Maximum Corrected QT Interval Research Articles

Is the development of arrhythmia predictable in rheumatoid arthritis?

Objectives: This study aimed to determine whether there is a difference in the electrocardiography (ECG) measurements of healthy controls and rheumatoid arthritis (RA) patients and to predict whether they can be used to determine the risk of arrhythmia in patients. Patients and methods: The prospective study included 50 cardiac asymptomatic RA patients (38 males, 12 females; mean age: 46.8±9.1 years; range, 18 to 60 years) who met the 2010 American College of Rheumatology/European Alliance of Associations for Rheumatology RA criteria and 50 healthy volunteers (34 males, 16 females; mean age: 43.4±10.4 years; range, 18 to 60 years) as a control group between June 1, 2022, and August 31, 2022. Disease activity of the patients was calculated with the Disase Activity Score (DAS28). Heart rate, minimum and maximum QT intervals, QT dispersion, minimum and maximum P waves, P wave dispersion (Pd), minimum and maximum Tp-e intervals, Tp-e dispersion, minimum and maximum corrected QT (QTc) intervals, QTc dispersion, and the Tp-e/QTc ratio in ECGs were calculated. Results: The mean disease duration of the RA group was 9.09±5.74 years. The mean C-reactive protein level was 9.83±8.29, the mean erythrocyte sedimentation rate was 26.12±16.28 mm/h, and the mean DAS28 was 3.03±0.37. There was a statistically significant increase in the maximum P wave, Pd, maximum QT, QT dispersion, maximum QTc, QTc dispersion, maximum Tp-e, Tp-e dispersion, and Tp-e/QTc dispersion parameters in the RA group compared to the control group, while there was a significant decrease in the minimum P wave, minimum QT, and minimum QTc parameters. Conclusion: In our study, the Pd, QTc dispersion, Tp-e dispersion, and Tp-e/QTc dispersion values of our patients, which indicate the risk of atrial and ventricular arrhythmia, were found to be significantly higher. This finding suggests that our patients had an increased risk of cardiac morbidity and mortality. Arrhythmias are the likely source of the increase in sudden cardiac death in RA, and these new indicators measured on ECG can be used as standardized cardiovascular morbidity and mortality indicators in the future.

Can indicators of myocardial damage predict carbon monoxide poisoning outcomes?

BackgroundCarbon monoxide causes electrical, functional, and morphological changes in the heart. It is unclear, however, whether the indicators of myocardial damage can predict the patient’s prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relationship between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient’s prognosis after carbon monoxide poisoning.MethodsCarboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated.ResultsThe correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P = 0.0072, R2 = 0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2358) and the corrected QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were corrected QT dispersion (P = 0.0042), and troponin I level (P = 0.0021).ConclusionsPatients’ prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.

Effect of Chloroquine, Hydroxychloroquine, and Azithromycin on the Corrected QT Interval in Patients With SARS-CoV-2 Infection.

Background:The novel SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) is responsible for the global coronavirus disease 2019 pandemic. Small studies have shown a potential benefit of chloroquine/hydroxychloroquine±azithromycin for the treatment of coronavirus disease 2019. Use of these medications alone, or in combination, can lead to a prolongation of the QT interval, possibly increasing the risk of Torsade de pointes and sudden cardiac death.Methods:Hospitalized patients treated with chloroquine/hydroxychloroquine±azithromycin from March 1 to the 23 at 3 hospitals within the Northwell Health system were included in this prospective, observational study. Serial assessments of the QT interval were performed. The primary outcome was QT prolongation resulting in Torsade de pointes. Secondary outcomes included QT prolongation, the need to prematurely discontinue any of the medications due to QT prolongation, and arrhythmogenic death.Results:Two hundred one patients were treated for coronavirus disease 2019 with chloroquine/hydroxychloroquine. Ten patients (5.0%) received chloroquine, 191 (95.0%) received hydroxychloroquine, and 119 (59.2%) also received azithromycin. The primary outcome of torsade de pointes was not observed in the entire population. Baseline corrected QT interval intervals did not differ between patients treated with chloroquine/hydroxychloroquine (monotherapy group) versus those treated with combination group (chloroquine/hydroxychloroquine and azithromycin; 440.6±24.9 versus 439.9±24.7 ms, P=0.834). The maximum corrected QT interval during treatment was significantly longer in the combination group versus the monotherapy group (470.4±45.0 ms versus 453.3±37.0 ms, P=0.004). Seven patients (3.5%) required discontinuation of these medications due to corrected QT interval prolongation. No arrhythmogenic deaths were reported.Conclusions:In the largest reported cohort of coronavirus disease 2019 patients to date treated with chloroquine/hydroxychloroquine±azithromycin, no instances of Torsade de pointes, or arrhythmogenic death were reported. Although use of these medications resulted in QT prolongation, clinicians seldomly needed to discontinue therapy. Further study of the need for QT interval monitoring is needed before final recommendations can be made.Visual Overview:A visual overview is available for this article.

