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PubMed2000

Non-invasive estimation of right atrial pressure by combined Doppler echocardiographic measurements of the inferior vena cava in patients with congestive heart failure.

BACKGROUND: In patients with congestive heart failure, evaluation of right atrial pressure (RAP) provides useful therapeutic, functional and prognostic information. The aim of this study was to investigate whether a combination of inferior vena cava variables measured by Doppler echocardiography could provide a reliable non-invasive estimate of RAP. METHODS: One hundred consecutive patients with severe congestive heart failure (ejection fraction 24 +/- 6%) due to dilated cardiomyopathy were evaluated by simultaneous Doppler echocardiography and hemodynamic studies. RAP, end-expiratory (IVCDmax) and end-inspiratory (IVCDmin) diameters of the inferior vena cava, its collapse index [CIIVC = (IVCDmax - IVCDmin/IVCDmax)*100] and systolic fraction of forward inferior vena cava flow were measured and correlated by both single and multilinear regression analysis. The accuracy of generated equations was tested in a separate testing group of 61 patients at baseline and a subgroup of 20 patients after loading manipulations, prospectively studied in the same methodological setting. RESULTS: All Doppler echocardiographic variables were correlated with RAP. The IVCDmin showed the strongest correlation (r = 0.84, p < 0.0001). Stepwise regression analysis identified two equations for predicting RAP: 1) RAP = (6.4*IVCDmin + 0.04*CIIVC - 2) (r = 0.82, p < 0.0001, SEE 1.7 mmHg) in all patients, and 2) RAP = (4.9*IVCDmin + 0.01*CIIVC - 0.2) (r = 0.92, p < 0.0001, SEE 1.2 mmHg) in patients without tricuspid regurgitation. In the testing group estimated and measured RAP was strongly correlated at baseline (r = 0.95, SEE 1.3 mmHg, p < 0.00001) and after loading manipulations (r = 0.96, SEE 1.2 mmHg, p < 0.00001). The agreement between invasive and non-invasive measurements of RAP in identifying patients with normal (< or = 5 mmHg), moderately increased (< 5 RAP < 10 mmHg) and markedly increased (> or = 10 mmHg) RAP was 81 or 93% using equation 1 or 2, respectively. CONCLUSIONS: Our results provide evidence that in patients with congestive heart failure indices derived from Doppler measurements of the inferior vena cava can be used to produce an accurate, strong and non-invasive estimate of RAP. This is another example of the usefulness of Doppler echocardiography in evaluating hemodynamic profile and its changes in patients with congestive heart failure. Echocardiographic assessment of the inferior vena cava should be included in the evaluation of patients with congestive heart failure.

Analysis of Variance↗
PubMed1989

An overview of integration of therapy for congestive heart failure.

Patients with symptoms of congestive heart failure look to treatment to relieve symptoms, improve the quality of life, and prolong life. They prefer a convenient dosing schedule, with minimal side effects and low cost. A wide variety of agents are available to treat patients with congestive heart failure. The three major classes of drugs that improve heart failure include the diuretics, inotropic drugs, and vasodilators. It appears that any one of these three classes are potential first-line candidates for treating patients with congestive heart failure. Patients with edema usually require long-term therapy with diuretic agents. Since the vasodilators are the only class of drugs which have been shown to prolong life, they should be used routinely in the management of patients with congestive heart failure. Since all three classes of drugs have additive beneficial hemodynamic effects, it makes sense to consider the use of all three in patients with at least moderate to severe heart failure. At the moment unanswered questions include the role of antiarrhythmic agents in reducing the incidence of sudden death, and the use of potent new inotropic vasodilators. Overall, the current therapeutic approach to patients with heart failure is effective in relieving symptoms, improving exercise tolerance and in prolonging life.

Heart Failure↗
PubMed1995

Hospital admissions and deaths due to congestive heart failure in New Zealand, 1988-91.

