Chronic Left-sided Heart Failure Research Articles

Pressure Volume Loop Analysis of the Right Ventricle in Heart Failure With Computed Tomography.

Right ventricular (RV) function is an important marker of mortality in chronic left-sided heart failure. Right ventricular function is particularly important for patients receiving left ventricular assist devices as it is a predictor of postoperative RV failure. RV stroke work index (RVSWI), the area enclosed by a pressure-volume (PV) loop, is prognostic of RV failure. However, clinical RVSWI approximates RVSWI as the product of thermodilution-derived stroke volume and the pulmonary pressure gradient. This ignores the energetic contribution of regurgitant flow and does not allow for advanced energetic measures, such as pressure-volume area and efficiency. Estimating RVSWI from forward flow may underestimate the underlying RV function. We created single-beat PV loops by combining data from cine computed tomography (CT) and right heart catheterization in 44 heart failure patients, tested the approximations made by clinical RVSWI and found it to underestimate PV loop RVSWI, primarily due to regurgitant flow in tricuspid regurgitation. The ability of RVSWI to predict post-operative RV failure improved when the single-beat approach was used. Further, RV pressure-volume area and efficiency measures were obtained and show broad agreement with other functional measures. Future work is needed to investigate the utility of these PV metrics in a clinical setting.

When Pulmonary Hypertension Complicates Heart Failure.

Pulmonary hypertension (PH) often complicates chronic left-sided heart failure, with a remarkable impact on quality of life, exercise capacity, and survival. PH in chronic left-sided heart failure (PH-LHD) is not only caused by backward transmission of pressures but also involves impairment of atrial function, inflammation, and vasoconstriction. Once the left atrium loses its reservoir capacity, usually pulmonary vascular resistances increase. Right atrial dilation commonly represents the first sign of PH-LHD, before right ventricle dilatation and systolic dysfunction develop, leading to right heart insufficiency, and ultimately, right heart failure.

THE EFFECT OF SPIRONOLACTONE ON SERUM ELECTROLYTES AND RENAL FUNCTION TESTS IN PATIENTS WITH SEVERE CHRONIC HEART FAILURE

The aim: To evaluate the effect of single daily 25 mg of spironolactone on serum electrolytes and kidney function tests in patients with severe chronic left sided heart failure. Materials and methods: 60 patients with severe chronic left sided heart failure were enrolled in this study and they were divided in to 2 equal groups’ one group with standard therapy of HF and the other with spironolactone in a dose of 25 mg / day, as an additive therapy to the standard one. Serum electrolytes and kidney function tests were assessed at the beginning of the study and after 3 months. Results: A significant increment in serum potassium (p<0.05) was observed in the spironolactone group after 3 months treatment, while no significant reduction in serum sodium (p>0.05) and no significant increase in serum creatinine and blood urea (p>0.05) was noticed in the same group, control group showed no significant changes (p>0.05), in both serum electrolytes (S.K and S.Na) and renal function tests (S.C and B.U). Conclusions: Spironolactone caused a significant elevation of serum potassium level but this elevation is still with the clinically accepted ranges when low dose of spironolactone is used and with intact renal function. Serum creatinine level was not significantly increased with 25 mgl day of spironolactone. We conclude that Renal function tests namely blood urea and serum Creatinine, and serum potassium should be closely monitored in patients on spironolactone therapy especially those patients who use ACEI and ARBs in addition.

