应用超声心动图评价高血压病患者收缩时间间期变化

目的 探讨高血压病患者左室收缩时间间期的变化及临床意义。方法 观察357例初诊高血压病患者及100例正常人左室射血分数(LVEF)、射血时间(LVET)、射血前期(PEP)，并对以上指标分别进行t检验。同时观察高血压病患者24小时平均动脉压(MABP)与左室收缩时间间期的相关性。结果 高血压病患者射血时间(LVET)、射血前期(PEP)、PEP／LVET与正常组有统计学差异。左室射血分数(LVEF)与正常组间无统计学差异。LVET与MABP呈负相关，PEP／LVET与MABP呈正相关。结论 本研究显示收缩时间间期可敏感的反映左室后负荷的升高。     

Effect of nebivolol on QT dispersion in hypertensive patients with left ventricular hypertrophy.

Hypertensive patients with left ventricular hypertrophy (LVH) have increased QT dispersion, which is considered an early indicator of end-organ damage and a non-invasive marker of risk for clinically important ventricular arrhythmias and cardiac mortality. The purpose of this study was to examine the effect of nebivolol antihypertensive therapy on QT dispersion in hypertensive subjects. Twenty-five subjects (15 men and 10 women, mean age 53.6 +/- 4.5 years) with essential arterial hypertension and mild-to-moderate LVH (blood pressure: 147.2 +/- 6.2/90.6 +/- 3.8 mmHg; left ventricular mass indexed: 149.1 +/- 10.7 g/m(2)) were compared with 25 age-matched healthy control subjects. All the participants underwent a complete clinical examination, including electrocardiogram for QT interval measurements. The QT dispersion was defined as the difference between the longest and the shortest QT interval occurring in the 12-lead electrocardiogram. The QT dispersion was corrected (QTc) with Bazett's formula. Hypertensive subjects were treated with 5 mg daily of nebivolol. The ECG and echocardiogram were repeated after four weeks of treatment. At baseline, hypertensive patients showed QT dispersion (56.9 +/- 6.4 vs. 31.7 +/- 8.4 ms, P < 0.001) and QTc dispersion (58.3 +/- 6.2 vs. 33.2 +/- 7.8 ms, P < 0.001) significantly higher than control subjects. Four-week nebivolol treatment reduced blood pressure from 147.2 +/- 6.2/90.6 +/- 3.6 mmHg to 136.3 +/- 3.1/83.3 +/- 2.5 mmHg (P < 0.0001), and resting heart rate from 75.3 +/- 4.7 to 64.2 +/- 3.0 bpm (P < 0.001), without significant change in left ventricular mass (LVMi: 149.1 +/- 10.7 vs. 151.4 +/- 9.8 g/m(2), ns). Nebivolol-based treatment improved QT dispersion (56.9 +/- 6.4 vs. 40.5 +/- 5.8 ms, P < 0.001) and QTc dispersion (58.3 +/- 6.2 vs. 42.2 +/- 5.6 ms, P < 0.001), which remained higher than in control subjects (P < 0.001 in both cases). The reduction of QT dispersion did not correlate with arterial BP reduction. In conclusion, nebivolol reduced increased QT dispersion in hypertensive subjects after four weeks. This effect, occurred without any change in LVM, did not seem to be related to the blood pressure lowering and could contribute to reduce arrhythmias as well as sudden cardiac death in at-risk hypertensive patients.     

Prolongation of the QT interval in heart failure occurs at low but not at high heart rates

