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John E. Madias - One of the best experts on this subject based on the ideXlab platform.
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The importance of the P-waves in the differentiation of attenuation of the QRS voltage due to pericardial effusion versus due to Peripheral Edema.
Journal of cardiac failure, 2008Co-Authors: John E. MadiasAbstract:Abstract Background The cases of the 3 patients reported herein show the role of the P-waves in the differential diagnosis of the attenuated voltage of QRS complexes from pericardial effusion (PEREF) and from those resulting from Peripheral Edema (PERED) of varying pathophysiologic etiology. Methods and Results Whereas the QRS complexes decrease similarly in these 2 conditions, the voltage of P-waves do not become attenuated in PEREF, but do so in PERED. The underlying mechanism preventing attenuation of the voltage of P-waves in PEREF is the lack of much fluid around the atria, particularly in the presence of less than massive PEREF (no local electrical short-circuiting influence), in contrast to the attenuating effect exerted to both ventricles and atria in patients with PERED, who as a result, show parallel decrease in the voltage of QRS complexes and P-waves. Conclusion Attenuation of the amplitude of the electrocardiogram QRS complexes occurs in both patients with PEREF and PERED; however, attenuation of the amplitude of the P-waves is seen only in patients with PERED, and this observation is useful in the differential diagnosis of these 2 clinical conditions.
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P-wave duration and dispersion in patients with Peripheral Edema and its amelioration.
Indian pacing and electrophysiology journal, 2007Co-Authors: John E. MadiasAbstract:BACKGROUND Attenuation of the P-wave amplitudes in patients with Peripheral Edema (PERED) has been recently reported, with P-waves regaining some of their amplitude in patients, who subsequently experienced amelioration of their PERED. Changes in the P-waves correlated with the corresponding alterations in the QRS complexes. Also since amplitudes and durations of QRS complexes changed in parallel in patients with PERED, it was hypothesized that similar changes in the P-wave amplitudes, mean P-wave duration (P-du-mean), and P-wave dispersion (P-d), would occur in such patients. METHODS Measurements of P-wave amplitude, P-du-mean and P-d in patients who developed, or experienced alleviation, of PERED, were carried out and analyzed. RESULTS Although P-wave amplitudes and P-wave areas decreased with development of PERED (N = 16), and increased with its amelioration (N = 6), P-dur-mean before PERED was 66.8+/-14.5 ms, and at peak weight gain it was 65.2+/-11.9 ms, p = 0.66; also at peak weight gain and subsequent lowest weight, in the patients who lost weight, it was 66.5+/-9.9 ms and 72.3+/-12.0 ms, respectively, p = 0.38. Similarly the P-d prior to PERED was 62.3+/-25.2 ms, and at peak weight gain it was 74.3+/-29.3 ms, p = 0.09; also at peak weight and subsequent lowest weight, in the patients who lost weight, it was 58.8+/-34.2 ms, and 61.3+/-13.6 ms, respectively, p = 0.87. CONCLUSION P-du-mean and P-d did not change in patients who developed PERED; their stability is attributed to the offsetting of the electrophysiologically-mediated real changes, by opposite apparent changes, imparted by PERED.
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T-wave amplitude attenuation/augmentation in patients with changing Edematous states: implications for patients with congestive heart failure.
Congestive heart failure (Greenwich Conn.), 2007Co-Authors: John E. MadiasAbstract:Since Peripheral Edema impacts the entire electrocardiographic curve, it was hypothesized that it would also affect T waves. The amplitude of T waves were measured in all electrocardiographic leads and a sum (ΣT) was calculated in 28 patients with and 28 patients without Peripheral Edema (controls). For patients with Peripheral Edema, ΣT on admission was 21.9±10.6 mm and ΣT at peak weight was 8.3±6.3 mm (P=.0005). For patients with Peripheral Edema who subsequently lost weight, ΣT at peak weight was 7.2±6.1 mm and ΣT at the lowest weight was 14.1±12.2 (P=.006). For controls, ΣT from admission and ΣT from discharge were 24.4±16.9 mm and 24.7±15.7 mm (P=.82), respectively. Percent change (Δ%ΣT) from admission to peak weight correlated with Δ% in weight (r=0.58; P=.001) and Δ% in the sum of QRS complexes (ΣQRS) (r=0.71; P=.00005). Δ%ΣT from peak weight to the lowest weight correlated with the corresponding Δ%ΣQRS (r=0.65; P=.02). Changes in T waves with development and alleviation of Peripheral Edema mirror the changes shown by the QRS complexes and may be useful in the treatment of patients with congestive heart failure or other Edematous states.
