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At least 163 records · Page 9Linked to original sources
PubMed1998

Effect of flecainide on heart rate variability in subjects without coronary artery disease or congestive heart failure.

Heart rate variability is a noninvasive indicator of autonomic nervous system activity. The role of the autonomic nervous system in the genesis of atrial or ventricular arrhythmias is now well established. Little is known about the effects of flecainide on heart rate variability in patients with normal heart structure, the main population receiving flecainide. This study was designed to evaluate the effects of flecainide on heart rate variability in patients without coronary artery disease or congestive heart failure. Time and frequency domain analysis of heart rate variability on 24-hour electrocardiogram recording were assessed in 40 patients with normal echocardiography and without evidence of coronary artery disease before and after 2 months of oral treatment with flecainide (321 +/- 57 mg/day) prescribed for Wolff Parkinson White syndrome with circus movement tachycardia. Flecainide significantly decreased all parameters of heart rate variability in the time domain (median delta% -10% to -25%) and in the frequency domain (median delta% -27% to -38%), including the markers of vagal activity. There was no correlation between plasma concentrations of flecainide and reduction in heart rate variability. It was concluded that in subjects without coronary artery disease or congestive heart failure, flecainide decreases all the measurements of heart rate variability and this decrease is not related to plasma concentrations of flecainide.

Adolescent↗
PubMed2005

[The novelty in the treatment of heart failure].

Heart failure is a very common clinical pathology. The treatment of heart failure is expensive; therefore, it is a large burden on the health care system in the world. Despite many recent advances in heart failure therapy, the prognosis remains poor. Levosimendan is a novel inotropic vasodilator agent. This drug induces enhanced contractility mainly via its calcium sensitizing actions. Levosimendan does not increase myocardial oxygen demand and also reduces significantly systemic vascular resistance, pulmonary artery pressure, and pulmonary vascular resistance. It causes venous, arterial, and coronary vasodilation. The drug is not proarrhythmic, has anti-ischemic and anti-stunning effects. It is well-tolerated drug for the treatment of cardiac failure. This review article discusses mechanism of action of levosimendan, its pharmacokinetics and metabolism, hemodynamic studies with this drug, effects on morbidity and mortality, therapeutic indication for its use, contraindications, special warnings and precautions for use, interactions with others medical products, undesirable effects of levosimendan.

Adolescent↗
PubMed1998

[Effects of cardiomegaly on the anatomical and functional state of the lung in chronic heart failure].

Heart and lungs might compete for the intrathoracic space in case of heart enlargement (as in heart failure). Therefore, the pulmonary abnormalities observed in patients with chronic heart failure (restrictive pattern and reduction of diffusion capacity) might be at least in part related to cardiomegaly. In 53 patients (11 women, 42 men, mean age 65 +/- 8 years) with stable heart failure and cardiac enlargement (cardiothoracic ratio-Ctr > or = 50%) we measured carbon monoxide lung diffusion (DLCO), lung tissue content (VT, single breath, expiratory regression of acetylene), alveolar volume (Va, single breath, expiratory regression of methane) and vital capacity (VC). In 16 patients the two subcomponents of DLCO, i.e. alveolar-capillary membrane diffusion (Dm) and diffusion related to capillary volume (Cv), were analyzed. Patients were grouped for Ctr (> or = 60%, Group 1, n = 28 and < 60%, Group 2, n = 25): VT (Group 1 0.62 +/- 0.2 l; Group 2 0.76 +/- 0.2 l, p < 0.01); Va (Group 1 4.21 +/- 0.97 l; Group 2 5.37 +/- 1.12 l, p < 0.0001); VC (Group 1 2.3 +/- 0.6 l; Group 2 3.1 +/- 0.6 l, p < 0.0001); DLCO (Group 1 16.15 +/- 3.95 ml/min x mmHg; Group 2 22.24 +/- 6.57 ml/min x mmHg, p < 0.0001). An inverse correlation was observed between Dm and Ctr (r = -0.47, p < 0.02), which disappeared when Va was accounted for Dm/Va (r = -0.12, NS). Cv was lower in Group 1 vs Group 2. In conclusion, in patients with Ctr > or = 60% (Group 1) "anatomy" (VT, Va, VC and Cv) and function (DLCO) of the lungs are impeded. This is likely due to reduction of space available for the lungs in the thorax by an enlarged heart (no correlation between Dm/Va vs Ctr).