Abnormal left ventricular structure and function as in, for example, left ventricular hypertrophy or chronic heart failure, is associated with sudden cardiac death and, when the ejection fraction is depressed, with prolongation of the QT interval. The dependence on heart rate of QT interval prolongation in these conditions, and the relationship of any abnormalities either to deranged autonomic nervous system function or to an adverse prognosis, has not been well studied. We therefore investigated (1) the dependence on heart rate of the QT interval, and (2) the relationship between both QT interval and the QT/heart rate slope and markers of adverse prognosis in these two conditions. The QT interval was measured at rest and during exercise in 34 subjects with heart failure, 16 subjects with left ventricular hypertrophy and 16 age-matched controls with normal left ventricular structure and function. QTc (corrected QT) intervals at rest were significantly longer in heart failure patients (471+/-10 ms) than in controls (421+/-6 ms) or in subjects with hypertrophy (420+/-6 ms) (P<0.05). At peak exercise, despite the attainment of similar heart rates, the QT intervals no longer differed from each other, being 281+/-7 ms for controls, 296+/-11 ms in hypertrophy and 303+/-10 ms in heart failure (no significant difference). The QT/heart rate slope was significantly increased in heart failure [2.3+/-0.1 ms.(beats/min)(-1)] compared with controls [1.55+/-0.06 ms.(beats/min)(-1)] and hypertrophy [1. 66+/-0.1 ms.(beats/min)(-1)] (P<0.001). In left ventricular hypertrophy, despite animal data suggesting that QT interval prolongation should occur, no abnormalities were found in QT intervals at rest or during exercise. The QT/heart rate slope did not relate to any markers for an adverse prognosis, except that of prolongation of QT interval. Long QT intervals were associated principally with impairment of left ventricular systolic function. Our data emphasize the dynamic nature of the QT interval abnormalities found in heart failure.     

Left ventricular function during sepsis

The prevalence and prognostic significance of left ventricular involvement in septic patients without shock was investigated. Systolic time intervals (STI) and preejection period/left ventricular ejection time ratio (PEP/LVET) were used to assess left ventricular function. Forty-nine patients, 22 of whom ultimately died, were studied. The group as a whole showed abnormal PEP/LVET ratio (0.40 +/- 0.02) that differed significantly (p less than .01) from reported normal values (0.345 +/- 0.002), demonstrating widespread left ventricular dysfunction in this population. In order to establish the prognostic significance of left ventricular impairment, the population was divided into two groups according to the PEP/LVET ratio. Group 1 (PEP/LVET less than or equal to 0.42) showed a mortality rate of 10/33 (30%), while group 2 (PEP/LVET greater than 0.42) had a significantly greater mortality (12/16 [75%], p less than .001). The test that has a sensitivity of 55%, a specificity of 85%, and a positive predictive value of 75% identifies a subset of septic patients with severe impairment of left ventricular function and high risk of dying.     

QT interval dispersion and autonomic modulation in subjects with anxiety

This study was designed to assess Q-T interval dispersion as a marker of electrical instability in subjects with anxiety. Recent observations have shown that the presence of anxiety symptoms increases the risk of sudden death. The Kawachi anxiety questionnaire identified 29 subjects (male/female ratio 13:16) who scored 0, 22 subjects (male/female ratio 14:8) who scored 1, and 37 subjects (male/female ratio 13:24) who scored 2 or more. In all subjects we measured electrocardiographic interlead QT dispersion and autonomic function through spectral analysis of R-R interval and blood pressure variabilities and left ventricular mass. Compared with subjects who scored 0, those reporting 2 or more symptoms showed increased heart rate-corrected QT dispersion (54.9+/-1.7 ms vs. 34.9+/-3.2 ms, P<.001), sympathetic modulation (normal logarithm low-frequency power/high-frequency power 0.59+/-0.1 vs. 0.12+/-0.04, P<.05), and left ventricular mass (120.7+/-3.5 g/m2 vs. 97.9+/-2.8 g/m2, P<.001). Probably because it augments sympathetic activity, anxiety causes left ventricular mass to increase and, like hypertension, increases heart rate-corrected Q-T interval dispersion. The consequent electrical instability could be the substrate responsible for inducing fatal ventricular arrhythmias.     

Temporary disturbances of the QT interval precede the onset of ventricular tachyarrhythmias in patients with structural heart diseases

