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

Congenital absence of the pulmonary valve appears to have a prolonged fate, despite substantial regurgitation, thus the optimal timing of surgical correction remains unclear. A 53-year-old man with isolated pulmonary regurgitation accompanied by obstructive sleep apnea developed progressive heart failure after reopening of the foramen ovale. Closure of the interatrial shunt and pulmonary valve replacement with a 25-mm mechanical prosthesis relieved his refractory left heart failure.
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PMID:Operative timing for absent pulmonary valve with obstructive sleep apnea. 1898 46

Using the Mueller maneuver (MM) to simulate obstructive sleep apnea (OSA), our aim was to investigate acute changes in left-sided cardiac morphologic characteristics and function which might develop with apneas occurring during sleep. Strong evidence supports a relation between OSA and both atrial fibrillation and heart failure. However, acute effects of airway obstruction on cardiac structure and function have not been well defined. In addition, it is unclear how OSA might contribute to the development of atrial fibrillation and heart failure. Echocardiography was used in healthy young adults to measure various parameters of cardiac structure and function. Subjects were studied at baseline, during, and immediately after performance of the MM and after a 10-minute recovery. Continuous heart rate, blood pressure, and pulse oximetry measurements were made. During the MM, left atrial (LA) volume index markedly decreased. Left ventricular (LV) end-systolic dimension increased in association with a decrease in LV ejection fraction. On release of the maneuver, there was a compensatory increase in blood flow to the left side of the heart, with stroke volume, ejection fraction, and cardiac output exceeding baseline. After 10 minutes of recovery, all parameters returned to baseline. In conclusion, sudden imposition of severe negative intrathoracic pressure led to an abrupt decrease in LA volume and a decrease in LV systolic performance. These changes reflected an increase in LV afterload. Repeated swings in afterload burden and chamber volumes may have implications for the future development of atrial fibrillation and heart failure.
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PMID:Dynamic changes of left ventricular performance and left atrial volume induced by the mueller maneuver in healthy young adults and implications for obstructive sleep apnea, atrial fibrillation, and heart failure. 1902 14

Obstructive sleep apnea is the most frequent sleep disorder. The prevalence of sleep apnea in the general population is 2-4% and the main characteristic of the disease is the intermittent cessation or substantial reduction of airflow during sleep, caused by complete, or near complete upper airway obstruction. Decreased airflow is followed by oxygen desaturation and intermittent arousals. The clinical presentation of the disorder is complex. Loud snoring with breathing pauses and daytime sleepiness should raise the suspicion of sleep apnea, but we have to consider this disease if the patient has therapy resistant hypertension, heart failure, arrhythmias, stroke, depression or memory problems. Family physicians have an important role in recognizing sleep apnea. High risk patients can easily be identified by the main symptoms and using the Berlin sleep apnea questionnaire. These patients should be referred to a sleep laboratory for polysomnographic assessment and, if necessary, for further treatment.
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PMID:[The role of family physicians in the recognition and screening of obstructive sleep apnea]. 1902 51

There is increasing awareness of sleep-disordered breathing, which may manifest as obstructive sleep apnea, central sleep apnea (CSA), or a mixture of the two. Obstructive sleep apnea and CSA are strongly associated with heart failure (HF) and risk factors for developing HF. CSA may be considered a manifestation of the pathophysiology of HF; hence, approaches to optimize pharmacologic and nonpharmacologic treatment of HF should help to ameliorate CSA. However, if CSA also contributes to HF progression, CSA may represent a potential therapeutic target. There was hope that CSA prevalence would decline with better HF therapies. However, contemporary studies of HF patients on optimal medical therapy have shown that CSA prevalence remains 30% to 40%. Treating CSA poses significant challenges. Presently, the role of routine continuous positive airway pressure remains unclear, although newer ventilatory strategies may prove effective. Currently, CSA treatment involves standard optimal HF therapies, although growing evidence indicates that newer ventilation modes and cardiac resynchronization therapy may prove to be useful.
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PMID:Prevalence and management of central sleep apnea in heart failure patients. 1903 19

Global risk assessment is the standard of care for coronary artery disease management. In this setting, sleep apnea syndrome, which includes obstructive sleep apnea and central sleep apnea, is being increasingly recognized as a potentially modifiable risk factor for coronary artery disease. Emerging evidence points toward a cause and effect relationship between sleep apnea syndrome and medical conditions like insulin resistance, hypertension, heart failure, and myocardial ischemia. The effects of sleep apnea on coronary artery disease can be independent of many traditional risk factors. Continuous positive airway pressure has been shown to decrease inflammatory markers that are elevated in sleep apnea syndrome. Well-designed randomized controlled clinical trials are needed to better establish the role of sleep apnea in the genesis and progression of coronary artery disease.
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PMID:Sleep apnea syndrome: implications on cardiovascular diseases. 1905 Apr 22

Peripartum cardiomyopathy is a potentially fatal form of heart failure associated with pregnancy. A 29-year-old African American woman, gravida 3, para 2, at 36 weeks' gestation had a history of cardiomyopathy, morbid obesity (body mass index > 70 kg/m2), uncontrolled hypertension, obstructive sleep apnea, and required a repeat cesarean delivery. The patient was admitted to the hospital several times throughout her pregnancy for congestive heart failure, pulmonary edema, and headaches. Two years previously the patient received a diagnosis of peripartum cardiomyopathy 3 weeks after the delivery of her second child. This case report illustrates the recognition of peripartum cardiomyopathy and the risks early in pregnancy. It also describes the appropriate medical management, including transesophageal echocardiography and the need for collaboration of multiple medical specialists before and during delivery to provide the best possible outcome for both mother and infant.
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PMID:Multidisciplinary management of peripartum cardiomyopathy during repeat cesarean delivery: a case report. 1909 Mar 14