Correlation of corrected QT interval with quantitative cardiac troponin-I levels and its prognostic role in Non-ST-elevation myocardial infarction

BackgroundNon-ST-elevation Myocardial Infarction (NSTEMI) subgroup of ACS has wide variability in patient prognosis. Risk stratification in NSTE-ACS is essential for deciding about early management. Corrected QT interval estimation is one tool which has utility in bedside risk stratification. Whether it differentiates NSTEMI patients into different risk groups is the contention of this study. ObjectiveTo assess (1) correlation between maximum corrected QT interval (QTc) and cardiac Troponin I (cTnI) levels; (2) if prolonged corrected QT interval is an independent predictor of higher MACE in NSTEMI patients. MethodsWe prospectively studied 301 NSTEMI patients. cTnI level and QTc were measured at 0, 12, 24 and 48h post-admission. Patients were followed for 30days post-discharge for incidence of major adverse cardiac events (MACE) defined as composite of cardiac death, non-fatal MI and urgent revascularization. We assessed correlation between cTnI level and maximum QTc value. Regression analysis was performed to identify independent predictors of MACE. ResultsWe found a strong positive linear correlation between maximum QTc interval and cTnI level with a correlation coefficient of 0.637 (p<0.001). Cut-off value of QTc>468ms predicted poor prognosis in form of MACE with 72% sensitivity and 61% specificity. Multivariate analysis revealed that after adjusting for different prognostic variables, TIMI score>2 and QTc>468ms, were the only independent predictors of MACE. ConclusionQTc-max interval has a strong positive linear correlation with cTnI level. Prolonged QTc has utility as an independent high risk predictor in NSTEMI population.

Dispersion Durations of P-Wave and QT Interval in Children Treated With a Ketogenic Diet

BackgroundLimited data are available on the effects of a ketogenic diet on dispersion duration of P-wave and QT-interval measures in children. We searched for the changes in these measures with serial electrocardiograms in patients treated with a ketogenic diet. MethodsTwenty-five drug-resistant patients with epilepsy treated with a ketogenic diet were enrolled in this study. Electrocardiography was performed in all patients before the beginning and at the sixth month after implementation of the ketogenic diet. Heart rate, maximum and minimum P-wave duration, P-wave dispersion, and maximum and minimum corrected QT interval and QT dispersion were manually measured from the 12-lead surface electrocardiogram. ResultsMinimum and maximum corrected QT and QT dispersion measurements showed nonsignificant increase at month 6 compared with baseline values. Other previously mentioned electrocardiogram parameters also showed no significant changes. ConclusionsA ketogenic diet of 6 months' duration has no significant effect on electrocardiogram parameters in children. Further studies with larger samples and longer duration of follow-up are needed to clarify the effects of ketogenic diet on P-wave dispersion and corrected QT and QT dispersion.