AIMS: Congestive heart failure is believed to be a major public health problem in most Western countries; however, little is known about the extent of morbidity and mortality from congestive heart failure in New Zealand. This paper reports data on hospital admissions and mortality due to congestive heart failure in New Zealand during the years 1988-91. METHODS: All data were obtained from the New Zealand Health Information Service. Deaths from congestive heart failure were identified from ICD-9 codes indicating a primary diagnosis of congestive heart failure. Hospitalisations for congestive heart failure were identified both from ICD-9 codes indicating a primary diagnosis of congestive heart failure and from codes indicating a diagnosis of congestive heart failure secondary to chronic rheumatic heart disease, ischaemic heart disease or valvular heart disease (nonrheumatic). RESULTS: Each year there was an average of about 850 deaths ascribed to heart failure; two-thirds of these occurred in patients over the age of 75 years. Each year there was also an average of about 8000 hospital admissions of about 5000 patients for congestive heart failure; 75% of these admissions involved patients over 65 years old. The mean duration of hospital stay for congestive heart failure was 16 days. On this basis, it is estimated that hospital admissions for congestive heart failure are likely to cost about NZ$50 million each year, or about 1% of the total health budget. CONCLUSIONS: Congestive heart failure is clearly a major public health problem in New Zealand with high hospitalisation and mortality rates. Several strategies have been proven to reduce mortality and hospital admissions for congestive heart failure and these should be utilised widely in patients at risk.

Aged↗
PubMed2003

Intraventricular conduction defects in patients with congestive heart failure: left but not right bundle branch block is an independent predictor of prognosis. A report from the Italian Network on Congestive Heart Failure (IN-CHF database).

BACKGROUND: In industrialized countries the prevalence of congestive heart failure (CHF) is increasing. Many clinical factors have been shown to influence the prognosis of CHF. The effect of a wide QRS on mortality is debated; while left bundle branch block (LBBB) has been already identified as a negative prognostic factor, the effect of right bundle branch block (RBBB) is still unknown. The aim of this study was to compare the association of these two intraventricular conduction defects on the prognosis of CHF. METHODS: Data were derived from the Italian Registry of CHF. Entry in the Registry required that patients had a diagnosis of CHF based on the European Society of Cardiology guidelines. We analyzed the 1-year follow-up data of 5517 outpatients with CHF of different etiologies. The presence of a wide QRS was defined if the duration was > 120 ms. RESULTS: A wide QRS was present in 2066 patients (37.5%), 25.2% with LBBB, 6.1% with RBBB, 6.2% with other intraventricular defects. At univariate analysis patients with complete LBBB had a significantly higher 1-year mortality than those without (16.1 vs 11.9%) but this was not true for complete RBBB (11.9 vs 11.9%). Even after multivariate adjustment, complete LBBB still remained an independent predictor of death (relative risk 1.36, 95% confidence interval 1.15-1.61). CONCLUSIONS: LBBB but not RBBB is an independent predictor of death in CHF.

Aged↗
PubMed1991

Limb vascular responsiveness to beta-adrenergic receptor stimulation in patients with congestive heart failure.

BACKGROUND: In patients with congestive heart failure, the chronotropic and inotropic responses to beta-adrenergic agonists are reduced. It is not known whether desensitization of peripheral beta-adrenoceptors accounts for impaired limb vasodilation in these patients. Accordingly, we studied 14 normal subjects and 13 age-matched patients with congestive heart failure. METHODS AND RESULTS: To distinguish vasodilation mediated by beta-adrenoceptors and adenylate cyclase from that mediated by stimulation of guanylate cyclase, each subject received intrabrachial artery infusions of isoproterenol (1-100 ng/min) and sodium nitroprusside (0.3-10 micrograms/min), respectively. Forearm blood flow was determined by venous occlusion plethysmography. Maximal vasodilative potential, determined during reactive hyperemia, was reduced in the patients with congestive heart failure. The maximal forearm blood flow response to isoproterenol was comparable in patients with heart failure and in normal subjects (8.0 +/- 1.1 versus 9.2 +/- 1.2 ml/100 ml of tissue/min, respectively, p = NS). Furthermore, the dose-response relation to isoproterenol was similar in both groups. Likewise, the forearm vasodilative response to sodium nitroprusside was preserved in the heart failure group. Plasma concentration of norepinephrine was higher in the patients with heart failure (436 +/- 34 versus 201 +/- 74 pg/ml, p less than 0.01). When both groups were considered, there was no correlation between norepinephrine levels and the maximal forearm blood flow response to isoproterenol (r = 0.10, p = NS). CONCLUSIONS: We conclude that beta-adrenoceptor desensitization does not occur in the limb vessels of patients with congestive heart failure.

