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PubMed1999

Potential benefit of biventricular pacing in patients with congestive heart failure and ventricular tachyarrhythmia.

Treatment of congestive heart failure (CHF) aims for symptomatic relief and reduction of mortality both from sudden death and pump failure. The implantable cardioverter defibrillator (ICD) is highly effective in the prevention of sudden death, but no mortality benefit in advanced CHF has yet been shown. Biventricular pacing may lead to functional improvement in selected patients with CHF. Thus, a biventricular pacemaker with defibrillation capabilities may be ideal for patients with advanced CHF. We retrospectively analyzed the data from 384 patients (age 59 +/- 12 years, 322 male and 62 female) with regard to New York Heart Association (NYHA) CHF class, mean QRS duration, mean PR interval, presence of a QRS > 120 msec and incidence of atrial fibrillation at the time of ICD implantation. Based on eligibility criteria from studies in biventricular pacing, we analyzed how many patients may benefit from biventricular pacing. Patients with CHF were older (NYHA class III: 60.9 +/- 9.7, class II: 61.3 +/- 10 versus class I: 50.8 +/- 13.6 years, p < 0.001 each) and mean QRS duration was longer with advanced CHF (NYHA class III 127.8 +/- 30 msec; class II 119.4 +/- 27.7 msec; class 0-1: 103.9 +/- 17.7 msec, p < 0.001, analysis of variance) as was the mean PR interval (NYHA class III 189.9 +/- 33.5 msec; class II 176.1 +/- 29.3 msec; class 0-1 162.7 +/- 45.9 msec, p < 0.001, analysis of variance). The incidence of atrial fibrillation was higher in class III (25.5%) compared with class 0-1 (16.9%) and class II patients (14.1%, p = 0.043, chi-square test). A total of 28 patients (7.3%) fulfilled eligibility criteria for biventricular pacing if NYHA class III patients were considered candidates and 48 (12.5%) if patients with NYHA II CHF and ejection fraction < or = 30% were included. Thus, biventricular pacing may offer a promising therapeutic approach for a significant proportion of patients with CHF at risk for ventricular tachyarrhythmia.

Aged↗
PubMed1999

A pharmacoeconomic assessment of torsemide and furosemide in the treatment of patients with congestive heart failure.

The management of patients with congestive heart failure (CHF) can place a significant economic burden on managed care organizations, leading providers to seek treatments that are cost-effective. Diuretics play a significant role in the treatment of edema associated with CHF. We evaluated the use of 2 loop diuretics, torsemide and furosemide, in patients with CHF in a managed care setting. This prospective study compared clinical, economic, and quality-of-life outcomes in 240 patients randomized to the 2 drugs. Patients with New York Heart Association (NYHA) class II or class III CHF requiring loop diuretic treatment, either alone or in conjunction with other therapy, were eligible. Patients were told about the study during an office visit, and those with an interest in participating and who met the eligibility criteria were given further information and the opportunity to participate. After investigators obtained informed consent, patients were enrolled, randomized to either treatment, and followed for 6 months. Outcomes included CHF/cardiovascular (CV)-related medical costs, change in NYHA class, change in sodium retention score, hospitalizations, physician visits, medication use, adverse events, and change in quality of life. A total of 103 patients were randomized to torsemide, and 137 patients were randomized to furosemide. Except for body weight, patient demographic characteristics did not differ between groups at baseline; patients in the torsemide group were significantly heavier (P = 0.004). The results showed that mean total CHF/CV-related medical costs did not differ between groups (torsemide, $1520.07; furosemide, $1503.26; P = 0.975), despite higher mean drug-acquisition costs for torsemide patients ($121.01 vs $42.95; P < 0.0001). Mean costs were similar for CHF/CV-related hospitalizations (torsemide, $845.84; furosemide, $893.33; P = 0.918) and CHF-related physician visits (torsemide, $138.80; furosemide, $164.09; P = 0.288). Quality of life was significantly better for patients in the torsemide group at month 4 (P = 0.017), but not at month 2 (P = 0.059) or month 6 (P = 0.269). The number of adverse events did not differ significantly between groups (torsemide, 221; furosemide, 287; P = 0.916). The results of this study appear to indicate that in a representative cross-section of managed care patients, those who received torsemide, despite higher drug-acquisition costs, had similar CHF/CV-related management costs compared with furosemide recipients.