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Increase in the QRS duration after amelioration of Peripheral Edema and after hemodialysis.
Congestive heart failure (Greenwich Conn.), 2006Co-Authors: John E. MadiasAbstract:Association among weights, amplitude of QRS complexes, and QRS duration in patients with Peripheral Edema has been described. This study explored whether increase in QRS duration occurs with amelioration of Peripheral Edema or after hemodialysis. Sums of the amplitudes of the 12 electrocardiographic leads and corresponding QRS duration were measured in 12 patients with Peripheral Edema before and after loss of weight, in 28 patients with a critical illness but without change in their weight ("controls"), and in 1 patient before and after hemodialysis. QRS duration increased from 90.1+/-25.0 milliseconds to 101.7+/-25.8 milliseconds (P=.001) in patients with Peripheral Edema, was unchanged in the controls, and increased from 87.8+/-5.9 milliseconds before to 92.7+/-6.7 milliseconds after hemodialysis (P=.007). It is proposed that these increases in QRS duration are only apparent (not electrophysiologically real), representing an extracardiac phenomenon mediated by alterations in the composite impedance of the passive body volume conductor, resulting in measurement of augmented QRS complexes after fluid removal. The clinical implications for patients with congestive heart failure are discussed.
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Reversible Attenuation of the ECG Voltage Due to Peripheral Edema Associated With Treatment With a COX‐2 Inhibitor
Congestive heart failure (Greenwich Conn.), 2006Co-Authors: John E. Madias, Nicolaos E. MadiasAbstract:A 74-year-old man developed Peripheral Edema as a side effect of the cyclooxygense-2 selective receptor inhibitor rofecoxib, which he had been taking for severe chronic arthritis. Discontinuation of rofecoxib led to augmentation of electrocardiographic (ECG) voltage and loss of weight gain (and reversibility of Peripheral Edema), which correlated well (r=0.82; p=0.0002). Other good correlations of the weight and other ECG variables and intercorrelations of ECG parameters underscore the multiple reversible influences Peripheral Edema has on the ECG. This case highlights an enhanced role of the ECG in monitoring patient therapy with other than strictly cardiovascular drugs. Recently, a syndrome pertaining to the influence of Peripheral Edema on the ECG was described; its mechanism is via the transforming effect of the body volume conductor on the surface transfer of the heart's potentials. The objective of this report is to describe a patient who developed Peripheral Edema as a side effect of a cyclooxygenase-2 selective receptor inhibitor.
Neil J. Douglas - One of the best experts on this subject based on the ideXlab platform.
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Peripheral Edema in the sleep apnea/hypopnea syndrome.
Sleep, 1991Co-Authors: K. F. Whyte, Neil J. DouglasAbstract:To clarify the roles of lung function, nocturnal hypoxemia and obesity in the development of Peripheral Edema in patients with the sleep apnea/hypopnea syndrome (SAHS), 65 consecutive SAHS patients had diagnostic sleep studies and respiratory function testing. Eighteen patients (27%) had Peripheral Edema without other explanation. Their sleep apnea/hypopnea index was similar to those without Edema, but they were more obese (p less than 0.01) and had worse lung function (p less than 0.01) and lower oxygen saturation (SaO2) awake (p less than 0.01). These 18 became more hypoxemic during sleep than predicted from their awake SaO2 (p less than 0.005). Eleven patients with Edema had evidence of pulmonary hypertension on cardiac catheterization, chest radiograph, or electrocardiograph and could be weight matched to 11 SAHS patients without Edema. Those with right heart failure were more hypoxic (p less than 0.01) when awake, desaturated more frequently during sleep (p less than 0.01), and had lower FEV1% predicted (p less than 0.01). Thus, extent of both daytime and nighttime hypoxemia are important in the development of right heart failure in patients with SAHS.
