Letter regarding article by Shvilkin et al, "T-vector direction differentiates postpacing from ischemic T wave inversion in precordial leads".
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Biomedical subjects
Publications and source records attributed to John E Madias.
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Increased ECG QRS duration (QRSd) in patients with dilated cardiomyopathy (DCM) or heart failure (HF) is a well-known phenomenon. The QRSd is not a static ECG measurement but shows fluctuations, and its recent inclusion among the parameters used in referring patients for implantable cardioverter/defibrillators (ICDs) or cardiac resynchronization therapy (CRT) has led to renewed interest in its natural course and its determinants. Although clinical deterioration has been traditionally associated with increasing QRSd, its changes often are left unexplained. Also, the recent description of a decrease in QRSd, well correlated with attenuated amplitude of QRS complexes in patients with peripheral oedema (PERO) in the context of a variety of illnesses, has added complexity to the matter. This communication aims at calling attention to the importance of a few clinical and ECG parameters when documenting changes in the QRSd in serial ECGs. Thus, presence or absence of PERO and change in the patients' weight, along with alteration in the amplitude of QRS complexes and shifts to/from incomplete/complete bundle branch block patterns, all should be considered when assessing changes in QRSd for meaningful follow-up of patients with DCM or CHF, or referral for ICD or CRT. Evaluation of the QRSd as a selection parameter for referring patients suitable for device implantation should continue along with the employment of mechanical analysis of ventricular dyssynchrony. Although reference here is made to QRSd particularly in connection with DCM and HF, the above apply to other oedematous states (i.e. patients with chronic renal failure, or those undergoing haemodialysis).
Nine patients aged 76.2 +/- 8.0 years, 3 males and 6 females, who had suffered anasarca due to various illnesses, and had bundle branch block (BBB) or intraventricular conduction delays (IVCD) on admission (3 with complete left BBB [LBBB], 2 with incomplete LBBB, 2 with complete right BBB, and 2 with complete IVCD), are described. After gaining 48.2 +/- 26.9 lb because of anasarca, their electrocardiograms revealed decreased QRS duration (112.7 +/- 18.9 milliseconds), as compared with the same measurement on admission (130.1 +/- 12.6 milliseconds) ( P = .015), with 4 patients showing apparent conversion of their complete BBB or IVCD to incomplete BBB, or normal IVC. Of these 9 patients, 5 lost subsequently 45.6 +/- 37.0 lb, and this was now associated with an increase in the QRS duration from 109.6 +/- 23.0 to 127.8 +/- 17.4 milliseconds ( P = .004), with 1 patient converting from normal IVC to incomplete LBBB, and 1 from incomplete to complete IVCD. These findings suggest that anasarca leads to apparent amelioration of the features of BBB or IVCD, with subsequent return to the baseline complete BBB or IVCD after loss of fluid overload; consequently, accurate characterization of a patient's BBB or IVCD is interfered with by the presence of anasarca. The pathophysiologic mechanism of this phenomenon has been traced to decreases of voltage across the entire electrocardiographic curve due to attenuation of the electrical impedance of the body volume conductor due to accumulation of the anasarca fluid.
Patients with congestive heart failure (CHF) responding to diuresis reveal marked augmentation of the QRS complexes (AUG-QRS) in their electrocardiograms (ECGs). Recently, such change in the ECG has been observed in patients with anasarca (AN) of varying etiology commensurate with partial alleviation of the volume overload; similar ECG change has been noted in patients with end-stage renal failure after hemodialysis. The mechanism for the AUG-QRS in patients with CHF has been debated, and many have ascribed this ECG change to the "Brody effect," linking the AUG-QRS to reduction of intracardiac blood volumes resulting from diuresis. However, the Brody effect (a theoretical formulation not fully validated by experimentation and associated with controversy in its clinical implementation) has not provided a satisfactory explanation for the AUG-QRS in patients with CHF. In contrast, the described association between amelioration of AN in a diverse patient population and AUG-QRS suggests that this ECG change in patients with CHF is due to an increased electrical resistance of the passive body volume conductor, resulting from water loss effected by diuresis. This thesis is supported by theoretical work, animal experimentation, and clinical evidence.
