

0.090

Ischemic heart disease

11

10.9

23

24.7

34

17.5

2.69:
(1.23 - 5.89)

0.011

Cerebrovascular disease

12

11.9

5

5.4

17

8.8

0.42:
(0.14 - 1.25)

0.109

Dyslipidemia

18

17.8

10

10.8

28

14.4

0.55:
(0.24 - 1.28)

0.162

Obesity

18

17.8

8

8.7

26

13.5

0.43:
(0.18 - 1.05)

0.060

Metabolic disease

6

5.9

4

4.3

10

5.2

0.71:
(0.19 - 2.61)

0.606

cQTI: corrected QT interval; PPH:  personal pathological history; HTN: Hypertension; OR: Odds ratio; CI: Confidence interval; LL: Lower limit; UL: Upper limit.

 
Table 2. Prolonged cQTI dispersion according to the presence
of personal pathological history

The logistic regression model that is shown in Table 3 was properly adjusted to the data (p>0.05). The variables that are associated significantly to cQTI dispersion were: ischemic heart disease, this time with an OR of 4.32 and a 95% CI (1.84 to 10.13); HTN, with an OR of 3.56 with a 95% CI (1.73 to 7.34); and diabetes mellitus with an OR of 3.21 and 95% CI (1.46 to 7.05). As we see, these three factors increased their OR when re-estimated by multivariate analysis.

Variables

ET

Wald

Sig.

OR

CI 95%

Lower

Upper

HTN

0.369

11.889

0.001

3.56

1.73

7.34

Diabetes Mellitus

0.402

10.398

0.002

3.21

1.46

7.05

Ischemic heart disease

0.435

11.347

0.001

4.32

1.84

10.13

Hosmer and Lemeshow: X2=0.425, p=0.935
HTN: Hypertension; OR: Odds ratio; CI: Confidence interval; Sig: Significance.

 
Table 3. Personal history showing a greater relation to corrected QT
interval in the model of logistic regression.


DISCUSSION
A study made in the School of Medicine of the Northwestern University of Chicago, where 40 healthy adults were studied (20 men and 20 women), with an age range of 35 to 67 years; they pointed that cQTI was greater in women than in men, p=0.006 with different circadian rhythm patterns (37±13 ms vs. 30±11 ms, p<0.001). In spite of the substantial differences, all the values were within the range of normalcy, so that gender did not constitute an independent risk factor for repolarization dispersion before coronary artery disease [11].

In 146 patients studied in the School of Medicine of the Hacettepe University in Ankara, Turkey, cases were divided in two groups, with an age of 65 years as cut-off point, with no evidence of coronary ischemic disease. As relevant findings, they obtained that QTI dispersion was significantly higher in the oldest group (35.6±15.6 ms vs. 24.2±12.4 ms; p<0.001). They also verified a greater QTI dispersion in women than in men (31.9±16.7 ms vs. 26.0±11.3 ms respectively, p=0.018). The argument of the first finding was based on the presence of myocardial fibrosis as a consequence of age, which may extend ventricular repolarization time or increase its dispersion.

Other hypothesis are supported on the loss of capillary density, loss of autonomic dysfunction and decline of baroreflex function as responsible for the greater QTI dispersion in the oldest group [12].

The absolute risk of ischemic heart disease increases with age, both in men and women, as a result from the increase in prevalence of coronary atherosclerosis. In fact, most of the new cases are observed above the 65 years of age, mainly in women. It is a well known fact that ischemic heart disease manifests later in women than in men. During the fertile period of women, the incidence of ischemic heart disease is very low, with a progressive increase of it after menopause. Thus, women have an incidence of ischemic heart disease similar to that of men, but with 6 to 10 years of delay, so that since the 75 years of age it is essentially the same. This fact, acknowledged since the 50s, had led to considering the hypothesis of a possible protective effect of female sexual hormones and has originated an intense investigation about it [13].

In HTN an increase in repolarization dispersion has been proven, mainly in those patients in whom left ventricular hypertrophy manifested. At the Harran University, Turkey, a research was carried out in hypertensive patients with a recent diagnosis, that showed values greater than cQTI and its dispersion (p=0.039 and p<0.001, respectively) before the control group. In the bivariate analysis, QTI correlated significantly and positively to parietal diameters, ventricular mass and systolic blood pressure [14]. Bugra et al [15], pointed out that the increase in ventricular mass is not the only reason explaining repolarization dispersion, but that it may also be influenced by a greater parietal stress that occurs in the presence of coronary atherosclerosis, changes in the geometry or normal space arrangement of myocytes (anisotropy), the loss of elastic properties of the aorta with a subsequent increase in differential pressure at the expense of the fall of diastolic pressure, which causes relative ischemia, among other factors.