Apicobasal gradient of left ventricular myocardial edema underlies transient T-wave inversion and QT interval prolongation (Wellens’ ECG pattern) in Tako-Tsubo cardiomyopathy

Tako-Tsubo cardiomyopathy (TTC) presents with chest pain, ST-segment elevation followed by T-wave inversion and QT interval prolongation (Wellens' electrocardiographic [ECG] pattern), and left ventricular dysfunction, which may mimic an acute coronary syndrome. To assess the pathophysiologic basis of the Wellens' ECG pattern in TTC by characterization of underlying myocardial changes by using cardiac magnetic resonance (CMR). The study population included 20 consecutive patients with TTC (95% women; mean age 65.3 ± 10.4 years) who underwent CMR studies both in the initial phase and after 3-month follow-up by using a protocol that included cine images, T2-weighted sequences for myocardial edema, and post-contrast sequences for late gadolinium enhancement. Quantitative ECG indices of repolarization, such as maximal amplitude of negative T waves, sum of the amplitudes of negative T waves, and maximum corrected QT interval (QTc max), were correlated to CMR findings. At the time of initial CMR study, there was a significant linear correlation between the apicobasal ratio of T2-weighted signal intensity for myocardial edema and the maximal amplitude of negative T waves (ρ = 0.498; P = .02), sum of the amplitudes of negative T waves (ρ = 0.483; P = .03), and maximum corrected QT interval (ρ = 0.520; P = .02). Repolarization indices were unrelated to either late gadolinium enhancement or quantitative cine parameters. Wellens' ECG abnormalities and myocardial edema showed a parallel time course of development and resolution on initial and follow-up CMR studies. Our study results show that the ischemic-like Wellens' ECG pattern in TTC coincides and quantitatively correlates with the apicobasal gradient of myocardial edema as evidenced by using CMR. Dynamic negative T waves and QTc prolongation are likely to reflect the edema-induced transient inhomogeneity and dispersion of repolarization between apical and basal left ventricular regions.

Prognostic Value of Corrected QT Interval and its Correlation with Cardiac Troponin T in Non

Background Presence of different risk groups in non-ST-elevation acute coronary syndrome (NSTE-ACS), indicate the need for new tools to perform early diagnosis and prognostic stratification. Thus, it has been shown that the corrected QT interval prolongation is an independent risk marker in NSTE-ACS with or without acute ischemic changes. However, there is scarce information about its relationship with other variables of known prognostic value, such as cardiac troponins. Objective The purpose of this study was to assess the correlation between the corrected QT interval prolongation and cardiac Troponin T in NSTE-ACS. Methods This prospective study included 106 patients admitted with NSTE-ACS. The corrected QT interval was measured on the admission ECG and at 6, 12, 18, 24, and 48 h. The cut-off point with best sensitivity and specificity to predict major clinical events was ³ 0.458 sec. Cardiac Troponin T ³ 0.04 ng/ml was considered positive. The composite end-point of cardiac death, non-fatal myocardial infarction and recurrent angina were the major clinical events up to 30 days after discharge. Patients were divided into two groups, according to the presence (group A) or absence (group B) of these events. Corrected QT interval on admission and maximum corrected QT interval were correlated with cardiac Troponin T in each group. Multivariate regression analysis was carried out to identify independent predictors of major clinical events. Results The correlation coefficient between cardiac Troponin T and maximum corrected QT interval was 0.38 (p <0.001) and maximum corrected QT ³ 0.458 sec was an independent predictor of major clinical events [OR=4.1 (IC 95% 1.7-11.2) p=0.002] with a negative predictive value of 80.8%. Conclusions Maximum corrected QT interval correlated with cardiac Troponin T values and was an independent predictor of risk in patients with NSTE-ACS.

