Hypernatremia and intercalated disc edema synergistically exacerbate long-QT syndrome type 3 phenotype.

Cardiac voltage-gated sodium channel gain-of-function prolongs repolarization in the long-QT syndrome type 3 (LQT3). Previous studies suggest that narrowing the perinexus within the intercalated disc, leading to rapid sodium depletion, attenuates LQT3-associated action potential duration (APD) prolongation. However, it remains unknown whether extracellular sodium concentration modulates APD prolongation during sodium channel gain-of-function. We hypothesized that elevated extracellular sodium concentration and widened perinexus synergistically prolong APD in LQT3. LQT3 was induced with sea anemone toxin (ATXII) in Langendorff-perfused guinea pig hearts (n = 34). Sodium concentration was increased from 145 to 160 mM. Perinexal expansion was induced with mannitol or the sodium channel ß1-subunit adhesion domain antagonist (ßadp1). Epicardial ventricular action potentials were optically mapped. Individual and combined effects of varying clefts and sodium concentrations were simulated in a computational model. With ATXII, both mannitol and ßadp1 significantly widened the perinexus and prolonged APD, respectively. The elevated sodium concentration alone significantly prolonged APD as well. Importantly, the combination of elevated sodium concentration and perinexal widening synergistically prolonged APD. Computational modeling results were consistent with animal experiments. Concurrently elevating extracellular sodium and increasing intercalated disc edema prolongs repolarization more than the individual interventions alone in LQT3. This synergistic effect suggests an important clinical implication that hypernatremia in the presence of cardiac edema can markedly increase LQT3-associated APD prolongation. Therefore, to our knowledge, this is the first study to provide evidence of a tractable and effective strategy to mitigate LQT3 phenotype by means of managing sodium levels and preventing cardiac edema in patients.NEW & NOTEWORTHY This is the first study to demonstrate that the long-QT syndrome type 3 (LQT3) phenotype can be exacerbated or concealed by regulating extracellular sodium concentrations and/or the intercalated disc separation. The animal experiments and computational modeling in the current study reveal a critically important clinical implication: sodium dysregulation in the presence of edema within the intercalated disc can markedly increase the risk of arrhythmia in LQT3. These findings strongly suggest that maintaining extracellular sodium within normal physiological limits may be an effective and inexpensive therapeutic option for patients with congenital or acquired sodium channel gain-of-function diseases.

Case of type 2 diabetes mellitus with edema resulting in subcutaneous insulin resistance syndrome.

Subcutaneous insulin resistance syndrome caused by obesity, induration at the injection site, skin temperature and other factors is common clinically, whereas resistance events caused by edema are relatively rare. This article introduced a case of a woman with type 2 diabetes mellitus with heart failure edema. Her blood glucose control was significantly associated with the level of edema. Excluding other factors, it can be concluded that edema might lead to subcutaneous insulin resistance syndrome, even if the edema at the injection site is not obvious.

Predictive Factors for Failure of Noninvasive Ventilation in Adult Intensive Care Unit: A Retrospective Clinical Study.

Background: Noninvasive ventilation (NIV) has been reported to be beneficial for patients with acute respiratory failure in intensive care unit (ICU); however, factors that influence the clinical outcome of NIV were unclarified. We aim to determine the factors that predict the failure of NIV in critically ill patients with acute respiratory failure (ARF). Setting. Adult mixed ICU in a medical university affiliated hospital. Patients and Methods. A retrospective clinical study using data from critical adult patients with initial NIV admitted to ICU in the period August 2016 to November 2017. Failure of NIV was regarded as patients needing invasive ventilation. Logistic regression was employed to determine the risk factor(s) for NIV, and a predictive model for NIV outcome was set up using risk factors. Results: Of 101 included patients, 50 were unsuccessful. Although more than 20 variables were associated with NIV failure, multivariate logistic regression demonstrated that only ideal body weight (IBW) (OR 1.110 (95%1.027-1.201), P=0.009), the maximal heart rate during NIV period (HR-MAX) (OR 1.024 (1.004-1.046), P=0.021), the minimal respiratory rate during NIV period (RR-MIN) (OR 1.198(1.051-1.365), P=0.007), and the highest body temperature during NIV period (T-MAX) (OR 1.838(1.038-3.252), P=0.037) were independent risk factors for NIV failure. We set up a predictive model based on these independent risk factors, whose area under the receiver operating characteristic curve (AUROC) was 0.783 (95% CI: 0.676-0.899, P < 0.001), and the sensitivity and specificity of model were 68.75% and 71.43%, respectively, with the optimal cut-off value of 0.4863. Conclusion: IBW, HR-MAX, RR-MIN, and T-MAX were associated with NIV failure in patients with ARF. A predictive model based on the risk factors could help to discriminate patients who are vulnerable to NIV failure.

