Effects of antiarrhythmics and hypokalemia on the rate adaptation of cardiac repolarization

Objectives. In normal conditions, sudden heart rate acceleration provokes a rapid reduction in ventricular action potential duration (APD). The protracted APD rate adaptation favors early afterdepolarizations and precipitates arrhythmia. Nevertheless, it is uncertain as to whether the rate-dependent changes of ventricular repolarization can be adversely modified by arrhythmogenic drugs (quinidine and procainamide) and hypokalemia, in comparison to the agents with safe therapeutic profile, such as lidocaine. Design. The rate adaptation of QT interval and monophasic APD obtained from the left ventricular (LV) and the right ventricular (RV) epicardium was examined during rapid cardiac pacing applied in isolated, perfused guinea-pig heart preparations. Results. At baseline, an abrupt increase in cardiac activation rate was associated with a substantial reduction of the QT interval and ventricular APD in the first two cardiac cycles, which was followed by a gradual shortening of repolarization over subsequent pacing intervals. The time constants of the fast (τ_fast) and slow (τ_slow) components of the APD dynamics determined from a double exponential fit were longer in RV compared to LV chamber. Quinidine, procainamide, and hypokalemia prolonged ventricular repolarization and delayed the rate adaptation of the QT interval and APD in LV and RV, as evidenced by increased τ_fast and τ_slow values. In contrast, lidocaine had no effect on the dynamic changes of ventricular repolarization upon heart rate acceleration. Conclusions. The rate adaptation of ventricular repolarization is delayed by arrhythmogenic interventions, such as quinidine, procainamide, and hypokalemia, but not changed by lidocaine, a clinically safe antiarrhythmic agent.     

Reduced intrinsic heart rate is associated with reduced arrhythmic susceptibility in guinea-pig heart

Objectives. In the clinical setting, patients with slower resting heart rate are less prone to cardiovascular death compared with those with elevated heart rate. However, electrophysiological adaptations associated with reduced cardiac rhythm have not been thoroughly explored. In this study, relationships between intrinsic heart rate and arrhythmic susceptibility were examined by assessments of action potential duration (APD) rate adaptation and inducibility of repolarization alternans in sinoatrial node (SAN)-driven and atrioventricular (AV)-blocked guinea-pig hearts perfused with Langendorff apparatus. Design. Electrocardiograms, epicardial monophasic action potentials, and effective refractory periods (ERP) were assessed in normokalemic and hypokalemic conditions. Results. Slower basal heart rate in AV-blocked hearts was associated with prolonged ventricular repolarization during spontaneous beating, and with attenuated APD shortening at increased cardiac activation rates during dynamic pacing, when compared with SAN-driven hearts. During hypokalemic perfusion, the inducibility of repolarization alternans and tachyarrhythmia by rapid pacing was found to be lower in AV-blocked hearts. This difference was ascribed to prolonged ERP in the setting of reduced basal heart rate, which prevented ventricular capture at critically short pacing intervals required to induce arrhythmia. Conclusions. Reduced basal heart rate is associated with electrophysiological changes that prevent electrical instability upon an abrupt cardiac acceleration.     

Pathogenesis of Arrhythmias in a Model of CKD

Patients with CKD have an increased risk of cardiovascular mortality from arrhythmias and sudden cardiac death. We used a rat model of CKD (Cy/+) to study potential mechanisms of increased ventricular arrhythmias. Rats with CKD showed normal ejection fraction but hypertrophic myocardium. Premature ventricular complexes occurred more frequently in CKD rats than normal rats (42% versus 11%, P=0.18). By optical mapping techniques, action potential duration (APD) at 80% of repolarization was longer in CKD rats (78±4ms) than normal rats (63±3 ms, P<0.05) at a 200-ms pacing cycle length. Calcium transient (CaT) duration was comparable. Pacing cycle length thresholds to induce CaT alternans or APD alternans were longer in CKD rats than normal rats (100±7 versus 80±3 ms and 93±6 versus 76±4 ms for CaT and APD alternans, respectively, P<0.05), suggesting increased vulnerability to ventricular arrhythmia. Ventricular fibrillation was induced in 9 of 12 CKD rats and 2 of 9 normal rats (P<0.05); early afterdepolarization occurred in two CKD rats but not normal rats. The mRNA levels of TGF-β, microRNA-21, and sodium calcium-exchanger type 1 were upregulated, whereas the levels of microRNA-29, L-type calcium channel, sarco/endoplasmic reticulum calcium–ATPase type 2a, Kv1.4, and Kv4.3 were downregulated in CKD rats. Cardiac fibrosis was mild and not different between groups. We conclude that cardiac ion channel and calcium handling are abnormal in CKD rats, leading to increased vulnerability to early afterdepolarization, triggered activity, and ventricular arrhythmias.     