Obstructive sleep apnoea (OSA) is a common disorder in which repetitive apnoeas expose the cardiovascular system to cycles of hypoxia, exaggerated negative intrathoracic pressure, and arousals. These noxious stimuli can, in turn, depress myocardial contractility, activate the sympathetic nervous system, raise blood pressure, heart rate, and myocardial wall stress, depress parasympathetic activity, provoke oxidative stress and systemic inflammation, activate platelets, and impair vascular endothelial function. Epidemiological studies have shown significant independent associations between OSA and hypertension, coronary artery disease, arrhythmias, heart failure, and stroke. In randomised trials, treating OSA with continuous positive airway pressure lowered blood pressure, attenuated signs of early atherosclerosis, and, in patients with heart failure, improved cardiac function. Current data therefore suggest that OSA increases the risk of developing cardiovascular diseases, and that its treatment has the potential to diminish such risk. However, large-scale randomised trials are needed to determine, definitively, whether treating OSA improves cardiovascular outcomes.
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PMID:Obstructive sleep apnoea and its cardiovascular consequences. 1910 Oct 28

Obstructive sleep apnea (OSA) is present in at least 2% to 4% of the general population. Central sleep apnea (CSA), though less common, is highly prevalent in patients with heart failure. Both forms of sleep apnea exert strong modulatory effects on the autonomic nervous system at night through a number of mechanisms including central respiratory-cardiac coupling in the brainstem, chemoreflex stimulation, baroreflexes, and reflexes relating to lung inflation. Arousals also contribute to the autonomic disturbance. Although sleep is normally a time when parasympathetic modulation of the heart predominates and myocardial electrical stability is enhanced, OSA and CSA disturb this quiescence, creating an autonomic profile in which both profound vagal activity leading to bradyarrhythmias, and sympatho-excitation favoring ventricular ectopy are observed. The resulting tendency toward cardiac arrhythmia may directly contribute to sudden cardiac death and premature mortality in patients with sleep apnea. Therapy consists largely of treatment with continuous positive airway pressure, which has been shown to improve autonomic profile and reduce nocturnal arrhythmias.
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PMID:Sleep-disordered breathing: autonomic mechanisms and arrhythmias. 1911 Jan 34

Sleep plays a large role in patients with heart failure. In normal subjects, sleep is usually in a supine position with reduced sympathetic drive, elevated vagal tone and as such a relatively lower cardiac output and minute ventilation, allowing for recuperation. Patients with heart failure may not experience the same degree of autonomic activity change and the supine position may place a large strain on the pulmonary system. More than half of all heart failure patients have one of two types of sleep apnea: either obstructive or central sleep apnea. Some patients have both types. Obstructive sleep apnea is likely to be a cause of heart failure due to large negative intrathoracic pressures, apnea related hypoxemia and hypercapnia, terminated by an arousal and surge in systemic blood pressure associated with endothelial damage and resultant premature atherosclerosis. Reversal of obstructive sleep apnea improves blood pressure, systolic contraction and autonomic dysfunction however mortality studies are lacking. Central sleep apnea with Cheyne Stokes pattern of respiration (CSA-CSR) occurs as a result of increased central controller (brainstem driving ventilation) and plant (ventilation driving CO2) gain in the setting of a delayed feed back (i.e., low cardiac output). It is thought this type of apnea is a result of moderately to severely impaired cardiac function and is possibly indicative of high mortality. Treatment of CSA-CSR is best undertaken by treating the underlying cardiac condition which may include with medications, pacemakers, transplantation or continuous positive airway pressure (CPAP). In such patients CPAP exerts unique effects to assist cardiac function and reduce pulmonary edema. Whether CPAP improves survival in this heart failure population remains to be determined.
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PMID:Sleep in heart failure. 1911 Jan 35

Background Carvedilol may reduce the severity of central sleep apnea (CSA) in patients with chronic heart failure (CHF). Methods and Results This study prospectively examined the effect of carvedilol on the severity of CSA in patients with CHF. Polysomnographic findings, left ventricular (LV) function, and plasma brain natriuretic peptide (BNP) level were evaluated before and 6 months after induction of carvedilol in 16 patients with CHF (New York Heart Association functional class II or III and LV ejection fraction <50%) who had CSA (central apnea index [CAI] >5 with dominant central apneic events). All patients tolerated carvedilol. The 6-month treatment with carvedilol increased the LV ejection fraction (32+/-7.4% to 45+/-9.8%, P<0.001) and decreased the BNP level (159 [69-458] pg/ml to 38 [16-193] pg/ml, P=0.017). The polysomnographic findings showed that the treatment decreased the apnea-hypopnea index (34+/-13 to 14+/-13, P=0.003) and CAI (13+/-11 to 1.9+/-4.3, P<0.001), whereas it increased the obstructive apnea index (1.1+/-1.5 to 3.1+/-3.4, P=0.04). Conclusion This preliminary study shows that treatment with carvedilol reduces the severity of CSA in patients with CHF, but that episodes of obstructive sleep apnea sometimes increase after the treatment.
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PMID:Carvedilol reduces the severity of central sleep apnea in chronic heart failure. 1912 6


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