QT Min Research Articles

Prognostic Value of QT Parameters in Patients with Acute Hemorrhagic Stroke: A Prospective Evaluation with Respect to Mortality and Post-hospitalization Bed Confinement

This prospective study was performed to evaluate the prognostic prediction value of QT parameters and clinical characteristics exhibited by patients with acute hemorrhagic stroke at the time of presenting to the emergency department (ED). One hundred and sixty-six patients admitted to the ED of Taipei Veterans General Hospital from January 2006 to October 2006 because of acute hemorrhagic stroke were enrolled. Glasgow Coma Scale (GCS) scores between 3 and 8 were taken to indicate severe neurologic deficits. QT parameters (QT max, QT min, QT dispersion, QTc max, QTc min, QTc dispersion) and other pertinent clinical variables were determined on admission. Logistic regression model was applied to evaluate prognostic prediction values. Mortality was higher among stroke patients with low GCS scores (p < 0.01). Leukocyte counts and systolic blood pressures were significantly higher among non-surviving patients (p = 0.04). No association was found between QT parameters and mortality (all p > 0.05). Among survivors, post-hospitalization bed confinement was required for those significantly older (p = 0.01) and those with higher QT max and QTc max values in multivariate analyses (p = 0.04 and p < 0.01, respectively). Low GCS scores, increased leukocyte counts, and elevated systolic blood pressures predict increased mortality for subjects with acute hemorrhagic stroke. Advanced age and prolongations in QTc and QT max at the time of stroke predicted poor functional recovery for these subjects.

Effect of Controlling Hyperglycemia With Diet on QT Abnormalities in Newly Diagnosed Patients With Type 2 Diabetes

Diabetic patients have an excess risk of dying from cardiovascular diseases. Recently, several studies have reported a high prevalence of QT prolongation and increased QT dispersion (QTd) in patients with diabetes. These abnormalities have been shown to be associated with sudden death and poor survival in both type 1 (1) and type 2 (2) diabetes. QTd, i.e., the difference between the maximum and minimum QT intervals on the 12-lead electrocardiogram (ECG) (QTd = QT max − QT min), is claimed to reflect the degree of inhomogeneity of myocardial repolarization. The role of hyperglycemia in causing QT abnormalities in people with diabetes is not clear. …

Patterns of QT Dispersion in Athletic and Hypertensive Left Ventricular Hypertrophy

The objective of this article is to assess whether left ventricular hypertrophy (LVH) due to physical training or of hypertensive patients shows similarities in QT length and QT dispersion. A total of 51 subjects were studied: 17 essential hypertensive patients (27.7 +/- 5.6 years), 17 athletes involved in agonistic activity (canoeing) (24.8 +/- 6.1 years), and 17 normotensive healthy subjects as control group (24.8 +/- 3.6 years). The testing protocol consisted of (1) clinic BP measurement, (2) echocardiography, (3) 12-lead electrocardiographic examination (QT max, QTc max, QT min, QTc min, DeltaQT, DeltaQTc). There were no significant differences between the body surface area, height, and age of the three groups. Clinic blood pressure was higher in hypertensives (146.5 +/- 45.2/93.5 +/- 4.9 mmHg) versus athletes (120.9 +/- 10.8/77.1 +/- 6.0 mmHg) and controls (123.5 +/- 4.8/78.8 +/- 2.9 mmHg) by definition. Indexed left ventricular mass (LVM/BSA) was significantly greater in both athletes (148.9 +/- 21.1 g/m2) and hypertensives (117.1 +/- 15.2 g/m2) versus controls (81.1 +/- 14.5 g/m2; P < 0.01), there being no statistical difference among them. LVH (LVMI > 125 g/m2) was observed in all athletes, while the prevalence in hypertensives was 50%. In spite of this large difference in cardiac structure there were no significant differences in QT parameters between athletes and the control group, while hypertensive patients showed a significant increase in QT dispersion versus the two other groups (DeltaQT 82 +/- 2.1, 48 +/- 1.3, 49 +/- 2.3 ms; P < 0.01; DeltaQTc 88 +/- 2.0, 47 +/- 1.4, 54 +/- 2.7; P < 0.01). LVH induced by physical training activity is not associated with an increase in QT dispersion, whereas pathological increase in LVM secondary to hypertension is accompanied by an increased QT dispersion.

