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PubMed1997

The delayed recovery of impaired endothelium-dependent vasodilatory response after hemodynamic improvement in dogs with congestive heart failure.

We investigated whether impaired endothelium-dependent vasodilatory response recovers as heart failure improves. The femoral blood flow responses to intra-arterial administration of nitroglycerin (NTG) and acetylcholine (ACh) were examined in dogs with 2-week pacing-induced chronic congestive heart failure (congestive heart failure group; CHF, n = 12). Thereafter, pacing was stopped and hemodynamic changes and femoral blood flow responses were re-examined either 1 week (recover 1 week group; Re 1W, n = 6) or 4 weeks (recover 4 weeks group; Re 4W, n = 6) after the cessation of pacing. Another group in which a pacemaker was implanted without pacing served as the control group (n = 8). In CHF, heart rate and pulmonary artery pressure increased, and echocardiography revealed increased left ventricular diastolic dimension and reduced percent fractional shortening compared with those in the control group. In Re 1W, all hemodynamic parameters returned to the basal levels and did not differ from those in the control group. Although there was no significant difference in the blood flow responses to NTG among the 4 groups, the responses to ACh in CHF were significantly reduced compared with those in the control group. Despite the recovered hemodynamics, femoral blood flow responses to ACh were still reduced in Re 1W, but they returned to the levels of the control group in Re 4W. Thus, vascular endothelial dysfunction recovers along with improvement in CHF, however, the recovery of endothelial function is delayed in comparison with improvement in cardiac function.

Acetylcholine↗
PubMed1977

The clinical recognition of congestive heart failure.

The recognition of early or mild congestive heart failure in the ambulatory patient is a common clinical challenge in everyday practice. Early diagnosis requires attention to symptoms, signs, and radiographic changes which may be minimal. This paper reviews basic pathophysiological principles involved in congestive heart failure and summarizes etiological factors which may cause or precipitate congestive heart failure. The symptoms, signs, and subtle radiological findings of early congestive heart failure are also described in some detail.

Cough↗
PubMed1994

Thyroid function in dogs with spontaneous and induced congestive heart failure.

The effects of spontaneous and experimentally induced congestive heart failure on serum thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3'5'-triiodothyronine (reverse T3), free T4, free T3 concentrations, and the serum T4 and T3 concentrations in response to administration of thyrotropin were studied. Serum thyroid hormone concentrations were not different between eight dogs with spontaneous congestive heart failure and normal age matched control dogs. Seven dogs with experimental heart failure were tested before and after induction of congestive heart failure by rapid ventricular pacing. Mean serum T4 and free T3 concentrations were decreased and mean serum reverse T3 concentration was increased following induction of heart failure. The serum T4 and T3 responses to thyrotropin were not altered. Thyroid gland morphology appeared normal in dogs with experimental heart failure. Experimental congestive heart failure, similar to some other nonthyroidal illnesses, alters thyroid hormone secretion and metabolism in dogs.

Animals↗
PubMed1997

Recognizing congestive heart failure in the neonatal period.

Signs of congestive heart failure can be subtle and vary in the time frame of presentation. As a result, this diagnosis is often missed in its early stages. This article reviews risk factors for myocardial dysfunction in the newborn period. Additionally, there is a comprehensive overview of cardiac physiology as it relates to the presentation of symptoms of congestive heart failure. This information is presented to provide a foundation of knowledge related to physiologic changes involved in congestive heart failure so that the health care provider can recognize congestive heart failure early.

Cyanosis↗
PubMed1998

Effect of heart transplantation on impaired peripheral microvascular perfusion and reactivity in congestive heart failure.

