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Biomedical subjects

M Malik

Publications and source records attributed to M Malik.

At least 37 records · Page 2Linked to original sources
PubMed2001

Increased QT dispersion in patients with Prinzmetal's variant angina and cardiac arrest.

OBJECTIVES: We sought to compare QT dispersion in patients presenting with Prinzmetal's variant angina complicated by cardiac arrest or syncope and patients with uncomplicated variant angina. BACKGROUND: Despite the usually benign course of treated Prinzmetal's variant angina, a proportion of vasospastic angina patients develop ventricular arrhythmias and sudden death in association with coronary spasm. Increased QT dispersion has been suggested to increase susceptibility to ventricular arrhythmias in patients with coronary artery spasm. METHODS: We studied 25 consecutive patients (mean age 58 years; 14 men) with classical Prinzmetal's variant angina and documented coronary artery spasm. None of the patients had coronary artery stenoses < or =40%. Five patients had suffered a documented cardiac arrest, two had recurrent syncope and 18 had no arrhythmic events or syncopal episodes. In all patients QT dispersion (QT maximum-QT minimum in every ECG lead) was measured on the baseline 12-lead electrocardiogram at study entry using a digitising board. RESULTS: Mean (+/-S.D.) QT dispersion of study patients was 62.3+/-19.5 ms. QT dispersion in patients with cardiac arrest and syncope (79.4+/-17.3 ms) was significantly higher compared to patients with no such events (56.3+/-16.9 ms), (95% CI 7.5-38.8, P=0.005). No significant clinical, biochemical or angiographic differences were found between patients with and those without cardiac arrest or syncope. CONCLUSION: QT dispersion is increased in patients with Prinzmetal's variant angina complicated by cardiac arrest and syncope compared to patients without such events. Increased QT dispersion may be both a substrate for sudden cardiac death and a marker of risk in patients with Prinzmetal's variant angina.

Adult↗
PubMed2001

Morphological algebraic models of the TU-wave patterns/in idiopathic long QT syndrome.

A computer-assisted analysis of the TU-complex morphology was employed to characterize repolarization abnormalities in LQTS and to assess arrhythmic risk. Electrocardiograms (ECGs) were collected from 14 idiopathic LQTS patients (seven without symptoms and seven with a history of syncope or cardiac arrest) and from 14 sex- and age-matched normal subjects. Digitized TU-wave patterns from V2-V6 precordial leads were analyzed. The morphologies of the T and U waves were modeled by an algebraic sum of differences between two pairs of action potential-like curves of different shape and duration so that the whole TU complex was approximated by (S1-S2)+(L1-L2). By finding the best fit model of the digitized TU-wave signal, the amplitude and duration of each decomposition curve were determined for each lead. The following 'secondary' parameters were then derived: (a) the ratio between the sum of the amplitudes of the two long (L1 and L2) and the two short (S1 and S2) decomposition curves (A-ratio), (b) the highest A-ratio found in V2 to V6 (A-ratio(max)), and (c) the model-derived durations of the T-wave, U-wave and TU-complex. Conventional measures of RR and QTc intervals and of QT dispersion did not differ between symptomatic and asymptomatic LQTS patients. Modeled QT interval was significantly longer in the symptomatic than in the asymptomatic LQTS patients and in asymptomatic LQTS patients than in the controls. In addition, symptomatic LQTS patients had a longer S2 and T-wave duration in most leads than normal subjects. Conversely, modeled QU interval and U-wave duration did not significantly differ between the three groups. Compared to normal subjects, the amplitudes of S1, S2, L1 and L2 in the LQTS patients were not significantly different in most leads. A-ratio and A-ratio(max) were greater in symptomatic than asymptomatic LQTS patients and in the latter than in controls. A cut-off value of 0.90 of A-ratio(max) separated all symptomatic (1.34+/-0.38) from all asymptomatic patients (0.60+/-0.21). Although the correlation between model parameters and cellular substrate is at present unclear, it is possible that the morphological alterations described by the model are related to the arrhythmogenic mechanism(s) of the idiopathic LQTS.

Adolescent↗
PubMed2001

Predictors of treatment response in patients with posttraumatic stress disorder.