Effect of ovulation induction on QT dispersion in electrocardiography

To investigate whether ovulation induction resulting in supra-physiological concentration range of ovarian hormones has an effect on interlead ventricular depolarization heterogeneity via QT dispersion measurements. Estrogens influence the duration of cardiac repolarization but there is no significant change in the QT interval duration within the range of physiological estradiol variations. Materials and methods: Included in the study were 40 subjects, in whom ovulation induction was planned, and 20 volunteers. During the study, a 12-lead electrocardiogram of each woman was carried out 3 times: for the first time on day 2-3 of the menstrual cycle (menstrual day), for the second time 36 h after hCG administration (ovulatory day), and for the third time at 6-8 days following ovulation (mid-luteal day). The RR and QT wave distances were measured. The QT interval corrected for heart rate (corrected QT) was calculated for each derivation. The difference between the longest and shortest corrected QT intervals was determined as corrected QT dispersion. Results: No difference was seen in the mean QT and corrected QT interval duration and the maximum corrected QT interval duration between menstrual phases. On the ovulatory day at peak estrogen level, the corrected QT dispersion was found to be lower than on mid-luteal and menstrual day. Conclusion: QT dispersion demonstrates the regional repolarization heterogeneity of the myocardium, which reflects the propensity of ventricular arrhythmia decreases on the ovulatory day of the ovulation induction cycle.

Serial Monitoring of the Physiological Effects of the Standard Pico-Salax® Regimen for Colon Cleansing in Healthy Volunteers

Sodium picosulfate⁄magnesium oxide⁄citric acid (Pico-Salax, Ferring Inc, Canada) is used widely in Canada and other countries for colon cleansing before colonoscopy. It is a low-volume osmotic⁄stimulant agent with the potential to deplete intravascular volume and alter electrolyte balance, yet there are little data regarding its effects on these clinically important end points. To serially measure parameters of intravascular volume and electrolyte status in healthy volunteers over a 24 h period using the standard two-sachet dosing. Twenty volunteers were given one sachet of Pico-Salax at time 0 h and another sachet 5 h later, as per usual bowel cleansing protocol. Subjects were continually monitored during the first 12 h of the study with postural vital signs, serum electrolytes and electrocardiograms obtained at intervals throughout this initial period and again at 24 h postingestion. No adverse events were reported nor were there any signs of intravascular volume depletion observed. There were decreases in potassium and calcium levels from baseline to 12 h, but these appeared minor and were corrected by 24 h. The proportions of patients with hypermagnesmia at 0 h, 5 h, 12 h and 24 h were 5%, 35%, 35% and 20%, respectively (P<0.05). However, the maximal values were only minimally elevated. Mean serum sodium, phosphate and creatinine levels remained within their respective reference ranges. There was a trend toward an increase in maximum corrected QT intervals from time 0 h (418 ms) to 5 h (430 ms) (P=0.06), but no significant change was seen subsequently at 12 h (419 ms). The subjects tolerated the medication well. The mean number of bowel movements per subject was 8.15 (range four to 15). Subjects consumed a mean (± SD) of 3.49±1.53 L of fluids during the observation period. The proportion of individuals with hypokalemia, hypocalcemia and hypermagnesemia following two sachets of Pico-Salax is significant, but the magnitude of the changes was not clinically relevant in this relatively small group, and both calcium and potassium levels normalized at 24 h. Nonetheless, this could have implications in patients with pre-existing electrolyte abnormalities and the safety of dosing with more than two sachets.

QT dispersion in patients with pulmonary embolism

Various ECG patterns have been associated with acute pulmonary embolism. However, there is no data regarding the association between QT interval measurements and pulmonary embolism. We aimed to investigate the association between QT dispersion and the severity of pulmonary embolism (PE). One hundred twenty-nine pulmonary embolism patients (mean age 58 ± 16.5 years) with ECGs obtained within the first 24 hours of hospital admission were included in the study. Patients were classified into low, intermediate and high-risk groups. We retrospectively measured ECG scores; maximum and minimum corrected QT intervals (QTc(max) and QTc(min)) and corrected QT interval dispersion (QTcd) in each risk group of patients. There was an increasing ECG score through from low to high-risk PE [3 (Interquartile Range, IQR: 2), 5 (IQR: 6) and 10 (IQR: 7) p < 0.0001]. QT interval analysis showed that QTcd was higher in high-risk group than in low and intermediate-risk groups (59.5 ± 23.4, 69.2 ± 21, 95.9 ± 33.2, p <0.001 and p = 0.01, respectively). Patients who died after diagnosis had significantly higher QTcd values at baseline compared with the QTcd values of surviving patients (89.1 ± 45.5 to 65 ± 22.9, p = 0.001). The sensitivity of QTcd > 71.5 ms for prediction of mortality was 71% with a specificity of 73% (p = 0.001). We observed a strong correlation between QTcd and ECG score values (r = 0.69, p< 0.001). There was also a correlation between QTcd values and pulmonary artery pressure (PAP) (r = 0.27, p = 0.05). QTcd is significantly increased in high-risk PE patients compared to intermediate and low-risk patients. In addition, QTcd is significantly correlated with ECG score and PAP.