Lung Ultrasound for the Diagnosis and Management of Acute Respiratory Failure.

For critically ill patients with acute respiratory failure (ARF), lung ultrasound (LUS) has emerged as an indispensable tool to facilitate diagnosis and rapid therapeutic management. In ARF, there is now evidence to support the use of LUS to diagnose pneumothorax, acute respiratory distress syndrome, cardiogenic pulmonary edema, pneumonia, and acute pulmonary embolism. In addition, the utility of LUS has expanded in recent years to aid in the ongoing management of critically ill patients with ARF, providing guidance in volume status and fluid administration, titration of positive end-expiratory pressure, and ventilator liberation. The aims of this review are to examine the basic foundational concepts regarding the performance and interpretation of LUS, and to appraise the current literature supporting the use of this technique in the diagnosis and continued management of patients with ARF.

Prognostic value of decreased peripheral congestion detected by Bioelectrical Impedance Vector Analysis (BIVA) in patients hospitalized for acute heart failure: BIVA prognostic value in acute heart failure.

OBJECTIVES: The objective of this study was to investigate the prognostic role of quantitative reduction of congestion during hospitalization assessed by Bioelectrical Impedance Vector Analysis (BIVA) serial evaluations in patients admitted for acute heart failure (AHF). BACKGROUND: AHF is a frequent reason for patients to be admitted. Exacerbation of chronic heart failure is linked with a progressive worsening of the disease with increased incidence of death. Fluid overload is the main mechanism underlying acute decompensation in these patients. BIVA is a validated technique able to quantify fluid overload. METHODS: a prospective, multicentre, observational study in AHF and no AHF patients in three Emergency Departments centres in Italy. Clinical data and BIVA evaluations were performed at admission (t0) and discharge (tdis). A follow-up phone call was carried out at 90 days. RESULTS: Three hundred and thirty-six patients were enrolled (221 AHF and 115 no AHF patients). We found that clinical signs showed the most powerful prognostic relevance. In particular the presence of rales and lower limb oedema at tdis were linked with events relapse at 90 days. At t0, congestion detected by BIVA was observed only in the AHF group, and significantly decreased at tdis. An increase of resistance variation (dR/H) >11 Ω/m during hospitalization was associated with survival. BIVA showed significant results in predicting total events, both at t0 (area under the curve (AUC) 0.56, p<0.04) and at tdis (AUC 0.57, p<0.03). When combined with clinical signs, BIVA showed a very good predictive value for cardiovascular events at 90 days (AUC 0.97, p<0.0001). CONCLUSIONS: In AHF patients, an accurate physical examination evaluating the presence of rales and lower limbs oedema remains the cornerstone in the management of patients with AHF. A congestion reduction, obtained as a consequence of therapies and detected through BIVA analysis, with an increase of dR/H >11 Ω/m during hospitalization seems to be associated with increased 90 day survival in patients admitted for AHF.

Pedal Edema as an Indicator of Early Heart Failure in the Community: Prevalence and Associations With Cardiac Structure/Function and Natriuretic Peptides (MESA [Multiethnic Study of Atherosclerosis]).