Adrenergic beta-Agonists↗
PubMed1992

Effects of prehospital medications on mortality and length of stay in congestive heart failure.

HYPOTHESIS: Prehospital medications for congestive heart failure should affect hospital outcomes (survival and length of stay). STUDY DESIGN: In a retrospective case series, hospital outcomes were compared for patients treated with prehospital nitroglycerin, furosemide, and/or morphine (252) versus those given no medications (241). SETTING: A rural/suburban emergency medical services system (population 140,000) served by three paramedic units. PARTICIPANTS: Four hundred ninety-three consecutive cases of congestive heart failure or pulmonary edema were identified by hospital discharge diagnosis from a data base of 8,315 paramedic transports with known outcome. INTERVENTIONS: Oxygen was given by protocol to 489 patients. Other medications were given by order of on-line physician medical command. RESULTS: Overall mortality was 10.9% (54 of 493). Treated and untreated patients were comparable in age, sex, cardiac rhythms, prior use of cardiac medications, and response and scene times; mortality was reduced in treated versus untreated patients (odds ratio for improved survival, 2.51; 95% confidence interval, 1.37 to 4.55; P less than .01). Positive treatment effect was greatest for 58 nonhypotensive, critical patients (odds ratio for survival, 10.25; P less than .01). No single drug combination was unique in terms of treatment benefit. Patients treated in the field received medications 36 minutes earlier than patients first treated in the emergency department. No survival benefit was evidence for noncritical, nonhypotensive patients, and patients with final diagnoses of asthma, chronic obstructive pulmonary disease, pneumonia, or bronchitis had a higher than expected mortality if erroneously treated for congestive heart failure. Differences in hospital length of stay were not significant for any group. CONCLUSION: Prehospital medications improve survival in congestive heart failure, especially in critical patients. More than one combination of medications seems effective, and early treatment is associated with improved survival. However, these medications appear to increase mortality in patients misdiagnosed in the field. Factors used in paramedica and medical command assessments require further study.

Academic Medical Centers↗
PubMed1996

Pulmonary hypertension caused by congestive heart failure is ameliorated by long-term application of an endothelin receptor antagonist. Increased expression of endothelin-1 messenger ribonucleic acid and endothelin-1-like immunoreactivity in the lung in congestive heart failure in rats.

OBJECTIVES: The purpose of this study was to investigate whether 1) endothelin-1, a potent vasoconstrictor peptide, is involved in progression of pulmonary hypertension caused by congestive heart failure (CHF); and 2) whether long-term treatment with BQ-123, an endothelin receptor antagonist, ameliorates pulmonary hypertension caused by CHF. BACKGROUND: Congestive heart failure accompanies pulmonary hypertension, and the severity of pulmonary hypertension is an important determinant of prognosis. Although we reported that production of endothelin-1 is increased in the failing heart in rats with CHF, it is not known whether production of endothelin-1 in the lung is altered by CHF. METHODS: Congestive heart failure was induced by coronary artery ligation in rats. Expression of preproendothelin-1 messenger ribonucleic acid (mRNA) in the lung and kidney was determined. Endothelin-1 staining (immunoreactivity) in the lung was studied by immunohistochemical analysis. Effects of long-term BQ-123 treatment on the rats were studied. RESULTS: Two weeks postoperatively, CHF accompanied by pulmonary hypertension developed in the rats (CHF rats). Expression of preproendothelin-1 mRNA in the lung was markedly higher in the CHF rats than in the sham-operated rats, whereas that in the kidney did not differ between the two groups. Endothelin-1 staining on the pulmonary vascular endothelial cells was more intense in the CHF rats. BQ-123 treatment over a 2-week period in the CHF rats greatly reduced right ventricular systolic pressure and central venous pressure, but it did not affect blood pressure or left ventricular contractility (peak positive first derivative of left ventricular pressure) in these rats. CONCLUSIONS: Long-term BQ-123 treatment greatly ameliorated pulmonary hypertension in the CHF rats. The present study suggests that endothelin-1 plays an important role in the progression of pulmonary hypertension caused by CHF and that an endothelin receptor antagonist may be a new therapeutic agent for CHF-induced pulmonary hypertension.