QT interval dispersion in North Indian children with Kawasaki disease without overt coronary artery abnormalities

Increased QT interval dispersion has been associated with an increased risk for ventricular arrhythmias and sudden cardiac events. We examined the QT interval dispersion in 20 North Indian children with Kawasaki disease (KD) with no coronary artery abnormalities on echocardiography compared the same with matched controls. The study population consisted of 20 children in convalescent phase of KD and 20 age and sex-matched healthy controls. Intervals were measured with the use of a digital caliper with least count of 0.01mm by a single blinded observer. The QTc dispersion was calculated as the difference between the maximum and minimum corrected QT intervals in 12 and 8 leads (i.e. the 6 precordial leads, the shortest extremity lead, and the median of the 5 other extremity leads). Of the 480 leads obtained (12 per subject), 36 were excluded from analysis (15 because of poor T wave formation and 11 because of presence of U waves). Children with KD had significantly higher QTc dispersion in 12 lead (67.08±17.72 ms compared to 47.63±16.48 ms in controls P≤0.001) as well as 8 lead (60.51±18.54 ms compared to 42.92±18.03 ms in controls P≤0.001) analysis. There was no correlation between delay in IVIG therapy and QT interval dispersion. In conclusion, QT interval dispersion is significantly increased in North Indian children with KD. The dispersion is indicative of inhomogenous ventricular repolarization and may represent increased risk for developing ventricular arrhythmia in this population.

Electrocardiographic Characterization of the QTc Interval in Patients with Advanced Solid Tumors: Pharmacokinetic- Pharmacodynamic Evaluation of Sunitinib

To evaluate the effects of sunitinib, a multitargeted tyrosine kinase inhibitor, on the QT interval in patients with cancer. Patients received sunitinib loading doses (150-200 mg) on days 3 and 9 and maintenance doses (50 mg/d) on days 4 to 8. Moxifloxacin (day 1), placebo (day 2), and granisetron [with placebo (day 2) or sunitinib (days 3 and 9)] were also administered. Treatment effects were evaluated by time-matched, serial electrocardiograms, and manually overread. Twenty-four of 48 patients were QT/PK evaluable. Moxifloxacin produced a time-matched, maximum mean placebo-adjusted corrected QT interval (QT(c)F) of 5.6 ms [90% confidence interval (CI), 1.9-9.3]. Sunitinib QT(c)F changes correlated with exposure, but not T(max). Maximum mean time-matched, placebo-adjusted QT(c)F was 9.6 ms (90% CI, 4.1-15.1) at steady state/therapeutic concentrations (day 3) and 15.4 ms (90% CI, 8.4-22.4) at supratherapeutic concentrations (day 9). No patient had a QT(c)F >500 ms. Concomitant granisetron produced no significant QT(c)F prolongation. Sunitinib-related adverse events were as previously described. Sunitinib has a dose-dependent effect on QT interval. The increased risk of ventricular arrhythmias must be weighed against the therapeutic benefit sunitinib provides to patients with advanced cancer.

