Diagnosis and long-term therapy of right-sided heart failure in a yellow-crowned amazon (Amazona ochrocephala).
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
AIMS: Transient systolic and diastolic abnormalities in ventricular function have previously been documented during endurance sports. However, these described alterations may be limited by the techniques applied. We sought, using less load-dependent methods, to characterize both the extent and the chronology of the cardiac changes associated with endurance events. METHODS AND RESULTS: Transthoracic echocardiography (TTE) was performed prior to, immediately after, and approximately 1 month after completion of the 2003 Boston Marathon in 20 amateur athletes. TTE included two-dimensional, spectral and tissue Doppler (TD) and flow propagation velocity (V(p)). After completion of the marathon, global measures of left ventricular (LV) systolic function were unchanged (EF 59 +/- 6 vs. 61 +/- 4% post, P = 0.14), whereas TD-derived measures of LV systolic function [septal strain -23 +/- 5 vs. -17 +/- 4%, P = 0.007; septal strain rate (SR) -1.5 +/- 0.3 vs. -1.1+/- 0.2 s(-1), P = 0.007] and right ventricular (RV) systolic function (RV apical strain -33 +/- 4 vs. -27 +/- 5%, P = 0.001; RV apical SR -2.4 +/- 0.7 vs. -1.8 +/- 0.5, P = 0.002) were reduced. Significant changes in transmitral velocity (E/A ratio 2.0 +/- 0.5 vs.1.3 +/- 0.3, P = 0.005) and TD indices of LV and RV diastolic function (E(a) septal 9.5 +/- 1.8 vs. 8.1 +/- 1.2 cm/s post-marathon, P = 0.01) were also observed, indicating an inherent alteration in LV relaxation. Although all indices of LV and RV systolic function had returned to normal on follow-up, there were persistent diastolic abnormalities (RV E(a), 11.5 +/- 1.5 cm/s pre-marathon vs. 10.0 +/- 1.6 cm/s follow-up, P = 0.01). CONCLUSION: Marathon running leads to transient systolic and more persistent diastolic dysfunction of both the LV and the RV.
In DDD pacing, the left-ventricular electromechanical latency period defines the duration between premature ventricular stimulation and the prematurely ending left-atrial contribution to left-ventricular filling. It has to be considered in diastolic AV delay optimization. Individual duration of this parameter seemed to reflect the ventricular function. Therefore, we compared the left-ventricular electromechanical latency period due to right ventricular stimulus with the documented ejection fraction of two groups, 33 congestive heart failure patients carrying biventricular systems and 13 right ventricular paced bradycardia patients. A mean latency period of 168+/-26 ms was found in the heart failure patients (ejection fraction: 25+/-5%) which was significantly longer (p=0.0039) compared to the bradycardia patients (ejection fraction: 51+/-12%) with a mean latency of 119+/-13 ms. Thus, an increasing latency period during right ventricular DDD pacing therapy indicates decreasing ejection fraction. A cut-off interval of 135 ms allowed the discrimination of 93% of our patients as having an individual ejection fraction of either up to 35% or above. Thus, the left ventricular electromechanical latency period can be used as an additional parameter indicating the necessity to upgrade from right to biventricular DDD pacing.
A 52-year-old man, living at home, had been on left ventricular assistance for 15 months with a Novacor pump (Worldheart, Ottawa, ON, Canada). Following the onset of effort dyspnea that had recently become worse, he was admitted to the hospital. A review of the pump showed that its flow rate had significantly decreased. An electrocardiogram showed a third-degree atrioventricular block. A pacemaker was implanted and the patient became asymptomatic immediately afterwards. This clinical case report shows the importance of satisfactory right ventricle filling in these patients. Right ventricle filling can be impaired by conduction disorders.
Primary tumors of the heart are rare with an incidence of 0.0017% to 0.19% in unselected patients at autopsy. Of those tumors, cardiac myxomas are the most commonly seen and account for about 50% of primary cardiac tumors. About 75% to 85% of myxomas originate in the left atrium, 15% to 20% in the right atrium, and only rare cases have been reported of myxomas originating in the left and right ventricles (5%). We present 3 cases in which right-sided myxomas were diagnosed echocardiographically and review the literature on primary cardiac myxomas.