Aged↗
PubMed2002

Hypomagnesemia and concurrent acid-base and electrolyte abnormalities in patients with congestive heart failure.

BACKGROUND: Patients with severe decompensated congestive heart failure (CHF) commonly exhibit acid-base and electrolyte disturbances mainly due to the activation of several neurohumoral mechanisms as well as to drugs regularly used in this population. Magnesium deficit is not infrequently observed in CHF patients but its pathophysiology remains less well-studied as compared with other electrolyte alterations, such as hypokalemia. However, there is evidence that early detection and correction of magnesium abnormalities could obviate potentially deleterious arrhythmogenic effects. AIM: To assess the incidence of magnesium level disorders and analyze the underlying pathophysiological mechanisms in patients with CHF. METHODS: Eighty-six consecutive CHF patients (NYHA class III or IV) admitted to our hospital over a period of 5 years were studied. Patients with diabetes mellitus, liver or renal failure, and chronic obstructive lung disease were excluded. All patients received conventional treatment with digoxin, diuretic agents and an angiotensin converting enzyme inhibitor. On admission, blood and urine electrolytes and renal function parameters were determined. Arterial blood gases and serum anion gap determinations were also performed. RESULTS: Hypomagnesemia was found in 15 [n=15 (17.4%)] CHF patients. The majority of these patients also exhibited other electrolyte abnormalities, such as hypokalemia, hypocalcemia and hypophosphatemia. Inappropriate magnesiuria (fractional excretion of magnesium >4%) was evident in eight hypomagnesemic patients. A variety of associated conditions, including poor dietary intake, also favored magnesium depletion. CONCLUSION: Magnesium deficit is a common electrolyte disorder in CHF (NYHA class III/IV) patients and several interrelated mechanisms are implicated in its pathogenesis. Clinicians' awareness of the incidence of hypomagnesemia in this population as well as its related pathophysiology could be useful for the early detection and appropriate treatment to inhibit its arrhythmogenic potential.

Acid-Base Imbalance↗
PubMed2006

The role of peritoneal dialysis in the management of treatment-resistant congestive heart failure: A European perspective.

Patients with congestive heart failure (CHF) resistant to conventional treatment have a poor prognosis. Extracorporeal ultrafiltration (UF) appears to be the therapy of choice for short-term management of such patients with severe fluid overload, whereas peritoneal dialysis (PD) may be the therapy of choice for the long-term treatment. Fluid removal results in reduction of plasma volume, improvement of hyponatremia, reduction in pulmonary capillary wedge pressure, improvement of New York Heart Association functional heart failure class, improvement of functional rehabilitation and quality of life, reduction of hospitalizations and readmissions, as well as improvement in diuretic responsiveness. Whether extracorporeal UF and/or PD modifies the survival rate of patients with refractory CHF needs to be determined in prospective randomized controlled trials.

Europe↗
PubMed2003

Neurohumoral activation and ventricular arrhythmias in patients with decompensated congestive heart failure: role of endothelin.

