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Table of Contents
Year : 2022  |  Volume : 12  |  Issue : 2  |  Page : 55-59

QT-dispersion and major adverse cardiovascular events prediction after percutaneous coronary intervention in patients with Type 2 diabetes mellitus

Department of Cardiology, Faculty of Medicine, Zagazig University, Zagazig, Egypt

Date of Submission19-Sep-2021
Date of Decision01-Oct-2021
Date of Acceptance04-Oct-2021
Date of Web Publication21-May-2022

Correspondence Address:
Prof. Ibtesam EL-Dosouky
Department of Cardiology, Faculty of Medicine, Zagazig University, Zagazig-44519
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jicc.jicc_53_21

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Objectives: The objective of this study investigated the relation between QT-dispersion (QTd) and both number of coronary artery disease and major adverse cardiovascular events (MACEs) among patients with type 2 diabetes after elective percutaneous coronary intervention (PCI). Methods: One hundred ischemic heart disease patients undergoing elective coronary angioplasty were included; 49 patients with diabetes (group I) and 51 patients without diabetes mellitus (group II). Based on the QTd parameter after PCI, both groups were subdivided into tertiles. Angiographic, electrocardiographic parameters, and MACE were compared. Results: Both QTd after PCI and delta QTd were correlated to the number of diseased coronary arteries and MACE in patients with diabetes compared to patients without diabetes. QTd was longer in patients with diabetes developing MACE than those without MACE (r = −0.31, P = 0.04). Conclusion: QTd after PCI and delta QTd are the independent predictors of MACE in patients with type 2 diabetes.

Keywords: Coronary angioplasty, diabetes, MACE, QT dispersion

How to cite this article:
Wageeh S, EL-Dosouky I, ELShabrawy AM, H Omar RE, Zein SG. QT-dispersion and major adverse cardiovascular events prediction after percutaneous coronary intervention in patients with Type 2 diabetes mellitus. J Indian coll cardiol 2022;12:55-9

How to cite this URL:
Wageeh S, EL-Dosouky I, ELShabrawy AM, H Omar RE, Zein SG. QT-dispersion and major adverse cardiovascular events prediction after percutaneous coronary intervention in patients with Type 2 diabetes mellitus. J Indian coll cardiol [serial online] 2022 [cited 2022 Jun 30];12:55-9. Available from: https://www.joicc.org/text.asp?2022/12/2/55/345627

  Introduction Top

Type 2 diabetes mellitus (DM) is a state of hyperglycemia giving rise to microvascular and macrovascular complications which increase cardiovascular morbidity and mortality.[1] The association between QT dispersion (QTd) and morbidity in patients with diabetes was investigated in many studies, and it was found that QTd represents summation of adverse conditions present in diabetic myocardium such as hypertrophy, fibrosis, dilatation, and autonomic dysfunction.[2]

Cardiac autonomic dysfunction in patients with diabetes is assumed to be of maximum importance because it leads to silent myocardial ischemia, intractable arrhythmias, and sudden cardiac death. Diabetic patients with autonomic neuropathy show longer corrected QT duration (QTc) compared with those without autonomic neuropathy.[3]

Over the past several years, QT duration and QTd (measured in surface electrocardiogram [ECG] recordings) have been explored as a potential simple bedside and noninvasive marker of the inhomogeneity in the ventricular repolarization. Its increase is a sign of electrical instability that reduces the threshold for ventricular fibrillation and facilitates the appearance of ventricular arrhythmias.[4]

As cardiovascular disease is the principal cause of death among patients with type 2 DM, the prediction and early diagnosis of MACE may decrease both morbidity and mortality. Several studies have demonstrated that QTd is increased in acute myocardial ischemia and that increased QTd predicts the risk of ventricular arrhythmias in acute myocardial infarction (AMI).[5]

However, the relationship between QTd and prognosis has not yet been fully elucidated in patients with diabetes and coronary artery disease (CAD).

Therefore, in our study, we investigated the predictive value of QTd after successful coronary stenting to major adverse cardiac events (MACEs) in patients with type 2 DM.

  Methods Top

This observational, case − control study was conducted at the cardiology department, Zagazig university hospitals, over a period from July 2020 to April 2021. One hundred ischemic heart disease patients undergoing elective coronary angioplasty and revascularization were included and divided into two groups: Group I included 49 patients with type 2 DM and Group II of 51 patients without DM as control. Hemoglobin A1C was used to define groups at a cutoff value ≥6.5%.[6] Patients with bundle branch block, atrial fibrillation, high-grade atrioventricular block, EF <45%, Wolff-Parkinson-White syndrome, congenital long QT syndromes, electrolytes imbalance, and diseases or drugs that modify the QT interval were all excluded from the study.