An increase in sinus rate prior to ventricular tachyarrhythmias has been demonstrated in previous studies. There is no clear data available concerning changes in ventricular de- and repolarization prior to ventricular tachyarrhythmias, especially in patients with structural heart disease. Therefore, the aim of this study was to analyze the QT and QTc interval (Bazett's formula immediately before the onset of ventricular tachyarrhythmias in stored electrograms of patients with ICDs. The study analyzed 228 spontaneous ventricular tachyarrhythmia episodes in 52 patients (mean age 64 +/- 10 years, 49 men, 3 women) and compared them with 146 electrograms of baseline rhythm recorded during regular ICD follow-up. Mean ventricular cycle length (CL), QT interval, and QTc were measured before the onset of ventricular tachyarrhythmia and during baseline rhythm. Prior to ventricular tachyarrhythmias onset, CL was significantly shorter than during baseline rhythm (714 +/- 139 vs 828 +/- 149 ms, P < 0.0001). By contrast, the QT interval (430 +/- 67 ms) and QTc interval (518 +/- 67 ms) were significantly prolonged before the onset of ventricular tachyarrhythmias as compared to baseline rhythm (QT 406 +/- 67 ms, QTc 450 +/- 61 ms; P < 0.0001). CL, QT, and QTc changes were independent of concomitant treatment with antiarrhythmic drugs. Ventricular tachyarrhythmias are preceded by a significant prolongation of the QT and QTc intervals. This phenomenon may represent a greater than normal disparity of repolarization recovery times possibly facilitating the development of ventricular tachyarrhythmias.     

Cardiovascular responses to dobutamine determined by systolic time intervals in preterm infants

We investigated the effects of dobutamine therapy on myocardial function in premature infants. Left ventricular performance was assessed by measuring left ventricular systolic time intervals: rate-corrected pre-ejection period (PEPI), rate-corrected left ventricular ejection time (LVETI), and pre-ejection period to left ventricular ejection time ratio (PEP/LVET) which was obtained by echocardiography. Measurements were performed in 17 hemodynamically unstable premature infants who had an elevated PEP/LVET ratio before and 30 min after starting dobutamine infusion (10 micrograms/kg.min). Dobutamine infusion resulted in a significant decrease in PEPI (from 108 +/- 16 [SEM] to 95 +/- 17 msec; p less than .01) and in PEP/LVET ratio (from 0.55 +/- 0.16 [SEM] to 0.45 +/- 0.17; p less than .01), and in a significant increase in LVETI (from 255 +/- 15.7 [SEM] to 264 +/- 16.2 msec; p less than .01). Heart rate increased significantly from 146 +/- 17 (SEM) to 163 +/- 16 beat/min; p less than .01. Mean arterial pressure increased in 12 of 14 infants. These results show that dobutamine enhances left ventricular performance in premature infants who have depressed left ventricular function.     

小儿急性心肌炎左室功能系统观察

我们对16例轻型心肌炎患儿用心机械图系统观察了发病6～12个月内的左室功能。结果发现发病第一个月PEP、ICT延长,LVET缩短,PEP/LVET、ICT/LVET升高,与对照组差异显著或非常显著,其中以PEP、PEP/LVET改变最明显。经正规治疗,以上指标多于3～4个月内逐渐恢复,PEP由79±6ms缩至69±9ms,PEP/LVET由0.265±0.02降为0.188±0.02。DTI无显著改变。说明轻型心肌炎发病一个月内左室收缩功能有所下降,至病程第三、四个月逐渐恢复正常。     

Influence of posture and handgrip on the QT interval in left ventricular hypertrophy and in chronic heart failure

In certain disease states prolongation of the QT interval has been shown to be arrhythmogenic. Whether QTc interval changes with position and thus whether certain positions are more arrhythmogenic than others is not known for different diseases that predispose to arrhythmias, and was therefore studied. Patients with left ventricular hypertrophy and heart failure, and the appropriate matched controls, were recruited. Subjects were studied in the lying, sitting, standing and squatting positions and had QT intervals determined by computer algorithm 2 min after each position change. After resting, QT interval was determined while the subjects performed maximum handgrip exercise with their dominant hand. QT intervals were rate-corrected using Bazett's method. QTc interval is prolonged in heart failure patients compared with either left ventricular hypertrophy or control subjects in the lying and sitting position, but not in the standing or squatting position. The QTc intervals for heart failure and control subjects were, respectively, 443+/-7 ms versus 421+/-6 ms when lying (P<0.05), 451+/-10 ms versus 419+/-6 ms when sitting (P<0.05), 429+/-10 versus 414+/-7 ms when standing (P not significant) and 437+/-10 versus 419+/-8 ms when squatting (P not significant). The values for patients with hypertrophy did not differ from control values. Maximum handgrip does not affect the QTc interval in heart failure, but prolongs it in both the hypertrophy and control groups. Position and static exercise are important modifiers of QTc interval and their effect depends on the condition of the left ventricle.     