Increased Persistent Sodium Current Due to Decreased PI3K Signaling Contributes to QT Prolongation in the Diabetic Heart

Diabetes is an independent risk factor for sudden cardiac death and ventricular arrhythmia complications of acute coronary syndrome. Prolongation of the QT interval on the electrocardiogram is also a risk factor for arrhythmias and sudden death, and the increased prevalence of QT prolongation is an independent risk factor for cardiovascular death in diabetic patients. The pathophysiological mechanisms responsible for this lethal complication are poorly understood. Diabetes is associated with a reduction in phosphoinositide 3-kinase (PI3K) signaling, which regulates the action potential duration (APD) of individual myocytes and thus the QT interval by altering multiple ion currents, including the persistent sodium current I_NaP. Here, we report a mechanism for diabetes-induced QT prolongation that involves an increase in I_NaP caused by defective PI3K signaling. Cardiac myocytes of mice with type 1 or type 2 diabetes exhibited an increase in APD that was reversed by expression of constitutively active PI3K or intracellular infusion of phosphatidylinositol 3,4,5-trisphosphate (PIP3), the second messenger produced by PI3K. The diabetic myocytes also showed an increase in I_NaP that was reversed by activated PI3K or PIP3. The increases in APD and I_NaP in myocytes translated into QT interval prolongation for both types of diabetic mice. The long QT interval of type 1 diabetic hearts was shortened by insulin treatment ex vivo, and this effect was blocked by a PI3K inhibitor. Treatment of both types of diabetic mouse hearts with an I_NaP blocker also shortened the QT interval. These results indicate that downregulation of cardiac PI3K signaling in diabetes prolongs the QT interval at least in part by causing an increase in I_NaP. This mechanism may explain why the diabetic population has an increased risk of life-threatening arrhythmias.Patients with diabetes are at increased risk of developing life-threatening cardiac arrhythmias, independent of other risk factors such as atherosclerosis and hypertension. Diabetes is an independent risk factor for sudden cardiac death, mortality after myocardial infarction, and major complications of acute coronary syndrome such as ventricular arrhythmias (1). However, pathophysiological mechanisms responsible for the increased risk of sudden cardiac death remain poorly understood, and consequently there has been relatively little progress in the prevention and treatment of this diabetes complication. QT interval prolongation on the electrocardiogram (ECG) is a well-established risk factor for lethal ventricular arrhythmias (2), and not only do diabetic patients have a greater prevalence of QT interval prolongation than control populations (3,4), but a prolonged QT interval corrected for heart rate (QTc) is an independent risk factor for cardiovascular death in diabetic people (5–7).The signaling defect that causes QT interval prolongation in diabetes has remained elusive. An interesting lead came from our recent demonstration that decreased cardiac phosphoinositide 3-kinase (PI3K) signaling results in QT interval prolongation and is responsible for the increased risk of long QT syndrome and lethal arrhythmias caused by some anticancer drugs (8). Our results raised the possibility that suppression of this signaling pathway might also play a role in QT interval prolongation associated with diabetes, where reduced production of or sensitivity to insulin results in decreased activation of PI3K and its downstream effector, Akt.Primary prolongation of the QT interval (i.e., that which is independent of an altered QRS complex on the ECG) results from lengthening of the action potential duration (APD) in individual cardiac myocytes. The APD is regulated by inward and outward ion currents, and our previous study demonstrated that PI3K signaling regulates both types. PI3K inhibition caused reductions in the L-type calcium current (I_CaL), the delayed rectifier potassium currents I_Kr and I_Ks, and the peak sodium current (I_Na), whereas it caused an increase in the persistent (late) sodium current (I_NaP) (8). In the current study, we used mouse models to investigate a possible connection between decreased cardiac PI3K signaling and the prolonged QT interval in diabetes. Whereas I_Kr and I_Ks play little or no role in regulating the APD in adult mouse myocytes (9,10), I_NaP has a major role, such that expression of gain-of-function mutant sodium channels that increase I_NaP prolongs the murine APD and QT interval (11,12). Therefore, we used I_NaP as a marker of PI3K effects on cardiac ion channels and asked whether an increase in I_NaP contributes to QT interval prolongation in these diabetic mouse models.     