Aged↗
PubMed2002

The role of inflammation in the pathogenesis of heart failure.

Heart failure is not a simple defect in the pumping function of cardiac muscle, but rather a complex systemic inflammatory disease affecting many organ systems. Recognition of this fact has led to new therapeutic interventions such as angiotensin-converting enzyme inhibitors and beta-blockers, which have a significant impact on the quality of life and survival of patients with heart failure. During the course of heart failure, the steps involved in the activation of inflammation are now better understood. As a result, new therapies will develop that block, modify, or prevent these inflammatory changes, and supplement our armamentarium for providing better and longer lives for patients.

Adrenergic beta-Antagonists↗
PubMed2001

Electrotherapeutic management of patients with heart failure.

Heart failure is associated with poor long term survival due to progressive refractory heart dysfunction and sudden cardiac death. Cardiac resynchronization through atrio-biventricular pacing has been introduced to treat patients affected by drug-refractory heart failure with desynchronized ventricular activation, as for complete left bundle branch block. The technique is aimed to overcome interventricular and intraventricular conduction delays leading to ventricular dysynchrony, paradoxical septal wall motion, presystolic mitral regurgitation and reduced diastolic filling times. Short term studies demonstrated that biventricular pacing (and perhaps left ventricular pacing alone) may improve both systolic and diastolic function. Initial studies in patients receiving long term pacing consistently showed significant QRS shortening associated with improvement in symptoms, left ventricular ejection fraction, exercise tolerance, quality of life and New York Heart Association functional class. As far as sudden cardiac death prevention in heart failure is concerned, implantable cardioverter defibrillator (ICD) implantation has been demonstrated to be the most effective therapy in patients with prior cardiac arrest due to ventricular fibrillation or poorly tolerated ventricular tachycardia. Low left ventricular ejection fraction, unsustained ventricular tachycardia and inducibility at electrophysiological study also may identify high risk patients requiring ICD implantation. Further studies are needed to evaluate the effect of cardiac resynchronization on hard end-points, such as survival and long term clinical outcome, and to upgrade risk stratification criteria to be used in selection of candidates for ICD implantation.

Clinical Trials as Topic↗
PubMed2002

Structural, functional, and molecular characterization of the SHHF model of heart failure.

Heart failure is a complex multifactorial disease resulting in a myriad of progressive changes at the molecular, cellular, and physiological level. To better understand the mechanisms associated with the development of congestive heart failure, a comprehensive examination of the aging lean male spontaneously hypertensive, heart failure-prone rat (SHHF) was conducted. Myocardial function and structural integrity progressively diminished as evidenced by decreased ejection fraction and increased left ventricular volume measured using echocardiography. Functional and structural changes were accompanied by elevations in circulating inflammatory markers, including tumor necrosis factor-alpha (TNF-alpha), IL-6, and TNF receptors type 1 and 2. Increased systemic inflammatory marker levels were consistent with age-dependent changes in the expression pattern of genes that contribute to stress, inflammation, and the extracellular matrix in SHHF animals analyzed from age 4 to 18 mo. In summary, the SHHF rat shares many hallmark features of the human disease state and represents a key experimental model for the dissection of complex human heart failure pathophysiology.

Animals↗
PubMed2000

Management of heart failure.

Heart failure imposes a major burden on society. Primary care physicians, who care for 70% of all heart-failure patients, have opportunities to reduce the economic and mortality impact of this disease by improved outpatient management. Management tasks for these patients are discussed. Successful completion of these tasks will lead to an improvement in functional capacity, fewer hospitalizations, and longer lives for heart-failure patients.

Adult↗
PubMed2006

[Importance of therapeutic education in the multidisciplinary management of heart failure].

Heart failure is a severe disease with high morbidity and mortality rates. The interest for multidisciplinary heart failure patient management is increasing in order to improve prescription of medical therapies and to allow a better quality of life. Proofs of reduction in morbi-mortality exist and some models of management have been assessed. The most important point remains the major role of therapeutic education. Training of health care professionals is needed. Tools for therapeutic education have been created and can be associated with complementary informative means. All these elements allow that a new approach of heart failure takes in place in France.

Delivery of Health Care, Integrated↗
PubMed2006

Clinical perspectives of heart rate slowing for coronary event reduction and heart failure.