Patients with congestive heart failure (CHF) have a high incidence of ventricular arrhythmias and sudden arrhythmic death. CHF entails profound and complex abnormalities in humoral responses that are thought to promote arrhythmic events. However, it is unknown which of the many endogenous mediators that accumulate as part of neurohormonal activation is important in arrhythmogenesis in the setting of CHF. The study included 83 patients admitted to the hospital for treatment of decompensated CHF. Neurohormonal and cytokine activation was assessed by measuring plasma renin activity, aldosterone, norepinephrine, endothelin-1, tumor necrosis factor-alpha, and interleukin-6 levels. Atrial and ventricular arrhythmic events were assessed by 24-hour Holter monitoring. In a univariate analysis, a highly significant, positive relationship was found between plasma endothelin-1 levels and the average hourly total premature ventricular beats (P = 0.003), the frequency of ventricular pairs (P = 0.0003), and the frequency of ventricular tachycardia episodes (P = 0.001). After inclusion of clinical variables, drug therapies, neurohormones, and cytokine levels in a multivariate analysis, the positive relationship between plasma endothelin-1 level and the average hourly total premature ventricular beats (P = 0.008), the frequency of ventricular pairs (P = 0.007), and ventricular tachycardia episodes (P = 0.009) remained independent. No association between other neurohormones or cytokines and arrhythmic events was demonstrated. The results of the present study suggest that increased endothelin-1 concentrations may be involved in promoting the occurrence of ventricular ectopy in patients with decompensated CHF. Proarrhythmic effects may account, in part, for the poor outcome associated with increased endothelin-1 levels in patients with decompensated CHF.

Arrhythmias, Cardiac↗
PubMed2000

The diagnostic and therapeutic approach to the patient in acute congestive heart failure.

The patient presented in acute congestive heart failure represents a diagnostic challenge. Life-threatening compromise of respiratory or cardiovascular function renders the patient vulnerable to the stresses associated with many diagnostic tests. Before risking any test in this situation, it is important to understand the information that each test will give, and how that will impact the diagnostic and therapeutic approach in this crucial early phase of patient management. This article describes the diagnostic tests commonly used in the evaluation of patients in acute heart failure and the information that each provides, and discusses how this information can be used to guide therapy. Pericardiocentesis is discussed in detail.

Acute Disease↗
PubMed2001

Overview: old and new controversies in the treatment of advanced congestive heart failure.

In 2001, patients with decompensated congestive heart failure can be treated with various intravenous inotropic agents, vasodilator agents, invasive hemodynamic monitoring, ventricular assist devices, and cardiac transplantation. The use of many of these agents is limited by toxicities and potentially incremental costs associated with intensive care unit stays. As new pharmacologic therapies become available, such as beta-blockers and natriuretic peptides, the combinatorial use of agents for the treatment of patients with decompensated heart failure presents new opportunities with potentially reduced toxicities. Finally, given the natural history of patients with advanced heart failure, it behooves all caregivers to understand the wishes and preferences of the patients who face life-threatening decompensation. This is particularly true with long-term intravenous inotropic therapy. This review article addresses some of the issues that can affect the balance between efficacy, toxicity, and patient preferences for end-of-life care.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Prehospital therapy for acute congestive heart failure: state of the art.

Acute congestive heart failure (CHF) is one of the most common syndromes encountered in emergency care settings. Correct diagnosis and treatment for pulmonary edema, the most common acute manifestation of CHF, are of primary importance as misdiagnosis can result in deleterious consequences to patients. The pathogenesis of acute pulmonary edema (APE) is currently believed to arise primarily from the redistribution of intravascular fluid to the lungs secondary to acutely elevated left ventricular (LV) filling pressures. This understanding has provided a basis for the management of acute APE, which entails reduction of LV preload, reduction of LV afterload, ventilatory support, inotropic support as needed, and identification and treatment of other underlying factors contributing to elevated LV filling pressures. The agent most applicable and effective for field treatment is nitroglycerin. Diuretics and morphine should be used with caution, as they carry higher risks, especially in misdiagnosed patients. The role of angiotensin-converting enzyme (ACE) inhibitors has yet to be demonstrated in a prehospital setting. Noninvasive positive pressure ventilation methods are effective adjuncts to current treatment, but their mode of delivery presents technical challenges. The development of novel rapid diagnostic tools, currently in progress, might prove valuable for emergency medical services (EMS) personnel in the future. But for now, EMS personnel must rely on their fundamental skills of history taking and physical examination for accurate diagnosis of CHF.

Emergency Medical Services↗
PubMed1995

Congestive heart failure: public and private burden.