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Peripheral Edema in the sleep apnea hypopnea syndrome
Sleep, 1991Co-Authors: K. F. Whyte, Neil J. DouglasAbstract:To clarify the roles of lung function, nocturnal hypoxemia and obesity in the development of Peripheral Edema in patients with the sleep apnea/hypopnea syndrome (SAHS), 65 consecutive SAHS patients had diagnostic sleep studies and respiratory function testing. Eighteen patients (27%) had Peripheral Edema without other explanation. Their sleep apnea/hypopnea index was similar to those without Edema, but they were more obese (p less than 0.01) and had worse lung function (p less than 0.01) and lower oxygen saturation (SaO2) awake (p less than 0.01). These 18 became more hypoxemic during sleep than predicted from their awake SaO2 (p less than 0.005). Eleven patients with Edema had evidence of pulmonary hypertension on cardiac catheterization, chest radiograph, or electrocardiograph and could be weight matched to 11 SAHS patients without Edema. Those with right heart failure were more hypoxic (p less than 0.01) when awake, desaturated more frequently during sleep (p less than 0.01), and had lower FEV1% predicted (p less than 0.01). Thus, extent of both daytime and nighttime hypoxemia are important in the development of right heart failure in patients with SAHS.
K. F. Whyte - One of the best experts on this subject based on the ideXlab platform.
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Peripheral Edema in the sleep apnea/hypopnea syndrome.
Sleep, 1991Co-Authors: K. F. Whyte, Neil J. DouglasAbstract:To clarify the roles of lung function, nocturnal hypoxemia and obesity in the development of Peripheral Edema in patients with the sleep apnea/hypopnea syndrome (SAHS), 65 consecutive SAHS patients had diagnostic sleep studies and respiratory function testing. Eighteen patients (27%) had Peripheral Edema without other explanation. Their sleep apnea/hypopnea index was similar to those without Edema, but they were more obese (p less than 0.01) and had worse lung function (p less than 0.01) and lower oxygen saturation (SaO2) awake (p less than 0.01). These 18 became more hypoxemic during sleep than predicted from their awake SaO2 (p less than 0.005). Eleven patients with Edema had evidence of pulmonary hypertension on cardiac catheterization, chest radiograph, or electrocardiograph and could be weight matched to 11 SAHS patients without Edema. Those with right heart failure were more hypoxic (p less than 0.01) when awake, desaturated more frequently during sleep (p less than 0.01), and had lower FEV1% predicted (p less than 0.01). Thus, extent of both daytime and nighttime hypoxemia are important in the development of right heart failure in patients with SAHS.
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Peripheral Edema in the sleep apnea hypopnea syndrome
Sleep, 1991Co-Authors: K. F. Whyte, Neil J. DouglasAbstract:To clarify the roles of lung function, nocturnal hypoxemia and obesity in the development of Peripheral Edema in patients with the sleep apnea/hypopnea syndrome (SAHS), 65 consecutive SAHS patients had diagnostic sleep studies and respiratory function testing. Eighteen patients (27%) had Peripheral Edema without other explanation. Their sleep apnea/hypopnea index was similar to those without Edema, but they were more obese (p less than 0.01) and had worse lung function (p less than 0.01) and lower oxygen saturation (SaO2) awake (p less than 0.01). These 18 became more hypoxemic during sleep than predicted from their awake SaO2 (p less than 0.005). Eleven patients with Edema had evidence of pulmonary hypertension on cardiac catheterization, chest radiograph, or electrocardiograph and could be weight matched to 11 SAHS patients without Edema. Those with right heart failure were more hypoxic (p less than 0.01) when awake, desaturated more frequently during sleep (p less than 0.01), and had lower FEV1% predicted (p less than 0.01). Thus, extent of both daytime and nighttime hypoxemia are important in the development of right heart failure in patients with SAHS.
