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Introduction Arrhythmia‐induced cardiomyopathy (AIC) is an underrecognized condition resulting in left ventricular systolic dysfunction (LVSD) that is primarily caused by atrial fibrillation (AFib). The relationship between AIC, right ventricular (RV) function, and quality of life (QoL) has not been well studied. Methods We performed a post‐hoc analysis of our AIC trial in which we prospectively screened for patients with tachyarrhythmia and newly diagnosed, otherwise unexplained LVSD. Following rhythm restoration, patients were followed up at 2, 4, and 6 months. Only patients with persistent sinus rhythm were analyzed. RV function was assessed via echocardiography (tricuspid annular plane systolic excursion [TASPE] and fractional area change [FAC]) and QoL by the Minnesota Living with Heart Failure Questionnaire. Results Of a total of 50 patients recovering from LVSD, 41 were diagnosed with AIC and 9 with non‐AIC. Initially, RV function was reduced in the AIC group and recovered after rhythm restoration, whereas no relevant changes were noted in the non‐AIC group. QoL was reduced in both groups and also improved after rhythm restoration. Regression analysis identified low TAPSE as a predictive parameter for AIC diagnosis and worse QoL in AIC patients. Conclusion We demonstrated that RV function and QoL are impaired in patients with AIC. Six months after rhythm restoration, TAPSE may serve as an early indicator of AIC while also correlating with QoL. This underscores the importance of detailed echocardiographic evaluation with a focus on RV function in patients with concomitant tachyarrhythmia and LVSD. Initial tricuspid annular plane systolic excursion (TAPSE), quality of life (QoL) as measured by the Minnesota Living with Heart Failure Questionnaire and left ventricular ejection fraction (LVEF) during atrial fibrillation (AFib) or atrial flutter (AFlut) were reduced in patients with arrhythmia‐induced cardiomyopathy (AIC) compared with values at the end of 6 months of follow‐up in sinus rhythm. In this paper we show that low TAPSE (optimal cut‐off 18.5 mm) has good predictive power for the diagnosis of AIC and that a low quality of life is associated with low TAPSE. Values in red indicate the relative percent the baseline values were reduced compared with the post‐recovery measurement at the end of follow‐up.

BackgroundShort-term improvements in quality of life (QOL) have been reported in adult congenital heart disease patients with systemic right ventricle (sRV) failure after treatment with sacubitril/valsartan. This study aimed to evaluate the medium-term QOL changes in sRV failure patients treated with sacubitril/valsartan.MethodsIn this single-centre, prospective cohort study, patients with symptomatic sRV failure completed the Netherlands Organisation for Applied Scientific Research/Academic Hospital Leiden Questionnaire for Adult’s Health-Related Quality of Life (TAAQOL) at baseline and after starting treatment with sacubitril/valsartan. The TAAQOL was taken at structured outpatient follow-up moments after 6, 12, 24 and 36 months of treatment. Linear mixed effects models were used to evaluate the medium-term changes in 12 QOL domains.ResultsOf 40 sRV failure patients initiated on sacubitril/valsartan, 35 completed the titration phase, and 31 filled in a total of 98 TAAQOL questionnaires (response rate 77.5%). Significant improvements in gross motoric functioning (p=0.008), cognitive function (p=0.002), sleep (p=0.041), social functioning (p<0.001) and daily activities (p=0.001) were observed during follow-up. No significant changes were observed in fine motoric functioning, pain, sexuality, vitality, positive, depressive or aggressive emotions. Of interest, periods with restrictions relating to the COVID-19 pandemic did not significantly influence changes over time in any of the 12 QOL domains.ConclusionsSacubitril/valsartan treatment was associated with persistent medium-term QOL improvements in gross motoric functioning, cognitive function, sleep, social functioning and daily activities domains in sRV failure patients. Self-perceived QOL of sRV failure patients may be amenable to improvement with sacubitril/valsartan.