Beat-to-beat systolic time-interval measurement from heart sounds and ECG

Systolic time intervals are highly correlated to fundamental cardiac functions. Several studies have shown that these measurements have significant diagnostic and prognostic value in heart failure condition and are adequate for long-term patient follow-up and disease management. In this paper, we investigate the feasibility of using heart sound (HS) to accurately measure the opening and closing moments of the aortic heart valve. These moments are crucial to define the main systolic timings of the heart cycle, i.e. pre-ejection period (PEP) and left ventricular ejection time (LVET). We introduce an algorithm for automatic extraction of PEP and LVET using HS and electrocardiogram. PEP is estimated with a Bayesian approach using the signal's instantaneous amplitude and patient-specific time intervals between atrio-ventricular valve closure and aortic valve opening. As for LVET, since the aortic valve closure corresponds to the start of the S2 HS component, we base LVET estimation on the detection of the S2 onset. A comparative assessment of the main systolic time intervals is performed using synchronous signal acquisitions of the current gold standard in cardiac time-interval measurement, i.e. echocardiography, and HS. The algorithms were evaluated on a healthy population, as well as on a group of subjects with different cardiovascular diseases (CVD). In the healthy group, from a set of 942 heartbeats, the proposed algorithm achieved 7.66 ± 5.92 ms absolute PEP estimation error. For LVET, the absolute estimation error was 11.39 ± 8.98 ms. For the CVD population, 404 beats were used, leading to 11.86 ± 8.30 and 17.51 ± 17.21 ms absolute PEP and LVET errors, respectively. The results achieved in this study suggest that HS can be used to accurately estimate LVET and PEP.     

Intravenous digoxin blunts the rise of inotropy induced by isometric exercise: a noninvasive study in healthy volunteers

Nine healthy volunteers were studied with echocardiography and systolic time intervals at rest and after 3 minutes' isometric exercise by hand grip. The recordings were repeated after intravenous administration of 1 mg digoxin before and after autonomic blockade induced with atropine and propranolol. During hand grip the heart rate rose from 61 +/- 3 (mean +/- SEM) to 73 +/- 5 bpm (p less than 0.05). Afterload, i.e. left ventricular systolic wall stress, increased by 21% from 260 +/- 19 x 10(3) dyn/cm2 (p less than 0.05). Preload, i.e. left ventricular end-diastolic diameter (LVEDD), fractional shortening and the ratio of the pre-ejection period to the left ventricular ejection time (PEP/LVET) did not change, indicating increased contractility. After digoxin heart rate rose during handgrip from 50 +/- 2 to 65 +/- 5 bpm, and wall stress increased by 19% from 274 +/- 21 x 10(3) dyn/cm2 (p less than 0.01 for both). Even though LVEDD rose from 44.8 +/- 1.4 to 46.6 +/- 1.3 mm (p less than 0.05), fractional shortening decreased from 33 +/- 2 to 30 +/- 2% (p less than 0.05) and PEP/LVET increased from 0.292 +/- 0.014 to 0.327 +/- 0.014 (p less than 0.01). This suggests that autonomic reflexes due to digoxin obscured the increase in inotropy during static exercise. Autonomic blockade raised heart rate under digoxin from 50 +/- 2 to 90 +/- 4 bpm and mean blood pressure from 87 +/- 2 to 99 +/- 3 mmHg (p less than 0.001 for both) without changes in loading conditions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Atrioventricular Sequential Pacing: Comparison with Ventricular Pacing Using Systolic Time Intervals

Nine patients with programmable atrioventricular sequential pacers were studied using systolic time intervals (QS2—the total electrical and mechanical systole, left ventricular ejection time, and pre-ejeclion period). These measurements were obtained by simultaneous recording of the electrocardiogram, phonocardiogram. and carotid pulse tracing. There was a dramatic fall of left ventricular ejection time (LVET) and an increase of the pre-ejection time (PEP) in all patients when the pacers were programmed from the atrioventricular to the ventricular mode at constant heart rate. This resulted in an increase of the ratio PEP/LVET from 428 to 574 suggesting loss of ventricular function. These measurements all reversed to baseline values when the pacers were reprogrammed back to the atrioventricular mode. This study suggests systolic time intervals might be useful to select non-invasively pacer parameters such as mode, rate, and effective PR interval in order to provide the best hemodynamics in a given patient.     

