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The heart in heart failure   总被引:1,自引:0,他引:1  
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Acute heart failure (AHF) is one of the most common causes for hospital admission and is associated with a high risk of mortality. Compared to chronic heart failure, there is less robust evidence to guide diagnosis, risk stratification and management of AHF. This state-of-the art review aims to summarize new developments in this field. We also highlight areas of ongoing work including novel vasoactive agents, alternative models to traditional hospital admission and strategies to improve patient engagement.  相似文献   

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Defining heart failure   总被引:4,自引:0,他引:4  
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Heart failure is a clinical syndrome which presents similarities and differences between children and adults; in pediatric age the spectrum of causes of heart failure is wide and congenital heart defects are the most common etiology. Volume and pressure overload on a 'normal myocardium' is the classical physiological pattern while myocardial contractile dysfunction of different etiology is much less observed in the pediatric population. However there are some peculiarities in clinical presentation of heart failure in infants and small children. The medical therapy cornerstones still remain loop diuretics, angiotensin-converting enzyme inhibitors, beta-blockers and digitalis. There are also some reported experiences with new inotropics drugs in acute heart failure. In pediatric cardiology there are few prospective studies on pharmacology of heart failure and the data are often extrapolated from adult large trials. Non pharmacological treatment with autonomic implantable cardioverter defibrillators and resynchronization therapy as well as the surgically implant of ventricular assist devices are increasingly employed in children. Cardiac transplantation is currently the treatment option with good outcome and long-term survival in pediatric patients with end-stage or refractory heart failure.  相似文献   

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Diastolic heart failure   总被引:7,自引:0,他引:7  
Diastolic heart failure is a distinct clinical entity increasingly seen in older patients and requires special awareness to make the diagnosis. Although no single laboratory test is identified for making a confident diagnosis of diastolic dysfunction as the pathogenetic mechanism for heart failure, a constellation of echocardiographic and radionuclear findings are helpful in most cases. Invasive assessment of LV diastole is laborious, requiring high-fidelity pressures and accurate measures of volumes, and these are rarely needed to diagnose the condition. It appears that prognosis is significantly better for those with normal systolic function, when compared with congestive heart failure caused by impaired systolic pump function. Finally, the therapeutic approaches are substantially different for the two groups. It must be emphasized that even patients with predominant myocardial systolic dysfunction have some combined diastolic dysfunction as well. This latter group is difficult to treat. However, improvement in systolic pump function, when markedly impaired, must take precedence in management strategies.  相似文献   

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A Nakanishi 《Naika》1971,27(6):1072-1075
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Drug-induced heart failure   总被引:2,自引:0,他引:2  
Heart failure is a clinical syndrome that is predominantly caused by cardiovascular disorders such as coronary heart disease and hypertension. However, several classes of drugs may induce heart failure in patients without concurrent cardiovascular disease or may precipitate the occurrence of heart failure in patients with preexisting left ventricular impairment. We reviewed the literature on drug-induced heart failure, using the MEDLINE database and lateral references. Successively, we discuss the potential role in the occurrence of heart failure of cytostatics, immunomodulating drugs, antidepressants, calcium channel blocking agents, nonsteroidal anti-inflammatory drugs, antiarrhythmics, beta-adrenoceptor blocking agents, anesthetics and some miscellaneous agents. Drug-induced heart failure may play a role in only a minority of the patients presenting with heart failure. Nevertheless, drug-induced heart failure should be regarded as a potentially preventable cause of heart failure, although sometimes other priorities do not offer therapeutic alternatives (e.g., anthracycline-induced cardiomyopathy). The awareness of clinicians of potential adverse effects on cardiac performance by several classes of drugs, particularly in patients with preexisting ventricular dysfunction, may contribute to timely diagnosis and prevention of drug-induced heart failure.  相似文献   

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Refractory heart failure   总被引:1,自引:0,他引:1  
Managing patients with heart failure is rooted in appropriate recognition of the syndrome and subsequent tailoring of therapies to individual patients based on the stage of the disease. An individual with asymptomatic left ventricular dysfunction (the earliest stage of heart failure) is treated quite differently than a patient with more advanced heart failure manifested by problematic fluid retention, peripheral organ hypoperfusion with dysfunction, and several comorbidities. The latter patient requires aggressive pharmacologic intervention coupled with other creative strategies that are individually tailored to each individual's unique clinical circumstance. The therapies available include long-term administration of parenteral inotropic therapy, dialysis, insertion of a ventricular assist device, cardiac transplantation, dynamic skeletal myoplasty, volume reduction surgery, or more standard (but higher risk) operative procedures. New drugs are constantly undergoing evaluation and may lead to additional therapeutic improvements in patients with advanced heart failure. The key is recognizing the appropriate place for more radical therapies.  相似文献   