1. This study examines the relation between baseline clinical characteristics in patients with posttraumatic stress disorder (PTSD) and response to treatment with a reversible monoamine oxidase A inhibitor (RIMA), brofaromine. 2. Data from two comparable, double-blind, placebo-controlled studies of brofaromine in patients with PTSD were combined. Bivariate analyses of variables of interest and outcome were performed. 3. Treatment response was significantly associated with lower baseline scores on the full scale Clinician-Administered PTSD Scale (CAPS) and on CAPS subscales B (re-experiencing) and C (avoidance/numbing), as well as to drug treatment with brofaromine. Placebo response was related to a history of past sexual trauma. 4. Brofaromine may have therapeutic benefit in treating PTSD, with lower baseline levels of reexperiencing and avoidance/numbing and overall less severe PTSD most predictive of outcome.

Adult↗
PubMed2001

Impact of electrocardiogram recording format on QT interval measurement and QT dispersion assessment.

The aim of this study was to determine the effect of recording conditions on the operator dependent measures of QT dispersion in patients with known and/or suspected repolarization abnormalities. Among several methods for risk stratification, QT dispersion has been suggested as a simple estimate of repolarization abnormalities. In a cohort of high and low risk patients, different components of the repolarization process were assessed in the 12-lead ECG using three different paper speeds and amplifier gains. To assess measurement error and reproducibility, a straight line was repeatedly measured. The operator error was 0.675 +/- 0.02 mm and the repeatability of the measurement error was 31 +/- 6%. The QT interval was most frequently measurable in V2-V5. Depending on the lead selected for analysis, the incidence of visible U waves was greatest in the precordial leads with high amplifier gain and low paper speed, strongly affecting QT interval measurement. The timing of the onset of the QRS complex (QRS onset dispersion) or offset of the T wave was strongly dependent on the paper speed. Paper speed, but not amplifier gain, had a significant shortening effect on the measurement of the maximum QT interval. As QT interval measurement in each ECG lead incorporates QRS onset and T wave offset (depending on the number of visible U waves), the dispersion of each of these parameters significantly affected QT dispersion. Thus, QT dispersion appears to reflect merely the presence of more complex repolarization patterns in patients at risk of arrhythmias.

Adult↗
PubMed2001

Problems of heart rate correction in assessment of drug-induced QT interval prolongation.

INTRODUCTION: Estimation of QT interval prolongation belongs to safety assessment of every drug. Among unresolved issues, heart rate correction of the QT interval may be problematic. This article proposes a strategy for heart rate correction in drug safety studies and demonstrates the strategy using a study of ebastine, a nonsedating antihistamine. METHODS AND RESULTS: Four-way cross-over Phase I study investigated 32 subjects on placebo, ebastine 60 mg once a day, 100 mg once a day, and terfenadine 180 mg twice a day. Repeated ECGs were obtained before each arm and after 7 days of treatment. The changes in heart rate-corrected QTc interval were investigated using (A) 20 published heart rate correction formulas, (B) a correction formula optimized by QT/RR regression modeling in all baseline data, and (C) individual corrections optimized for each subject by drug-free QT/RR regression modeling. (A) Previously published correction formulas found QTc interval increases on terfenadine. The results with ebastine were inconsistent. For instance, Bazett's and Lecocq's correction found significant QTc increase and decrease on ebastine, respectively. The results were related (absolute value(r) > 0.95) to the success of each formula (independence of drug-free QTc and RR intervals). (B) The pooled drug-free QT/RR regression found an optimized correction QTc = QT/RR(0.314). QTc interval changes on placebo, ebastine 60 mg, ebastine 100 mg, and terfenadine were -1.95 +/- 6.87 msec (P = 0.18), -3.91 +/- 9.38 msec (P = 0.053), 0.75 +/- 8.23 msec (P = 0.66), and 12.95 +/- 14.64 msec (P = 0.00025), respectively. (C) Individual QT/RR regressions were significantly different between subjects and found optimized corrections QTc = QT/RR(alpha) with alpha = 0.161 to 0.417. Individualized QTc interval changes on placebo, ebastine 60 mg, ebastine 100 mg, and terfenadine were -2.76 +/- 5.51 msec (P = 0.022), -3.15 +/- 9.17 msec (P = 0.11), -2.61 +/- 9.55 msec (P = 0.19), and 12.43 +/- 15.25 msec (P = 0.00057, respectively. Drug-unrelated QTc changes up to 4.70 +/- 8.92 msec reflected measurement variability. CONCLUSION: Use of published heart rate correction formulas in the assessment of drug-induced QTc prolongation is inappropriate, especially when the drug might induce heart rate changes. Correction formulas optimized for pooled drug-free data are inferior to the formulas individualized for each subject. Measurement imprecision and natural variability can lead to mean QTc interval changes of 4 to 5 msec in the absence of drug treatment.