Nocturnal Hypoxemia, But Not Sleep Apnea, Is Associated With a Poor Prognosis in Patients With Pulmonary Arterial Hypertension

Sleep apnea (SA) can cause repeated nocturnal arterial oxygen desaturation and result in acute increase in pulmonary arterial pressure (PAP). The presence of SA is associated with a poor prognosis in patients with chronic left-sided heart failure, but little is known for patients with pulmonary arterial hypertension (PAH). Methods and Results: We enrolled 151 patients with PAH (44±16 years old, male/female=37/114). They were all in the Nice Classification group 1 (idiopathic PAH/associated PAH=52/48%, mean PAP of 46±16 mmHg). They underwent right-heart catheterization and a sleep study with simplified polysomnography. Averaged percutaneous oxygen saturation (SpO2) during sleep was measured and an apnea-hypopnea index >5 was defined as SA. SA was noted in 58 patients (obstructive SA/central SA: 29/29). Over an average follow-up of 1,170±763 days, 32 patients died. By Kaplan-Meier analysis, there was no significant difference in deaths of patients with and without SA (χ2=2.82, P=0.093). On the other hand, the mortality in patients with lower averaged SpO2 was significantly higher than in those with higher averaged SpO2 (χ2=14.7, P<0.001) and that was the only independent variable related to death in multivariate Cox proportional hazards analysis. SA in patients with PAH was not associated with worse prognosis, unlike left ventricular heart failure, but nocturnal hypoxemia was related to poor prognosis.

Assessment of right ventricular function by echocardiography in patients with chronic heart failure.

BackgroundThe main focus of most of the studies in heart failure (HF) is the assessment of the left ventricular functions, while the right ventricle was much less studied. Much of this neglect is due to the complexity of anatomy and physiology of the right ventricle which are considered challenges during assessment of RV.Objective[1] To review the alterations of right ventricular dimensions & function associated with chronic heart failure. [2] To predict the prevalence of right ventricular systolic dysfunction in patients with chronic heart failure, based on echocardiographic parameters.Methods100 chronic left sided heart failure patients with LVEF less than 40% were evaluated in Ain Shams University hospitals from April 2015 to March 2016. All patients were subjected to full history taking & clinical evaluation. ECG was done mainly to exclude presence of ischemic heart disease. Complete trans-thoracic echocardiography study was done for assessment of [B] Left ventricular dimensions, systolic and diastolic functions [B] Assessment of the right side of the heart: [1] Measurement of the right ventricular dimensions [basal – mid cavity and the longitudinal diameters]. [2] Right ventricular area and calculation of the fractional area change (FAC). [3] Tricuspid annular plane systolic excursion (TAPSE). [4] Tissue Doppler derived tricuspid lateral annular systolic velocity (S′ wave velocity). [5] Tissue Doppler derived Myocardial Performance Index (MPI) (Tei index). [6] Grading of tricuspid regurgitation severity, and assessment of right ventricular systolic pressure.ResultsRight ventricle was dilated at the basal level in 36% of the studied patients & at the mid cavity level in 23% of the patients. Longitudinal RV diameter was enlarged in 20% of the patients.Right ventricular systolic dysfunction was found in 36% of patients with DCM in the current study. Patients who had right ventricular systolic dysfunction had significantly higher incidence of elevated JVP, significantly lower EF and significantly higher grade of LV Diastolic dysfunction. They showed significantly larger RV dimensions at different levels, significantly worse degree of TR and significantly higher mean value of RVSP.ConclusionsThe occurrence of right ventricular systolic dysfunction in patients with DCM is common [Approaching 40% in this study] and is independent of age and sex, and is proportionate to the degree of LV dilatation, and EF impairment.