BACKGROUND: Inhaled nitric oxide (NO), a selective pulmonary vasodilator, reduces pulmonary artery pressure in patients with acute respiratory distress syndrome (ARDS). In spite of the reduction of right ventricular afterload, the effect of NO on cardiac output remains unclear. METHODS: A patient with ARDS and echocardiographically determined severe acute right heart failure was treated with increasing concentrations of inhaled nitric oxide (NO). Haemodynamic and gas exchange variables were determined for each concentration of NO. NO treatment was continued for 3 days. RESULTS: During initial right heart failure, administration of NO resulted in a large increase (32%) in cardiac output in a dose-dependent manner. When right ventricular function had improved, inhalation of NO did not increase cardiac output. CONCLUSION: Our observations suggest that inhalation of NO is likely to increase cardiac output in ARDS when severe acute right heart failure is present.
Hypertrophic cardiomyopathy (HCM) is a disease characterized by an unknown cause of hypertrophy in the left or right ventricle. The dilated phase of HCM shows disease conditions resembling dilated cardiomyopathy, such as ventricular dilation, thin ventricular wall, and reduction of the ejection fraction. A patient presented with left ventricular concentric hypertrophy accompanied by right ventricular dilatation of unknown cause. Right ventricular endomyocardial biopsy specimens showed characteristic myocardial disarray. Therefore, there is the possibility that the patient had right and left ventricular HCM in the process toward the dilated phase, in which dilatation first occurred in the right ventricle.
Explore the source record for details and available documents.
OBJECTIVES: The purpose of this study was to determine, in a large referral population, the rate of echocardiographic change in mitral valve area (MVA) without interim intervention, to determine which factors influence progression of narrowing and to examine associated changes in the right side of the heart. BACKGROUND: Little information is currently available on the echocardiographic progression of mitral stenosis, particularly on progressive changes in the right side of the heart and the ability of a previously proposed algorithm to predict progression. METHODS: We studied 103 patients (mean age 61 years; 74% female) with serial two-dimensional and Doppler echocardiography. The average interval between entry and most recent follow-up study was 3.3 +/- 2 years (range 1 to 11). RESULTS: During the follow-up period, MVA decreased at a mean rate of 0.09 cm2/year. In 28 patients there was no decrease, in 40 there was only relatively little change (< 0.1 cm2/year) and in 35 the rate of progression of mitral valve narrowing was more rapid (> or = 0.1 cm2/year). The rate of progression was significantly greater among patients with a larger initial MVA and milder mitral stenosis (0.12 vs. 0.06 vs. 0.03 cm2/year for mild, moderate and severe stenosis, p < 0.01). Although the rate of mitral valve narrowing was a weak function of initial MVA and echocardiographic score by multivariate analysis, no set of individual values or cutoff points of these variables or pressure gradients could predict this rate in individual patients. There was a significant increase in right ventricular diastolic area (17 to 18.7 cm2) and tricuspid regurgitation grade (2 + to 3 +; p < 0.0001 between entry and follow-up studies). Progression in right heart disease occurred even in patients with minimal or no change in MVA. Patients with associated aortic regurgitation had a higher rate of decrease in MVA than did those with trace or no aortic regurgitation (0.19 vs. 0.086 cm2/year, p < 0.05). CONCLUSIONS: The rate of mitral valve narrowing in individual patients is variable and cannot be predicted by initial MVA, mitral valve score or transmitral gradient, alone or in combination. Right heart disease can progress independent of mitral valve narrowing.
Chronic right heart failure determines cardiac liver sclerosis as a consequence of the hepatic venous congestion that is easily detectable with pulsed Doppler sonography measuring hepatic venous pulsatility. These Doppler parameters profoundly change on the basis of the causative agent of the liver sclerosis. In fact, on pulsed Doppler examination, we detected a flat waveform in hepatic veins of subjects with viral liver cirrhosis whereas we only observed biphasic waveforms in subjects with cardiac liver sclerosis. On the contrary, a pulsed Doppler sonography pattern in subjects with viral cirrhosis and associated chronic right heart failure is unknown. We suppose that splanchnic pulsed Doppler sonography has an important role both in differentiating cardiac liver sclerosis from viral cirrhosis with chronic right heart failure and in the follow-up of the seriousness of the right ventricular failure.