Associations have been described among weight, amplitude of QRS complexes, and QRS duration (QRSd) in patients with anasarca (AN), and changes in the amplitude of the QRS complexes, QRSd, and QTc after hemodialysis (HD) and in patients with heart failure with associated peripheral edema congestive heart failure. The objective of this study was to evaluate the hypothesis that changes in QTc in patients with AN and after HD are at least partially apparent, due to changing edematous states, and not totally due to altered electrophysiology. QTc was measured in patients with AN on admission, at peak weight (N = 28), and at their subsequent lowest weight (N = 12), in 28 control patients without change in weight during hospitalization, and in one patient before and after 26 HD sessions. In the patients with AN, the QTc was 451 +/- 36 ms on admission and dropped to 423 +/- 46 ms at peak weight (P = 0.005). QTc was 421 +/- 44 ms at peak weight and raised to 434 +/- 30 at subsequent lowest weight (P = 0.32). In the controls, QTc on admission and at discharge were 435 +/- 34 and 428 +/- 23 ms, correspondingly (P = 0.18). QTc increased from 472 +/- 18 ms before to 489 +/- 36 ms after HD (P = 0.017). Alterations in QTc in AN, or HD suggest that the changes in the QTc may be partially only apparent, and due to the electrocardiogram machine-based measurement of the attenuated/augmented QRST complexes resulting from fluid shifts.
BACKGROUND: A diagnostic ECG sign of a ventricular aneurysm (VA) consequent to a myocardial infarction (MI) in the presence of complete left bundle branch block was recently described, and consists of the presence of ST-segment elevation (+ST), instead of the expected ST-segment depression (-ST), in leads V4-6. Generally, complete right bundle branch block (RBBB) is associated with -ST in ECG leads V1-3. We hypothesized that stable +ST, instead of the expected -ST in leads V1-3 in patients with RBBB could be also diagnostic of a VA and other severe segmental left ventricular dysfunction (VA/SSD). Thus, this study was performed to explore the feasibility of using the ECG to diagnose a VA/SSD in the presence of RBBB, and to evaluate the determinants of such diagnosis. METHODS: The frequency of +ST > or =1 mm in leads V1-3 was assessed in patients with RBBB, prior MI, and a VA/SSD diagnosed by echocardiography and/or contrast left cine-ventriculography. The ECG correlates for a positive or negative diagnosis of a VA/SSD were explored. RESULTS: Out of 4197 files of our cohort of the Cardiology Clinic, RBBB was detected in 175 patients. Of these, 28 had an old MI, and had a VA/SSD diagnosed by > or =1 of noninvasive and/or invasive non-ECG tests. Twenty-one of these 28 patients had stable +ST in > or =1 of leads V1-3 (Group 1), and 7 did not (Group 2). Thus, the sensitivity of this ECG criterion for the diagnosis of VA/SSD was 75%, and the specificity was 100% in this highly selective group. VA/SSD in the septal and anterior myocardial regions was more frequent in the patients of Group 1, than in the patients of Group 2 (P = 0.03 and 0.02, correspondingly). The number of myocardial territories involved with the VA/SSD, or the ejection fraction were not different in the two groups (P = 0.65 and 0.55, correspondingly). CONCLUSION: VA/SSD can be diagnosed in the presence of RBBB by the concordant to the QRS repolarization changes (+ST) in leads V1-3. Positivity of this ECG marker for VA/SSD correlates with involvement of the septal or anterior myocardial regions, and represents mechanistically a superimposition of primary repolarization alterations, overcoming the secondary such changes.