Right Ventricular Function in Cardiovascular Disease, Part II

Right ventricular (RV) function may be impaired in pulmonary hypertension (PH), congenital heart disease (CHD), and coronary artery disease and in patients with left-sided heart failure (HF) or valvular heart disease. In recent years, many studies have demonstrated the prognostic value of RV function in cardiovascular disease. In the past, however, the importance of RV function has been underestimated. This perception originated from studies on open-pericardium dog models and from the observation that patients may survive without a functional subpulmonary RV (Fontan procedure). In the 1940s, studies using open-pericardium dog models showed that cauterization of the RV lateral wall did not result in a decrease in cardiac output or an increase in systemic venous pressure.1–3 As was later demonstrated, the open-pericardium model did not take into account the complex nature of ventricular interaction. In 1982, Goldstein and colleagues2 showed that RV myocardial infarction (RVMI) in a closed-chest dog model led to significant hemodynamic compromise. These findings were further supported by clinical studies demonstrating an increased risk of death, arrhythmia, and shock in patients with RVMI.4 The study of the RV is a relatively young field. In 2006, the National Heart, Lung, and Blood Institute identified RV physiology as a priority in cardiovascular research.5 The goal of this review is to present a clinical perspective on RV physiology and pathobiology. In the first article of the series, the anatomy, physiology, embryology, and assessment of the RV were discussed. In this second part, we discuss the pathophysiology, clinical importance, and management of RV failure. RV failure is a complex clinical syndrome that can result from any structural or functional cardiovascular disorder that impairs the ability of the RV to fill or to eject blood. The cardinal clinical manifestations of RV failure are (1) fluid retention, which may lead …

Plasma atrial natriuretic polypeptide as an index of left ventricular end-diastolic pressure in patients with chronic left-sided heart failure

To evaluate the relationship between plasma atrial natriuretic polypeptide (ANP), hemodynamic parameters, and plasma catecholamines and, in addition, to determine whether circulating ANP is metabolized in the pulmonary circulation, plasma concentrations of ANP were determined in 40 patients with chronic left-sided heart failure. After at least 30 minutes of bed rest with the patient in the supine position, blood samples were drawn simultaneously from both the main pulmonary artery (mPA) and the ascending aorta (Ao) before administration of contrast medium. The plasma ANP concentrations significantly decreased from the mPA to the Ao (135.3 ± 18.1 pg/ml vs 127.4 ± 19.4 pg/ml; mean ± SEM, p < 0.05). The plasma ANP level in the mPA correlated with the plasma norepinephrine level in the Ao ( r = 0.71, p < 0.01), right atrial pressure ( r = 0.34, p < 0.05), mean pulmonary capillary wedge pressure ( r = 0.829, p < 0.001), and left ventricular end-diastolic pressure (LVEDP) ( r = 0.88, p < 0.001). Of the various hemodynamic parameters and plasma catecholamine concentrations in the Ao, only LVEDP was found to be an independent and significant predictor of plasma ANP levels in the mPA. These results indicate that ANP released from the heart is regulated mainly by preload (LVEDP) in cases of left-sided heart failure and that circulating ANP is metabolized in the pulmonary circulation. In conclusion, the plasma ANP concentration may be a useful noninvasive index of LVEDP in patients with chronic left-sided heart failure.

Bronchoalveolar lavage cellular analysis and gallium lung scan in the assessment of patients with amiodarone-induced pneumonitis.

Seven patients suffering from amiodarone-induced pneumonitis were followed after diagnosis over a period of 16 +/- 6 months. All of them showed clinical, radiographic and functional manifestations of interstitial lung disease. Bronchoalveolar lavage was performed on 6 of them and disclosed lymphocytosis in 2 cases (associated to eosinophilia in 1 of them), neutrophilia in 1 and normal differential count in 2. In 1 case there were abundant hemosiderin-laden macrophages. In addition, all patients evidenced an increased 67Ga lung scan uptake. After discontinuation of amiodarone therapy (with or without corticosteroid therapy), 67Ga lung uptake normalized in 3 cases, but remained increased in 3. Bronchoalveolar lavage was repeated only in 2 cases, showing disappearance of lymphocytosis in one and abundant hemosiderin-laden macrophages in the other. Our results suggest that (1) hemosiderin-laden macrophages can be found in bronchoalveolar lavage in patients with amiodarone-induced pneumonitis, probably related to subclinical chronic left-sided heart failure; (2) 67Ga lung scan appears to be a sensitive marker of amiodarone pneumonitis, although it can remain abnormal after pulmonary clinical, radiographic and functional normalization.