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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 4-year-old Thoroughbred gelding racehorse was referred to the Onderstepoort Veterinary Academic Hospital (OVAH) with a history of post-race distress and collapse. In the absence of any obvious abnormalities in the preceding diagnostic work-up, a standard exercise test was performed to determine an underlying cause for the post-race distress reported. In this particular case oxygen desaturation became evident at speeds as slow as 6 m/s, where PO2 was measured at 82.3 mm Hg. Similarly at a blood pH of 7.28, PCO2 had dropped to 30.0 mm Hg indicating a combined metabolic acidosis and respiratory alkalosis. The cause of the distress was attributed to a severe hypoxia, with an associated hypocapnoea, confirmed on blood gas analyses, where PO2 levels obtained were as low as 56.6 mm Hg with a mean PCO2 level of 25.4 mm Hg during strenuous exercise. Arterial oxygenation returned to normal immediately after cessation of exercise to 106.44 mm Hg, while the hypocapnoeic alkalosis, PCO2 25.67 mm Hg, persisted until the animal's breathing normalized. The results obtained were indicative of a dynamic cardiac insufficiency present during exercise. The combination of an aortic stenosis and a mitral valve insufficiency may have resulted in a condition similar to that described as high-altitude pulmonary oedema, with respiratory changes and compensation as for acute altitude disease. The results obtained were indicative of a dynamic cardiac insufficiency present during exercise and substantiate the fact that an extensive diagnostic regime may be required to establish a cause for poor performance and that the standard exercise test remains an integral part of this work-up.
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PMID:The use of the standard exercise test to establish the clinical significance of mild echocardiographic changes in a Thoroughbred poor performer. 1545 67

55 patients with congenital heart diseases (CHD) in phase of Eisenmereger's syndrome (ES) (11 patients with ductus arteriosus (DA), 28--ventricular septal defect (VSD), 16--atrial septal defect (ASD)) at age of 14-53 (mean 29.7+/-3.2) were examined. Heart failure corresponded to I-II functional classes (NYHA) in 28 (50.9%) patients, III-IV--in 27 (49.1%). Diagnosis of ES was confirmed by ECG, Doppler-Echo-CG, catheterization and ventriculography. Moderate right ventricle systolic dysfunction was revealed and confirmed by its dilation and deterioration of inferior vena cava (IVC) (for 156.0% in comparision with healthy people, P<0.001) in patients DA and ASD collapse after inspiration. Unchanged indices of Vmax and Accmax in PA and IVC diameter showed good compensatory potential of RV. There was the initial stage of LV systolic dysfunction (decrease EF for 7.0%, Vmax for 16.7% and Accmax for 21.4%, P<0.05). Diastolic dysfunction of both ventricles in patients with ES is unidirectional and corresponds to relaxation type.
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PMID:[Systolic and diastolic function of heart ventricles and their remodeling in adult patients with congenital heart disease in phase of Eisenmenger's syndrome]. 1560 15

Despite recent therapeutic advances, chronic cardiac failure is still associated with a significant morbidity and mortality. Sleep apnoea syndrome is common in this population, affecting almost half of these patients. However, it is rarely diagnosed and treated. There are two types of sleep apnoea syndrome, which can sometimes co-exist: the obstructive apnoea syndrome with collapse of the upper airways, and the central apnoea syndrome with cyclical Cheyne-Stokes respiration, linked with anomalies of central control. Apnoea leads to sympathetic stimulation and an increase in the left ventricular post-charge which can alter cardiac function and the prognosis. Diagnosis of sleep apnoea syndromes is now made with small ambulatory oxymeters which do not disturb sleep and which allow precise detection of episodes of desaturation. Treatment with positive pressure ventilation brings an improvement in daytime symptoms (fatigue, drowsiness) as well as an improvement in cardiac function. Screening for sleep apnoea is thus essential in patients with chronic heart failure, especially in those resistant to optimal drug treatment, in order to improve their management.
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PMID:[Sleep apnoea syndrome and cardiac failure]. 1581 21

Intracardiac haemangioma is a very rare primary benign tumour. A 20 year old female patient, with no significant previous medical history, presented to the emergency department with cardiovascular collapse and vague abdominal pains, with no peripheral signs of cardiac failure. The electrocardiogram showed sinus rhythm with diffuse reploarisation disturbances. Chest radiography revealed cardiomegaly (cardiothoracic index of 0.67) with a right paracardial opacity. Abdominal ultrasound showed a moderate peritoneal effusion and transthoracic ultrasound showed a tumour occupying the right atrial cavity but sparing the interatrial septum. The patient underwent emergency open heart surgery for tumour resection and right atrial wall repair with autologous pericardium. Histology confirmed a haemangioma. Follow-up at one month was uneventful. The clinical, diagnostic and therapeutic features of this case are underlined.
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PMID:[Haemangioma of the right atrium revealed by cardiogenic shock]. 1588 51