BACKGROUND: The prevalence of pedal edema (PE) and its associations with abnormal cardiac structure/function, natriuretic peptides, and incident heart failure (HF) is unknown, especially in community-dwelling adults without a history of cardiovascular disease. METHODS AND RESULTS: Out of 5004 MESA (Multiethnic Study of Atherosclerosis) participants who had cardiac magnetic resonance imaging, 4196 had complete data and were included in this analysis (3501 for the right ventricle analysis). Logistic regression and Cox proportional hazard analyses were used to assess the associations among self-reported PE, 2-pillow orthopnea, paroxysmal nocturnal dyspnea, left and right ventricular structure and function, natriuretic peptide levels, and incident HF. PE was present in 28% of the participants. PE was not associated with overt left or right ventricular systolic dysfunction (ejection fraction <50%). PE was associated with 2-pillow orthopnea (odds ratio 1.66; 95% confidence interval [CI], 1.30-2.12), paroxysmal nocturnal dyspnea (odds ratio 1.95; 95% CI, 1.55-2.44), and abnormal N-terminal pro-B-type natriuretic peptide levels (defined as >400 pg/mL; odds ratio 1.80; 95% CI, 1.21-2.68) in adjusted models. After a mean of 10.2 years of follow-up, 184/4196 (4.4%) participants had an adjudicated incident HF hospitalization. PE was associated with incident HF hospitalization in models adjusted for age, sex, and race (hazard ratio 1.44; 95% CI, 1.05-1.97). This association persisted after adding additional covariates, including comorbidities, baseline left ventricular ejection fraction, and antecedent myocardial infarction (hazard ratio 1.43; 95% CI, 1.02-1.99). The association of PE with incident HF was attenuated by further adjustment for N-terminal pro-B-type natriuretic peptide. CONCLUSIONS: PE is prevalent in community-dwelling adults without clinically recognized cardiovascular disease and associated with future hospitalized HF.

Relationship between T-wave inversion and transmural myocardial edema as evidenced by cardiac magnetic resonance in patients with clinically suspected acute myocarditis: clinical and prognostic implications.

BACKGROUND: The pathophysiologic mechanisms and the prognostic meaning of electrocardiographic (ECG) T-wave inversion (TWI) occurring in a subgroup of patients with clinically suspected acute myocarditis remain to be elucidated. Contrast-enhanced cardiac magnetic resonance (CMR) offers the potential to identify myocardial tissue changes such as edema and/or fibrosis which may underlie TWI. METHODS AND RESULTS: We studied 76 consecutive patients (median age 34years) with clinically suspected acute myocarditis, using a comprehensive CMR protocol which included T2 weighted sequences for myocardial edema. At the time of CMR, TWI was observed in 21 (27%) patients. There was a statistically significant association of TWI with the median number of left ventricular (LV) segments showing both any pattern of myocardial edema (transmural and non-transmural) [5 (3-7) vs. 3 (2-4); p=0.015] and myocardial late-gadolinium-enhancement [4 (3-7) vs. 3 (2-4); p=0.002]. Transmural myocardial edema involving ≥2 LV segments was found in 17/21 (81%) patients with TWI versus 13/55 (24%) patients without TWI (p<0.001) and remained the only independent predictor of TWI at multivariable analysis (OR=9.96; 95%CI=2.71-36.6; p=0.001). Overall, topographic concordance between the location of TWI across the ECG leads and the regional distribution of transmural myocardial edema was 88%. There was no association between acute TWI and reduced LV ejection fraction (<55%) at 6-months of follow-up. CONCLUSIONS: This is the first study to demonstrate an association between LV transmural myocardial edema as evidenced by CMR sequences and TWI in clinically suspected acute myocarditis. As an expression of reversible myocardial edema, development of TWI during the acute disease phase was not a predictor of LV systolic dysfunction at follow-up.

A fast and effective method to assess myocardial hyperemia in acute myocarditis by magnetic resonance.