Effect of a single oral dose of moxifloxacin (400 mg and 800 mg) on ventricular repolarization in healthy subjects

BACKGROUND: Moxifloxacin is a new fluoroquinolone. In vitro studies have suggested that it could prolong ventricular repolarization. The main objective of this study was to measure the actual effect of single oral doses of moxifloxacin on QT interval duration in healthy volunteers. METHODS: Nine men and 9 women participated in a double-blind, randomized, placebo-controlled, crossover study. Each participant received single oral doses (400 mg and 800 mg) of moxifloxacin or placebo. At the time of expected moxifloxacin maximum concentration, several electrocardiographic recordings were obtained at rest and during the course of a submaximal exercise test. QT interval and the corresponding RR interval value were measured within a wide range of RR intervals in each subject. RESULTS: ANOVA showed that both moxifloxacin doses increased mean QT intervals compared with placebo. The mean QT interval duration at RR = 1000 ms was 379 +/- 24 ms during placebo, 394 +/- 33 ms during moxifloxacin 400 mg (P < .05), and 396 +/- 28 ms during moxifloxacin 800 mg (P < .05). Moxifloxacin-induced QT interval prolongation remained significant at all tested heart rates. The increase in QT interval duration relative to placebo remained between 2.3% +/- 2.8% and 4.5% + 3.8% across the range of RR intervals tested. CONCLUSION: Moxifloxacin prolongs QT interval duration. The amplitude of this effect is small, and the risk of moxifloxacin-induced torsades de pointes is expected to be minimal when the drug is administered at the recommended dose of 400 mg/d. However, moxifloxacin should not be used in patients with predisposing factors of torsades de pointes such as electrolyte disturbances and bradycardia or during coadministration of proarrhythmic drugs.     

Epinephrine-induced QT interval prolongation: a gene-specific paradoxical response in congenital long QT syndrome

OBJECTIVE: To determine the effect of epinephrine on the QT interval in patients with genotyped long QT syndrome (LQTS). PATIENTS AND METHODS: Between May 1999 and April 2001, 37 patients (24 females) with genotyped LQTS (19 LQT1, 15 LQT2, 3 LQT3, mean age, 27 years; range, 10-53 years) from 21 different kindreds and 27 (16 females) controls (mean age, 31 years; range, 13-45 years) were studied at baseline and during gradually increasing doses of intravenous epinephrine infusion (0.05, 0.1, 0.2, and 0.3 microg x k(-1) x min(-1)). The 12-lead electrocardiogram was monitored continuously, and heart rate, QT, and corrected QT interval (QTc) were measured during each study stage. RESULTS: There was no significant difference in resting heart rate or chronotropic response to epinephrine between LQTS patients and controls. The mean +/- SD baseline QTc was greater in LQTS patients (500+/-68 ms) than in controls (436+/-19 ms, P<.001). However, 9 (47%) of 19 KVLQT1-genotyped LQT1 patients had a nondiagnostic resting QTc (<460 milliseconds), whereas 11 (41%) of 27 controls had a resting QTc higher than 440 milliseconds. During epinephrine infusion, every LQT1 patient manifested prolongation of the QT interval (paradoxical response), whereas healthy controls and patients with either LQT2 or LQT3 tended to have shortened QT intervals (P<.001). The maximum mean +/- SD change in QT (AQT [epinephrine QT minus baseline QT]) was -5+/-47 ms (controls), +94+/-31 ms (LQT1), and -87+/-67 ms (LQT2 and LQT3 patients). Of 27 controls, 6 had lengthening of their QT intervals (AQT >30 milliseconds) during high-dose epinephrine. Low-dose epinephrine (0.05 microg x kg(-1) x min(-1)) completely discriminated LQT1 patients (AQT, +82+/-34 ms) from controls (AQT, -7+/-13 ms; P<.001). Epinephrine-triggered nonsustained ventricular tachycardia occurred in 2 patients with LQTS and in 1 control. CONCLUSIONS: Epinephrine-induced prolongation of the QT interval appears pathognomonic for LQT1. Low-dose epinephrine infusion distinguishes controls from patients with concealed LQT1 manifesting an equivocal QTc at rest. Thus, epinephrine provocation may help unmask some patients with concealed LQTS and strategically direct molecular genetic testing.     