Detailed history taking, full clinical examination, routine laboratory investigations, and ECG recording with measurement of QTd were done. QTd was calculated from the QT max minus QT min.[7]

We measured QTd twice, 24 h before and 7 days postpercutaneous coronary intervention (PCI), the difference was measured (QTd before PCI–QTd after PCI) and was recorded as delta (Δ) QTd.

All patients were followed up for 6 months for MACEs; MACEs were defined as cardiac death, nonfatal myocardial infarction, ischemic stroke, and ischemic symptoms leading to hospital admission. Written informed consent was obtained from all participants, and protocols were approved by the Medical Research and Ethics committee.

Statistical analysis

The demographic, clinical, and laboratory parameters were collected, and calculations were performed, summarized, tabulated, and analyzed using the computerized software statistical packages (SPSS for Windows® version 16 IBM SPSS (Statistical Package for the social sciences) statistics for windows, version 16.0 IBM Corp., Armonk, NY: USA. The continuous variables were expressed as mean and standard deviation and discrete variables were presented as frequencies and percentages.

The continuous variables were compared between the groups using the one-way analysis of variance. Discrete variables were compared using the Chi-squared test (X2) with Fisher's exact correction. Multivariate logistic regression analysis was performed for MACE prediction. Receiver operating characteristic (ROC) curve analysis was used to identify the optimal cutoff values. A two-tailed P < 0.05 was considered statistically significant.

  Results Top

Our study included 100 patients divided into two groups: Group I for patients with diabetes (n = 49) and Group II for patients without diabetes (n = 51), each was subdivided into three subgroups (tertiles) according to the QTd measured after PCI. Diabetic group (I); 1st ≥27 ± 7, (n = 16), 2nd ≥50 ± 7 (n = 17), and 3rd ≥80 ± 23, (n = 16). Nondiabetic group (II); 1st ≥34.5 ± 9, (n = 17), 2nd ≥54.7 ± 5 n = 18, and 3rd (74.3 ± 13) n = 16.

The demographic and clinical parameters of the study groups are shown in [Table 1].
Table 1: Demographic, clinical, laboratory, electrocardiography, and coronary angiography of studied groups

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Both groups showed significant reduction of the QTd after PCI in comparison to QTd measured before PCI (52.3 ± 23.9 after PCI vs. 58.6 ± 19 before PCI in Group I and 54 ± 18 after PCI vs. 61.5 ± 23 before PCI in Group II, P = 0.002) [Table 1].

MACE was higher at diabetic group (10 (20.4%) vs. 5 (9.8%) in nondiabetic, P = 0.07 (near significance) [Table 1].

Diabetic patients with MACE had longer QTd than those without MACE with statistically significant difference between tertiles (P = 0.04), [Table 2].
Table 2: Analysis of QT dispersion after percutaneous coronary intervention with other parameters

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In the diabetic group, QTd after PCI was longer among patients who developed MACE (10 patients), while patients without MACE (39 patients) were distributed among lower tertiles; representing negative correlation between the number of patients developed MACE and QTd after PCI (r = −0.3, P = 0.02), [Table 2].

Dyslipidemic patients were distributed among higher tertiles, (P = 0.011). Furthermore, the number of diseased coronary vessels showed positive correlation with QTd; two and three vessel disease was distributed at higher tertiles; (r = 0.318, P = 0.026), [Table 2].

The nondiabetic group showed higher distribution of the left anterior descending artery (LAD) as a culprit at 1st tertile while higher number of the non-LAD culprit was found among 3rd tertile with positive correlation (r = 0.32, P = 0.022), while there was no relation between QTd after PCI and MACE occurrence in that population [Table 2].

On multivariate logistic regression analysis of risk factors to determine the independent risk parameters, [Table 3], only QTd after PCI dispersion (B Coefficient = −0.012 (0.022), 95% confidence interval [CI] 0.925–0.992 with an odds ratio = 1 and P = 0.017), and so delta QT (B Coefficient = −0.052 [1.162], 95% CI 0.913–0.982 with an odds ratio = 1 and P = 0.003) were found to be the independent predictor of MACE in diabetic patients [Table 3].
Table 3: Logistic regression analysis for predictors of major adverse cardiac event in diabetic group

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ROC analysis of these independent predictors showed that QT after PCI at a cutoff value ≥53.5 ms is a good predictor (area under the curve [AUC] =0.76, P = 0.011) with 80% sensitivity and 61.5% specificity for MACE, and so the delta QTd at a cutoff value ≥6 ms (AUC = 0.82, P = 0.002) with 90% sensitivity and 80% specificity to predict MACE [Figure 1].
Figure 1: Receiver operating characteristic analysis of the independent predictors of MACE, showed that QT after percutaneous coronary intervention at a cutoff value ≥53.5 m and so the delta QT dispersion at a cutoff value ≥6 ms can predict MACE