Robert R. Henry - One of the best experts on this subject based on the ideXlab platform.
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thiazolidinediones Peripheral Edema and type 2 diabetes incidence pathophysiology and clinical implications
Endocrine Practice, 2003Co-Authors: Face Sunder Mudaliar, Anna R. Chang, Robert R. HenryAbstract:ABSTRACT Objective: To present an objective, evidence-based review of Edema associated with thiazolidinedione use in patients with type 2 diabetes. Methods: We review the incidence, pathophysiology, and clinical significance of Edema associated with the use of thiazolidinediones, with specific emphasis on the two currently available thiazolidinediones, rosiglitazone and pioglitazone. Results: Both pioglitazone and rosiglitazone have been associated with increased development of Edema in clinical trials. The incidence of Edema in these trials varies from about 3.0 to 7.5% with the thiazolidinediones compared with 1.0 to 2.5% with placebo or other oral antidiabetic therapy. The highest incidence of Edema has been reported when thiazolidinediones are used in combination with insulin. In clinical studies, these patients have an incidence of Edema of 15.3% when treated with insulin plus pioglitazone and 14.7% when treated with insulin plus rosiglitazone (compared with 7.0% and 5.4% in the insulin-only groups, respectively). In addition to Peripheral Edema, reports have described pulmonary Edema associated with thiazolidinedione therapy. In all such reports, patients failed to respond to diuretics during use of thiazolidinediones. Clinical improvement ensued only after discontinuation of thiazolidinedione therapy. Therefore, thiazolidinediones either may have some effect on the delivery of diuretics to the lumen of the nephron or may induce tubular alterations that impair the ability of the nephrons to respond to diuretics. Several potential causes have been postulated to precipitate Edema in patients with diabetes who are treated with these agents: increased plasma volume, increased renal sodium reabsorption, reflex sympathetic activation, alteration of intestinal ion transport, and increased production of vascular endothelial growth factor. Conclusion: Available evidence suggests that Edema is a class effect of the thiazolidinediones and is multifactorial in origin. Thiazolidinedione-associated Edema seems to be dose related and occurs most frequently when thiazolidinediones are used in combination with insulin. Hence, therapy with these agents should be initiated at low doses, and patients should undergo assessment for Edema and congestive heart failure during the first few weeks of treatment. Caution should be exercised when thiazolidine- diones are used in those at risk for or with a history of heart failure. Options for management thiazolidinedione- associated Edema include dose reduction, drug discontinuation, and symptomatic therapy with diuretics. Further studies are needed to elucidate the mechanisms responsible for the cause of Edema in patients with type 2 diabetes treated with thiazolidinediones and to determine whether certain factors might predict susceptibility to development of Edema and congestive heart failure. (Endocr Pract. 2003;9:406-416)
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Thiazolidinediones, Peripheral Edema, and type 2 diabetes: incidence, pathophysiology, and clinical implications.
Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists, 2003Co-Authors: Face Sunder Mudaliar, Anna R. Chang, Robert R. HenryAbstract:OBJECTIVE To present an objective, evidence-based review of Edema associated with thiazolidinedione use in patients with type 2 diabetes. METHODS We review the incidence, pathophysiology, and clinical significance of Edema associated with the use of thiazolidinediones, with specific emphasis on the two currently available thiazolidinediones, rosiglitazone and pioglitazone. RESULTS Both pioglitazone and rosiglitazone have been associated with increased development of Edema in clinical trials. The incidence of Edema in these trials varies from about 3.0 to 7.5% with the thiazolidinediones compared with 1.0 to 2.5% with placebo or other oral antidiabetic therapy. The highest incidence of Edema has been reported when thiazolidinediones are used in combination with insulin. In clinical studies, these patients have an incidence of Edema of 15.3% when treated with insulin plus pioglitazone and 14.7% when treated with insulin plus rosiglitazone (compared with 7.0% and 5.4% in the insulin-only groups, respectively). In addition to Peripheral Edema, reports have described pulmonary Edema associated with thiazolidinedione therapy. In all such reports, patients failed to respond to diuretics during use of thiazolidinediones. Clinical improvement ensued only after discontinuation of thiazolidinedione therapy. Therefore, thiazolidinediones either may have some effect on the delivery of diuretics to the lumen of the nephron or may induce tubular alterations that impair the ability of the nephrons to respond to diuretics. Several potential causes have been postulated to precipitate Edema in patients with diabetes who are treated with these agents: increased plasma volume, increased renal sodium reabsorption, reflex sympathetic activation, alteration of intestinal ion transport, and increased production of vascular endothelial growth factor. CONCLUSION Available evidence suggests that Edema is a class effect of the thiazolidinediones and is multifactorial in origin. Thiazolidinedione-associated Edema seems to be dose related and occurs most frequently when thiazolidinediones are used in combination with insulin. Hence, therapy with these agents should be initiated at low doses, and patients should undergo assessment for Edema and congestive heart failure during the first few weeks of treatment. Caution should be exercised when thiazolidine-diones are used in those at risk for or with a history of heart failure. Options for management thiazolidinedione-associated Edema include dose reduction, drug discontinuation, and symptomatic therapy with diuretics. Further studies are needed to elucidate the mechanisms responsible for the cause of Edema in patients with type 2 diabetes treated with thiazolidinediones and to determine whether certain factors might predict susceptibility to development of Edema and congestive heart failure.
Gerasimos Filippatos - One of the best experts on this subject based on the ideXlab platform.
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Effects of serelaxin on the outcome of patients with or without substantial Peripheral Edema: A subgroup analysis from the RELAX-AHF trial.
American heart journal, 2017Co-Authors: Claudio Gimpelewicz, Marco Metra, John G.f. Cleland, Peter Szecsödy, Chuan Chuan Chang Wun, Leandro Boer-martins, Gad Cotter, Beth A. Davison, G.m. Felker, Gerasimos FilippatosAbstract:Background Acute heart failure (AHF) is a heterogeneous disorder, with most of the patients presenting with breathlessness along with varying degrees of Peripheral Edema. The presence of Peripheral Edema suggests that volume overload is the cause of decompensation leading to AHF, whereas breathlessness in the absence of Edema may reflect a “vascular phenotype.” This analysis investigated the characteristics, therapeutic response, and outcome of patients with AHF, with and without overt Peripheral Edema in the RELAX-AHF trial. Methods Physician-assessed Edema scores at baseline were used to categorize the population into those with no/mild Edema (score 0 or 1+) and moderate/severe Edema (score 2+ or 3+). The effect of serelaxin vs placebo was assessed within each subgroup. Results Patients with moderate/severe Edema (n = 583; 50.5%) were more likely to have severe dyspnea, orthopnea (>30°), rales (≥1/3), and elevated jugular venous pressure (>6 cm) than the patients with little or no Peripheral Edema (n=571; 49.5%). The relative benefits of serelaxin in terms of reduction in breathlessness, lower diuretic requirements, decreased length of initial hospital stay and days in intensive care unit/cardiac care unit, and improved prognosis (180-day cardiovascular and all-cause mortality) were generally similar for patients with or without Peripheral Edema. However, because patients with moderate/severe Peripheral Edema had worse outcomes, the absolute benefit was generally greater than in patients with no/mild Edema. Conclusions Overall, patients with AHF and moderate/severe Peripheral Edema have a worse prognosis but appear to receive similar relative benefit and perhaps greater absolute benefit from serelaxin administration.