Exercise-induced changes in QT interval duration and dispersion in patients with isolated myocardial bridging

Background: Isolated myocardial bridging (MB) often is considered to be an unimportant angiographic finding; however, its association with cardiovascular event has been shown. In this study we aimed to assess exercise-induced electrocardiographic (ECG) changes and susceptibility to arrhythmia in patients with MB. Method: 21 consecutive patients who had angiographically proven MB (group I) and 25 subjects (group II) who had normal coronary arteries underwent exercise test using Bruce protocol. Before and after the exercise test the changes in QT interval duration and dispersion were compared. Results: Baseline characteristics of both groups were similar. Heart rate significantly increased after exercise test in both groups. In group I, after exercise mean QT max and QT min durations did not change significantly compared to baseline values, respectively. (QT max: 411±20 vs. 421±18 ms, p>0.05 and QT min: 380±12 vs. 378±10 ms, p>0.05). However, following exercise test QT dispersion (QT d) and corrected QT dispersion (QT cd) significantly increased when compared to baseline values, respectively. (34±13 vs. 66±14 ms, p<0.05 and 37±14 vs. 69±17 ms, p<0.05) On the other hand, in control group QT max and QT min durations, QT c and QT cd did not change significantly compared to baseline values, respectively. (QT max: 408±18 vs. 412±17 ms, p>0.05 and QT min: 390±11 vs. 387±10 ms, p>0.05; QT d: 25±14 vs. 31±16 ms, p>0.05; QT cd: 27±15 vs. 33±17 ms, p>0.05). Conclusion: Treadmill exercise test significantly increased QT dispersion in patients with MB. This increase may result from exercise-induced ischemia at the area perfused by bridged artery.

Haemodialysis increases QT(c) interval but not QT(c) dispersion in ESRD patients without manifest cardiac disease.

HD has been reported to determine an increase in QTc interval and QTc dispersion (QT(max)-QT(min))-risk factors that predispose to severe ventricular arrhythmias and sudden death. However, most studies have included end-stage renal disease (ESRD) patients with significant heart pathology. We therefore aimed to study the impact of a single HD session in subjects without manifest cardiac disease. Sixty-eight stable, non-diabetic HD patients (47.1% males, age 40.2+/-12.7 years, HD duration 57+/-36 months and 37% hypertensive), with normal maximal ECG stress test and sub-endocardiac viability index and without ECG left ventricular hypertrophy were included. QT interval was calculated 10 min pre- and post-HD, as an average of three consecutive complexes, and corrected for heart rate using Bazett's formula (QTc=QT/(R-R)(1/2)). Na(+), K(+), Ca(2+), PO(4), pH and BP levels were also determined pre- and post-HD. The QTc interval increased significantly post-HD to 434+/-29 from 421+/-26 ms pre-HD (P=0.005); an abnormally prolonged QTc (>440 ms) was recorded in 34% cases pre-HD and in 46% post-HD, i.e. 1.5-2.3 times higher than in the high risk EURODIAB IDDM population. However, this effect was not homogeneous. Only 47 subjects had an increase in QTc duration after a dialysis session, while in 21 a decrease in QTc duration was recorded. The increase in QTc post-HD correlated with Ca(2+) homeostasis. Patients with greater increases in QTc after dialysis had higher baseline plasma calcium levels (r=0.47, P<0.001); also, a larger decrease in Ca(2+) post-HD correlated with higher increases in QTc interval (r=0.33, P<0.05). In contrast with QTc behaviour and with data from the literature, in this young HD population without manifest cardiac disease and with a low prevalence of HTA, post-HD QTc dispersion was similar to pre-HD values, increasing in only 39 patients. Furthermore, changes in QTc dispersion were not related to changes in electrolytes and BP following dialysis. However, changes in QTc dispersion and in QTc interval were directly correlated (r=0.37, P=0.42). There were no relationships between pre-HD measured echocardiographic variables, including: LV ejection fraction, internal diameters, wall thickness, mass and mass index and baseline or changes in QTc or QTc-d. Haemodialysis increases the QTc interval in ESRD patients, mainly related to rapid changes in electrolyte plasma concentrations. However, the impact on QTc dispersion is less important in the absence of significant coexisting cardiac disease.