Animals↗
PubMed1991

Impaired suppression of plasma norepinephrine during head-down tilt in patients with congestive heart failure.

Neurohumoral activation is present in congestive heart failure and may contribute to vasoconstriction in this syndrome. The mechanisms leading to and maintaining neurohumoral activation in long-standing congestive heart failure are as yet undefined. The present study addresses the possibility that baroreceptor-mediated suppression of plasma norepinephrine may be abnormal in patients with long-standing congestive heart failure. Eight normal subjects and 12 patients with long-standing congestive heart failure were studied during 15 minutes of 30 degrees head-down tilt. There were no significant changes in heart rate or arterial blood pressure in either group during these maneuvers. In normal subjects, plasma norepinephrine declined from 257 +/- 38 pg/ml at control to 208 +/- 39 pg/ml during head-down tilt (p less than 0.005). Plasma norepinephrine was elevated in the patients with congestive heart failure, 475 +/- 189 pg/ml, and did not change during head-down tilt. These observations suggest that baroreflex loading maneuvers, which in this study included increased central blood volume and hydrostatic effects on the sinoaortic baroreceptor, do not suppress increased plasma norepinephrine in patients with long-standing congestive heart failure. Impaired baroreflex responsiveness could therefore contribute to either the generation or maintenance of high plasma norepinephrine in this syndrome.

Adult↗
PubMed1982

The renin-angiotensin-aldosterone system, antidiuretic hormone and sympathetic nerve activity in an experimental model of congestive heart failure in the dog.

1. Congestive heart failure was induced in dogs by rapid pacemaker stimulation of the heart (240-280/min) for 14 days. This represents a model of low output heart failure which permits the study of the development and reversal of congestive heart failure in an anatomically intact circulation in the unanaesthetized animal. 2. Cardiac output was reduced by 54%. Pulmonary artery pressure gradually increased by a factor of 2.4 and pulmonary capillary pressure rose to 4.6 times basal values. The animals retained a mean of 1.1 litres of fluid. 3. At the same time there was a gradual increase of plasma levels of renin, angiotension II, aldosterone, noradrenaline and adrenaline. After the pacemaker stimulation was discontinued all hormone levels returned to normal, the retained fluid was excreted, and intracardiac pressures and cardiac output returned to baseline values. 4. When heart failure was established at the end of the pacemaker stimulation period an inappropriately high secretion of antidiuretic hormone in relation to plasma osmolality was observed in five of six dogs. 5. It is concluded that beside the well-known non-hormonal renal factors, these hormone systems may be involved in the formation of oedema in congestive heart failure. The inappropriately high levels of antidiuretic hormone may cause hyponatraemia by water retention, representing a state of 'dilutional hypo-osmolality'.

Animals↗
PubMed2000

Acute Congestive Heart Failure and Tumor Necrosis Factor Alpha.