Butyrophenones↗
PubMed2001

The role of atrial ectopics in initiating paroxysmal atrial fibrillation.

AIMS: To characterize the nature and timing of atrial ectopics preceding clinical episodes of paroxysmal atrial fibrillation. METHODS AND RESULTS: Holter recordings (n= 177, 60 patients, 58% male, mean age 61.7 +/- 11.5 years) were performed on patients with paroxysmal atrial fibrillation. These were subjected to standard analysis and recordings containing atrial fibrillation episodes suitable for analysis were identified (n = 74). Beat interval files differentiating sinus rhythm from atrial fibrillation were generated and atrial ectopics were identified. Atrial ectopics preceding atrial fibrillation were found to be more frequent (5.07 +/- 7.39 min(-1)) and more premature (ratio of coupling interval to that of surrounding sinus cycles = 0.56 +/- 0.08) compared to ectopics occurring remote from atrial fibrillation episodes (frequency = 3.60 +/- 7.32 min(-1) P = 5 x 10(-24), prematurity ratio = 0.60 +/- 0.10, P = 2 x 10(-73)). Atrial ectopic coupling interval frequency histograms were generated and analysed visually and by an automated statistically based test. Many ectopics were seen to occur at one coupling interval in 27 recordings (in eight this occurred only preceding atrial fibrillation onset, while in a further 19 cases this was also seen remote from atrial fibrillation onset). Overall 45% of ectopics preceding atrial fibrillation episodes occurred in isolation, 13% as part of a bigeminal rhythm, 22% as couplets and 20% as runs. This pattern did not differ from that seen remote from atrial fibrillation episodes. CONCLUSION: Paroxysmal atrial fibrillation is preceded by ectopics of a fixed coupling interval in a significant proportion of patients. If, as seems likely, this is a marker of 'focally mediated' atrial fibrillation, then Holter techniques may provide a useful screening tool with which to identify patients suitable for fuller electrophysiological assessment.

Adult↗
PubMed2001

Predictive value of T-wave morphology variables and QT dispersion for postmyocardial infarction risk assessment.

Different attempts have been made to use the 12-lead surface electrocardiogram (ECG) for risk stratification of patients prone to sudden cardiac death. Among others, QT dispersion (QTd) has been proposed as a simple risk marker, eg, in patients postmyocardial infarction (MI). To overcome the methodological limitations of QTd, novel T-wave morphology variables have been recently developed based on technologies that better quantify the substrate of a pathologically changed repolarization. In 280 post-MI patients with 27 events (death or nonfatal sustained ventricular tachycardia/ventricular fibrillation) during long-term follow-up (32 +/- 10 months), a 12-lead ECG was recorded before discharge and converted into a digital format. The prognostic value of digitally measured QTd and other conventional variables, and that of novel ECG variables of T-wave loop morphology was assessed. The latter included fully automatic and reproducible analysis of variables defining spatial and temporal T-wave variation as well as its wavefront direction. Among the 5 variables studied, the total cosine R to T (TCRT--describing the global angle between repolarization and depolarization orientations) and the T-wave loop dispersion were univariately associated (P = .0002 and P < .002) with events. Comparison of Kaplan Meier curves for patient strata above and below the median confirmed the strong discrimination of risk by TCRT and T-wave loop dispersion values (P < .003 and P < .001). On Cox regression analysis entering other univariately predictive risk stratifiers including age, left ventricular ejection fraction, heart rate, reperfusion therapy, beta adrenergic blocker treatment, and SDNN from Holter, TCRT (P < .03) yielded independent predictive value while T-wave loop dispersion was of borderline independence (P = .064). Heart rate (P < .02), left ventricular ejection fraction (P < .02), and reperfusion therapy (P <.02) also remained in the final model. In contrast, none of the conventional variables of repolarization dispersion including QTd and rate-corrected QTd revealed prognostic value on univariate or Kaplan Meier analysis despite optimized digital processing techniques. Computerized analysis of T-wave loop morphology from the 12-lead resting ECG permits independent assessment of post-MI risk and should replace the poorly conceptualized measurement of QTd.

Death, Sudden, Cardiac↗
PubMed2001

T-wave morphology differences between patients with and without arrhythmic complication of ischemic heart disease.