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  Discussion Top

Atherosclerotic cardiovascular disease is the leading cause of morbidity and mortality in diabetic patients. Hence, the prediction and early diagnosis of MACE is of outstanding clinical importance to decrease both morbidity and mortality.[8]

Numerous markers for both microvascular and macrovascular complications of DM had been studied. In an effort to identify easily available and reliable predictors for cardiovascular risk and mortality in DM, QTd is considered a simple bedside test with particular interest reflecting myocardial repolarization, as it is associated with increased risk of arrhythmia and death.[9]

The purpose of this study is to evaluate prospectively whether QTd is associated with MACEs at 6 months follow-up after successful elective coronary stenting in patients with type 2 diabetes.

In the diabetic group, we observed that QTd was longer post PCI in patients with MACE than those who did not developed MACE. The non-MACE group showed significant reduction of both QTd and delta QTd post PCI compared to the MACE group.

Multiple logistic regression analysis, Δ QTd and QTd after PCI was independent predictor of MACE with odds ratio = 1 for each with 95% CI (0.925–0.992), (P = 0.017) for QTd after PCI, while 95% CI (0.913–0.982), (P = 0.003) for Δ QTd. Our results were concordant with Pan et al.[10] who showed that the absolute cQTd change after primary PCI was an independent predictor of the development of MACE.

We detected that QTd after PCI can be used as a good predictor for MACE with 80% sensitivity and 61.5% specificity at a cutoff value ≥53.5 ms (AUC = 0.763, P = 0.011). Furthermore, delta QTd is a good predictor for MACE in this population at a cutoff value ≥6 ms with 90% sensitivity and 79.5% specificity.(AUC = 0.824, P = 0.002). While Hiroyasu Ueda et al.[11] concluded that corrected QTd before PCI is associated with an increased risk of MACE and mortality after successful PCI in patients with AMI.

In our study, it was observed that QTd after PCI was positively correlated with the number of diseased vessels in patients with diabetes (r = 0.318, P = 0.026). This is in agreement with NI Sharafat et al.[12] who studied the relationship between the extent of coronary vessel involvement in acute ST-elevated myocardial infarction patients with QTd. They proved that the longer the QTc dispersion, the higher the number of coronary artery involvement (r = 0.75, P < 0.001). Furthermore, Shafiqul et al.[13] results agree with ours; QTd post PCI was associated with the severity of coronary artery stenosis, and the number of coronary vessels involved.

Significant reduction in QTd after PCI in both groups was observed, this is concordant with Choi et al.[14] and Alasti et al.[15] who found that QTd decreases in patients with CAD but without a history of myocardial infarction at 1 month following successful PCI. This suggests that PCI facilitates a favorable recovery from inhomogeneous repolarization due to myocardial ischemia.

In our study, we observed that in patients without diabetes, QTd after PCI was correlated to culprit lesion. Patients with LAD culprit have higher QTd while lower values were recorded among non-LAD culprit with significant difference (P = 0.022, r = 0.319). This was concordant with Kilic et al.[16] who found that the greatest QTd was observed in the LAD lesions.

While in our diabetic group, no relation was found between culprit lesion and QTd, this may be explained by the extended pathological effects of diabetes on microcirculation which can prolong QTd independent of large vessels affection. This was concordant with Tikiz et al.[17] who concluded that the severity of localized ischemia rather than extent of CAD would be expected to have a greater effect on inducible QTd. In contrary of Ramadan and Hosam[18] who observed that there is predictive value of QTd for the early detection of LAD coronary artery lesions (they studied isolated T-wave inversion in lead aVL only).

Limitations of the study

Week correlations in our study are mainly attributed to small number of patients; however, we overcome this problem using the appropriate statistical tests. Furthermore, we measured QT intervals manually in this study, but Goldenberg et al.[19] suggested that the accuracy of automatic measurements of QT interval was questionable in many cases.

  Conclusion Top

In our study, we found that QTd was longer in patients with type 2 diabetes than those without diabetes. Furthermore, QTd post PCI was predictive of MACE in the diabetic population with 80% sensitivity and 61.5% specificity at cutoff value of ≥53.5 ms, whereas delta QTd at cutoff value of ≥6 ms had sensitivity and specificity of 90% and 79.5%, respectively. However, no correlation was found in nondiabetics.