Current cardiac magnetic resonance (CMR) quantitative signs for the diagnosis of myocarditis include myocardial edema, fibrosis and myocardial hyperemia (Hyp). Methods for the assessment of Hyp are actually complex and time-consuming. To test a simple and fast method to assess Hyp, using contrast enhancement steady state free precession (ceSSFP) technique. CMR imaging at 1.5T was performed on 39 patients with diagnosis of acute myocarditis and in 20 healthy controls. Hyp was evaluated in systolic and diastolic frames (Hyp-SYS and Hyp-DIA) as areas of myocardial hyperintensity in ceSSFP images early after gadolinium injection. Myocardial edema was evaluated using T2-STIR images. Myocardial fibrosis was assessed in conventional late gadolinium enhancement (LGE) images. A value of ≤12.1 g of Hyp-DIA was obtained as cut-off of normality in healthy controls. Using this threshold, Hyp was detected in 30 patients (77 %) with myocarditis. LGE was detected in 36 patients (92 %), and myocardial edema in 38 (97 %) patients with myocarditis A linear relation was found between Hyp-DIA and the extent of myocardial edema (R(2) 0.48, 95 % CI 0.47-0.85, p < 0.001) and the extent of LGE (R(2) 0.41, 95 % CI 0.31-0.61, p < 0.001). Patients with hyperemia had higher levels of C-reactive protein (p < 0.001), a higher extent of LGE (p < 0.05) and a larger left atrial area (p < 0.05). ceSSFP sequence at CMR is a novel and fast method to assess myocardial hyperemia in patient with acute myocarditis. Compared with non-Hyp subjects, patients with Hyp had more signs of inflammation and myocardial damage.

[Changes of the hemodynamics, heart structure and functional state in patients with reactive arthritis].

Our investigation showed for the patients with reactive arthritis typical is hyperkinetic type of haemodynamic, and also structural changes of the heart which manifestate by interventricular partition's thickness as a result of inflammatory edema and it's valve consolidation frequently whithout expressed blood regurgitation, and diastolic dysfunction's development of the left and right heart ventricles in hypertrophic type with disorders of their active relaxation and growth their chamber's rigidity. These changes, probably, evidence about development of the inflammatory cardiopathy in these patients and can be preconditions of the heart failure.

Equal performance of novel N-terminal proBNP (Cardiac proBNP®) and established BNP (Triage BNP®) point-of-care tests.

BACKGROUND: Recently, a novel point-of-care test (POCT) for N-terminal proBNP (NTproBNP) has been introduced (Cardiac proBNP®, Roche). AIM: The aim was to compare the novel POCT for NTproBNP with the established POCT for BNP. METHODS: NTproBNP and BNP were assessed in 222 individuals with chronic heart failure (n = 151) or controls (n = 71) with both POCTs. RESULTS: NTproBNP and BNP were closely correlated upon regression analysis (r = 0.93; p < 0.01). NTproBNP and BNP were both correlated with ejection fraction and New York Heart Association stage. Receiver operating characteristic analysis yielded satisfying and equivalent predictive values for the detection of left ventricular dysfunction (ejection fraction <40%; NTproBNP: area under the curve 0.97; BNP: area under the curve 0.96; p > 0.05) and presence of New York Heart Association stage >2 (area under the curve 0.92 vs 0.91 for NT-proBNP and BNP, respectively; p > 0.05). CONCLUSION: The NTproBNP POCT allows biochemical detection of heart failure with satisfactory predictive values, is equivalent to the BNP POCT and will improve near-patient testing.

A CMR study of the effects of tissue edema and necrosis on left ventricular dyssynchrony in acute myocardial infarction: implications for cardiac resynchronization therapy.