The prevalence of congestive heart failure has increased in the world. Despite advances in pharmacological treatment, some patients have progression of the disease and deterioration of their functional class. In this group of patients cardiac resynchronization therapy has been accepted as a treatment option. However, some patients are non-responders to cardiac resynchronization, and others who respond favorably, will experience reappearance of their symptoms. For these patients, multisite stimulation with the implant of a second electrode in the right ventricle has been published as a new option. We report a 76 year-old woman with a dilated cardiomyopathy, who was treated with resynchronization therapy with good clinical response during two years, but symptoms of congestive heart failure reappeared and her functional class deteriorated to NYHA class IV. She was successfully treated with right ventricular multisite stimulation, with a reduction of symptoms that has lasted during the two months of follow up after the procedure.
An echocardiographic study of right ventricular myocardial contractility in 123 patients with chronic obstructive bronchitis (COB) confirmed the suggestion that in COB patients symptoms of right ventricular failure (cyanosis, acrocyanosis, crural edema, dilated liver) may have extracardiac origin. In echocardiographic diagnosis of right ventricular failure one should measure the speed of the anterior wall movements in the systole, diastole and ejection fraction.
UNLABELLED: In patients with pulmonary hypertension (PH) the right ventricular (RV)-to-left ventricular (LV) ratio of fatty acid uptake is reduced. In animal studies, such a finding was combined with an increased glucose uptake in RV myocardium. The aim of this study was to measure the metabolic rates of glucose uptake for the RV and LV myocardium in patients in relationship to parameters of RV and LV function. METHODS: Thirty patients with PH underwent PET with (18)F-FDG and SPECT with (99m)Tc-tetrofosmine. The metabolic rate of glucose uptake was determined for RV and LV myocardium using the method of Patlak. A right heart catheter, thermodilution, and Doppler sonography were used to characterize RV and LV function. From these methods, the stroke work of both ventricles and the RV Tei index were calculated. RESULTS: RV-to-LV ratios of (18)F-FDG-uptake increased with rising pulmonary arteriolar resistance (PAR). With increasing PAR, the metabolic rate of glucose uptake of the left ventricle decreased (r = -0.547; P < 0.01) together with LV stroke work (r = -0.838; P < 0.001). The metabolic rate of glucose uptake of the right ventricle, however, correlated neither with RV stroke work (r = 0.124) nor with PAR (r = 0.189) but with the Tei index (r = 0.78; P < 0.001). CONCLUSION: Increasing right-to-left ratios of glucose uptake with an increasing pressure load in the right ventricle in PH are caused mainly by a significant reduction in the LV metabolic rate of glucose uptake. This is obviously due to a reduced energy demand of the LV myocardium caused by reduced stroke work. An increased metabolic rate of glucose uptake in the right ventricle presumably indicates RV impairment, correlating with the Tei index, which is an established prognostic parameter for cardiac dysfunction and poor survival.
Explore the source record for details and available documents.
Isolated noncompaction of the ventricular myo-cardium (INVM) is a rare congenital disorder characterized by an arrest of myocardial morphogenesis. We experienced a case of a 23-year-old man, referred to our emergency room, whose symptoms included shortness of breath. ECG-gated cardiac magnetic resonance imaging depicted distinctive features of INVM in both the left and right ventricles. We present the clinical characteristics and morphological features of this case in comparison with some recent reports.
Right ventricular failure after left ventricular assist device implantation sometimes requires additional mechanical right ventricular support. The effectiveness of nitrates, prostaglandin, or nitric oxide inhalation in such cases has already been reported. However, there are few reports on the administration of phosphodiesterase inhibitor for right ventricular failure after left ventricular assist device implantation. We report two patients with right ventricular failure after left ventricular assist device implantation successfully treated with milrinone. Both had residual pulmonary hypertension due to high pulmonary vascular resistance after left ventricular assist device implantation. However, intravenous milrinone caused a significant reduction in pulmonary vascular resistance and an increase in left ventricular assist device flow. Milrinone acts as both an inotropic agent and a direct vasodilator, and thus may avoid the need for mechanical support for right ventricular failure due to residual pulmonary hypertension after left ventricular assist device implantation.
We found a significant ABD-assisted right ventricular hypokinetic regression after thrombolytic therapy in acute pulmonary embolism but could not demonstrate a linear relation between improvement in early right ventricular function and angiography.