Whether reduced peripheral blood flow in congestive heart failure is reversed after heart transplantation, has not been closely examined. We therefore studied skin microvascular resting perfusion and reactivity in patients pre- and postoperatively. Resting digital skin perfusion, together with the responses to cold pressor test, postocclusive reactive hyperemia and direct skin heating were examined with laser Doppler perfusion measurements. We examined 28 patients with congestive heart failure and 14 of these patients after heart transplantation and compared them to 13 healthy controls. Measurements were performed within 3 months preoperatively and 12 days, 1, 2, 3 and 6 months postoperatively. Patients with congestive heart failure had significantly lower resting perfusion levels than controls and demonstrated attenuated responses to both stimuli of vasodilation (all P<0.01). While peak hyperemic responses improved significantly after transplantation, postocclusive area under the hyperemic curve decreased further, and none of these variables were normalized after 6 months. In contrast, minimal perfusion during cold pressor test increased from a significantly lower level in the patients with congestive heart failure (P<0.05), to a level similar to that of the controls within 12 days postoperatively. Thus, skin microvascular perfusion and reactivity improve, but are not normalized within 6 months of transplantation. Both pre- and postoperative factors may be involved in maintaining a dysfunction of the peripheral microcirculation, which may contribute to exercise intolerance and hypertension in heart transplant recipients.

Adult↗
PubMed1990

Neurohumoral activation in congestive heart failure.

This article reviews the evidence that congestive heart failure is accompanied by an increased plasma norepinephrine concentration and that this is due not only to a reduced tissue clearance of the substance but also to a marked increase in sympathetic nerve activity. It also reports data that indicate that the sympathetic activation is associated with an activation of the renin-angiotensin system and an increased plasma level of vasopressin. At which degree of congestive heart failure these phenomena become manifest is not clear, but some studies suggest that the sympathetic and renin-angiotensin systems may be normal in asymptomatic congestive heart failure but already somewhat activated when this condition reaches New York Heart Association class II. There is also evidence that this activation, though initially compensatory, is eventually responsible for a number of adverse cardiovascular effects that account for the negative relationship between this event and survival. Finally, the article discusses the inability of the increased plasma level of atrial natriuretic peptide that characterizes congestive heart failure to offset the adverse effects of the neurohumoral activation and the variable influence of drug treatment on this phenomenon. This is not impossible to achieve, however, because heart transplantation appears to rapidly normalize a major factor in the increased sympathetic activity observed before surgical intervention, that is, impairment of the arterial baroreflex.

Animals↗
PubMed1991

Left ventricular diastolic dysfunction in patients with congestive heart failure.

This study reviewed 372 male patients with congestive heart failure. Two hundred and eighty-three (77%) had congestive heart failure due to systolic dysfunction as demonstrated by radionuclide angiography. Eighty-seven (23%) with congestive heart failure were identified who had normal ejection fractions. All patients met the Framingham criteria for congestive heart failure. These 87 individuals had unrecognized diastolic heart failure. It is important to distinguish between systolic and diastolic heart failure because the pathophysiology, treatment, and prognosis differ significantly. The most frequent cause of diastolic heart failure in this study was hypertension. Diastolic dysfunction should be considered in patients with acute heart failure and severe uncontrolled hypertension, or in patients with ischemic heart disease who develop acute pulmonary edema. Patients who do not respond or deteriorate when treated for heart failure using conventional therapy may also have diastolic dysfunction. These patients warrant special recognition and tailored management.

Aged↗
PubMed1996

[Heart transplantation--one possibility in the treatment of advanced congestive heart failure].

The authors present epidemiological data about congestive heart failure, its most common etiology and prognosis. They justify the performance of heart transplantation (HTx) in the treatment of congestive heart failure. They analyze the present state of HTx in the world and describe also the history of HTx in Slovakia. They present the review of contraindications and indications for the inclusion of recipients into the HTx programme and describe the further fates of these patients. They regard the HTx as an integral component of the therapeutical approach to the precisely defined group of patients with otherwise refractory congestive heart failure. (Tab. 4, Fig. 6, Ref. 38.)

Animals↗
PubMed2003

Congestive heart failure and the elderly.

As patients age, congestive heart failure becomes an increasingly important problem and accounts for up to 20% of hospital admissions for patients over 65 years. With technological improvements in the treatment of coronary artery disease, improved survival after myocardial infarction, and better hypertension therapy, patients are living longer, thus the need for successful management of older patients with chronic heart failure. The elderly, especially minorities, tend to be under-represented in congestive heart failure trials. This article will focus on the care of the geriatric patient with congestive heart failure.

Adrenergic beta-Antagonists↗
PubMed1990

Excess purine degradation caused by an imbalance in the supply of adenosine triphosphate in patients with congestive heart failure.