BACKGROUND: In acute myocardial infarction (AMI), both tissue necrosis and edema are present and both might be implicated in the development of intraventricular dyssynchrony. However, their relative contribution to transient dyssynchrony is not known. Cardiovascular magnetic resonance (CMR) can detect necrosis and edema with high spatial resolution and it can quantify dyssynchrony by tagging techniques. METHODS: Patients with a first AMI underwent percutaneous coronary interventions (PCI) of the infarct-related artery within 24 h of onset of chest pain. Within 5-7 days after the event and at 4 months, CMR was performed. The CMR protocol included the evaluation of intraventricular dyssynchrony by applying a novel 3D-tagging sequence to the left ventricle (LV) yielding the CURE index (circumferential uniformity ratio estimate; 1 = complete synchrony). On T2-weighted images, edema was measured as high-signal (> 2 SD above remote tissue) along the LV mid-myocardial circumference on 3 short-axis images (% of circumference corresponding to the area-at-risk). In analogy, on late-gadolinium enhancement (LGE) images, necrosis was quantified manually as percentage of LV mid-myocardial circumference on 3 short-axis images. Necrosis was also quantified on LGE images covering the entire LV (expressed as % LV mass). Finally, salvaged myocardium was calculated as the area-at-risk minus necrosis (expressed as % of LV circumference). RESULTS: After successful PCI (n = 22, 2 female, mean age: 57 ± 12y), peak troponin T was 20 ± 36ug/l and the LV ejection fraction on CMR was 41 ± 8%. Necrosis mass was 30 ± 10% and CURE was 0.91 ± 0.05. Edema was measured as 58 ± 14% of the LV circumference. In the acute phase, the extent of edema correlated with dyssynchrony (r2 = -0.63, p < 0.01), while extent of necrosis showed borderline correlation (r2 = -0.19, p = 0.05). PCI resulted in salvaged myocardium of 27 ± 14%. LV dyssynchrony (=CURE) decreased at 4 months from 0.91 ± 0.05 to 0.94 ± 0.03 (p < 0.004, paired t-test). At 4 months, edema was absent and scar %LV slightly shrunk to 23.7 ± 10.0% (p < 0.002 vs baseline). Regression of LV dyssynchrony during the 4 months follow-up period was predicted by both, the extent of edema and its necrosis component in the acute phase. CONCLUSIONS: In the acute phase of infarction, LV dyssynchrony is closely related to the extent of edema, while necrosis is a poor predictor of acute LV dyssynchrony. Conversely, regression of intraventricular LV dyssynchrony during infarct healing is predicted by the extent of necrosis in the acute phase.

Impact of manual lymphatic drainage on hemodynamic parameters in patients with heart failure and lower limb edema.

Manual lymphatic drainage (MLD), intermittent sequential pneumatic therapy (ISPT), multilayered bandages (MLB), and compression garments are main techniques in conservative treatment of peripheral lymphedema. Since 1990, it has been thought that ISPT applied to both lower limbs simultaneously should not be used for patients with heart failure because right atrial, pulmonary arterial, and pulmonary wedge pressures may increase to a critical point. In 2005, these same results were observed in patients with heart failure wearing MLB. For these reasons, MLB and ISPT have been contraindicated during lymphedema treatment in cardiac patients. The aim of this study was to determine if we may continue the treatment of lower limb lymphedema using MLD in patients with heart failure. We evaluated hemodynamic parameters using echography during MLD in patients with cardiac disease and obtained circumferential measurements of the edematous limb before and after treatment. MLD treatment significantly decreased the limbs as expected. The heart rate also decreased following MLD in contrast with all other hemodynamic parameters which were not affected by MLD. The findings suggest that there is no contraindication to use MLD in patients with heart failure and lower limb edema.

Cardiac sarcoidosis complicated with atrioventricular block and wall thinning, edema and fibrosis in left ventricle: confirmed recovery to normal sinus rhythm and visualization of edema improvement by administration of predonisolone.