COPD, a systemic illness associated with the impairment of different organs, affects patient prognosis and quality of life. The aim of this study was to evaluate the association between right ventricle (RV) function, the BODE (body mass index, airflow obstruction, dyspnea, and exercise capacity) index (a multifunctional scale for the assessment of mortality risk), and quality of life in patients with COPD. A cross-sectional study was carried out in 107 outpatients presenting with stable COPD who underwent clinical assessment, spirometry, arterial blood gas analyses, a 6-minute walk test, electrocardiography, and echocardiogram and who responded to the Saint George's Respiratory Questionnaire (SGRQ). Among the study subjects, 53% (57/107) were males, and the mean age was 65.26±8.81 years. A positive correlation was observed between RV dysfunction measured by the myocardial performance index using tissue Doppler (MPIt) and the BODE index, even after adjustment for age and partial pressure of oxygen ( =0.47; <0.01). Patients with alterations in the MPIt had worse quality of life, and a statistically significant difference was found for different domains of the SGRQ. Patients with a normal MPIt had a mean total score of 46.2±18.6, whereas for those with MPIt alterations, the mean total score was 61.6±14.2 ( =0.005). These patients had a 1.49-fold increased risk of exhibiting SGRQ total score above the upper limit of the 95% CI ( =0.01). The findings of this study suggest that RV dysfunction as measured by the MPIt was associated with impairment in quality of life and a worse BODE index in COPD patients, irrespective of age and hypoxemia status.

Pulmonary embolism (PE) is caused by emboli, which have originated from venous thrombi, travelling to and occluding the arteries of the lung. PE is the most dangerous form of venous thromboembolism, and undiagnosed or untreated PE can be fatal. Acute PE is associated with right ventricular dysfunction, which can lead to arrhythmia, haemodynamic collapse and shock. Furthermore, individuals who survive PE can develop post-PE syndrome, which is characterized by chronic thrombotic remains in the pulmonary arteries, persistent right ventricular dysfunction, decreased quality of life and/or chronic functional limitations. Several important improvements have been made in the diagnostic and therapeutic management of acute PE in recent years, such as the introduction of a simplified diagnostic algorithm for suspected PE as well as phase III trials demonstrating the value of direct oral anticoagulants in acute and extended treatment of venous thromboembolism. Future research should aim to address novel treatment options (for example, fibrinolysis enhancers) and improved methods for predicting long-term complications and defining optimal anticoagulant therapy parameters in individual patients, and to gain a greater understanding of post-PE syndrome. Pulmonary embolism (PE) is a form of venous thromboembolism in which an embolus occludes pulmonary arteries. This Primer by Huisman and colleagues discusses the epidemiology, mechanisms, diagnosis and prevention of PE and describes patient management and quality of life.

Objective This study aims to examine the impact of chronic intermittent hypoxia on hearts in patients with obstructive sleep apnea (OSA). Methods Two hundred twenty patients were divided into groups based on (1) severity of the disease, (2) years of disease history, and (3) with or without secondary hypertension. All subjects underwent blood pressure measurements, polysomnogram monitoring, and cardiac Doppler ultrasound examinations. Results The left ventricular ejection fraction (LVEF), fractional shortening (FS), and the ratio of early to late diastolic filling (E/A) in patients with severe OSA were lower than in those with moderate OSA and in healthy controls. The inner diameters of the main pulmonary artery (inD of MPA), the inner diameters of the right cardiac ventricle (inD of RV), and the thickness of anterior wall of the right ventricle (TAW of RV) were increased in patients with severe OSA compared to those with moderate disease and worsened as a function of time with disease. The tissue Doppler imaging-derived Tei index and pulmonary artery systolic pressure were also increased along with the severity of OSA. LVEF and FS in patients who had suffered from OSA for >10 years were decreased compared with those suffering from OSA for a shorter time. LVEF and FS in patients with secondary hypertension were decreased significantly relative to non-hypertensive OSA patients and healthy controls. E/A was decreased in OSA patients whether they had secondary hypertension or not. Conclusion OSA affected the left ventricular diastolic function in the early stage of the disease. Extended exposure to OSA resulted in left ventricular dysfunction with increased hypertension. Right ventricle dysfunction and abnormalities became more severe as the disease progressed.

During the course of chronic obstructive pulmonary disease (COPD), pulmonary hypertension (PH) and right ventricular (RV) failure may develop due to elevated afterload of the RV. In those patients, exercise capacity is reduced due to pulmonary and cardiac limitations. We investigated relationships between serum N-terminal of proB-type natriuretic peptide (NT-proBNP) and RV functions with exercise capacity and quality of life in patients COPD. An observational case-control study was conducted. We enrolled 31 moderate and severe COPD patients, and 20 subjects without chronic diseases as control group. Parameters reflecting the right ventricular diastolic and systolic functions by echocardiography along with serum NT-proBNP levels were assessed. Cardiopulmonary exercise testing and Short Form-36 (SF-36) were applied. Serum NT-proBNP levels were higher in COPD patients than control group (p=0.003). Serum NT-proBNP level was found to be related with pulmonary arterial pressure. Serum NT-proBNP levels were negatively correlated with anaerobic threshold oxygen uptake (AT VO2) and peak oxygen uptake (PVO2) values. Early ventricular filling velocity (Em) was lower in COPD patients. Em wave was significantly correlated with O2 pulse. There was a positive relationship between tricuspid E/A ratio and VO2 value at AT. SF-36 domains of physical functioning, general health and role limitation due to physical disorder were significantly correlated with AT VO2, PVO2 and O2 pulse. Exercise limitation may be predicted by assessment of right ventricule functions and NT-proBNP levels and exercise limitation impairs quality of life in COPD patients.