To evaluate purine degradation in patients with congestive heart failure concentrations of serum hypoxanthine, lactate, and noradrenaline were measured before and after submaximal treadmill exercise in 12 patients with chronic congestive heart failure and nine healthy volunteers. In four patients the concentration of hypoxanthine was significantly higher than in the controls or in the remaining eight patients with congestive heart failure. Venous lactate and noradrenaline in the four patients with high concentrations of hypoxanthine were also significantly higher than those in the eight patients with normal concentrations of hypoxanthine. Patients who responded normally were also more likely to have been treated with vasodilators and angiotensin converting enzyme inhibitors. Exercise induced arrhythmias were more common in the patients with high concentrations of hypoxanthine. These results suggest that the excess purine degradation in patients with congestive heart failure might be the result of a "relative" disturbance in the supply of adenosine triphosphate caused by the shift of cellular metabolism from aerobic glycolysis to anaerobic glycolysis during submaximal exercise and that hypoxanthine (a substrate for xanthine oxidase and a source of free radicals) was increased after submaximal exercise in some patients with congestive heart failure.

Adenosine Triphosphate↗
PubMedDate not supplied

Mode of death in patients with congestive heart failure: comparison between possible candidates for heart transplantation and patients with less advanced disease.

To study whether the relative incidence of sudden death versus progressive congestive heart failure is related to the severity of congestive heart failure as assessed by determination of peak oxygen consumption, we followed 90 ambulatory patients with moderate to severe congestive heart failure for 24.1 +/- 13.1 months. All patients had a left ventricular ejection fraction of 40% or less (mean, 22.6% +/- 9.2%) and a peak oxygen consumption of 20 ml/min/kg or less (mean, 14.7 +/- 3.5 ml/min/kg). Patients with severe congestive heart failure who might be eligible for heart transplantation (group I: n = 37; peak oxygen consumption < or = 14 ml/min/kg, mean, 11.0 +/- 1.8 ml/min/kg; mean left ventricular ejection fraction, 22.3% +/- 9.3%) were compared with those considered too well for heart transplantation (group II: n = 53; peak oxygen consumption > 14 < or = 20 ml/min/kg, mean, 17.1 +/- 1.6 ml/min/kg; mean left ventricular ejection fraction, 22.9% +/- 9.1%). During follow-up, 15 patients (41%) in group I died; 11 patients (21%) in group II died. In group I, seven of the 15 deaths (47%) were sudden; in group II, nine of the 11 deaths (82%) occurred suddenly. Patients who died suddenly had a significantly higher peak oxygen consumption (14.0 +/- 3.5 ml/min/kg) than those who died of progressive congestive heart failure (11.0 +/- 3.1 ml/min/kg; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Death, Sudden↗
PubMed1987

Hypocalcemic congestive heart failure.

We have described a patient who had congestive heart failure associated with hypocalcemia. The heart failure improved as the serum calcium increased. We conclude that severe hypocalcemia may produce congestive failure in the normal heart.

Adult↗
PubMed2005

Impact of care at a multidisciplinary congestive heart failure clinic: a randomized trial.

BACKGROUND: Although multidisciplinary congestive heart failure clinics in the United States appear to be effective in reducing the number of hospital readmissions, it is unclear whether the same benefit is seen in countries such as Canada, where access to both general and specialized medical care is free and unrestricted. We sought to determine the impact of care at a multidisciplinary specialized outpatient congestive heart failure clinic compared with standard care. METHODS: We randomly assigned 230 eligible patients who had experienced an acute episode of congestive heart failure to standard care (n = 115) or follow-up at a multidisciplinary specialized heart failure outpatient clinic (n = 115). The intervention consisted of a structured outpatient clinic environment with complete access to cardiologists and allied health professionals. The primary outcomes were all-cause hospital admission rates and total number of days in hospital at 6 months. The secondary outcomes were total number of emergency department visits, quality of life and total mortality. RESULTS: At 6 months, fewer patients in the intervention group had required readmission to hospital than patients in the control group (45 [39%] v. 66 [57%], crude hazard ratio [HR] 0.59, 95% confidence interval [CI] 0.38-0.92. Patients in the intervention group stayed in hospital for 514 days compared with 815 days required by patients in the control group (adjusted HR 0.56, 95% CI 0.35-0.89). The number of patients seen in the emergency department and the total number of emergency department visits were similar in the intervention and control groups. At 6 months, quality of life, which was self-assessed using the Minnesota Living with Heart Failure questionnaire, was unchanged in the control group but improved in the intervention group (p < 0.001). No difference in mortality was observed, with 19 deaths in the control group and 12 in the intervention group (HR 0.61, 95% CI 0.24-1.54). INTERPRETATION: Compared with usual care, care at a multidisciplinary specialized congestive heart failure outpatient clinic reduced the number of hospital readmissions and hospital days and improved quality of life. When our results are integrated with those from other, similar trials, multidisciplinary disease management strategies for congestive heart failure are associated with clinically worthwhile improvements in survival.