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Diastolic heart failure   总被引:13,自引:0,他引:13  
Primary diastolic failure is typically seen in patients with hypertensive or valvular heart disease as well as in hypertrophic or restrictive cardiomyopathy but can also occur in a variety of clinical disorders, especially tachycardia and ischemia. Diastolic dysfunction has a particularly high prevalence in elderly patients and is generally associated, with low mortality but high morbidity. The pathophysiology of diastolic dysfunction includes delayed relaxation, impaired LV filling and/or increased stiffness. These conditions result typically in an upward displacement of the diastolic pressure-volume relationship with increased end-diastolic, left atrial and pulmo-capillary wedge pressure leading to symptoms of pulmonary congestion. Diagnosis of diastolic heart failure requires three conditions: (1) presence of signs or symptoms of heart failure; (2) presence of normal or slightly reduced LV ejection fraction (EF > 50%) and (3) presence of increased diastolic filling pressure. Assessment of diastolic function can be performed with several non-invasive (2D- and Doppler-echocardiography, color Doppler M-mode, Doppler tissue imaging, MR-myocardial tagging, radionuclide ventriculography) and invasive techniques (micromanometry, angiography, conductance method). Doppler-echocardiography is the most useful tool to routinely measure diastolic function. Different techniques can be used alone or in combination to assess LV diastolic function, but most of them are dependent on heart rate, pre- and afterload. The transmitral flow pattern remains the starting point, since it is easy to acquire and rapidly categorizes patients into normal (E > A), delayed relaxation (E < A), and restrictive (E > A) filling patterns. Invasive assessment of diastolic function allows determination of the time constant of relaxation from the exponential pressure decay during isovolumic relaxation, and the evaluation of the passive elastic properties from the slope of the diastolic pressure-volume (= constant of chamber stiffness) and stress-strain relationship (= constant of myocardial stiffness). The prognosis of diastolic heart failure is usually better than for systolic dysfunction. Diastolic heart failure is associated with a lower annual mortality rate of approximately 8% as compared to annual mortality of 19% in heart failure with systolic dysfunction, however, morbidity rate can be substantial. Thus, diastolic heart failure is an important clinical disorder mainly seen in the elderly patients with hypertensive heart disease. Early recognition and appropriate therapy of diastolic dysfunction is advisable to prevent further progression to diastolic heart failure and death. There is no specific therapy to improve LV diastolic function directly. Medical therapy of diastolic dysfunction is often empirical and lacks clear-cut pathophysiologic concepts. Nevertheless, there is growing evidence that calcium channel blockers, beta-blockers, ACE-inhibitors and AT2-blockers as well as nitric oxide donors can be beneficial. Treatment of the underlying disease is currently the most important therapeutic approach.  相似文献   

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Opinion statement  
–  The diagnosis of diastolic heart failure (DHF) can be made when a patient has both symptoms and signs on physical exam of congestive heart failure (CHF), and normal left ventricular volume and ejection fraction. Documentation of abnormal diastolic function is confirmatory but not mandatory.
–  Diastolic heart failure is a frequent cause of CHF (prevalence is 35% to 50%) and has a significant effect on mortality (5-year mortality rate is 25% to 35%) and morbidity (1-year readmission rate is 50%).
–  Treatment should be targeted at symptoms, causal clinical disease, and underlying basic mechanisms.
–  Symptom-targeted therapy: decrease pulmonary venous pressure using diuretics and long-acting nitrates, maintain atrial contraction and atrial ventricular synchrony, reduce heart rate using beta-adrenergic blockers and calcium channel blockers; increase exercise tolerance by reducing exerciseinduced increases in blood pressure and heart rate using angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, and calcium channel blockers.
–  Disease-targeted therapy: prevent or treat myocardial ischemia, prevent or regress left ventricular hypertrophy.
–  Mechanism-targeted therapy (future directions): modify neurohumoral activation using renin, angiotensin, and aldosterone system antagonists (ACE inhibitors, angiotensin II receptor blockade, aldosterone and renin antagonist); endothelin antagonists; nitric oxide agonists; and atrial natruretic peptide agonists; alter intracellular mechanisms; alter extracellular matrix structures.
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T Takatsu 《Naika》1970,25(6):1057-1066
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