A 65 year-old female had a node of some kind in her right leg five years ago and was diagnosed with sarcoidosis by gallium scintigraphy. Serum angiotension-converting enzyme levels had gradually increased, and three months ago she felt palpitations and dizziness when standing. On electrocardiogram, 2:1 atrioventricular (AV) block was observed. On transthoracic echocardiogram, the basal portion of the interventricular septum (IVS) revealed wall thinning with dyskinetic motion and lack of systolic thickening, and low attenuation. The basal portion of the left ventricular (LV) posterior inferior wall revealed mild wall thickening with low attenuation. Enhanced multislice-CT revealed a thickened LV posterior wall and thinned basal portion of IVS with interstitial change suggesting presence of fibrosis or edema. Late enhancement was also observed in the basal portion of the LV posterior inferior wall and basal IVS in T1 weighted magnetic resonance imaging (MRI); in addition, an area, the center of which indicated low attenuation surrounded by high attenuation, was observed in the basal portion of the LV posterior inferior wall in T2 weighted MRI. Positron emission tomography (PET) imaging using F-18 fluoro-deoxyglucose with the subject fasted for 6 h beforehand, revealed strong uptake in the basal portion of IVS and a thickened LV posterior wall, suggesting the presence of inflammation. Administration of predonisolone was started before pacemaker implantation and clinical symptoms immediately disappeared; in addition AV block recovered to normal sinus rhythm. On a repeat MRI performed four months later, the late enhancement in T1 weighted MRI and the high attenuation surrounding low attenuation in the basal portion of the LV posterior inferior wall in T2 weighted MRI both disappeared, and we confirmed that temporary edema had also disappeared.

Relation between signal intensity on T2-weighted MR images and presence of microvascular obstruction in patients with acute myocardial infarction.

OBJECTIVE: In experimental animal models and human autopsy studies, hemorrhagic infarction caused by microvascular injury has been detected after coronary reperfusion. The purpose of this study was to determine whether detection of myocardial edema with T2-weighted MRI is influenced by the presence of microvascular obstruction. SUBJECTS AND METHODS: Thirty-seven patients underwent black-blood fat-suppressed T2-weighted, rest perfusion, and late gadolinium-enhanced MRI 5.4 +/- 3.1 days after the onset of acute myocardial infarction. On T2-weighted MR images, the signal intensity in relation to that of remote myocardium was determined in the late gadolinium-enhanced and periinfarction areas. Segment-based analysis was performed to determine whether the presence of microvascular obstruction influences the detection of myocardial edema. RESULTS: The averaged signal intensity in the late gadolinium-enhanced area without microvascular obstruction was significantly higher than the signal intensity in remote normal myocardium (relative signal intensity, 1.83 +/- 0.50; p < 0.001). In contrast, the signal intensity in the microvascular obstruction area on T2-weighted images was not significantly different from the signal intensity in remote myocardium (relative signal intensity, 1.14 +/- 0.26). The percentages of late gadolinium-enhanced segments with high signal intensity on T2-weighted MR images were 95% (73/77) without microvascular obstruction and 30% (22/73) with microvascular obstruction. CONCLUSION: With T2-weighted MRI, infarction-associated edema can be reliably detected in infarct lesions without microvascular obstruction. Microvascular obstruction, however, does not necessarily exhibit high signal intensity on T2-weighted MRI. Careful attention is required in interpretation of cardiac MR images of patients who have experienced acute myocardial infarction and undergone percutaneous coronary intervention. The findings on T2-weighted MR images can be substantial underestimates of the extent of acute myocardial infarction.

Dysfunction induced by ischemia versus edema: does edema matter?

OBJECTIVES: Recovery from pediatric cardiac surgery is affected by ischemia-reperfusion injury, cardiac edema, and in some cases a low cardiac output syndrome. Although association has been made between the development of edema and dysfunction, modeling is confounded by intercurrent injurious stimuli that also cause cardiac edema and dysfunction. We tested whether a true causal relationship exists between edema and cardiac dysfunction. METHODS: We induced either ischemia or edema alone in isolated cardiomyocytes and whole Langendorff-perfused hearts. Function was measured as shortening dynamics and developed pressure, respectively. RESULTS: Ischemic injury impaired function in both cardiomyocytes and whole hearts. Isolated cells showed significant reduction in peak shortening and departure and relaxation velocities. Whole hearts displayed severely reduced developed pressures. Hyposmotic solution forced cardiomyocytes to swell to 7% greater than their normal size. No significant effect on shortening was seen. Similarly, Langendorff-perfused hearts were induced to take on 3% more water than control-perfused hearts and 9% more water than nonperfused hearts. This additional water was associated with mild dysfunction. CONCLUSIONS: We demonstrate the capacity of the heart to tolerate edema greater than that seen in clinical settings without residual effect. Ischemia results in ongoing contractile dysfunction of both isolated cardiomyocytes and whole hearts. We conclude that dysfunction resulting from edema in ex vivo cardiac models is mild and suggest review of the importance given to edema-mediated dysfunction after cardiac surgery.