Sleep-disordered breathing is very common and is associated with an increased risk of cardiovascular disease, cardiac arrhythmia and stroke. There are two types of sleep apnea: obstructive and central. The objective of this review is to provide a broad perspective of the pathophysiological and clinical aspects of the two types of apnea and to discuss their cardiovascular adverse effects. The diagnosis of sleep apnea syndrome is based on polysomnography, and severity is measured with an apnea-hypopnea index that counts the total number of apneas per hour of sleep. Recent large epidemiologic studies have shown that sleep apnea affects about 16% of men and 5% of women between 30 and 65 years of age. Obstructive sleep apnea is characterized by abnormal collapse of the pharyngeal airway during sleep, snoring, vigorous inspiratory efforts causing frequent arousal, and excessive daytime drowsiness. Central sleep apnea with Cheyne-Stokes respiration is a form of periodic breathing with frequent periods of hyperventilation, and carries a poor prognosis in patients with heart failure. Obstructive apnea can also have substantial health consequences. Although the exact mechanism linking sleep apnea with cardiovascular disease is unknown, there is evidence that obstructive apnea is associated with a group of proinflammatory and prothrombic factors that are also important in the development of atherosclerosis. Nocturnal and daytime sympathetic activity is elevated after sleep apnea. Autonomic abnormalities include an increased resting heart rate, decreased cardiac rhythm activity, and increased blood pressure variability. Obstructive apnea is associated with endothelial dysfunction, increased C-reactive protein and cytokine expression, elevated fibrinogen levels and decreased fibrinolytic activity. Enhanced platelet activity and aggregation, leukocyte adhesion and accumulation of endothelial cells are common in both obstructive apnea and atherosclerosis. Surges in sympathetic activity, blood pressure, ventricular wall tension and afterload adversely affect ventricular function. Many studies have shown that patients with obstructive apnea have an increased incidence of daytime hypertension, and this syndrome is recognized as an independent risk factor for hypertension. Obstructive apnea is associated with myocardial ischemia (silent or symptomatic), acute coronary events, stroke and transient ischemic attacks, cardiac arrhythmia, pulmonary hypertension and heart failure. Central sleep apnea is frequent in severe heart failure. Most heart failure patients with pulmonary congestion chronically hyperventilate because of stimulation of vagal irritant receptors and central and peripheral chemosensitivity. When PaCO2 falls below the threshold required to stimulate breathing, the central drive to respiratory muscles and air inflow ceases and central apnea ensues. Apnea, hypoxia, CO2 retention and arousals provoke elevated sympathetic activity, increased afterload and elevated left ventricular transmural pressure, and promote the progression of heart failure. Tentative relationships have been identified between central apnea and markers of inflammation, oxidative stress and endothelial dysfunction. Recent mid-terms trials showed that nocturnal use of positive airway pressure in patients with the two types of apnea alleviates symptoms, reduces sympathetic activity, improves ventricular function and quality of life, and reduces daytime drowsiness. More studies are needed to understand the mechanisms underlying the relationship between sleep apnea and cardiovascular disease, but clinicians should be aware of this link and should attempt to identify patients with these syndromes.
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PMID:[Sleep apnea syndromes and cardiovascular disease]. 1614 10

Ventricular assist devices now clinically used for treatment of end-stage heart failure require responsive and reliable hemodynamic control to accommodate the continually changing demands of the body. This is an essential ingredient to maintaining a high quality of life. To satisfy this need, a control algorithm involving a trade-off between optimal perfusion and avoidance of ventricular collapse has been developed. An optimal control strategy has been implemented in vitro that combines two competing indices: representing venous return and prevalence of suction. The former is derived from the first derivative of diastolic flow with speed, and the latter derived from the harmonic spectra of the flow signal. The responsiveness of the controller to change in preload and afterload were evaluated in a mock circulatory simulator using a HeartQuest centrifugal blood pump (CF4b, MedQuest Products, Salt Lake City, UT). To avoid the need for flow sensors, a state estimator was used, based on the back-EMF of the actuator. The multiobjective algorithm has demonstrated more robust performance as compared with controllers relying on individual indices.
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PMID:In vitro evaluation of multiobjective hemodynamic control of a heart-assist pump. 1615 94

Pericardial effusion is a potentially life-threatening problem leading to a rise in the intrapericardial pressure resulting in varying degrees of hemodynamic compromise. Cardiac tamponade occurs when the intrapericardial pressure equals or exceeds right ventricular diastolic filling pressures leading to a decreased cardiac output. In dogs, the most common causes of pericardial effusion that require pericardiocentesis are cardiac neoplasia and idiopathic pericardial effusion (IPE). The incidence of cardiac neoplasia in dogs is low, and it is rare in cats. In dogs, hemangiosarcoma and chemodectoma are the two most common types of cardiac neoplasia. In cats, lymphosarcoma is the most common form of cardiac neoplasia, but they are more likely to develop pericardial effusion secondary to congestive heart failure or feline infectious peritonitis. Common histories include lethargy, dyspnea, anorexia, collapse, and abdominal distension. Pericardiocentesis is used to stabilize animals with life-threatening cardiac tamponade, relieve the pressure leading to right-sided heart failure, and obtain fluid samples for diagnostic evaluation. The fluid should be quantified and characterized. Serious complications associated with pericardiocentesis are rare. Complications include cardiac puncture, arrhythmias, and laceration of a tumor or coronary artery resulting in intrapericardial hemorrhage or sudden death.
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PMID:Therapeutic pericardiocentesis in the dog and cat. 1618 Mar 97