BACKGROUND: Increase in the amplitude of electrocardiogram (ECG) QRS complexes has been observed in patients treated for heart failure (HF), but the underlying mechanism has not been delineated. Also, correlation of augmentation of the QRS potentials with loss of weight has been noted in patients recovering from anasarca of varying etiology, or after hemodialysis. We assessed the effect of diuresis-based fluid loss in patients treated for HF on the amplitude of ECG QRS complexes. METHODS: This is a cohort study based on ECG and other data from a previously published investigation of patients with HF conducted at a university affiliated hospital, which used new measurements and analysis, performed by a totally blinded investigator based at another institution. Twenty-one patients (10 men) aged 70.5+/-12.7 years, 13 with ischemic, and 8 with nonischemic cardiomyopathy, were admitted to the hospital for management of exacerbated HF and were observed for 48 hours. The patients received diuresis, and had routine laboratory testing, documentation of the net fluid lost, and recording of ECGs prior to the initiation of therapy and at 24 and 48 hours. Percent change (%Delta) over the course of observation in the sums of the amplitude of QRS complexes from 12 leads (SigmaQRS12), 6-limb leads (SigmaQRS6), and leads 1+2 (SigmaQRS2) in mm of standard ECGs were correlated with net fluid loss corrected for admission weight in mL/kg. RESULTS: Fluid loss amounted to 3204.9+/-1399.5 mL in the course of 40+/-23 hours of diuresis. SigmaQRS12 was 160.9+/-42.3 mm before and 170.0+/-50.7 mm after diuresis (P=0. 024). Percent change in SigmaQRS12, SigmaQRS6, and SigmaQRS2 correlated well with the net fluid loss (r=-0.70, -0.82, -0.61, and P=0.002, 0.0005, 0.001) correspondingly. CONCLUSION: Changes in sums of the amplitude of QRS complexes of the standard ECG correlates well with net fluid loss in response to short-term diuresis in patients with HF. Change in the SigmaQRS12, SigmaQRS6, and SigmaQRS2 from ECGs before and after diuresis can be used as an easily obtainable and universally available bedside index of the net fluid loss experienced by bedridden patients with HF undergoing therapy.
Increases in the P-wave duration (P-du) and P-wave dispersion (P-d) following hemodialysis (HD) are attributed to changes in the electrolytic milieu with HD, or are considered to be due to an unknown mechanism. Such changes are thought to be proarrhythmic, and thus have potential clinical implications. Increase in the amplitude of QRS complexes following HD has been amply documented in the literature. Also, recent work linking attenuation/augmentation of amplitude of QRS and P-wave complexes in patients with increase/subsequent decrease weights due to anasarca peripheral edema/and its alleviation, or before/after hemodialysis (HD) suggests that the increase in the P-du and P-d after HD may be totally (or partially) mediated by the alleviation of the fluid overload by the procedure. This is supported by the decrease/increase in the QRS duration noted with anasarca/and its alleviation. To further clarify this issue, and prove or refute the above hypothesis, it is recommended that correlations of changes in the P-du and P-d with the loss of weight or net fluid dialyzed are carried out, in addition to the traditional considerations of electrolytic alterations after HD.
Since research is concentrated to a large extent on patients with left bundle branch block, we aimed at evaluating the hypothesis that measurements of certain intervals and other characteristics of the ECG may change over time in patients with right bundle branch block (RBBB), and to design a model, which could be implemented in research and clinical practice, irrespective of the specific ECG features present. The duration of the QRS complex, QT, QTc, and PR intervals, the frontal QRS axis, the heart rate and the presence of hemiblocks, atrioventricular blocks, and atrial fibrillation were compared in the 1st and last of all available ECGs for each patient. Also, a subgroup of patients who had a ventricular aneurysm (VA) was compared with the remaining patients, with respect to the above variables. This longitudinal analysis included all of the patients with RBBB followed in our Cardiology Clinic. There were no significant changes in the ECG variables from the two ECGs recorded 487.6 +/- 410.1 (range 0-1,476) days apart, in the two comparisons carried out in 151 patients with RBBB. Comparison of the above-described ECG intervals and characteristics of patients with RBBB were found to be stable over the time course of the investigation. This methodological study is presented as a model to be used serially and prospectively in research and clinical practice for the follow-up of patients with bundle branch block, VA, dilated cardiomyopathy, congestive heart failure, or those considered for cardiac resynchronization therapy.