Heart rate is a major determinant of myocardial oxygen consumption. There is ample evidence of an association between high heart rate and poor outcome in numerous clinical settings. Experimental studies in monkeys have shown a link between increased heart rate and development of atherosclerosis. In the clinical setting, increased heart rate has been found associated with coronary plaque rupture. A causal relationship is further supported by the fact that Beta-blockers have a well-documented efficacy after myocardial infarction, although the other properties of these agents may also participate in their protective effect. Beyond the potential benefits of heart rate lowering in patients with coronary artery disease, medications capable of decreasing heart rate without altering left ventricular function, such as the I(f) current inhibitor ivabradine, might prove particularly helpful in patients with chronic heart failure associated with coronary artery disease, but also in heart failure without systolic dysfunction, or in patients needing inotropic support for acute heart failure.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

The district nurse's role in managing patients with heart failure.

Heart failure is a complex disorder that affects patients and their carers in many ways. Recommendations for improving the quality of care for people with heart failure are set out in the government's National Service Framework for Coronary Heart Disease (Department of Health (DH) 2000a) and in the guideline commissioned by the National Institute for Clinical Excellence (NICE 2003a), which describes best practice for the management of patients with heart failure. This article discusses the role of the district nurse in meeting the challenges of the NICE guideline, and suggests that district nurses are better placed than other health professionals in primary care to have a central role in delivering such care. The contribution of district nurses to the management of patients with chronic diseases and those who are terminally ill at home is also discussed. The impact of The NHS Cancer Plan (DH 2000b) on the care of cancer patients in primary care is examined briefly to ascertain whether the NICE guideline is likely to have a similar impact on the scope and capacity of district nursing.

Chronic Disease↗
PubMed1995

Advanced practice nurses can refine the management of heart failure.

Heart failure is a prevalent problem with increasingly high rates of mortality and morbidity. Frequent exacerbation of heart failure leads to multiple rehospitalizations and interferes with patients' quality of life. In addition, it induces excessive consumption of health care resources. This leads to detrimental repercussions for these patients. Studies that have looked at causes of heart failure exacerbation determine an implicit need for more nursing influence. This nursing influence requires the expertise of Master's-prepared advanced practice nurses (APNs) who have exceptional knowledge of cardiovascular disease. APNs can enhance quality and efficiency through coordination and provision of care in the hospital and outpatient settings. Future research is needed to support the role of the APN in the delivery of health care.

Heart Failure↗
PubMed2003

Cardiac transplantation of skeletal myoblasts for heart failure.

Heart failure has become the most prevalent cardiovascular syndrome, and its incidence continues to increase. Most cases of heart failure develop as a result of myocardial infarction. Although current treatment modalities have brought us the opportunity to reduce mortality and morbidity after myocardial infarction, our progress has plateaued due to our inability to treat the underlying problem, death of cardiomyocytes. Recently, a new option has emerged. Transplantation of undifferentiated cells into the damaged heart is a promising new treatment modality. These cells may have the capability of adapting to the cardiac environment, regenerating the damaged muscle, restoring cardiac function and preventing transition to heart failure. During the last few years many cell types have been proposed for cardiac repair and promising pre-clinical studies have moved some of these into the clinic. The most widely studied cell type is the progenitor cell of adult muscle, or the myoblast. When transplanted into the heart myoblasts are able to engraft and to a large degree regenerate the infarcted area. Although the feasibility of myoblast transplantation has been proven in animal models of infarction, many questions remain unanswered. In this review we will try to present an overview of where intracardiac myoblast transplantation stands and where it is heading. We also provide our insight into the future potential for myoblast transplantation clinically.

Animals↗
PubMedDate not supplied

Cognitive impairment in heart failure.

Heart failure is reaching epidemic proportions in the United States, causing a constellation of disabling symptoms. Cognitive impairment in people with heart failure may be more common than previously known with multiple etiologies from both the disease process and the treatment. Exemplars from a research study are used to illustrate the perspective of heart failure patients. Given the critical importance of memory deficits on patient education, potential nursing interventions to address the issue of cognitive impairment are described.

Cardiac Output, Low↗
PubMed2004

[Signal transduction in heart failure].