Flecainide is effective against premature supraventricular and ventricular contractions during general anesthesia

The effect of intravenously administered flecainide on premature supraventricular (PSCs) and ventricular contractions (PVCs) which developed under general anesthesia was evaluated. Flecainide was infused intravenously at a rate of 0.2 mg/kg/min until the efficacy of this drug appeared or for 10 min; thus, the maximum dose was determined to be 2 mg/kg. Flecainide was administered to 10 patients who experienced more than 5 supraventricular and/or ventricular contractions/min for a period of more than 5 min (PVCs, 4 patients; PSCs, 6 patients). PVCs in 4/4 cases and PSCs in 5/6 cases disappeared following administration of flecainide. The average dose of flecainide was 1.08±0.17 mg/kg (SE). This dose of flecainide did not affect the heart rate and QRS interval, but caused a transient decrease in systolic blood pressure from 127±6 mmHg (SE) to 114±6 mmHg, a 14% increase in the PQ interval, and a 6.3% increase in the QT interval. These results suggest that flecainide is a promising drug for the treatment of PSCs and PVCs which develop during general anesthesia. Transient hypotension and cardiac conduction disturbances immediately after injection may occur when flecainide is used intravenously.     

Acute effects of intravenous magnesium on ventricular refractoriness and monophasic action potential duration in humans.

The objective of this study was to examine the antiarrhythmic mechanisms of magnesium (Mg). The 12 patients who were selected for the study were given 12 mmol Mg sulphate followed by an infusion of 8 mmol/h. Ventricular effective refractory period (VERP). monophasic action potential duration at 50% and 90% repolarization during spontaneous rhythm (MAPD50, MAPD90) and atrial pacing at a cycle length of 600 ms (MAPD(50)600, MAPD(90)600) were measured before and after the intervention. Plasma magnesium concentration rose from 0.83 +/- 0.05 to 1.85 +/- 0.24 mmol/l (p < 0.001). Shortening of MAPD(50) (250 +/- 45 vs 240 +/- 46 ms; p < 0.05), MAPD(90) (294 +/- 42 vs 283 +/- 41 ms; p < 0.05) and shortening of sinus cycle length (SCL) (783 +/- 153 vs 742 +/- 160 ms; p < 0.01) were detected. During controlled cycle length, magnesium decreased MAPD(50)600 (230 +/- 28 vs 221 +/- 28 ms; p < 0.01), MAPD(90)600 (274 +/- 25 vs 261 +/- 29 ms; p < 0.01) and VERP (247 +/- 25 vs 241 +/- 21 ms: p < 0.05). QRS duration, QT interval and blood pressure remained unchanged. The change in SCL correlated with the change in MAPD(50) (r = 0.58; p < 0.05) and MAPD(90) (r = 0.55; p = 0.06 ) but not with MAPD(50)600, MAPD(90)600 or VERP. Magnesium acutely shortens ventricular monophasic action potential duration and refractoriness. This effect is partly mediated by mechanisms that increase heart rate. The reductions might bring salutary effects in arrhythmias evoked by prolonged repolarization.     

QT dispersion in patients with end-stage renal failure and during hemodialysis.