Chronic congestive heart failure (CHF) is a common yet devastating syndrome. CHF is a leading cause of morbidity and mortality in the United States and other industrialized countries. The incidence and prevalence of CHF is increasing, placing a growing burden on the health care system. Patients suffering from CHF report a poor quality of life because of physical symptoms, functional disability, emotional and economic burdens, frequent hospitalizations, and poor prognosis. Nurses play a key role in the identification of strategies for effective management of CHF.

Cost of Illness↗
PubMed2000

Brain blood flow patterns after the development of congestive heart failure: effects of treadmill exercise.

OBJECTIVE: Congestive heart failure (CHF) is associated with left ventricular (LV) failure, neurohormonal system activation, and diminished exercise capacity. Although alterations in systemic vascular resistive properties have been recognized to occur with CHF, whether and to what degree perfusion abnormalities occur within the brain after the development of CHF remain poorly understood. Accordingly, the present study measured brain blood flow patterns in pigs after the development of pacing-induced CHF at rest and after treadmill-induced exercise. MEASUREMENTS AND MAIN RESULTS: Adult pigs (n = 6) were studied before and after the development of pacing-induced CHF (240 beats/min, 3 wks) at rest and with treadmill exercise (3 mph, 15 degrees incline, 10 mins). At rest, LV stroke volume was reduced nearly 45% with CHF compared with normal (20+/-2 vs. 36+/-3 mL; p<.05) and was associated with a more than four-fold increase in plasma catecholamines, renin activity, and endothelin concentration. At rest, global brain blood flow was reduced with CHF compared with the normal state (1.06+/-0.13 vs. 0.81+/-0.06 mL/min/g; p<.05). At rest, blood flow to the frontal lobe, cerebellum, and medullary regions was reduced by approximately 30% in the CHF group (p<.05). With treadmill exercise, LV stroke volume remained lower and neurohormonal concentrations remained higher in the pacing CHF state. Global brain blood flow increased significantly with treadmill exercise in both the normal and CHF states (4.58+/-1.36 and 2.01+/-0.29 mL/min/g; p<.05) but remained reduced in the CHF state compared with normal values (p<.05). In the CHF group, the relative increase in blood flow with exercise was significantly blunted in the parietal and occipital regions of the cerebrum and the suprapyramidal region of the medulla. CONCLUSIONS: The development of pacing-induced CHF was associated with diminished brain perfusion under resting conditions and with treadmill exercise. These perfusion abnormalities with pacing CHF were pronounced in specific regions of the brain. The defects in brain perfusion with the development of CHF may contribute to abnormalities in centrally mediated processes of cardiovascular regulation.

Animals↗
PubMed1986

Preliminary observations of chronic indoramin therapy in congestive heart failure.

Twenty-one patients with congestive heart failure (New York Heart Association functional class III) underwent a double-blind, parallel, placebo-controlled, randomized trial of indoramin (average dose of 50 mg every 12 h in 11 patients) versus placebo (n = 10). The study lasted 2 months and was initiated and terminated with the measurement of resting and exercise hemodynamics. Compared with baseline values, chronic administration of indoramin caused a mild reduction in resting mean systemic blood pressure (mean change of -10 mm Hg), and postdosing results included a drop in systemic and pulmonary vascular resistances and pulmonary capillary wedge pressure and a mild increase in stroke volume. Compared with baseline responses, chronic indoramin administration (postdosing) elicited a mild reduction in systemic and pulmonary vascular resistances and pulmonary capillary wedge pressure during submaximal exercise. At this dose, chronic indoramin administration did not alter hemodynamics at maximal exercise or exercise duration to maximal exercise. While certain individual patients experienced clinical improvement on chronic indoramin therapy, the overall clinical status (symptoms, signs, diuretic requirements) of the indoramin-treated group did not change significantly when compared with that of the placebo control group.

Blood Pressure↗
PubMed1981

Acute hemodynamic and long-term clinical effects of prazosin in the treatment of chronic congestive heart failure.