The hemodynamic effects of ventilation are complex but can be grouped under four clinically relevant concepts. First, spontaneous ventilation is exercise, and critically ill patients may not withstand the increased work of breathing. Initiation of mechanical ventilatory support will improve oxygen delivery to the remainder of the body by decreasing oxygen consumption. To the extent that mixed venous oxygen also increases, Pao(2) will increase without any improvement in gas exchange. Similarly, weaning from mechanical ventilatory support is a cardiovascular stress test. Patients who fail to wean also manifest cardiovascular insufficiency during the failed weaning attempts. Improving cardiovascular reserve or supplementing support with inotropic therapy may allow patients to wean from mechanical ventilation. Second, changes in lung volume alter autonomic tone and pulmonary vascular resistance (PVR), and at high lung volumes compress the heart in the cardiac fossa. Hyperinflation increases PVR and pulmonary artery pressure, impeding right ventricular ejection. Decreases in lung volume induce alveolar collapse and hypoxia, stimulating an increased pulmonary vasomotor tone by the process of hypoxic pulmonary vasoconstriction. Recruitment maneuvers, positive end-expiratory pressure, and continuous positive airway pressure may reverse hypoxic pulmonary vasoconstriction and reduce pulmonary artery pressure. Third, spontaneous inspiration and spontaneous inspiratory efforts decrease intrathoracic pressure (ITP). Since diaphragmatic descent increases intra-abdominal pressure, these combined effects cause right atrial pressure inside the thorax to decrease but venous pressure in the abdomen to increase, markedly increasing the pressure gradient for systemic venous return. Furthermore, the greater the decrease in ITP, the greater the increase in left ventricular (LV) afterload for a constant arterial pressure. Mechanical ventilation, by abolishing the negative swings in ITP, will selectively decrease LV afterload, as long as the increases in lung volume and ITP are small. Finally, positive-pressure ventilation increases ITP. Since diaphragmatic descent increases intra-abdominal pressure, the decrease in the pressure gradient for venous return is less than would otherwise occur if the only change were an increase in right atrial pressure. However, in hypovolemic states, positive-pressure ventilation can induce profound decreases in venous return. Increases in ITP decrease LV afterload and will augment LV ejection. In patients with hypervolemic heart failure, this afterload reducing effect can result in improved LV ejection, increased cardiac output, and reduced myocardial oxygen demand.
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PMID:Cardiovascular issues in respiratory care. 1630 58

Computed tomographic (CT) pulmonary angiography has been established as a first-line diagnostic technique in patients suspected of having pulmonary embolism. Risk stratification is important in patients with pulmonary embolism because optimal management, monitoring, and therapeutic strategies depend on the prognosis. Acute right-sided heart failure is known to be responsible for circulatory collapse and death in patients with severe pulmonary embolism. Acute right-sided heart failure can be assessed at CT pulmonary angiography by measuring the dimensions of right-sided heart cavities or upstream venous structures, such as the superior vena cava or azygos vein. The magnitude of pulmonary embolism can be calculated at CT pulmonary angiography by applying angiographic scores adapted for CT (Miller and Walsh scores) or dedicated CT scores (Qanadli and Mastora scores). The advent of CT pulmonary angiography performed with electrocardiographic gating permits new advances in assessment of acute right-sided heart failure, such as measurement of the ventricular ejection fraction. Although such findings may be useful for assessment of treatment effectiveness, their effect on prognosis in patients with severe pulmonary embolism is debated in the literature.
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PMID:Can CT pulmonary angiography allow assessment of severity and prognosis in patients presenting with pulmonary embolism? What the radiologist needs to know. 1641 40

Cardiac resynchronization therapy (CRT) has been proposed to improve hemodynamics in patients with heart failure and left bundle branch block (LBBB) by resynchronization of left ventricular (LV) dyssynchrony. The current report concerns a patient with narrow QRS complex without LV dyssynchrony who experienced an acute exacerbation of heart failure following exercise. Careful analysis revealed that an increase of heart rate induced acceleration-dependent LBBB with severe LV dyssynchrony and mitral regurgitation followed by acute heart failure and hemodynamic collapse. CRT prevented these adverse reactions. Accordingly, optimal evaluation for CRT may include testing for LV dyssynchrony during exercise.
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PMID:Acceleration-dependent left bundle branch block with severe left ventricular dyssynchrony results in acute heart failure: are there more patients who benefit from cardiac resynchronization therapy? 1642 11


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