Interlead variability of the QT interval in surface electrocardiogram (ECG), i.e., QT dispersion, reflects regional differences in ventricular recovery time, and it has been linked to the occurrence of malignant arrhythmias in different cardiac diseases. The purpose of the study was to assess the effect of hemodialysis on QT and corrected QT (QTc) interval and dispersion in chronic hemodialyzed patients. Data of 34 nondiabetic patients (male/female = 21/13; mean age, 54 +/- 15 yr) on chronic hemodialysis were studied. Polysulfone capillaries and bicarbonate dialysate containing (in mEq/L) 135 Na+, 2.0 K+, 1.5 Ca2+, and 1.0 Mg2+ were used. Simultaneous 12-lead ECG were recorded before and after hemodialysis in a standard setting. The QT intervals for each lead were measured manually on enlarged (x3) ECG by one observer using calipers. Each QT interval was corrected for patient heart rate: QTc = QT/square root of RR (in milliseconds [ms]). The average cycle intervals were 853 +/- 152 ms predialysis and 830 +/- 173 ms postdialysis; the difference was not significant. The maximal QT interval changed significantly from 449 +/- 43 to 469 +/- 41 ms (P < 0.01). The corrected maximal QT interval increased significantly from 482 +/- 42 to 519 +/- 33 ms (P < 0.01). The QT dispersion changed from 56 +/- 15 to 85 +/- 12 ms (P < 0.001) and the corrected QT interval dispersion from 62 +/- 18 to 95 +/- 17 ms (P < 0.001). During hemodialysis, the serum potassium and phosphate levels decreased from 5.5 +/- 0.8 to 3.9 +/- 0.5 (mM) and from 2.3 +/- 0.5 to 1.6 +/- 0.4 (mM), respectively, whereas calcium increased from 2.2 +/- 0.23 to 2.5 +/- 0.22 (mM). It is concluded that hemodialysis increases the QT and QTc interval and QT and QTc dispersion in patients with end-stage renal failure. Thus, it may be stated that the nonhomogeneity of regional ventricular repolarization increases during hemodialysis. Measurement of QT and QTc dispersion is a simple bedside method that can be used for analyzing ventricular repolarization during hemodialysis.     

Heart rate and dyssynchrony in patients with cardiac resynchronization therapy: a pilot study

Objectives: The objective of this pilot study was to describe the impact of paced heart rate on left ventricular (LV) mechanical dyssynchrony in synchronous compared to dyssynchronous pacing modes in patients with heart failure.

Methods: Echocardiography was performed in 14 cardiac resynchronization therapy (CRT) patients at paced heart rates of 70 and 90 bpm in synchronous- (CRT), and dyssynchronous (atrial pacing?+?wide QRS activation) pacing modes. LV dyssynchrony was quantified using the 12-segment standard deviation model (Ts-SD) derived from Tissue Doppler Imaging. In addition, cardiac cycle intervals were assessed using cardiac state diagrams and stroke volume (SV) and filling pressure were estimated.

Results: Ts-SD decreased significantly with CRT at 90 bpm (25?±?12?ms) compared to 70 bpm (35?±?15?ms, p?=?.01), but remained unchanged with atrial pacing at different paced heart rates (p?=?.96). The paced heart rate dependent reduction in Ts-SD was consistent when Ts-SD was indexed to average Ts and systolic time interval. Cardiac state diagram derived analysis of cardiac cycle intervals demonstrated a significant reduction of the pre-ejection interval and an increase in diastole with CRT compared to atrial pacing. SV was maintained at the higher paced heart rate with CRT pacing but decreased with atrial pacing.

Discussion: Due to the small sample size in this pilot study general and firm conclusions are difficult to render. However, the data suggest that pacing at higher heart rates acutely reduces remaining LV dyssynchrony during CRT, but not during atrial pacing with dyssynchronous ventricular activation. These results need confirmation in a larger patient cohort.     

Increased prevalence of prolonged QT interval in males with primary or secondary hypogonadism: A pilot study

Symptoms and signs of male hypogonadism span all organ systems, including the cardiovascular apparatus. The electrocardiographic QT interval reflects cardiac ventricular repolarization and, if prolonged, increases the risk of malignant arrhythmias. QT interval duration is similar in boys and girls during childhood, but shortens in males after puberty and experimental studies suggest that testosterone is a major contributor to shortening of QT interval in men. The aim of the present pilot study was to assess the duration of ventricular repolarization in adult males with primary or secondary hypogonadism. Standard ECG recordings were performed in 26 men (mean age 39.2 ± 2.17 years) with pituitary or testicular hypogonadism and repeated in 15 patients during testosterone replacement. Twenty-six age-matched control men were also analysed. Measured QT intervals were corrected for heart rate according to Bazzett's formula (QTc = QT/√RR interval). The prevalence of prolonged QTc was considerably higher in hypogonadal patients (four of 26 men) than in control men (none, p  < 0.05) and in the general, healthy population (<2.5%). QTc interval normalized on hormone replacement therapy in the four patients presenting prolonged QTc in the hypogonadal state. Heart rate and left ventricular mass did not differ among the two groups and no known QT-prolonging factor was apparent in patients with abnormal QTc interval. In conclusion, a high number prolonged QT interval measurements was observed in hypogonadal men who may therefore be at increased risk for cardiac arrhythmias. This observation reveals an additional feature of male hypogonadism, which may benefit from testosterone replacement therapy.     