Heart failure is the final culmination of protracted disease status precipitated by underlying ischemic disease, valvular insufficiency and viral myocarditis. The factors that lead to the development of heart failure are still not fully understood. In mammalian cells, four parallel kinase cascades have been described that finally lead to the activation of members of the mitogen-activated protein kinase(MAPK) family, such as ERKs (p42 and p44), JNK and p38 protein kinase. Apoptosis signal-regulating kinase 1 (ASK1), an upstream activator of JNK and p38, was shown to promote heart dysfunction and dilation as well as cardiac fibrosis. Meanwhile, not only myocyte apoptosis but also myocardial interstitial changes such as extracellular matrix deposition, activation of fibroblasts, and narrowing of vessel lumens play important roles for the progression of heart failure.

Animals↗
PubMed2003

A mechanistic role for cardiac myocyte apoptosis in heart failure.

Heart failure is a common, lethal condition whose pathogenesis is poorly understood. Recent studies have identified low levels of myocyte apoptosis (80-250 myocytes per 10(5) nuclei) in failing human hearts. It remains unclear, however, whether this cell death is a coincidental finding, a protective process, or a causal component in pathogenesis. Using transgenic mice that express a conditionally active caspase exclusively in the myocardium, we demonstrate that very low levels of myocyte apoptosis (23 myocytes per 10(5) nuclei, compared with 1.5 myocytes per 10(5) nuclei in controls) are sufficient to cause a lethal, dilated cardiomyopathy. Interestingly, these levels are four- to tenfold lower than those observed in failing human hearts. Conversely, inhibition of cardiac myocyte death in this murine model largely prevents the development of cardiac dilation and contractile dysfunction, the hallmarks of heart failure. To our knowledge, these data provide the first direct evidence that myocyte apoptosis may be a causal mechanism of heart failure, and they suggest that inhibition of this cell death process may constitute the basis for novel therapies.

Animals↗
PubMed2000

The economic burden of heart failure.

Heart failure, a major cause of morbidity and mortality among the elderly, is a serious public health problem. As the population ages and the prevalence of heart failure increases, expenditures related to the care of these patients will climb dramatically. As a result, the health care industry must develop strategies to contain this staggering economic burden. Strategies may include adopting approaches for preventing heart failure and implementing new treatment modalities with proven efficacy into large-scale clinical practice. Successful implementation of these strategies will require intensive physician and patient education and development of innovative approaches to fund support services.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Myocardial revascularization for the treatment of post-ischemic heart failure.

Heart failure due to coronary artery disease is a major public health problem. Medical treatment ameliorates symptoms and prognosis, although mortality remains high. Heart failure occurs when a sizeable number of myocytes do not contract. This may be due to irreversible myocyte loss (infarct) and/or dysfunctional but viable myocytes (hibernating), which can resume function following coronary artery bypass surgery. The presence of hibernating myocardium can be predicted by noninvasive nuclear imaging using both single photon (SPECT) and positron emission tomography, and also by stress echocardiography. A number of uncontrolled studies have demonstrated a promising role for coronary artery bypass surgery in patients with heart failure in whom a substantial amount of hibernating myocardium is present. These findings, particularly the magnitude of the benefits reported, justify the need for a randomized trial in this patient population.

Angina, Unstable↗
PubMed1990

Regional blood flow supply and demand in heart failure.

Heart failure results not only in a fall in cardiac output but also in a redistribution of blood flow favoring some regional beds (the brain and the heart) at the expense of others (the kidney and working skeletal muscle). The chronic resting hypoperfusion of striated muscle is further compromised with exercise. Maladaptive vasoconstrictor control mechanisms prevent the redirection of blood flow from nonworking muscle and liver to working muscle. This inappropriate preservation of nonworking organ perfusion further compromises the functional capacity of working muscle and is associated with evidence for metabolic deconditioning with reduced oxygen extraction and impaired oxidative phosphorylation. It is becoming increasingly clear that the clinical response to the inotropic and vasodilator therapy used in heart failure is in part dependent on the differing regional blood flow profiles of the various agents studied. The ability of the angiotensin-converting enzyme inhibitors to redirect blood flow away from nonworking regional beds to exercising muscle, and thereby to reestablish an appropriate physiologic response to changing metabolic needs, may be the overriding reason for their long-term efficacy. Certainly in the future the comprehensive therapy of heart failure will have to take into consideration not only central hemodynamic but also regional blood flow/supply and demand issues.

Heart Failure↗