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Background: Hemodialysis (HD) leads to an augmentation in the amplitude of QRS complexes (QRS-c), and R waves (R-w); some correlates of this phenomenon have been identified, but the exact mechanism for these ECG changes remains elusive. The objective of this study is to search for the underlying mechanism(s) of the post-HD augmentation of QRS-c and R-w.Methods: The sum of the amplitudes of ECG QRS-c and R-w, along with a host of other parameters (body weight, fluid volumes, echocardiographically-derived left ventricular dimensions and volumes, serum potassium, hemoglobin, hematocrit, and others) was measured, before and after HD, in 17 patients with end-stage renal failure.Results: While there were many correlations noted between the changes in the QRS-c and R-w and some of the above variables in numerous univariate analyses carried out, multivariate analyses did not identify any of the examined variables as exerting an independent influence on the observed ECG changes after HD.Conclusion: Augmentation of QRS-c and R-w following HD is engendered by an interplay of a decrease in the LVEDD/LVEDV, and K+, loss of fluid volume, and a rise in Hb and Ht, without any of the above being an independent variable; also other factor(s) (e.g., increase in the body electrical impedance) exerting an influence in this ECG phenomenon cannot be excluded. [ABSTRACT FROM AUTHOR]

Background: Increased QT dispersion (QTd) has been associated with an increased risk for ventricular arrhythmias and sudden death in the general population and in various clinical states.Methods: We investigated the impact of hemodialysis (HD) on QT, QTd, and T-wave amplitude in subjects with end-stage renal failure. Data on 49 patients on chronic HD were studied. The QT, QTd, and the sum of amplitude of T waves (SigmaT) in millimetre in the 12 ECG leads, along with a host of other ECG parameters, body weight, blood pressure, heart rate, electrolytes, and hemoglobin/hematocrit were measured before and immediately after HD.Results: QT decreased (380.9 +/- 38.4-363.5 +/- 36.8 ms, P = 0.001), the QTc did not change (406.2 +/- 30.8-405.4 +/- 32.2 ms, P = 0.8), the QTd increased (31.3 +/- 14.6-43.9 +/- 18.6 ms, P = 0.003), and the SigmaT decreased (32.3 +/- 15.7-25.9 +/- 12.6 mm, P = 0.0001) after HD. There was no correlation between the change in QTd and the changes in serum cations, heart rate, the subjects' weight, T-wave duration, and SigmaT. However, the change in QTc correlated inversely with the change in serum Ca(++) (r =-0.339, P = 0.021).Conclusion: QTd increased, the SigmaT decreased, and the QTc and T-wave duration remained stable, after HD. The QTd increase, although may be real, could also reflect measurement errors stemming from the decrease in the amplitude of T waves (as shown recently), imparted by HD; this requires clarification, to use QTd in patient on HD. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Hemodialysis (HD) is often administered in critical care areas to patients with chronic renal failure as a continuation of the HD they are receiving on an ambulatory basis, and to patients who develop such a need for the first time or may require HD only transiently. The double-lumen Shiley central venous catheter (SCVC), inserted via the brachiocephalic veins, is often employed for HD, and it is customary to obtain a chest radiograph to ensure proper positioning of the tip of the SCVC within the superior vena cava (SVC) or high right atrium (RA). This practice is implemented to evaluate for complications stemming from the insertion of the SCVC and subsequent mishaps due to low positioning of the tip of the catheter in the RA or right ventricle. Intracardiac ECGs obtained via a saline solution-filled SCVC as the conductive medium can be easily recorded serially and periprocedurally to ensure proper positioning of the tip of the SCVC in the SVC or high RA based on the evaluation of the appearance and amplitude of atrial depolarization, thus rendering chest radiographs redundant. [ABSTRACT FROM AUTHOR]

Objective: Precordial ECGs reveal significant intrasubject variability due to the inexact employment of the recommended V(1)-V(6) chest landmarks. Also, as per the Einthoven law, the six limb leads can be derived from leads 1 and 2. The purpose of this study was to evaluate whether the 12-lead ECG could be substituted by ECG sets with a limited number of leads.Materials and Methods: The performance of three ECG systems (ie, the 12-lead ECG, a 6-lead ECG comprising the limb leads, and a 2-lead ECG comprising exclusively leads 1 and 2) was evaluated in data from 28 patients with anasarca (AN), 28 control patients, 10 patients who had undergone hemodialysis, and 3 patients with idiopathic dilated cardiomyopathy.Results: Linear regression analyses of changes in ECG data with the weight gain of patients with AN and the intercorrelations of the three ECG systems in the various patient subgroups were found to be statistically significant at p = 0.0005 and r values ranging from 0.61 to 0.99, which are suggestive of good/excellent correlations. However, regression analyses of peak weight (PW) gain with changes in the 2-lead ECG (r = 0.43; p = 0.02) and 6-lead ECG (r = 0.48; p = 0.01), and half of PW gain and 12-lead ECG (r = 0.41; p = 0.03), 6-lead ECG (r= 0.18; p = 0.35), and 2-lead ECG (r = 0.43; p = 0.02) revealed poor correlations.Conclusion: ECG systems, comprising 2 or 6 leads, can be substituted for the 12-lead ECG for certain clinical and research applications (pertaining to the amplitude of QRS complexes), attesting to the inherent redundancy of the information from the 12-lead ECG. [ABSTRACT FROM AUTHOR]