The study investigated the differences in T-wave morphology between normal controls, patients with an uncomplicated follow-up after a myocardial infarction (MI), and patients with ischaemic heart disease and a history of ventricular tachycardia/fibrillation (VT/VF). The study population consisted of 164 healthy patients (age 53.4 +/- 18.7 years old, 80 women), 123 VT/VF patients (age 63.8 +/- 10.1 years old, 15 women), and 196 MI patients (age 59.2 +/- 10.0 years old, 23 women). In all patients, supine resting signal-averaged orthogonal electrocardiograms were obtained. After singular value decomposition of electrocardiogram signal, 2 T-wave morphology descriptors were calculated: total cosine R to T describing the global angle between repolarisation and depolarisation loops, and percentage of loop area expressing the irregularity of the T-wave loop (a more irregular wave results in a lower percentage of loop area value). Both parameters were practically uncorrelated (Controls: r = - .106, MI r = .161, and VT/VF r = .173) and different between individual groups of patients: total cosine R to T (Control vs. MI: P = 4.3 x 10(-8), Control vs. VT/VF: P = 2.7 x 10(-16), MI vs. VT/VF: P = 3.1 x 10(-6)), percentage of loop area (Control vs. MI: P = 0.07, Control vs. VT/VF: P = 1.1 x 10(-8), MI vs. VT/VF: P = 2.9 x 10(-5), all nonparametric Mann-Whitney test). The comparisons of cumulative histograms also revealed significant differences between all three groups for both parameters (Kruskal-Wallis ANOVA test). Thus, these numerical descriptors of T-wave morphology are powerful indicators of arrhythmic complications among patients with ischaemic heart disease. They also differentiate between patients with stable uncomplicated ischaemic heart disease and healthy controls.

Electrocardiography↗
PubMed2001

Circadian behavior of P-wave duration, P-wave area, and PR interval in healthy subjects.

BACKGROUND: The prolongation of P-wave duration has long been shown to indicate the presence of high risk for atrial fibrillation. The circadian variation of P-wave characteristics and their dynamic adaptation to heart rate changes was not tested before. METHODS: To evaluate the diurnal pattern of P-wave duration, P area, and PR interval and of their linearly fitted relation with RR interval, 50 healthy volunteers (25 men, mean age 34 +/- 10 years) underwent 24-hour ambulatory electrocardiographic (ECG) recording with digital 12-lead Holter recorders. The median P-wave duration, P area, and PR interval were calculated from the average 12-lead ECG constructed from each 10-second ECG recording. Single harmonic regression analysis was performed to reveal the presence of circadian variation in the aforementioned ECG parameters. RESULTS: The P area (P < 0.0001, R(2) = 0.78), the PR interval (P < 0.0001, R(2) = 0.92), the P area / RR slope (P < 0.0001, R(2) = 0.55), and the PR/RR slope (P < 0.0001, R(2) = 0.42) showed a highly significant circadian variation while the periodic nature of P-wave duration (P = 0.016, R(2) = 0.32) and of the P duration / RR slope (P = 0.011, R(2) = 0.18) was only indicated by harmonic regression analysis. CONCLUSIONS: P-wave duration, P area, and PR interval show a significant circadian variation in healthy subjects. The relations between P area/RR,PR/ RR, and P duration/RR also demonstrate a significant diurnal pattern.

Adult↗
PubMed2001

Is QT dispersion associated with sudden cardiac death in patients with hypertrophic cardiomyopathy?