QTc interval length and QT dispersion as predictors of mortality in patients with non-insulin-dependent diabetes

Patients with non-insulin-dependent diabetes (NIDDM) are at independent risk of cardiovascular death. The reason is only partially understood. The aim of our study was therefore to evaluate the impact of corrected QT interval length (QTc) and QT dispersion (QT-disp) on mortality in a cohort of 324 Caucasian NIDDM patients. A resting 12-lead ECG was recorded at baseline. Maximum (QT-max) and minimum QT (QT-min) intervals were measured, and QT-max was corrected for heart rate (QTc-max). QT-disp was defined as the difference between QT-max and QT-min. QTc-max was 454 (376-671) ms½ (median (range)) and QT-disp 61 (0-240) ms. Prolonged QTc interval (PQTc), defined as QTc-max>440 ms½, was present in 67% of the patients and prolonged QT-disp (PQT-disp), defined as QT-disp>50 ms, was present in 51%. During the 9-year follow-up period, 100 patients died (52 from cardiovascular diseases). Thirty-seven percent of the patients with PQTc died compared with 17% with normal QTc interval (p<0.001). The Cox proportional hazard model, including putative risk factors at baseline, revealed the following independent predictors of all cause mortality; QTc-max (p<0.05), age (p<0.0001), albuminuria (p<0.01), retinopathy (p><0.01), HbA1c (p<0.05), insulin treatment (p<0.01), total cholesterol (p<0.01), serum creatinine (p<0.05) and presence of cardiac heart disease based on Minnesota coded ECG (p<0.001). Whereas QT-disp was not a predictor. QTc-max interval was an independent predictor of cardiovascular mortality. Our study showed a high prevalence of QTc and QT-disp abnormalities and indicated that QTc-max but not QT-disp is an independent predictor of all cause and cardiovascular mortality in NIDDM patients.

Effect of coronary angioplasty on QT dispersion

Increased QT dispersion (QT max – QT min [QTd]) reflects inhomogeneous ventricular repolarization that may provide a substrate for serious arrhythmias and is associated with adverse clinical outcomes in patients with heart disease. Effective treatment of acute myocardial infarction or ventricular arrhythmias may reduce QTd, but the effect of coronary revascularization on QTd in patients without these conditions is unknown. In this study, QTd was measured before and 4 and 24 hours after successful angioplasty in 94 patients without ongoing symptomatic myocardial ischemia or malignant arrhythmias. QTd decreased from 434 ± 17 msec before angioplasty to 354 ± 15 msec 4 hours ( p < 0.05) and 33 ± 14 msec 24 hours after angioplasty ( p < 0.05). QTd was improved in 64% of patients, worse in 28%, and unchanged in 8%. Thus angioplasty significantly improves QTd. This may reflect increased myocardial perfusion and may be inherently beneficial by reducing the propensity for arrhythmias. (Am Heart J 1997;134:399-405.)

901–46 QT Dispersion Predicts Mortality in Treated Patients with Life-threatening Ventricular Tachyarrhythmias

QT dispersion (QTD = QT max – QT min), measured from the 12-lead ECG, reflects regional variations in ventricular repolarization and has been associated with an increased risk of arrhythmic events in some patient (pt) groups, but has not been applied as a predictor in patients at risk for recurrent, sustained ventricular tachyarrhythmias (VT/VF). Thus, we sought to determine the predictive value of QTD in consecutive pts presenting with life threatening ventricular arrhythmias and treated with antiarrhythmic drugs predicted to be effective by electrophysiologic testing (n = 11) or Holter monitoring (n = 18). The study group comprised 29 pts of age 66 ± 13 years with ejection fraction 37 ± 13%; 24 were males, 23 had coronary artery disease; 22 had failed previous antiarrhythmic therapy; treatment was with class I drugs in 16 and class III (sotalol) in 13. Follow-up lasted up to 5.7 years (x ± SD, 2.1 ± 1.7). Arrhythmia recurred in 15 pts; there were 4 arrhythmic and 7 total deaths. Parameters on 12 lead ECG tested for long-term predictive value included QRS, QT. QTc, JT, JTc, QTD, QTcD, JTD, and JTcD. Measurements were made within 1 mo of initiating “effective” antiarrhythmic therapy by an experienced observer using electronic calipers and blinded to clinical course. Only measures of dispersion of recovery were predictors of arrhythmic and total mortality: QTD (p ≤ 0.005, 0.0001), QTcD (p ≤ 0.01, 0.0001), JTD (p ≤ 0.005, 0.0000), and JTcD (p ≥ 0.005, 0.0000). In patients dying vs surviving, QTD was 147 ≤ 42 vs 74 ≤ 34 ms and JTcD, 141 ≤ 33 vs 76 ± 30 ms, respectively. Predictive value was independent of antiarrhythmic therapy (ie, sotalol vS other) in a multivariate model. Thus, excessive dispersion of repolarization is a powerful predictor of arrhythmic and total deaths, despite “effective” drug therapy, in patients with life-threatening ventricular arrhythmias. QTD should be further tested in larger groups of high-risk pts, including the selection of pts for further therapies (eg, defibrillators).