The effect of prazosin in congestive heart failure was assessed in 10 patients (age 39--69) years) with ischemic heart disease or cardiomyopathy in functional class II-IV (NYHA). All patients were treated with digitalis and diuretics in optimal doses. Mean (+/- S.E.M.) cardiac index (CI) was 2.2 +/- 0.2 l/min/m2 before and 2.3 +/- 0.1 one hour after oral administration of 2--4 mg prazosin (given as tablets) (p less than 0.10). Mean pulmonary capillary wedge pressure (PWP) fell from 24 +/- 4 to 20 +/- 4 mmHg (p greater than 0.10). Prazosin seemed to have a more beneficial effect on patients with markedly elevated PWP or reduced CI before prazosin administration. The effect of prazosin on heart rate and systolic blood pressure was insignificant. During a follow-up period of 1--20 months (mean 7.3), 2 of 7 patients treated with prazosin (2--4 mg daily) improved their clinical condition, one patient was unchanged and 4 patients died in progressive cardiac failure. The results indicate that some patients with severe heart failure may benefit from prazosin when conventional treatment has failed.

Adult↗
PubMed2006

Right bundle branch block and long-term mortality in patients with acute congestive heart failure.

OBJECTIVES: Risk stratification in acute congestive heart failure (ACHF) is poorly defined. The aim of the present study was to assess the impact of right bundle brunch block (RBBB) on long-term mortality in patients presenting with ACHF. METHODS AND RESULTS: The initial 12-lead electrocardiogram was analysed for RBBB in 192 consecutive patients presenting with ACHF to the emergency department. The primary endpoint was all-cause mortality during 720-day follow-up. This study included an elderly cohort (mean age 74 years) of ACHF patients. RBBB was present in 27 patients (14%). Age, sex, B-type natriuretic peptide levels and initial management were similar in patients with RBBB when compared with patients without RBBB. However, patients with RBBB more often had pulmonary comorbidity. A total of 84 patients died during follow-up. Kaplan-Meier analysis revealed that mortality at 720 days was significantly higher in patients with RBBB when compared with patients without RBBB (63% vs. 39%, P = 0.004). In Cox proportional hazard analysis, RBBB was associated with a two-fold increase in mortality (hazard ratio 2.18, 95% CI 1.26-3.66; P = 0.003). This association persisted after adjustment for age and comorbidity. CONCLUSIONS: RBBB is a powerful predictor of mortality in patients with ACHF. Early identification of this high-risk group may help to offer tailored treatment in order to improve outcome.

Aged↗
PubMed1990

Effects of desipramine on norepinephrine clearance in congestive heart failure.

Elevated plasma norepinephrine (NE) in congestive heart failure (CHF) is caused by increased NE spillover and decreased NE clearance. To evaluate the effects of neuronal uptake blockade on NE clearance, we studied NE kinetics during steady-state infusions of [3H]NE, before and after oral desipramine (DMI, 50 mg) in 11 patients with CHF and 8 normal volunteers. Baseline plasma NE was greater in the CHF group (637 +/- 56 vs. 271 +/- 32 pg/ml; P less than 0.001), NE clearance was lower in CHF (1.31 +/- 0.21 vs. 1.94 +/- 0.17 l.min-1.m-2; P = 0.026), and NE spillover was greater in CHF (4.71 +/- 0.78 vs. 3.04 +/- 0.35 nmol.min-1.m-2, P = 0.054). After DMI, plasma NE rose significantly in CHF (778 +/- 67; P = 0.008), and NE clearance decreased further in CHF (0.97 +/- 0.16; P = 0.024), but neither changed in normal subjects. NE spillover did not change in either group. There appears to be an enhanced effect of DMI on NE clearance in CHF patients. Two general mechanisms may be responsible for this finding, an increased concentration of drug, possibly caused by a decreased volume of distribution, and an increased sensitivity of neuronal amine pumps to DMI. Both mechanisms may reflect a more general abnormality of clearance of drugs and hormones related to abnormalities of tissue perfusion in CHF.

Adult↗
PubMed2004

Atrial ionic remodeling induced by atrial tachycardia in the presence of congestive heart failure.