QT dispersion is significantly greater in patients with hypertrophic cardiomyopathy (HCM) than that in healthy subjects. Few data exist regarding the prognostic value of QT dispersion in HCM. In this study, we retrospectively investigated the association between QT dispersion and sudden cardiac death in 46 patients with HCM (mean 33.1 +/- 15.5 years, 32 men). The case group consisted of 23 HCM patients who died suddenly, and the control group consisted of 23 HCM patients who survived uneventfully during follow-up. Study patients were pair-matched for age, gender, and maximum left ventricular wall thickness. QT dispersion (maximum minus minimum QT interval) was manually measured on early 12-lead ECGs using a digitizing board. An in-house program was used for calculating QT interval, QT dispersion, JT interval, and JT dispersion (maximum minus minimum J point to T end interval). Patients in the case group tended to have shorter RR intervals than those in the control group (777 +/- 171 vs 856 +/- 192 ms, P = 0.08). Maximum corrected QT and JT intervals did not discriminate the case group from controls (489 +/- 29 vs 479 +/- 27 ms, P = NS; 375 +/- 36 vs 366 +/- 22 ms, P = NS, respectively). Greater QT dispersion and JT dispersion were found in the case group compared with controls (74 +/- 28 vs 59 +/- 21 ms, P = 0.02 and 76 +/- 32 vs 59 +/- 26 ms, P = 0.03, respectively). The measurements of maximum QT, JT, and T peak to T end intervals, precordial QT and JT dispersion, and T peak and T end dispersion were all comparable between the two groups (P = NS for all). No systematic changes in ECG measurements were found from late ECGs of the case group compared to those from early ECGs (P = NS). No correlation between maximum left ventricular wall thickness and QT dispersion, JT dispersion, maximum QTc or JTc intervals was observed (r < 0.29, P > 0.05 for all). Our results show that increased QT dispersion and JT dispersion is weakly associated with sudden cardiac death in the selected patients with HCM.

Adolescent↗
PubMed2001

Diurnal variations of the dominant cycle length of chronic atrial fibrillation.

High-resolution digital Holter recording was carried out in 21 patients (15 men, 64 +/- 12 yr) with chronic atrial fibrillation. Dominating atrial cycle length (DACL) was derived by frequency domain analysis of QRST-reduced electrocardiograms. Daytime mean DACL was 150 +/- 17 ms, and nighttime mean was 157 +/- 22 ms (P = 0. 0002). Diurnal fluctuation in DACL differed among patients: it tended to be virtually absent in those with a short mean DACL, but in those with longer DACL the night-day difference was as much as 23 ms (R = 0.72, P < 0.001, correlation of mean DACL to night-day difference). Mean DACL also correlated with ventricular cycle length (R = 0.40, P < 0.001), particularly at night (r = 0.49). The shorter cycle lengths found in this study during the day are consistent with sympathetic and/or other physiological modulation, but since increased vagal tone shortens atrial refractoriness in most models, parasympathetic influences are not likely to play a major role. Alternatively, atrial effective refractory period may not be the sole determinant of atrial cycle length during atrial fibrillation.

Adult↗
PubMed2001

Evaluation of drug-induced QT interval prolongation: implications for drug approval and labelling.

Assessment of proarrhythmic toxicity of newly developed drugs attracts significant attention from drug developers and regulatory agencies. Although no guidelines exist for such assessment, the present experience allows several key suggestions to be made and an appropriate technology to be proposed. Several different in vitro and in vitro preclinical models exist that, in many instances, correctly predict the clinical outcome. However, the correspondence between different preclinical models is not absolute. None of the available models has been demonstrated to be more predictive and/or superior to others. Generally, compounds that do not generate any adverse preclinical signal are less likely to lead to cardiac toxicity in humans. Nevertheless, differences in likelihood offer no guarantee compared with entities with a preclinical signal. Thus, the preclinical investigations lead to probabilistic answers with the possibility of both false positive and false negative findings. Clinical assessment of drug-induced QT interval prolongation is crucially dependent on the quality of electrocardiographic data and the appropriateness of electrocardiographic analyses. An integral part of this is a precise heart rate correction of QT interval, which has been shown to require the assessment of QT/RR relationship in each study individual. The numbers of electrocardiograms required for such an assessment are larger than usually obtained in pharmacokinetic studies. Thus, cardiac safety considerations need to be an integral part of early phase I/II studies. Once proarrhythmic safety has been established in phase I/II studies, large phase III studies and postmarketing surveillance can be limited to less strict designs. The incidence of torsade de pointes tachycardia varies from 1 to 5% with clearly proarrhythmic drugs (e.g. quinidine) to 1 in hundreds of thousands with drugs that are still considered unsafe (e.g. terfenadine, cisapride). Thus, not recording any torsade de pointes tachycardia during large phase III studies offers no guarantee, and the clinical premarketing evaluation has to rely on the assessment of QT interval changes. However, since QT interval prolongation is only an indirect surrogate of predisposition to the induction of torsade de pointes tachycardia, any conclusion that a drug is safe should be reserved until postmarketing surveillance data are reviewed. The area of drug-related cardiac proarrhythmic toxicity is fast evolving. The academic perspective includes identification of markers more focused compared with simple QT interval measurement, as well as identification of individuals with an increased risk of torsade de pointes. The regulatory perspective includes careful adaptation of new research findings.