An altered repolarizing potassium current in rat cardiac myocytes after subtotal nephrectomy

Renal failure in humans is associated with electrocardiographic changes including altered QT interval dispersion, which suggests that cardiac myocyte repolarization is abnormal and which appears to correlate with cardiac prognosis. In this study, cardiac myocyte repolarizing currents have been studied in isolated cells from rats 8 wk after subtotal nephrectomy (SNx), using sham-operated animals as controls. In addition, monophasic cardiac action potentials were recorded from the epicardial surface of the left ventricle (LV) apex, LV base, and the right ventricle of isolated perfused hearts paced at 320/min. SNx was associated with cardiac hypertrophy and histologic evidence of myocardial fibrosis, but SNx rats were not hypertensive. Repolarizing K(+) currents were measured using whole-cell patch-clamp, and 4-aminopyridine (4-AP)-sensitive transient outward (I(to)) and 4-AP-insensitive sustained outward (I(so)) components were quantified. After SNx, I(to) was increased by two to threefold at voltages from -30 to +60 mV and showed increased heterogeneity. For example, at 0 mV voltage clamp pulse, the median I(to) was increased from 3.23 pA/pF in control myocytes (interquartile range 3.20 pA/pF, n = 24) to 5.86 pA/pF in SNx myocytes (interquartile range 7.32 pA/pF, n = 21, P: < 0.005). The kinetics of inactivation of I(to) were altered after SNx with slowing both of the onset and the recovery from inactivation. The mean time constant of inactivation at +30 mV after SNx was 14.2 +/- 1.6 ms (n = 20) compared with control values of 9.8 +/- 0.6 ms (n = 23, P: < 0.05). Neither I(so) nor inward rectifier K(+) currents were altered after SNx. The action potential duration (APD(50)) at the left ventricular base was approximately 20% shorter (P: < 0.02) in hearts from SNx rats compared with controls. 4-AP (2 mM) prolonged the APD(50) in all regions in hearts from both SNx and control rats and abolished the APD(50) shortening in SNx. These results indicate that abnormalities of the cardiac transient outward K(+) current contribute to alterations in the cardiac action potential in renal failure and warrant further investigation because they may contribute to altered repolarization and arrythmogenesis.     

Mechanisms of abnormal cardiac repolarization during insulin-induced hypoglycemia

Prolonged cardiac repolarization causes fatal cardiac arrhythmias. There is evidence that these contribute to sudden death associated with nocturnal hypoglycemia in young people with diabetes. We measured cardiac repolarization (QT interval [QTc] and QT dispersion [QTd]) during experimental hypoglycemia with and without beta-blockade and potassium infusion to establish possible mechanisms. Two groups of 10 nondiabetic men (study 1 and study 2) each underwent four hyperinsulinemic clamps: two euglycemic (5 mmol/l) and two hypoglycemic (5 mmol/l and 2.5 mmol/l for 60 min each). Study 1 was performed with and without potassium infusion to maintain normal concentrations and study 2 with and without beta-blockade (atenolol, 100 mg/day for 7 days). QTd was unchanged during euglycemia but increased during hypoglycemia (55 ms, P < 0.0001 vs. baseline), which was prevented by potassium (6 ms, P = 0.78). QTc increased significantly during hypoglycemia alone (67 ms, P < 0.0001) and during potassium replacement (46 ms, P = 0.02). In study 2, the increase in QTd during hypoglycemia (68 ms, P < 0.0001) was prevented by beta-blockade (3 ms, P = 0.88). The increase in QTc during hypoglycemia (55 ms, P < 0.0001) was prevented by beta-blockade (1 ms, P = 0.98). Our data indicate that hypoglycemia causes an acquired long QT syndrome. Sympathoadrenal stimulation is the main cause, through mechanisms that involve but are not limited to catecholamine-mediated hypokalemia. These abnormalities are prevented by selective beta-blockade.     

Torsade de pointes and long QT syndrome following major blood transfusion

We report a rare complication following transfusion of a large volume of blood in an adult patient. An electrophysiological disturbance of the cardiac cycle with prolongation of the QT interval developed, which was followed by recurrent episodes of torsade de pointes, a unique form of ventricular tachycardia. The most likely cause of this acquired long QT syndrome was hypomagnesaemia secondary to massive blood transfusion. Treatment with a magnesium infusion restored the QT interval to normal and temporary ventricular pacing prevented further ventricular arrhythmias.     