Hence, QTd after PCI and delta QTd can be utilized as a simple, nonexpensive tool for the prediction of outcome in patients with type 2 diabetes.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Orasanu G, Plutzky J. The pathologic continuum of diabetic vascular disease. J Am Coll Cardiol 2009;53:S35-42.  Back to cited text no. 1
Naas AA, Davidson NC, Thompson C, Cummings F, Ogston SA, Jung RT, et al. QT and QTc dispersion are accurate predictors of cardiac death in newly diagnosed non-insulin dependent diabetes: Cohort study. BMJ 1998;316:745-6.  Back to cited text no. 2
Mahwi TO, Hasan RM, Faraj HI. Incidence of QTc prolongation in type 2 diabetes mellitus and its relation to cardiac autonomic neuropathy. Jordan Med J 2014;48:102-11. DOI:10.12816/0024900  Back to cited text no. 3
Zhang Y, Post WS, Blasco-Colmenares E, Dalal D, Tomaselli GF, Guallar E. Electrocardiographic QT interval and mortality: A meta-analysis. Epidemiology 2011;22:660-70.  Back to cited text no. 4
Yunus A, Gillis AM, Duff HJ, Wyse DG, Mitchell LB. Increased precordial QTc dispersion predicts ventricular fibrillation during acute myocardial infarction. Am J Cardiol 1996;78:706-8.  Back to cited text no. 5
American Diabetes Association. Standards of medical care in diabetes-2020. Diabetes Care 2020;43 Suppl 1:S1-2.  Back to cited text no. 6
Malik M, Batchvarov VN. Measurement, interpretation and clinical potential of QT dispersion. J Am Coll Cardiol 2000;36:1749-66.  Back to cited text no. 7
Christensen PK, Gall MA, Major-Pedersen A, Sato A, Rossing P, Breum L, et al. QTc interval length and QT dispersion as predictors of mortality in patients with non-insulin-dependent diabetes. Scand J Clin Lab Invest 2000;60:323-32.  Back to cited text no. 8
Stettler C, Bearth A, Allemann S, Zwahlen M, Zanchin L, Deplazes M, et al. QTc interval and resting heart rate as long-term predictors of mortality in type 1 and type 2 diabetes mellitus: A 23-year follow-up. Diabetologia 2007;50:186-94.  Back to cited text no. 9
Pan KL, Hsu JT, Chang ST, Chung CM, Chen MC. Prognostic value of QT dispersion change following primary percutaneous coronary intervention in acute ST elevation myocardial infarction. Int Heart J 2011;52:207-11.  Back to cited text no. 10
Ueda H, Hayashi T, Tsumura K, Kaitani K, Yoshimaru K, Nakayama Y, et al. QT dispersion and prognosis after coronary stent placement in acute myocardial infarction. Clin Cardiol 2007;30:229-33.  Back to cited text no. 11
Sharafat N, Khalequzzaman M, Akhtaruzzaman M, Choudhury S, Hasem S, Choudhury T, et al. Prolonged QTc dispersion correlates with coronary artery disease in acute ST elevated myocardial infarction (STEMI). Cardiovasc J 2013;5:173-81.  Back to cited text no. 12
Islam MS, Mondal SK, Jahan J, Arefin M, Ahmed N, Das PR, et al. Effect of PCI on QTC dispersion in patients with angina. Univ Heart J 2020;16:33-9. DOI:10.3329/uhj.v16i1.44820  Back to cited text no. 13
Choi KJ, Lee IS, Lee SK, Hong MK, Park SW, Park SJ, et al. Change of QT dispersion following PTCA in angina patients. Korean Circ J 1998;28:1487-92.  Back to cited text no. 14
Alasti M, Adel MH, Torfi E, Noorizadeh M, Bahadoram S, Moghaddam MA, et al. QT dispersion: Does it change after percutaneous coronary intervention? J Tehran Heart Cent 2011;6:19-23.  Back to cited text no. 15
Kilic H, Atalar E, Necla O, Ovunc K, Aksoyek S, Ozmen F. QT interval dispersion changes according to the vessel involved during percutaneous coronary angioplasty. J Natl Med Assoc 2007;99:914-6.  Back to cited text no. 16
Tikiz H, Terzi T, Balbay Y, Demir AD, Soylu M, Keles T, et al. QT dispersion in single coronary artery disease: Is there a relation between QT dispersion and diseased coronary artery or lesion localization? Angiology 2001;52:43-51.  Back to cited text no. 17
Ghaleb R, Mansour H. Predictive value of QT dispersion and isolated T-wave inversion in lead aVL for early detection of left anterior descending coronary artery lesions. Oman Med J. 2010 Apr; 25(2): 124–127. doi: 10.5001/omj.2010.33.  Back to cited text no. 18
Goldenberg I, Moss AJ, Zareba W. QT interval: How to measure it and what is “normal”. J Cardiovasc Electrophysiol 2006;17:333-6.  Back to cited text no. 19


  [Figure 1]

  [Table 1], [Table 2], [Table 3]


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