Congestive heart failure is prevalent in the elderly; recurrent hospital admissions for acute deterioration is a major health care problem. We examined tumor necrosis factor alpha levels in 31 congestive heart failure patients who were admitted to the hospital due to acute cardiogenic pulmonary edema. Blood samples were taken within 24 hours of admission and at the time of discharge after recovery. Tumor necrosis factor alpha levels were also measured in 10 stable congestive heart failure outpatients and 16 healthy controls. Tumor necrosis factor alpha level at admission was higher than at time of discharge (4.6Â+/-1.9 vs. 3.4Â+/-1.1 (rg/mL, p is less than 0.02). Mean tumor necrosis factor alpha level of stable congestive heart failure outpatient was 2.6Â+/-0.7 rg/mL healthy controls had significantly lower tumor necrosis factor alpha levels (1.7Â+/-0.7 rg/mL) than congestive heart failure patients (p is less than 0.01). tumor necrosis factor alpha levels were highest among acute congestive heart failure patients. Elevated tumor necrosis factor alpha appears to be related to the exacerbation of congestive heart failure and may be a marker for deterioration. (c) 2000 by CVRR, Inc.

Journal Article↗
PubMed1990

[Efficacy of long-term treatment with enalapril in patients with congestive heart failure].

Effects of enalapril on congestive heart failure and survival until 12 months have been evaluated in 60 patients with congestive heart failure (II, III, IV NYHA class) versus 60 control patients. Enalapril has been administered with digitalis and diuretic for 12 months 5 mg twice a day; in 60 control patients only digitalis and diuretic have been administered. Patients have been controlled every month during 12 months evaluating: NYHA class, time of exercise at treadmill, ejection time of left ventricle, speed index of ejection, cardiac output, systolic output, ECG, blood pressure, creatinine, BUN and electrolytes. After 12 months a significant increase (p less than 0.001) of systolic and cardiac output in patients with enalapril has been recorded. Also the increase of exercise time was more evident in patients with enalapril (p less than 0.01). The results show that long term treatment with enalapril in patients with congestive heart failure, improving cardiac performance, gives an hemodynamic and symptomatic benefit.

Adult↗
PubMed1979

Operative treatment of cerebral arteriovenous aneurysm of vein of Galen complicated by congestive heart failure.

A rare cause of congestive heart failure in the neonatal period is an intracranial arteriovenous malformation, but this condition should be borne in mind when there is unexplained right-sided congestive heart failure. A case is reported of an aneurysm of the great vein of Galen, complicated by congestive heart failure. Successful surgical treatment was carried out using a two-stage procedure.

Female↗
PubMed2003

Cognitive impairment: a key feature of congestive heart failure in the elderly.

Congestive heart failure (CHF) has been proposed as a possible cause of cognitive dysfunction but only a few studies have directly assessed cognitive performance in CHF. The aim of the present study was to compare the cognitive patterns of patients with CHF and patients having cardiovascular diseases uncomplicated by CHF (no-CHF group). In a multicenter observational case-control study, we studied 149 hospitalized elderly CHF patients in the New York Heart Association (NYHA) class II (CHFm, m: moderate), 159 CHF patients in NYHA class III-IV (CHFs, s: severe), and 207 no-CHF patients. Patients underwent a multidimensional assessment and neuropsychological tests for the following cognitive domains: attention, visual-spatial intelligence, verbal attainment, verbal and visuo-spatial memory. Neuropsychological performances of groups were compared by multivariate analysis. Correlates of an abnormal performance on at least three neuropsychological tests were assessed by logistic regression analysis. CHFs performed worse than no-CHF patients on 4 of the 7 neuropsychological measures, the largest difference being in tests of attention and verbal learning (p < 0.001). Prevalence of abnormal performance on at least 3 tests was 57.9 % in CHFs, 43% in CHFm and 34.3 % in no-CHF groups (chi square = 17.3, p < 0.0001). The following qualified as independent correlates of the outcome at logistic regression analysis: CHFs group membership (Odds Ratio-OR = 2.56, 95% Confidence Interval-CI = 1.49-4.40), depression (OR = 2.37, 95% CI = 1.54-3.66), hypertension (OR = 1.88, 95% CI = 1.18-2.99). Our results demonstrate that cognitive impairment is common among CHF patients and seems to be causally related to CHF severity, depression and hypertension. The cognitive dysfunction also characterizes a relevant fraction of patients with cardiovascular diseases uncomplicated by CHF.