2型糖尿病患者心电图QT间期的变化及卡托普利对其影响

目的　探讨 2型糖尿病患者心电图QT间期的变化及卡托普利对其影响。方法　对 189例糖尿病患者心电图QT间期进行测量 ,并按Bazett公式进行校正 ,取其校正的QT间期QTc与 12 0例正常人进行对照。给糖尿病患者卡托普利治疗 ,观察治疗 1、2、3、6个月后QTc间期的变化。结果　正常人QTc间期 ,男性 396± 1.7ms ,女性 418± 2 .3ms。糖尿病患者QTc ,男性 40 7± 1.9ms、女性 42 7± 2 .2ms。糖尿病患者卡托普利治疗 3、6个月后QTc间期缩短 ,分别为 :男性40 3± 2 .1ms、40 2± 1.6ms ,女性 413± 2 .3ms、412± 1.9ms。与治疗前相比具有显著性差异。结论　 2型糖尿病患者QTc间期延长 ,卡托普利可使延长的QTc间期缩短。提示卡托普利有助于防治糖尿病心血管并发症     

Dispersion in ventricular repolarization in patients with severe intraventricular conduction disturbances

Increased dispersion of repolarization, measured invasively or by QT interval measurements, is associated with an increased risk for ventricular arrhythmias and sudden death. Most studies on this issue have included patients with normal intraventricular conduction, and it is not known if this finding has a predictive value also in patients with intraventricular conduction disorders. An invasive electrophysiological study, including programmed ventricular stimulation and assessment of effective refractory periods at two RV sites, was performed in 103 patients with bifascicular block (mean age 67 +/- 12 years). QT dispersion was measured from standard 12-lead ECGs. In patients with inducible sustained polymorphic VT or VF the dispersion in refractoriness between the two RV sites was significantly greater (46 +/- 11 ms, n = 13) than in noninducible patients (14 +/- 14 ms, n = 84) and in patients with inducible sustained monomorphic VT (16 +/- 5 ms, n = 6) (P < 0.01). Similarly, QT dispersion was 104 +/- 46 ms, 66 +/- 31 ms, and 77 +/- 33 ms, respectively, in the three groups (P < 0.05). Dispersion in repolarization, neither measured invasively nor by QT interval measurements, predicted sudden death, all cause mortality, or ventricular arrhythmia during a mean follow-up period of 3 years. In patients with bifascicular block, there is a relation between the degree of dispersion of ventricular repolarization and the inducibility of polymorphic ventricular arrhythmia, but this outcome did not occur during follow-up.     

Polymorphous Ventricular Tachycardia and Atrioventricular Block

Nine patients are presented who had polymorphous ventricular tachycardia (PMVT) occurring during atrioventricular (AV) block. There were five men and four women with a mean age of 80 +/- 9 years. Five patients had organic heart disease and the remaining four had primary conduction disease (bundle branch block). AV block was complete in four patients (2:1 in three, and paroxysmal in two). The mean ventricular cycle length (of the AV block rhythm) was 1567 +/- 203 ms. The mean QT interval was 0.64 +/- 0.09 s and the mean QTc was 0.51 +/- 0.06 s. When compared to a similar control group with AV block but without PMVT, the ventricular cycle length was similar but the QT and QTc were significantly longer. PMVT was usually of short duration (eight beats to 12 s) and in seven of these nine patients, frequent premature ventricular beats (PVBs) were recorded at various times from the occurrence of PMVT. This is in contrast to the control patients in whom PVBs were detected in one patient only. In conclusion, patients with AV block who develop PMVT usually have longer QT intervals and have detectable PVBs on routine ECGs, unlike similar patients with AV block but without PMVT. In a patient with AV block, a QT interval above 0.60 s and PVBs on the ECG seem to indicate an increased risk for the development of PMVT.     