We describe two patients with posterior myocardial infarction (PMI) with unusually atypical clinical presentations and cardiac enzymatic profiles, but with the abrupt development of complete AV block in patient 1, and Mobitz II second-degree AV block with paroxysmal phases of higher degrees of AV block in patient 2, and mitral regurgitation leading to symptomatic pulmonary congestion. Also, both patients had complete right bundle-branch block (RBBB) [old in patient 1, new in patient 2], the pattern of which was altered due to the associated PMI. The alteration included tall R waves involving the early part of the QRS complex, and tall T waves, both noted in the right precordial leads. The mechanism of these ECG modulations of the RBBB pattern was believed to be a superimposition of the early depolarization and repolarization consequences of the PMI. The significance of this observation lies in the ECG detection of PMI, frequently underdiagnosed particularly in patients with an atypical presentation, and with the RBBB adding further to the complexity. Thus, it is gratifying to note the contribution of the ECG to diagnostics, the only modality that provided a pathophysiologic insight in these two patients who appeared to be abruptly deteriorating clinically without an apparent reason. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To establish whether hypomagnesemia at admission predicts excessive morbidity, particularly cardiac arrhythmias, and mortality in patients with acute myocardial infarction. METHODS: We compared hypomagnesemic and normomagnesemic patients with acute myocardial infarction in 517 patients admitted to the coronary care unit. The serum magnesium concentration, along with a large array of other parameters, was measured on admission to the emergency department. Other baseline attributes and variables related to the patients' hospital course were used to compare the 2 groups. RESULTS: The 132 patients (25.9%) with low serum magnesium concentrations at admission (mean +/- SD, 0.61 +/- 0.06 mmol/L [1.48 +/- 0.15 mg/dL]) were comparable to the patients with normal serum magnesium concentrations (0.81 +/- 0.11 mmol/L [1.96 +/- 0.26 mg/dL]) except for a higher rate of prehospital use of diuretic agents (32.6% vs 22.5%, P = .02) and earlier presentation after onset of symptoms (mean +/- SD, 3.2 +/- 4.1 vs 4.8 +/- 6.6 hours, P = .003). There was no correlation between serum magnesium and potassium concentrations in the emergency department (r = 0.14). No difference was detected between the hypomagnesemic and normomagnesemic cohorts in rates of total mortality (18.9% vs 18.5%, P = .91), cardiac mortality (15.2% vs 15.3%, P = .99), atrial fibrillation (13.6% vs 13.8%, P = .97), ventricular tachycardia (18.2% vs 15.3%, P = .44), or ventricular fibrillation (15.2% vs 13.5%, P = .63). Management of the 2 cohorts was not different, except for higher rates of use of magnesium (17.4% vs 1.3%, P < .001) and potassium (59.8% vs 42.1%, P < .001) supplements and antiarrhythmic drugs (62.9% vs 48.7%, P = .005) in the hypomagnesemic patients. An endogenous rise in serum magnesium level was documented in a subgroup of 161 patients who had a repeated measurement (0.74 +/- 0.12 mmol/L [1.79 +/- 0.29 mg/dL] in the emergency department vs 0.77 +/- 0.09 mmol/L [1.88 +/- 0.23 mg/dL] in the coronary care unit, P < .001). CONCLUSIONS: We conclude that hypomagnesemia is seen in approximately one fourth of patients with myocardial infarction, is not linked to hypokalemia, has some relationship to preadmission use of diuretic agents, is associated with early presentation to the hospital, and is not a predictor of increased morbidity or mortality. [ABSTRACT FROM AUTHOR]

There is recent evidence that anasarca peripheral edema, irrespective of its etiology, attenuates ECG QRS potentials. Pulmonary edema (PE) also is thought to cause reduction in the amplitude of QRS complexes. The case reported herein is of a patient with severe PE, hypertension, left ventricular diastolic dysfunction, and no peripheral edema who did not show changes in the QRS complexes with the management of her pulmonary edema. Thus it appears that PE does not attenuate the amplitude of QRS complexes, and alleviation of this condition does not cause augmentation of QRS voltage. This is in contrast to alterations of peripheral edematous states in the setting of congestive heart failure, which result in changes in the QRS amplitude, as shown previously. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article titled "Dynamic Left Ventricular Outflow Tract Obstruction in Apical Ballooning Syndrome (Takotsubo Cardiomyopathy)" by J. Liang, C. Janish, K. Bishu, and G. Reeder published in the May 21, 2014 issue of "Perfusion."