QT Interval Measurement: Evaluation of Automatic QTc Measurement and New Simple Method to Calculate and Interpret Corrected QT Interval

Background: Assessment of repolarization duration is often recommended to avoid administration of QT-prolonging drugs in patients with prolonged QTc interval, a frequent situation in the postoperative period. Bazett QT correction inappropriately increases QTc when heart rate is increased, and the use of the Fridericia formula may avoid a falsely prolonged QTc interval. The authors assessed automatic QT interval measurement to detect prolonged QTc interval (women >450 ms; men >440 ms) in the postoperative setting.

Methods: Automatic and manual electrocardiograms were performed in 108 patients after anesthesia. Automatic electrocardiographic measurement used the Bazett formula. Manual measurements were made from each electrocardiogram and used as the reference. Agreement between the two methods was analyzed. Bazett and Fridericia QT corrections were compared in this population.

Results: Agreement between automatic and manual measurements was low. The Fridericia correction, but not the Bazett correction, was independent from heart rate and allowed adequate QT correction. Sensitivity of automatic measurements to detect prolonged QTc-Bazett interval was 54%. Automatic QTc-Bazett interval less than 430 ms ruled out a manual prolonged QTc interval. When automatic QTc-Bazett was greater than 430 ms, this value was converted according to Fridericia. Automatic QTc-Fridericia greater than 430 ms identified all patients with prolonged manual QTc with a negative predictive error of 0% (95% confidence interval, 0-7%). QTc-Fridericia can be approximated by respectively adding or subtracting 5% to the uncorrected QT for each increase or decrease by 10 beats/min in heart rate from 60 beats/min.     

Relationships between Brain Natriuretic Peptide,Troponin I and QT Dispersion in Asymptomatic Dialysis Patients

Objectives. The relationships between increased wall stress, myocyte death, and ventricular repolarization instability in patients with heart failure were reported. Design and Methods. The relationships between brain natriuretic peptide (BNP), a predictor of increased wall stress of hearth; troponin I (cTnI), a predictor of myocyte death; and QT dispersion (QT_d), a reflection of ventricular repolarization instability were evaluated in age- and sex-matched asymptomatic 29 hemodialysis (HD) patients and 26 peritoneal dialysis (PD) patients, and the finding were compared. Results. Serum BNP and cTnI levels in HD patients (722.9 ± 907.9 pg/mL, 0.05 ± 0.07 μg/L, respectively), just before HD, were significantly higher than those of PD patients (255.4 ± 463.7 pg/mL, 0.02 ± 0.02 μg/L, respectively; p < 0.05). There was no significant difference between groups with regard to corrected QT_d and maximum and minimum QT intervals (p > 0.05). Serum cTnI levels were significantly and positively correlated with serum BNP levels in both dialysis groups (r = 0.447, p = 0.048). No relationship was found between plasma BNP and ECG parameters studied in both groups (p > 0.05). Conclusion. Increased serum cTnI levels were associated with elevated BNP levels in both dialysis groups. The increases in BNP and troponin I are more likely to reflect hypervolemia. Although CAPD patients were receiving dialysis daily and HD patients were more hypervolemic, CAPD patients have similar QT_dc and accordingly a similar tendency toward arrhythmias. This suggests that factors other than electromechanical interaction may be important in determining the QT interval length in patients on dialysis.     

QT and JT dispersion and cardiac performance in children with neonatal Bartter syndrome: a pilot study

Background

QT dispersion and JT dispersion are simple noninvasive arrhythmogenic markers that can be used to assess the homogeneity of cardiac repolarization. The aim of this study was to assess QT and JT dispersion and their relation with left ventricular systolic and diastolic functions in children with Bartter syndrome (BS).

Methods

Nine neonatal patients with BS (median age 9.7 years) and 20 controls (median age 8 years) were investigated at rest. Both study and control subjects underwent electrocardiography (ECG) in which the interval between two R waves and QT intervals, corrected QT, QT dispersion, corrected QT dispersion, JT, corrected JT, JT dispersion and corrected JT dispersion were measured with 12-lead ECG. Two-dimensional, Doppler echocardiographic examinations were performed.