QT Duration and Dispersion in Patients with Anomalous Origins of Coronary Arteries

Coronary artery anomalies have been reported to show various symptoms ranging from chest pain and dyspnea to cardio-respiratory arrest and sudden death. In this study, we attempted to assess the changes in QT interval duration and dispersion in anomalous origins of coronary arteries (AOCA). Nineteen AOCA patients (mean age: 52 +/- 11 years) and 30 healthy control subjects (mean age: 50 +/- 12 years) were included in the study. Minimum and maximum corrected QT intervals, and corrected QT dispersion were calculated. The two groups were compared in terms of QT dispersion and QT duration. There was no difference between the two groups in terms of baseline demographic characteristics. Maximum corrected QT intervals (QTc max), minimum corrected QT intervals (QTc min), and corrected QT dispersion were higher in AOCA patients than controls (452 +/- 38 vs 411 +/- 25 ms [P = 0.0001], 402 +/- 31 vs 383 +/- 28 ms [P = 0.048], and 51 +/- 30 vs 28 +/- 12 ms [P = 0.001], respectively). In the patients with anomalous origins of coronary arteries, QT dispersion that is an indicator of sudden cardiac death and arrhythmias frequency increased. QTc max, QTc min, and corrected QT dispersion are higher in patients with anomalous origin of the coronary artery than in control subjects.

The Effect of Altitude on P‐Wave and QT Duration and Dispersion

Short-term and long-term exposure to high altitude has been reported to change the surface electrocardiogram. We aimed to compare P-wave and QT parameters between healthy people living at high altitude and sea level. Twelve-lead electrocardiographies of 38 healthy people living at sea level (Antalya,Turkey) and 38 healthy people living at high altitude (Van, Turkey; 1,700-1,800 m) were obtained. Minimum and maximum P-wave durations, P-wave dispersion, minimum and maximum corrected QT intervals, and corrected QT dispersion were calculated. There was no significant difference between the two groups in respect to heart rate and QT variables. Mean Pminimum values were slightly but significantly lower in the high altitude group (P = 0.029). Mean Pmaximum values tended to be lower at high altitude but did not reach statistical significance (P = 0.085). However, there was no significant difference in respect to P-wave dispersion values. In a sample of men and women living at high altitude in Turkey, significant reduction of Pminimum and borderline reduction of Pmaximum duration, but no significant change of P-wave and QT dispersion, were observed.

Human antibodies with muscarinic activity modulate ventricular repolarization: Basis for electrical disturbance

Introduction In chronic chagasic patients sudden death has been reported when QT interval dispersion is increased and antibodies with muscarinic-like activity have been demonstrated to trigger arrhythmias. The aims were to investigate, in vivo and in vitro, relation between these antibodies and heterogeneity of ventricular repolarization and to identify predictors of cardiac death in chronic chagasic patients. Methods and results Clinical, electrocardiograph and echocardiograph variables from 32 chronic chagasic patients with moderate to severe left ventricular dysfunction, followed-up for 10 years were analyzed. Sera from chronic chagasic patients with or without muscarinic activity were tested in isolated rabbit hearts to study ventricular repolarization. Stepwise multivariate logistic analysis was applied to identify independent predictors of cardiac death. QT interval dispersion of patients with muscarinic activity (75.9 ± 5.5 ms) was larger than that of patients without muscarinic activity (51.3 ± 4.0 ms, p < 0.001). Maximum uncorrected and corrected QT intervals were not significantly different between groups of patients. Sera from patients with muscarinic activity significantly and reversibly increased QT interval in isolated rabbit hearts ( p = 0.002). This effect was abolished in the presence of the muscarinic antagonist atropine. Multivariate analysis identified maximum corrected QT intervals and left ventricular end diastolic index as independent predictors of cardiac death ( p = 0.03 and p = 0.02, respectively). Conclusions Sera with muscarinic activity from chagasic patients have a strong contribution to evoke ventricular repolarization rhythm disorder. In these patients, ventricular repolarization heterogeneity is increased significantly. In vitro, muscarinic sera reversibly increased repolarization duration. Maximum corrected QT intervals and left ventricular end diastolic index are independent predictors of cardiac death.

A prognostic index to predict long-term mortality in patients with mild to moderate chronic heart failure stabilised on angiotensin converting enzyme inhibitors.