BACKGROUND: Atrial fibrillation (AF) and congestive heart failure (CHF) produce discrete forms of atrial ionic remodeling. The in vivo effects of atrial tachycardia (AT) remodeling are altered by CHF. This study evaluated underlying mechanisms at the level of ionic remodeling. METHODS AND RESULTS: We studied 4 groups of dogs: (1) unpaced controls (CTLs); (2) CHF caused by 2-week ventricular tachypacing (VTP, 240 bpm); (3) AT (400 bpm x 7 days); and (4) CHF+AT (2-week VTP with AT for the last 7 days). CHF and CHF+AT groups equally increased left atrial pressure. AF duration was increased in all paced groups. Effective refractory period (ERP) was decreased by 42% in AT versus CTL but by only 24% in AT+CHF versus CHF. CHF reduced L-type Ca2+ (I(Ca)), transient-outward (I(to)), and the slow delayed-rectifier (I(Ks)) currents while increasing the Na+-Ca2+ exchanger (I(NCX)) and not affecting the inward-rectifier (I(K1)) current. AT reduced I(to) and I(Ca) while increasing I(K1) and leaving I(Ks) unaltered. The addition of AT to CHF failed to alter I(to), I(Ks), or I(NCX) beyond the effect of CHF alone, decreased I(Ca) slightly compared with CHF alone, but had smaller effects on I(Ca) and I(K1) compared with AT alone. Thus, CHF+AT, as would occur in a CHF patient who develops AF, produced an ionic remodeling pattern different from that of CHF or AT alone and from what would have been predicted from additive effects of CHF and AT. CONCLUSIONS: The presence of CHF alters AT-induced ionic remodeling. Thus, the ionic remodeling caused by cardiac arrhythmias in the presence of cardiac pathology is not necessarily predictable from the effects of either alone, with important potential implications for understanding the pathophysiology of arrhythmias in the diseased heart.

Animals↗
PubMedDate not supplied

Sustained improvement in flow-mediated vasodilation after short-term administration of dobutamine in patients with severe congestive heart failure.

BACKGROUND: In patients with severe congestive heart failure (CHF), short-term administration of dobutamine exerts sustained clinical benefits that are partially mediated by a training-like effect on skeletal muscle. Recently, physical training has been shown to enhance endothelial function in the skeletal muscle vasculature by improving endothelial function. Whether the dobutamine-induced training effect is also associated with an improvement in endothelial function in the skeletal muscle vasculature is currently unknown. METHODS AND RESULTS: Flow-mediated vasodilation in response to peak reactive hyperemia was evaluated in the forearms of 9 patients with severe CHF who were treated with dobutamine for 72 hours. Resting and peak hyperemic brachial artery blood flow and diameter (BABF [mL/min] and BAD [mm], respectively) were measured by 2-dimensional and Doppler ultrasonography at baseline, at 3 and 72 hours during dobutamine infusion, and at 2 and 4 weeks after discontinuation of dobutamine therapy. In addition, the brachial artery response to sublingual (SL) administration of nitroglycerin (NTG) was evaluated at baseline and at 2 and 4 weeks after discontinuation of dobutamine therapy. Ten patients with severe CHF who did not receive dobutamine served as control subjects. Resting BABF was significantly increased at 3 and 72 hours (391.2+/-31.8 and 366.8+/-31.0 mL/min, respectively, compared with 289.8+/-18.6 mL/min at baseline; P<0.05). Peak hyperemic BABF was not altered by dobutamine infusion compared with baseline values. The increase in BAD during peak hyperemic response was greater after infusion of dobutamine for 72 hours (15.2+/-2.7% versus 9.1+/-1.8%, P<0.05) and remained significantly greater for >/=2 weeks after discontinuation of dobutamine (12.3+/-2.2% versus 9.1+/-1.8%, P<0.05). In contrast to the peak hyperemic response, the increase in BAD (%) induced by SL NTG was unchanged by administration of dobutamine for 72 hours. Two and 4 weeks after discontinuation of dobutamine, NTG-induced increases in BAD were similar to the BAD noted at baseline. CONCLUSIONS: In patients with severe CHF, short-term administration of dobutamine for 72 hours selectively improves vascular endothelial function for >/=2 weeks.

Blood Flow Velocity↗