Greater quinidine-induced QTc interval prolongation in women

BACKGROUND: Prolongation of the electrocardiographic QT interval by drugs is associated with the occurrence of a potentially lethal form of polymorphic ventricular tachycardia termed torsades de pointes. Women are at greater risk than men for development of this adverse event when taking drugs that prolong the QT interval. To determine whether this may be the result of gender-specific differences in the effect of quinidine on cardiac repolarization, we compared the degree of quinidine-induced QT interval lengthening in healthy young men and women. METHODS: Twelve women and 12 men received a single intravenous dose of quinidine (4 mg/kg) or placebo in a single-blind, randomized crossover trial. Total plasma and protein-free concentrations of quinidine and 3-hydroxyquinidine were measured in serum. QT intervals were determined and corrected for differences in heart rate with use of the method of Bazett (QTc = QT/RR1/2). RESULTS: As expected, the mean QTc interval at baseline was longer for women than for men (mean +/- SD; 407 +/- 7 versus 395 +/- 9 ms, P < .05). The slope of the relationship between change in the QTc interval (delta QTc) from baseline to the serum concentration of quinidine was 44% greater for women than for men (mean +/- SE; 42.2 +/- 3.4 versus 29.3 +/- 2.6 ms/microg per mL, P < .001). These results were not influenced by analysis of 3-hydroxyquinidine, free concentrations of quinidine and 3-hydroxyquinidine, or the JT interval. CONCLUSIONS: Quinidine causes greater QT prolongation in women than in men at equivalent serum concentrations. This difference may contribute to the greater incidence of drug-induced torsades de pointes observed in women taking quinidine and has implications for other cardiac and noncardiac drugs that prolong the QTc interval. Adjustment of dosages based on body size alone are unlikely to substantially reduce the increased risk of torsades de pointes in women.     

Hyperbaric oxygen therapy decreases QT dispersion in diabetic patients

Diabetes mellitus is frequently associated with the malignant ventricular arrhythmias and sudden death. The QT dispersion is the difference between the longest and shortest QT interval calculated from the standard 12-lead electrocardiogram. The QT dispersion is suggested as an index of myocardial electrical activity. An increase in QT dispersion is associated with the malignant ventricular arrhythmias and sudden cardiac death. Diabetic patients receive hyperbaric oxygen (HBO) therapy for non-healing lower extremity ulcers. The aim of this study was to determine the effect of HBO therapy on QT dispersion in diabetic patients. Thirty diabetic patients (18 male and 12 female, 59.9 +/- 10 years), who were planning to undergo ten sessions of HBO therapy in two weeks for non-healing lower extremity ulcers, were consecutively enrolled into the study. The 12-lead resting electrocardiography recordings were taken before the first HBO therapy and after the 10th HBO-therapy session. QT intervals were measured on electrocardiogram. QT intervals were corrected for heart rate by using Bazett's formula (corrected QT [QTc] = QT/ radical R - R [seconds]). QTc dispersion was significantly decreased from 59.8 +/- 17.4 msec to 52.2 +/- 15.5 msec after ten sessions of HBO therapy (p < 0.05). However, maximum QTc, minimum QTc and mean QTc did not change significantly after HBO therapy. We have concluded that HBO therapy may reduce the risk of malignant ventricular arrhythmia and sudden cardiac death in diabetic patients when applied repetitively.     

Automatic detection of left ventricular ejection time from a finger photoplethysmographic pulse oximetry waveform: comparison with Doppler aortic measurement

Left ventricular ejection time (LVET) is a useful measure of ventricular performance and preload. The present study explores a novel method of continuous LVET monitoring using a noninvasive finger photoplethysmographic pulse oximetry waveform (PPG-POW). A method for the automatic beat-to-beat detection of LVET from the finger PPG-POW is presented based on a combination of derivative analysis, waveform averaging and rule-based logic. The performance of the detection method was evaluated on 13 healthy subjects during graded head-up tilt. Overall, the correlation between the PPG-POW derived LVET and the aortic flow derived LVET was high and significant (r = 0.897, p < 0.05). The bias was -14 +/- 14 ms (mean +/- SD), and the percentage error was 9.7%. Although these results would not be sufficient to satisfy the requirement for clinical evaluation of LVET when absolute accuracy was demanded, the strong correlation between the PPG-POW LVET and the aortic LVET on an intra-subject basis (r = 0.945 +/- 0.043, mean +/- SD) would support the application of PPG-POW to detect the directional change in LVET of an individual. This could be very useful for the early identification of progressive hypovolaemia or blood loss. The present study has demonstrated a promising approach to extract potentially useful information from a noninvasive, easy-to-obtain signal that could be readily acquired either from existing patient monitoring equipment or from inexpensive instrumentation. More extensive investigation is necessary to evaluate the applicability of the present approach in clinical care monitoring.