Results

Patients and controls did not differ for gender and for serum levels of potassium, magnesium, and calcium (p?>?0.05). Both study and control subjects had normal echocardiographic examination and baseline myocardial performance indexes. The QT dispersion and JT dispersion were significantly prolonged in patients with BS compared to those of the controls {37.5 ms [interquartile range (IQR) 32.5–40] vs. 25.5 ms (IQR 20–30), respectively, p?=?0.014 and 37.5 ms (IQR 27.5–40) vs. 22.5 ms (IQR 20–30), respectively, p?=?0.003}.

Conclusions

Elevated QT and JT dispersion during asymptomatic and normokalemic periods may be risk factors for the development of cardiac complications and arrhythmias in children with BS. In these patients the need for systematic cardiac screening and management protocol is extremely important for effective prevention.     

Shortening of the QT Interval is Observed Soon after Sleeve Gastrectomy in Morbidly Obese Patients

Background

Morbidly obese patients have an increased risk of sudden cardiac death. It is well known that obesity prolongs the QT interval, which in turn may cause ventricular arrhythmia and sudden cardiac death. The objective of this study was to establish whether sleeve gastrectomy shortens the QT interval.

Methods

Twenty-eight consecutive patients underwent sleeve gastrectomy at our institution between September 2010 and March 2011 and were included in the study. The indications for bariatric surgery were in accordance with French national guidelines. For each patient, an electrocardiogram was recorded before and then 3 months after surgery. The corrected QT (QTc) was determined independently by two physicians.

Results

The mean body mass index was 45.27?±?6.09 kg/m² before surgery and 38.32?±?5.19 kg/m² 3 months after surgery. The mean weight loss over this period was 20.71?±?7.57 kg. The QTc interval was 427?±?18.6 ms (415.7?±?12.06 in men and 428.4?±?18.96 in women) prior to surgery and was significantly lower 3 months after surgery (398.6?±?15.5 ms overall, 391.3?±?7.63 in men, and 399.6?±?16.02 in women). The QTc interval decreased in all individual patients (by an average of 28.5?±?15.6 ms overall, 24.3?±?8.38 in men, and 29?±?16.23 in women). Weight loss and decreased QTc interval were not significantly correlated (p?=?0.88).

Conclusion

Sleeve gastrectomy in morbidly obese patients was associated with a significantly lower QTc interval 3 months after surgery. These findings imply that bariatric surgery might reduce the risk of sudden cardiac death in this patient population.     

Gender differences in QTc interval in young, trained individuals with lower spinal cord injury

STUDY DESIGN: Cross-sectional comparison. OBJECTIVE: To examine gender differences in rate-corrected QT interval (QTc), an index of ventricular depolarization/repolarization, in young, trained men and women with lower spinal cord injury (SCI) and able-bodied (AB) controls. SETTING: University of Illinois at Urbana-Champaign, Exercise and Cardiovascular Research Lab, USA. METHODS: Subjects consisted of 16 athletes with SCI (eight men and eight women) and 16 age-matched AB active controls (eight men and eight women). QT interval dynamics was derived from ECG recordings and rate corrected using the Bazett formula. RESULTS: Men with SCI had QTc similar to that of AB men (369.3+/-7.5 versus 357.9+/-3.0 ms, P>0.05). Women with SCI had QTc similar to that of AB women (400.0+/-4.6 versus 385.2+/-6.5 ms, P>0.05). AB women had longer QTc interval than AB men, and SCI women had longer QTc than SCI men (P<0.05). CONCLUSIONS: Gender differences in ventricular depolarization/repolarization are present in trained individuals with SCI. Thus, similar to their AB gender-matched peers, women with SCI have longer QTc intervals and may be at greater risk for the development of untoward cardiac arrhythmias than men with SCI.     