Mortality in acute cardiogenic pulmonary edema treated with continuous positive airway pressure.

OBJECTIVE: To investigate mortality in acute cardiogenic pulmonary edema (ACPE) patients treated with continuous positive airway pressure (CPAP) and to identify clinical and laboratory characteristics associated with mortality. DESIGN: Observational, retrospective study. SETTING: Emergency Medicine Department. PATIENTS AND PARTICIPANTS: A total of 454 consecutive ACPE patients treated with CPAP. MEASUREMENTS AND RESULTS: Demographics, past medical history, clinical characteristics, laboratory evaluation, in-hospital mortality data were collected. Potential predictors of in-hospital mortality that were considered of clinical relevance and immediately accessible on admission were investigated by multivariable logistic regression. ACPE-related mortality rate was 3.8% (17/452 patients) and the in-hospital mortality rate was 11.4% (50/440 patients). Significant independent predictors of increased risk of in-hospital mortality were: advanced age (P = 0.012), normal-to-low blood pressure (P < 0.001), low PaO(2)/FiO(2) ratio (P = 0.020), hypocapnia (P = 0.009) and anemia (P = 0.05). CONCLUSIONS: Values recorded within few minutes from arrival to the hospital can predict mortality in ACPE patients treated with CPAP who has been tested, for the first time, in a real life study. This can allow physicians to quickly recognize more severe ACPE patients treated with CPAP and plan for aggressive monitoring and treatment and for deciding the better site of care.

Platypnea-orthodeoxia syndrome associated with patent foramen ovale and aortic ectasia.

A 59-year-old man was admitted for dyspnea on exertion and edema. The patient did not have any pulmonary diseases that could cause dyspnea. Transesophageal echocardiography on the tilting bed with contrast infusion revealed a right-to-left shunt through the patent foramen ovale. Therefore, he was diagosed as platypnea-orthodeoxia syndrome due to the patent foramen ovale. Surgical closure was done and all of his symptoms had improved.

Mechanics of the left ventricular myocardial interstitium: effects of acute and chronic myocardial edema.

Myocardial interstitial edema forms as a result of several disease states and clinical interventions. Acute myocardial interstitial edema is associated with compromised systolic and diastolic cardiac function and increased stiffness of the left ventricular chamber. Formation of chronic myocardial interstitial edema results in deposition of interstitial collagen, which causes interstitial fibrosis. To assess the effect of myocardial interstitial edema on the mechanical properties of the left ventricle and the myocardial interstitium, we induced acute and chronic interstitial edema in dogs. Acute myocardial edema was generated by coronary sinus pressure elevation, while chronic myocardial edema was generated by chronic pulmonary artery banding. The pressure-volume relationships of the left ventricular myocardial interstitium and left ventricular chamber for control animals were compared with acutely and chronically edematous animals. Collagen content of nonedematous and chronically edematous animals was also compared. Generating acute myocardial interstitial edema resulted in decreased left ventricular chamber compliance compared with nonedematous animals. With chronic edema, the primary form of collagen changed from type I to III. Left ventricular chamber compliance in animals made chronically edematous was significantly higher than nonedematous animals. The change in primary collagen type secondary to chronic left ventricular myocardial interstitial edema provides direct evidence for structural remodeling. The resulting functional adaptation allows the chronically edematous heart to maintain left ventricular chamber compliance when challenged with acute edema, thus preserving cardiac function over a wide range of interstitial fluid pressures.