Aged↗
PubMed1998

Coronary artery bypass surgery as treatment for ischemic heart failure: the predictive value of viability assessment with quantitative positron emission tomography for symptomatic and functional outcome.

OBJECTIVES: To determine the predictive value of quantitative evaluation of myocardial viability on changes in left ventricular function, exercise capacity, and quality of life after coronary artery bypass grafting in patients with ischemic heart failure (congestive heart failure, New York Heart Association class > or = III) with and without angina. METHODS: Thirty-five patients, 14 with congestive heart failure and angina (CHF-angina) and 21 with congestive heart failure without angina (CHF-no angina) were studied at baseline and 6 months after coronary bypass grafting. Left ventricular function was evaluated with transthoracic echocardiography and radionuclide ventriculography. Myocardial viability was assessed with [18F]-2-fluoro-2-deoxy-D-glucose using positron emission tomography. Peak aerobic capacity (peak oxygen consumption) and anaerobic threshold were assessed with treadmill exercise test and quality of life with a questionnaire. RESULTS: A total of 286 of 336 dysfunctional left ventricular segments were viable. There were two perioperative deaths (5.7%) and three late deaths. Left ventricular ejection fraction increased from 23% +/- 7% to 32% +/- 9% (p < 0.0001), and a linear correlation was found between the number of viable segments and the changes in ejection fraction (r = 0.65; p = 0.0001). Receiver operating characteristics curve identified eight viable segments as the best predictor for increase of ejection fraction more than 5 percentage points. Peak oxygen consumption increased from 15 +/- 4 to 22 +/- 5 ml/kg per minute (p < 0.0001). Preoperatively, anaerobic threshold was identified in one patient from the CHF-angina group and in all from the CHF-no angina group and increased from 13 +/- 4 to 19 +/- 4 ml/kg per minute (p < 0.0001). Quality of life scores improved significantly in both groups. No correlation was found between the amount of viable dysfunctional myocardium and changes in exercise capacity or quality of life. CONCLUSIONS: In patients with postischemic congestive heart failure the amount of viable myocardium dictates the degree of improvement in left ventricular function after revascularization.

Angina Pectoris↗
PubMed1993

Vasodilator therapy for congestive heart failure. Lessons from mortality trials.

Congestive heart failure is a major clinical and public health problem affecting between 2 and 3 million people in the United States. Whereas myocardial dysfunction assumes a central pathophysiologic role in the development of chronic heart failure, alterations in the peripheral vasculature and neurohormonal systems serve to modulate the heart failure state. Short-term studies of nonspecific vasodilators and angiotensin-converting enzyme inhibitors demonstrate a beneficial effect of these agents on left ventricular function, hemodynamics, exercise tolerance, and quality of life in patients with congestive heart failure and depressed left ventricular systolic function. More recently, several large-scale multicenter trials have documented improved survival in patients with heart failure who received vasodilating agents. These studies, in conjunction with hemodynamic and functional studies, argue strongly for the widespread use of vasodilator therapy, notably the angiotensin-converting enzyme inhibitors, for congestive heart failure and left ventricular systolic dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Newer drug therapy for congestive heart failure.

BACKGROUND: The management of congestive heart failure has undergone a number of modifications over the past 5 to 10 years. METHODS: These include assaying the role of inotropic drugs, evaluating the role of phosphodiesterase inhibitors, considering the role of intermittent inotropic infusion in ambulatory patients, and recognizing the importance of angiotensin-converting enzyme inhibitors. Very recently, the important role of angiotensin II receptor blocking agents and the use of beta blockade have provided additional modalities for the control of congestive heart failure. The relative usefulness of such therapy has been reviewed in this article. CONCLUSION: The management of congestive heart failure has undergone considerable change with the use of newer and more effective drugs.

Adrenergic beta-Antagonists↗