Introduction In 70 consecutive male patients with obstructive sleep apnea (OSA) diagnosed at the Northport VA Medical Center Sleep Disorders Center, we have characterized the association between obesity, OSA, and pulmonary hypertension (PH). Materials and methods By including anthropometric, pulmonary function, and sleep study parameters in a multivariate logistic regression model, we found that a BMI of >40 kg/m 2 and the minimum oxygen saturation in non-rapid eye movement (NREM) sleep predicted the presence of pretibial edema in this sleep apnea population. We then characterized the hemodynamics of those OSA patients that had lower extremity edema. Twenty-nine of the 70 consecutive patients with sleep apnea (41%) had pretibial edema, and right heart catheterization data was obtained for 28 (97%) of these patients. Results and discussion Ninety-three percent (26/28) of the patients had right heart failure (mean RAP > 5 mm Hg; RAP range = 0–32 mmHg) and PH (PA mean ≥ 20 mm Hg) was present in 86% (24/28.) The OSA patients with lower extremity edema had an increased cardiac output (7.0 + 1.4 l/min) with a normal cardiac index (2.9 + 0.5 l/min/m 2 ) in the setting of an elevated pulmonary capillary wedge pressure (PCWP 17 ± 7 mmHg) and a normal pulmonary vascular resistance (122 + 70 dynes s cm −5 ). While PCWP, FEV 1 % predicted, and the minimum oxygen saturation in NREM sleep all independently predicted PH, PCWP was the most important predictor of PH. Conclusion We conclude that pulmonary hypertension is commonly seen in patients with OSA with pretibial edema and that pretibial edema is a highly specific sign of PH in OSA patients. Pulmonary hypertension appears to result from an elevated back pressure and diastolic dysfunction with contributions from lung function and nocturnal oxygen saturation.

Homocyst(e)ine injured vascular endothelium and modulated endothelial-dependent vascular function. Endothelium plays an analogous role in both the vessel and the endocardium. Therefore, we hypothesized that homocyst(e)ine modulated endocardial endothelium (EE) dependent cardiac function. The ex vivo cardiac rings from normal male Wistar-Kyoto rats were prepared. The contractile responses of left and right ventricular rings were measured in an isometric myobath, using different concentrations of CaCl 2 . The response was higher in the left ventricle than right ventricle and was elevated in endocardium without endothelium. The half effective concentration (EC 50 ) and maximum tension generated by homocyst(e)ine were 10 6 and 5-fold lower than endothelin (ET) and angiotensin II (AII), respectively. However, in endothelial-denuded endocardium, homocyst(e)ine response was significantly increased (p < 0.005, compared with intact endothelium) and equal to the response to ET and AII. To determine the physiological significance of ET, AII, homocyst(e)ine, and endothelial nitric oxide in EE function, cardiac rings were pretreated with AII (10 -10 M) or ET (10 -13 M) and then treated with homocyst(e)ine (10 -8 M). Results suggested that at these concentrations AII, ET, or homocyst(e)ine alone had no effect on cardiac contraction. However, in the presence of 10 -10 M AII or 10 -13 M ET, the cardiac contraction to homocyst(e)ine (10 -8 M) was significantly enhanced (p < 0.01, compared with without pretreatment) and further increased in the endocardium without endothelium. The pretreatment of cardiac ring with the inhibitor of nitric oxide, N ω -nitro-L-arginine methyl ester (L-NAME), increased contractile response to homocyst(e)ine. These results suggested that homocyst(e)ine impaired EE-dependent cardiac function and acted synergistically with AII and ET in enhancing the cardiac contraction.Key words: endocardial remodeling, homocyst(e)ine, contraction, endothelin, angiotensin, endothelial-derived relaxing factor (EDRF), N ω -nitro-L-arginine methyl ester (L-NAME), endothelial dysfunction, ex vivo cardiac function, heart failure.