Animals↗
PubMed2001

Development of a thermoresistant tissue culture rinderpest vaccine virus.

The currently used Plowright's tissue culture rinderpest vaccine (RBOK strain) gives full protection and lifelong immunity, but it is highly thermolabile and requires maintenance of cold chain from vaccine production till delivery. Keeping in view the need for a thermostabile vaccine in tropical developing countries with limited refrigeration facilities, we passaged serially the RBOK strain of rinderpestvirus (RPV) at gradually elevated temperature up to 40 degrees C to obtain a thermoresistant RPV (TR-RPV) mutant. The thermoresistance (thermostability) and antigenicity of TR-RPV were compared with those of the vaccine virus by various methods, confirming the acquired properties. Thus, the infectivity titres of the TR-RPV mutant and vaccine virus were determined after incubation for various times at 37 degrees C. Regression analysis indicated that TR-RPV had a half-life of 1.81 hr and a degradation constant of 0.1656, while the parent vaccine virus had a half-life of 1.11 hr and a degradation constant of 0.2686. In capture ELISA with four different monoclonal antibodies (MAbs) to the N protein of RPV, TR-RPV showed a 10-fold higher reactivity with one MAb as compared to the vaccine virus. Although TR-RPV did react also with the other three MAbs, its reactivity was only 4-5 times higher than that of the vaccine virus. A treatment of the virus with Triton X-100 resulted in 2-4 times higher reactivity with the MAbs. The 35S-methionine-labeled vaccine virus-and TR-RPV-infected Vero cell lysates showed 6 polypeptide bands with identical pattern of migration in polyacrylamide gel electrophoresis in the presence of SDS (SDS-PAGE). Radioimmunoprecipitation assay (RIPA) of the TR-RPV and vaccine virus with a rabbit anti-RPV immune serum (RHIS) and bovine anti-RPV hyperimmune serum (BHIS) showed the presence of four identical antigenic proteins, namely H, N, F and M, for both viruses. It can be concluded that TR-RPV has indeed retained the antigenic properties of the parental vaccine virus besides acquiring thermoresistance.

Animals↗
PubMed2000

Measurement, interpretation and clinical potential of QT dispersion.

QT dispersion was originally proposed to measure spatial dispersion of ventricular recovery times. Later, it was shown that QT dispersion does not directly reflect the dispersion of recovery times and that it results mainly from variations in the T loop morphology and the error of QT measurement. The reliability of both automatic and manual measurement of QT dispersion is low and significantly lower than that of the QT interval. The measurement error is of the order of the differences between different patient groups. The agreement between automatic and manual measurement is poor. There is little to choose between various QT dispersion indices, as well as between different lead systems for their measurement. Reported values of QT dispersion vary widely, e.g., normal values from 10 to 71 ms. Although QT dispersion is increased in cardiac patients compared with healthy subjects and prognostic value of QT dispersion has been reported, values are largely overlapping, both between healthy subjects and cardiac patients and between patients with and without adverse outcome. In reality, QT dispersion is a crude and approximate measure of abnormality of the complete course of repolarization. Probably only grossly abnormal values (e.g. > or =100 ms), outside the range of measurement error may potentially have practical value by pointing to a grossly abnormal repolarization. Efforts should be directed toward established as well as new methods for assessment and quantification of repolarization abnormalities, such as principal component analysis of the T wave, T loop descriptors, and T wave morphology and wavefront direction descriptors.

Animals↗
PubMed2000

Analysis of 12-lead T-wave morphology for risk stratification after myocardial infarction.