Mortality in patients with mild to moderate chronic heart failure remains high. At present there is no easy way of identifying patients within this population at increased risk of death in the medium to long term. To develop a prognostic index to identify outpatients with mild to moderate chronic heart failure at increased risk of death. Five hundred and fifty-three outpatients mean (S.D.) age 63(+/-10) years with symptoms of chronic heart failure (mean New York Heart Association functional class, 2.3(+/-0.5)), were recruited between December 1993 and April 1995. By April 2000, 201 patients had died. Using data from non-invasive measurements of cardiac size, electrical and autonomic function, renal function and plasma biochemistry we identified eight independent predictors of mortality (all P<0.01). To develop a prognostic index, predictors were dichotomised by group median and awarded 0 or 1 point accordingly. Serum sodium </=140 mmol/l (1 point), creatinine >/=111 micromol/l (1 point), cardiothoracic ratio >/=0.52 (1 point), SDNN </=112 ms (1 point), maximum corrected QT interval >/=487 ms (1 point), QRS dispersion>/=42.7 ms (1 point), the presence of non-sustained ventricular tachycardia (1 point) and voltage criteria for left ventricular hypertrophy on 12-lead ECG (1 point). We calculated risk scores for patients by adding the points of each independent risk factor. In the low-risk group (0-3 points) mortality at 5 years was 20% and in the high-risk group (4-8 points) 53%. The area under the receiver-operator characteristic curve using dichotomised variables was 0.74 and for continuous model 0.78. Our prognostic index which uses eight non-invasive measurements and a straightforward additive points system, has good discrimination and stratifies outpatients with chronic heart failure into high and low risk. This index may be useful in clinical care and risk stratification.

Effects of slow coronary artery flow on QT interval duration and dispersion.

The coronary slow-flow phenomenon is an angiographic phenomenon characterized by delayed opacification of vessels in the absence of any evidence of obstructive epicardial coronary disease. Several studies have demonstrated myocardial ischemia in patients with slow coronary artery flow. In the present study, we aimed at evaluating the effects of slow coronary artery flow on QT interval duration and QT dispersion as a possible indicator of increased risk for ventricular arrhythmias and sudden cardiac death. The study population included 49 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (group I, 33 males, 16 females, mean age = 48 +/- 9 years), and 71 patients with angiographically proven normal coronary arteries without associated slow coronary flow (group II, 47 males, 24 females, mean age = 50 +/- 8 years). Coronary flow rates of all subjects were documented by thrombolysis in myocardial infarction frame count (TIMI frame count). QT interval duration and QT dispersion of all subjects were measured on the standard 12-lead electrocardiogram. There was no statistically significant difference between the two groups in respect to age, gender, presence of hypertension, and diabetes mellitus. There was a significant difference between the two groups in respect to the presence of cigarette smoking, typical angina, and positive exercise test results. TIMI frame counts of group I patients were significantly higher than those of group II patients for all three coronary arteries (P < 0.001). Maximum corrected QT interval (QTcmax) of group I did not differ from the QTcmax of group II (P > 0.05). However, minimum corrected QT interval (QTcmin) of group I was significantly lower than that for group II (P = 0.008). Consequently, corrected QT dispersion (QTcd) in group I was found to be significantly higher than in group II (P < 0.001). QTcd, indicating increased risk for ventricular arrhythmias and cardiovascular mortality, was found to be significantly higher in patients with slow coronary artery flow. However, further long-term prospective studies should be carried out to establish the significance of QTcd as a risk factor for ventricular arrhythmias and subsequent sudden cardiac death in patients with slow coronary artery flow.

Relationship between infarction location and size to QT dispersion in patients with chronic myocardial infarction.