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The feasibility of recording the intracardiac electrocardiogram (IC-ECG) through a saline-filled central venous catheter has been demonstrated. The importance of identifying P waves for the accurate characterization of arrhythmias has long been emphasized. The "Lewis lead" has been occasionally employed when the standard electrocardiogram (SECG) fails to detect P waves. The objectives of this study were to compare the amplitude of P waves recorded by intracardiac and standard ECGs and the Lewis lead and to explore whether the latter has any advantages over either type of electrocardiography. The amplitudes of P wave (in millimeters) measured on SECG, the Lewis lead, and IC-ECG obtained through a saline-filled central venous catheter were compared; recordings were obtained through the intracardiac electrocardiographic distal, medial, and proximal ports of the central venous catheter in 28 patients who underwent 62 measurements. P waves were larger on the distal port of the IC-ECG than on the medial and proximal ports, on lead V(1), the lead with the tallest P wave on SECG, and the Lewis lead (all p = 0.0005). P waves were also larger on the medial port than on the proximal port of the IC-ECG (p = 0.0005). P waves were larger on the proximal port of the IC-ECG than on lead V(1), the lead with the tallest P wave on SECG, and the Lewis lead (p = 0.0005 for the 2 leads), and P waves were larger with the Lewis lead than on lead V(1) (p = 0.0005) but did not differ from the lead with the tallest P wave on a SECG (p = 0.124). Augmented P waves can be secured by employment of an intracardiac electrocardiographic lead; the Lewis lead has no advantages over the SECG for detecting P waves. These data are useful when the amplitude of P waves is an issue of concern in clinical practice and research.
BACKGROUND: Diagnosis of left ventricular hypertrophy (LVH) is primarily based on measurements of R- and S-waves from various electrocardiographic (ECG) leads. Recent information has shown that anasarca peripheral edema (AN) (defined as fluid accumulation diagnosed by weight gain, positive fluid intake/output records, and pitting edema in the lower extremities and rest of the body, particularly in the dorsal region) leads to attenuation in the amplitude of QRS complexes and consequently could interfere with the diagnosis of LVH. The objective of this study was to evaluate whether the diagnosis of LVH is concealed by AN. METHODS: Conventional ECG measurements and diagnostic binary characterization according to the Cornell, Sokolow-Lyon, and Romhilt-Estes systems were carried out in 14 patients with LVH (six patients with AN and eight patients admitted contemporaneously who did not gain weight during their hospitalization and who served as control subjects). The patients with AN were evaluated on admission (before the development of AN), and on the days of half of peak weight (HF-W) gain, peak weight (P-W) gain, and the lowest subsequent weight (L-W). The control subjects were evaluated on admission and at discharge. Analyses included the following: characterization by the three LVH diagnostic instruments mentioned previously; QRS amplitude measurements for the assessment of LVH before and after development of AN; and comparisons of the AN patients with the control subjects. RESULTS: Measurements and binary characterization was diagnostic of LVH on admission by design for all 14 patients. However, although such characterization remained unaltered for the control subjects, the patients with AN revealed statistically significant drops in all ECG measurements on the days of HF-W gain (P = .016 to .0005) and P-W gain (P = .02 to .0005), at which points the diagnosis of LVH could no longer anymore substantiated. CONCLUSIONS: The results of this study indicate that AN interferes with electrocardiographically based diagnosis of LVH. This has clinical implications because accurate characterization of the presence or absence of LVH is unattainable in patients with AN and should await abatement of the edematous state. The previously stated can be extrapolated to the patients with congestive heart failure who have gone on to develop right heart failure and AN, or to patients with end-stage renal failure who also reveal attenuation of the ECG QRS potentials at the stage of poor compensation of their edematous state.
The criterion of ST-segment elevation (+ST) > or=5.0 mm in leads V1-V3 for the diagnosis of acute myocardial infarction (AMI) in patients with paced ventricular rhythm lacks specificity, since it is also encountered in patients with pacemakers and QRS complexes of large amplitudes in leads V1-V3 but without an AMI. This report is based on 2 such patients with electronically-paced rhythms and excessive +ST who did not have an AMI although this diagnosis would have been made if proposed criteria had been strictly employed. Consequently, it is recommended that in such instances the amplitudes of QRS complexes are taken into account when ST-segment elevations in leads V1-V3 are used in the diagnostic algorithm of AMI.