Aged↗
PubMed1989

The role of endogenous dopamine in congestive heart failure.

Although the effects of epinephrine and norepinephrine in congestive heart failure have been extensively studied, and exogenous dopamine, another of the catecholamines, has been widely used for the treatment of congestive heart failure, little attention has been paid to the physiological significance of endogenous dopamine in this condition. The present study was therefore designed to assess the physiological significance of endogenous dopamine in congestive heart failure. Nineteen patients with congestive heart failure caused by such conditions as acute myocardial infarction, valvular disease and dilated cardiomyopathy were examined before and after treatment with diuretics, digitalis and vasodilators. Electrolyte, creatinine and catecholamine concentrations in plasma and urine were analyzed. Urinary dopamine levels were increased in 13 out of 19 cases before treatment and returned to the normal range after treatment, falling from 2448 +/- 950.7 to 528.8 +/- 56.3 micrograms/day (normal level, less than 700 micrograms/day). Urinary dopamine excretion was markedly elevated within 24 hours after the onset of symptoms of heart failure, such as chest pain, palpitations and dyspnea. The relationship between urinary dopamine excretion and time after the onset of symptoms showed a strong statistical correlation (r = 0.55, p less than 0.001). Urinary dopamine excretion was also well correlated with plasma dopamine concentration, urinary norepinephrine excretion and venous pressure. From these results, it is concluded that endogenous dopamine seems to play an important role during the acute phase of congestive heart failure.

Adult↗
PubMed1996

Congestive heart failure revisited: new concepts in treatment.

Congestive heart failure is a major cause of morbidity and mortality as the population ages. This article reviews the progress made in treating the two major causes of heart failure--mechanical and myocardial. New approaches to relieving mitral stenosis and guidelines for the treatment of congestive heart failure are reviewed. Appropriate assessment and management leads to major improvement in prognosis.

Cardiomyopathies↗
PubMed2004

Urinary excretion of aquaporin-2 water channel exaggerated dependent upon vasopressin in congestive heart failure.

BACKGROUND: Impaired water excretion occurs in patients with congestive heart failure. The present study was undertaken to determine whether urinary excretion of aquaporin-2 (AQP-2) water channel is exaggerated in patients with congestive heart failure dependent upon arginine vasopressin (AVP). METHODS: Sixty-five patients with congestive heart failure and eight age- and gender-matched control subjects were examined. The patients were divided into four groups according to the criteria of New York Heart Association (NYHA). Plasma AVP levels, urinary excretion of AQP-2, and cardiac index were determined. RESULTS: Plasma AVP levels were progressively increased following the severity of NYHA class in the patients with congestive heart failure. Cardiac index was inversely decreased, and there was a negative correlation between plasma AVP levels and cardiac index (r=-0.430, P < 0.02). Urinary excretion of AQP-2 was 187.3 +/- 50.2 fmol/mg creatinine in the control subjects. It was markedly increased in the patients. Urinary excretion of AQP-2 was elevated to 1144.4 +/- 257.5 and 990.5 +/- 176.0 fmol/mg creatinine in the patients with NYHA class III and class IV, respectively, values significantly greater than the control subjects (P < 0.05). Urinary excretion of AQP-2 had a positive correlation with plasma AVP levels (r= 0.280, P < 0.02). CONCLUSION: The present study indicates that exaggerated urinary excretion of AQP-2 is dependent on baroreceptor-mediated release of AVP in patients with congestive heart failure.

Adult↗