The relationship between the location and size of an infarction and QT dispersion was investigated in 84 Japanese patients with chronic myocardial infarction (54 with anteroseptal infarction and 30 with inferior infarction). The control group consisted of 23 subjects without ischemic heart disease (13 normal subjects and 10 hypertensive patients). Corrected QT dispersion (maximum corrected QT interval minus minimum corrected QT interval: QTc dispersion), was significantly larger in the anterior infarction group than in the control group (69.9+/-21.5 msec vs 53.0+/-17.6 msec), while the inferior infarction group showed no significant difference from control subjects. QTc dispersion was significantly greater in the patients with large anterior infarcts than in those with small anterior infarcts (80.5+/-20.5 msec vs 61.9+/-18.8 msec). In patients with chronic myocardial infarction, QT dispersion is influenced by the infarct location and size. Accordingly, interpretation of QT dispersion data should take these factors into consideration.

Effect of coronary angioplasty on precordial QT dispersion

Dispersion of the QT interval is a measure of inhomogeneity of ventricular repolarization. Because ischemia is associated with regional abnormalities of conduction and repolarization, we hypothesized that the surface electrocardiographic interval dispersion would increase in patients with symptomatic coronary artery disease in the absence of myocardial infarction and that successful revascularization would reduce QT interval dispersion. Thirty-seven consecutive patients with ischemia due to 1-vessel coronary artery disease without prior myocardial infarction who underwent percutaneous transluminal coronary angioplasty (PTCA) were evaluated. Standard 12-lead electrocardiograms were performed 24 hours before, 24 hours after, and late (>2 months) after PTCA. Precordial QT interval dispersions were determined from differences in the maximum and minimum corrected QT intervals. Mean QT interval dispersion before PTCA was 60 ± 9 ms, immediately after PTCA 23 ± 14 ms (p < 0.001), and late after PTCA 29 ± 18 ms (p < 0.001 vs before PTCA). The shortest precordial QT interval increased immediately after PTCA (367 ± 40 vs 391 ± 39 ms; p < 0.02) and then remained stable late after PTCA (376 ± 36 ms, p = NS vs immedately after PTCA). Symptomatic recurrent ischemia in 8 patients with documented restenosis increased QT interval dispersion (56 ± 15 ms [p < 0.01] vs 25 ± 14 ms immediately after PTCA), which decreased again after successful repeat PTCA (22 ± 13 ms [p < 0.01] vs before the second PTCA). QT interval dispersion decreases after successful coronary artery revascularization and increases with restenosis. Therefore, QT interval dispersion may be a marker of recurrent ischemia due to restenosis after PTCA.

966-45 QT Dispersion in Essential Hypertension

Increased QT dispersion (QTd) reflects regional variation in ventricular repolarisation, and has been shown in heart failure and hypertrophic cardiomyopathy to relate to an increased incidence of sudden death. As essential hypertensives (EH) are also at increased risk of sudden death we aimed to determine whether increased QTd is found in those EH who are known to be at the highest risk of sudden death. In 50 EH we measured QTd (maximum corrected QT interval minus minimum corrected QT interval), echocardiographic left ventricular mass index (LVMI) (n = 46 as 4 patients non-echogenic), office systolic and diastolic blood pressure (SSP, DSP), and 24 hour ambulatory systolic and diastolic blood pressure (24 SSP, 24 DSP) (n = 40). Univariate analysis demonstrated no relationship between QTd and age, sex, height, weight, 24 SSP or 24 DBP. Significant relationships existed between QTd and LVMI (R 2 = 0.25, P &lt; 0.001), SSP (R 2 = 0.16, P &lt; 0.01), DSP (R 2 = 0.08, P &lt; 0.05). Multiple linear regression analysis revealed the only relationships to QTd were LVMI (p &lt; 0.01) and SSP (p &lt; 0.05). Excluding 4 patients with electro-cardiographic left ventricular hypertrophy (ECG-LVH) from the analysis a significant relationship between QTd and LVMI (R 2 = 0.13, P &lt; 0.05) and SSP (R 2 = 0.10, P &lt; 0.05) persists. These demonstrate that increased QTd is found in EH with the highest risk of sudden death (greatest SSP and LVMI). This relationship persists in the absence of ECG-LVH. Further study of QTd, as a predictor of sudden death in EH is warranted.