We describe a patient with coronary artery disease who showed transiently augmented R-waves in his electrocardiogram (ECG) during the course of an exercise treadmill test (ETT), an ECG pattern occasionally associated with the hyperacute phase of myocardial infarction and variant angina. This change in the R-waves was noted in II, III, and aVF ECG leads and was associated with ST-segment elevation; both changed gradually and were normalized during the recovery period. Cardiac enzymes after ETT were negative, and arteriography revealed 3-vessel coronary artery disease, with a completely occluded right coronary artery. The ventriculogram showed very mild hypokinesis of the inferior left ventricular wall, while the global ejection fraction was 75%. These ECG changes, noted previously during ETT in precordial ECG leads, are herein reported to occur also in II, III, and aVF ECG leads. The generation of these ECG changes, which hinges upon a late unopposed depolarization occurring in the course and at the site of severe ischemic injury, constitutes a transient focal ventricular conduction abnormality.
The author describes his experience with a "saline-filled central venous catheter electrocardiographic lead" for the recording of intracardiac electrocardiograms provides a brief description of the methodology, refers to this modality's clinical usefulness, furnishes 2 examples illustrating the contribution of the method to clinical diagnosis, and outlines his literature search to find the discoverer/originator of the employment of a saline-filled intracardiac catheter as an electrocardiogram recording lead.
Although the ECG diagnosis of cardiac pathology is well served by the employment of the standard 12 ECG leads, an occasional need arises that additional leads might provide a diagnostic advantage. To this effect it is proposed that a space is provided in the standard 12-lead ECG printed report for a "13th multiuse ECG lead"; such a lead, which will be referenced to the "central Wilson's terminal," would provide additional information from various chest wall locations (V3R-V6R, posterior [left parascapular]) or other regions. Also such a lead could provide intracardiac electrograms via intracardiac recording wires or metallic or normal saline-filled catheters.
Reported associations between weight and amplitude of QRS complexes in patients with anasarca and those undergoing hemodialysis (HD) led to the hypothesis that similar alterations in the P waves may occur with changing edematous states. The objective of this study was to explore whether anasarca or the state prior to HD are associated with attenuated P waves. The sum of P wave amplitude in millimeters measured in the 12 leads of the ECG (SigmaP) was calculated in 28 patients with anasarca, 28 "controls," without change in their weight during hospitalization, and in 1 patient before and after 26 HD sessions. Admission SigmaP (10.5 +/- 4.9 mm) decreased at peak weight (3.8 +/- 2.0 mm, P = 0.0005) in patients with anasarca and increased at subsequent lowest weight in those who lost weight (2.3 +/- 1.3 vs 6.15 +/- 1.6 mm, P = 0.002). Admission and discharge SigmaPs were 10.9 +/- 4.5 and 9.8 +/- 3.8 mm, P = 0.062 in the controls, and 13.7 +/- 2.8 mm before and 18.2 +/- 3.0 mm after HD, P = 0.0005. In the patients with anasarca, the percent of decrease in SigmaP correlated well with the percent of increase in weight (r = 0.70, P = 0.0028) and percent of decrease in the sum of QRS complexes from all 12 ECG leads (r = 0.62, P = 0.01). After HD, the percent of increase in SigmaP correlated with percent of increase in the body electrical resistance (r = 0.44, P = 0.029), reactance (r = 0.46, P = 0.020), and impedance (r = 0.44, P = 0.029). Alterations in P wave amplitudes, commensurate with the ones affecting the corresponding QRS complexes, occur in patients developing anasarca, and those undergoing HD. This observation suggests that accurate measurement of the P wave amplitudes in such patients cannot be made until the fluid overload is alleviated, and this factor should be taken into consideration when repeat P wave measurements are compared.