BACKGROUND: The stratification of post-myocardial infarction (MI) patients at risk of sudden cardiac death remains important. The aim of the present study was to assess the prognostic value of novel T-wave morphology descriptors derived from resting 12-lead ECGs. METHODS AND RESULTS: In 280 consecutive post-MI patients, a 12-lead ECG was recorded before discharge, optically scanned, and digitized. For the present study, 5 T-wave morphology descriptors were automatically calculated after singular value decomposition of the ECG signal. The total cosine R-to-T (TCRT [describes the global angle between repolarization and depolarization wavefront]) and the T-wave loop dispersion were univariately associated (P:=0.0002 and P:<0.002, respectively, U: test) with 27 prospectively defined clinical events in 261 patients (mean follow-up 32+/-10 months). Kaplan-Meier event probability curves for strata above and below the median confirmed the strong risk discrimination by TCRT and T-wave loop dispersion (P:<0.003 and P:<0.001, respectively, log-rank test). On Cox regression analysis, with the entering of age, left ventricular ejection fraction, heart rate, QRS width, reperfusion therapy, beta-adrenergic-blocker treatment, and standard deviation of R-R intervals on 24-hour Holter monitoring, TCRT (P:<0.03) yielded independent predictive value, whereas T-wave loop dispersion was of borderline independence (P:=0.064). Heart rate (P:<0.02), left ventricular ejection fraction (P:<0.02), and reperfusion therapy (P:<0.02) also remained in the final model. CONCLUSIONS: Computerized T-wave morphology analysis of the 12-lead resting ECG permits independent assessment of post-MI risk and an improved risk stratification when combined with other risk markers.

Analysis of Variance↗
PubMed2000

Stability of the noninvasive baroreflex sensitivity assessment using cross-spectral analysis of heart rate and arterial blood pressure variabilities.

BACKGROUND: Depressed baroreflex sensitivity (BRS), usually estimated using the invasive phenylephrine method or the nitroprusside test, is significantly and independently associated with an increased risk of malignant ventricular arrhythmias and sudden cardiac death in patients surviving acute myocardial infarction. Several investigators have compared the standard phenylephrine test and different noninvasive methods. HYPOTHESIS: This study evaluated the influence of different body positions with different breathing regimes on cross-spectral baroreflex indices (coherence between the spectral densities of blood pressure and cardiac cycle variabilities) in both low- and high-frequency bands. METHODS: The data were obtained in 103 patients (73 males, aged 53 +/- 12 years) with coronary artery disease and/or hypertension. Simultaneous electrocardiographic and noninvasive blood pressure recordings were obtained in each subject in both supine and sitting positions during both spontaneous and slow and fast controlled respiration (0.1 and 0.33 Hz). RESULTS: The results show a significant bias and disagreement between noninvasive baroreflex sensitivity (BRS) indices. The mean values of the baroreflex in low frequency ranged from 5.0 +/- 5.3 to 10.1 +/- 7.9 ms/mmHg, while in high frequency, the mean values ranged from 6.6 +/- 6.1 to 10.1 +/- 7.9 ms/mmHg. The limits of agreement ranged from +/-1.7 to +/-4.1 ms/mmHg with bias from -1.0 to +0.7 ms/mmHg. CONCLUSION: A comprehensive comparison of different methods shows that BRS estimated in low-frequency band in sitting position during spontaneous respiration is the most representative part of the global baroreflex gain.

Adult↗
PubMed2000

Changes of the T-wave amplitude and angle: an early marker of altered ventricular repolarization in hypertension.

BACKGROUND: The heterogeneity of ventricular repolarization is an important proarrhythmic factor. QT dispersion has been proposed to reflect the inhomogeneity of ventricular repolarization, but a poor reproducibility limits its clinical applicability. Reliable noninvasive methods to quantify abnormalities in ventricular repolarization are still lacking. The T-loop morphology analysis is a novel method aimed at quantifying ventricular repolarization. HYPOTHESIS: To test the ability of the T-loop morphology analysis to discriminate between hypertensive patients and healthy subjects, 105 hypertensive patients (mean age 63.6 +/- 12.3 years) and 110 healthy controls (mean age 49.7 +/- 14.3 years) were evaluated. METHODS: The maximum QT interval (QT maximum), the minimum QT interval (QT minimum), and their difference (QT dispersion) were calculated from a digitally recorded 12-lead electrocardiogram (ECG) in both study groups. X, Y, and Z leads were reconstructed from the 12-lead ECG, and the amplitude of the maximum T vector (T amplitude) and the angle between the maximum T vector and X axis (T angle) were calculated from the projection of the T loop in the frontal plane. RESULTS: T amplitude (p < 0.001), T angle (p = 0.05), and QT dispersion (p = 0.04) were significantly different between hypertensive patients and controls, while QT maximum (p = 0.14) and QT minimum (p = 0.35) did not differ between the groups. T amplitude was the only marker which differed between hypertensive patients without ECG criteria for left ventricular hypertrophy and controls (p = 0.002). CONCLUSIONS: T-loop features and particularly T amplitude are significantly different between hypertensive patients and healthy controls and may serve as early markers of repolarization abnormalities in a hypertensive population.

Action Potentials↗