Relationship between QT interval prolongation and structural abnormalities in cirrhotic cardiomyopathy: A change in the current paradigm

It is postulated that cardiac structural abnormalities observed in cirrhotic cardiomyopathy (CCM) contribute to the electrophysiologic abnormality of QT interval (QTc) prolongation. We sought to evaluate whether QTc prolongation is associated with intrinsic abnormalities in cardiac structure and function that characterize CCM. Consecutive patients undergoing liver transplant work-up between 2010 and 2018 were included. Measures of cardiac function on stress testing including cardiac reserve and chronotropic incompetence were collected prospectively and a corrected QTc ≥ 440 ms was considered prolonged. Overall, 439 patients were included and 65.1% had a prolonged QTc. There were no differences in markers of left ventricular and atrial remodeling, or resting systolic and diastolic function across QTc groups. The proportion of patients that met the criteria for a low cardiac reserve (39.2 vs 36.6%, p = .66) or chronotropic incompetence (18.1 vs 21.3%, p = .52) was not different in those with a QTc ≥ 440 vs <440 ms. Further, there was no association between QTc prolongation and CCM by either the 2005 World College of Gastroenterology or modified 2020 Cirrhotic Cardiomyopathy Consortium criteria. QT interval prolongation was not associated with structural or functional cardiac abnormalities that characterize CCM. These findings suggest that CCM and QT interval prolongation in cirrhosis may be two separate entities with distinct pathophysiological origins.     

QT interval measurement: evaluation of automatic QTc measurement and new simple method to calculate and interpret corrected QT interval

BACKGROUND: Assessment of repolarization duration is often recommended to avoid administration of QT-prolonging drugs in patients with prolonged QTc interval, a frequent situation in the postoperative period. Bazett QT correction inappropriately increases QTc when heart rate is increased, and the use of the Fridericia formula may avoid a falsely prolonged QTc interval. The authors assessed automatic QT interval measurement to detect prolonged QTc interval (women >450 ms; men >440 ms) in the postoperative setting. METHODS: Automatic and manual electrocardiograms were performed in 108 patients after anesthesia. Automatic electrocardiographic measurement used the Bazett formula. Manual measurements were made from each electrocardiogram and used as the reference. Agreement between the two methods was analyzed. Bazett and Fridericia QT corrections were compared in this population. RESULTS: Agreement between automatic and manual measurements was low. The Fridericia correction, but not the Bazett correction, was independent from heart rate and allowed adequate QT correction. Sensitivity of automatic measurements to detect prolonged QTc-Bazett interval was 54%. Automatic QTc-Bazett interval less than 430 ms ruled out a manual prolonged QTc interval. When automatic QTc-Bazett was greater than 430 ms, this value was converted according to Fridericia. Automatic QTc-Fridericia greater than 430 ms identified all patients with prolonged manual QTc with a negative predictive error of 0% (95% confidence interval, 0-7%). QTc-Fridericia can be approximated by respectively adding or subtracting 5% to the uncorrected QT for each increase or decrease by 10 beats/min in heart rate from 60 beats/min. CONCLUSIONS: Automatic QTc-Bazett measurement, if abnormal, associated with calculation of QTc-Fridericia reliably identifies patients in whom manual QTc measurement must be performed to confirm postoperative prolonged QTc interval.     

Carbon monoxide poisoning - a cause of increased QT dispersion

BACKGROUND: Carbon monoxide (CO) poisoning is associated with direct cardiovascular toxicity. QT dispersion (QTd) of the ECG is an indirect measure of heterogeneity of ventricular repolarization, which may contribute to ventricular arrhythmias. Our aim was to study QTd in patients with acute CO poisoning. METHODS: CO intoxication was confirmed by arterial blood gas analysis. A control group consisted of age- and sex-matched individuals admitted to the hospital for unrelated clinical conditions. 12-lead ECG's were recorded on admission and repeated 1 week after discharge from the hospital. QT dispersion was defined as the difference between the greatest and the least QT intervals in any of the 12 leads. RESULTS: Seventeen intoxicated patients, aged 5-46 years, had mean carboxyhemoglobin levels of 22.5 +/- 11.1%. On admission, corrected QT intervals of the intoxicated patients were significantly increased compared to the control group (431 +/- 18 ms vs. 404 +/- 28 ms, P = 0.008), but not the QT interval (358 +/- 25 ms vs. 345 +/- 20 ms, P = 0.17). Mean QTd and cQTd values (46 +/- 15 ms and 62 +/- 13 ms) of the intoxicated patients were significantly increased compared to the control group (17 +/- 4 ms and 33 +/- 15 ms, P < 0.0001 for both). Both QTd and cQTd decreased significantly after discharge from the hospital (P = 0.0001). CONCLUSION: Although QT dispersion increased in patients with CO poisoning, none of ECG's showed ventricular arrhythmia. Increased QTd in the absence of QT interval prolongation may have a lowered arrhythmogenic potential of CO poisoning.