Besides highlighting the potential mechanisms of HTN in QTI dispersion, it has been of vital clinical important to publish this electrocardiographic parameter as revealing of major cardiac events, shown in the Dimopoulos studies [16,17], who took as cut-off point, cQTI dispersion of 45 ms. Values above this figure were translated in a higher rate of adverse events (p<0.001) and a greater left ventricular mass index (p<0.001). Multivariate analysis found this parameter as the greater predictor of mortality (OR: 4.9, CI 95%: 2.0-12.1; p=0.001).

Korantzopoulos et al, analyzed in patients with stable CAD, the influence of diabetes in electrocardiographic predictors of arrhythmic risk, showing that the Tpeak-Tend/QT ratio was increased in regard to non-diabetic individuals (p=0.030)[0.030] [18]. Subbalakshmi et al, in a study of cases and controls, compared cQTI dispersion between diabetic and non-diabetic patients, and showed a greater increase in the dispersion group of diabetic subjects (115±36 ms vs. 34±12 ms; p<0.001). The maximal cQTI was not significantly modified (415.2±4.1 ms vs. 401.4±6.6 ms, ns)[19].

Diabetes mellitus represents a world epidemic; it is currently considered an equivalent of CAD. There is epidemiological evidence that points diabetes as a strong predictor of sudden cardiac death in ischemic patients; and it has even been associated to the presence of diabetic autonomic neuropathy. The relation between autonomic function and hyperglycemia has been extensively described. In diabetic neuropathy, vegetative regulation is lost, with a predominance of the sympathetic tone and a decrease in the protective vagal properties [20-24].

It is stated that insulin resistance plays a central role in the mechanism of cQTI dispersion in diabetes mellitus. It has been reported that hyperinsulinemia is capable of increasing QTI and its dispersion both in diabetic and non-diabetic patients. The clinical result of this finding is not completely clear. High levels of insulin were associated with an increase in sympathetic activity, which causes changes in cellular refractory periods. Insulin hyperpolarizes cell membranes in excitable and non-excitable tissues with the corresponding consequences, from baroreflex desensitization to refractoriness alterations. It is very well known that insulin causes hypokalemia; one of the most common influences of this electrolytic disorder is cQTI prolongation. The other mechanism that could explain these repolarization alterations is the presence of diabetic macroangiopathy, responsible for coronary circulatory affection [25]. Hyperglycemia stimulates the production of free radicals and reduces the availability of nitric oxide; the decrease in nitric oxide may cause a decrease in the Na/K and Na/CA ATPase pumps with a subsequent increase in cytosolic Ca and prolongation of ventricular repolarization [26].

There was an attempt to determine the links between chronic ischemic heart disease and repolarization dispersion in several studies. Pan et al, in Taiwan, used the coronary score of calcium as a marker for atherosclerosis, obtaining significantly higher values of cQTI dispersion in patients with a high calcium score (≥200) than in the cases with a low score (1-199) p<0.005 [27].

This effect, in which the most recognizable risk factors act in a plausible synergy through a common pathological process, highlights the need of a comprehensive strategy for risk control, both in individuals and in populations; there is even the criterion that considering them is most significant, not as an addition or a multiplication among themselves, but their presence and interactions during the process health-disease in the individual.

Different papers [28-30] showed that the greater presence of ventricular arrhythmias and new acute coronary ischemic events in the follow-up of acute ischemic heart disease, in patients that show prolonged cQTI values; so, knowing  these risk factors that extend cQTI in acute coronary syndrome, guides a better control of them to prevent recurrent acute coronary ischemia and severe electrical complications of the ventricular arrhythmias type.

 

CONCLUSIONS
The result of this investigation significantly illustrates that the risk factors most associated to prolonged repolarization dispersion in the first ECG of an acute coronary event are hypertension, diabetes mellitus and chronic ischemic heart disease. Moreover, it is important to know that they, per se, extend ventricular repolarization and in the presence of acute ischemic event, in a patient with these risk factors, cQTI dispersion may be more substantial; so, controlling these risk factors would help to prevent an acute coronary event, besides preventing the complications generated when ventricular repolarization is increased, thus decreasing the morbi-mortality associated to hypertension, diabetes mellitus and chronic ischemic heart disease.

 

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Publication: March 2014

 
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