911-37 Quinidine or Sotalol-induced Changes in QT-Dispersion During Pharmacological Conversion Therapy of Atrial Fibrillation: Link to Proarrhythmia as Assessed in a Prospective, andomized Trial

QT dispersion (QTD;QT max -QT min ) is considered to reflect inhomogeneous ventricular recovery. In pts with atrial fibrillation (AF), however, the effects of antiarrhythmic drugs on QTD have not been systematically evaluated particularly with respect to their association with drug-induced proarrhythmia. Thus, QTD was assessed in a prospective, randomized trial including 50 pts with AF receiving quinidine (Q; 1000 mg/day) or sotalol (S;320 mg/day) in an attempt to restore sinus rhythm (SRI. Precordial QTD was measured by means of a digitizer-based software before and during drug therapy. 22/25 Q-treated pts converted to SR compared to 17/25 S pts (p = ns). There were 4 cases of proarrhythmia (torsade de pointes in 3 pts, monomorphic VT in 1 pt) in the Q- but none in the S-pts. Whereas ventricular depolarization (QRS) was not affected by either drug, Q and S caused a comparable increase in QTmax. QTD, however, increased only in the Q group whereas no significant changes were observed in S pts. QTD increased by &gt; 50% in all 3 pts with Q-associated torsade de pointes. QRS (msec) QTmax (msec) QTD (msec) control drug control drug control drug Q 86 ± 17 90 ± 17 363 ± 38 4 ± 39 # 34 ± 9 43 ± 14 * S 89 ± 21 89 ± 18 367 ± 40 425 ± 58 # 36 ± 18 40 ± 17 * p &lt; 0.05 # p &lt; 0.01 In pts with AF, precordial QTD increases significantly during Q- but not during S-therapy desp te a comparable increase in QT max .This finding may reflect a greater propensity for the development of proarrhythmia associated with Q therapy. Determination of QTD may help to increase the safety of pharmacological therapy in this patient population.

901-9 QT Dispersion and Prognosis After Myocardial Infarction

QT dispersion (QT max minus QT min) is an important measure of arrhythmia risk, providing information about heterogeneity of ventricular repolarisation. We studied QT dispersion for all cause mortality in patients from the placebo arm of a large therapeutic intervention trial in acute myocardial infarction. Standard 12 lead electrocardiograms (ECGs) were analysed from day 2 or 3 of the acute infarction; and if available, from a later period of life (more than 1 month post infarct). The only exclusions were patients with chronic atrial fibrillation or paced rhythm, or those with ECGs of too poor quality to be analysed. The ECGs were scanned, and the image divided into12 files corresponding to the 12 leads of the standard ECG. Specially designed software then skeletonised and joined each file, which is then available for either user-interactive or automatic measurement of QT dispersion, again using specially designed software. The following results are all user interactive, and are rate and lead corrected (rate corrected QT max minus QT min divided by the square root of the number of leads with a measureable QT interval). For the group known to have deceased 163 patients had ECGs analysed during the early stage of acute myocardial infarction, and 53 had ECGs recorded later in life. 163 age and sex matched survivors in the same study have been analysed, of these 82 have had ECGs recorded later in life. Mean adjusted QT dispersion for the death group is 36.6 ms (SD 14.7), andfor survivors 35.2 ms (SD 13.9), p-NS; for ECGs recorded on day 2 or 3 of acute myocardial infarction. ECGs recorded later in life have an adjusted OT dispersion of 31.2 ms (SD 13.9) for the deceased group, and for survivors of 24.5 ms (SD 9.5), p &lt; 0.01. QT dispersion is prolonged in the early stages of acute myocardial infarction, and for long term survivors then falls towards more normal values. The failure of QT dispersion to normalise in patients who subsequently decease is an important observation, and may provide insight into the causes of mortality in this group.