Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CONGESTIVE HEART FAILURE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMed1993

Regional specificity of peak hyperemic response in patients with congestive heart failure: correlation with peak aerobic capacity.

OBJECTIVES: The aim of this study was to compare peak reactive hyperemic blood flows in the forearm and calf of patients with congestive heart failure and in age- and gender-matched normal subjects. In addition, we attempted to correlate peak oxygen consumption with forearm and calf peak reactive hyperemic flows in the patients with heart failure. BACKGROUND: Disparate results have been reported regarding forearm peak reactive hyperemia in patients with congestive heart failure. Because training significantly increases peak reactive hyperemic flow in normal subjects, we hypothesized that in patients with congestive heart failure who curtail walking because of exertional symptoms, calf peak reactive hyperemic flow would be preferentially attenuated and that impairment of calf vasculature may correlate with peak oxygen consumption. METHODS: Forearm and calf blood flows were measured by venous occlusive plethysmography at rest and after 5 min of arterial occlusion in 46 patients with congestive heart failure and 7 age- and gender-matched normal subjects. Peak oxygen consumption was measured during graded exercise on a bicycle ergometer. RESULTS: Calf peak reactive hyperemic flow was lower in patients with congestive heart failure than in normal subjects (22 +/- 1 vs. 32.5 +/- 3.5 ml/min per 100 ml, p < 0.001), whereas forearm peak reactive hyperemic flows were similar in the two groups. Calf peak reactive hyperemic flow was linearly related to peak oxygen consumption (r = 0.58, p < 0.0001), but forearm peak reactive hyperemic flow was not. Forearm and calf peak reactive hyperemic flows were not related at rest or after 5 min of arterial occlusion in the patients with heart failure. CONCLUSIONS: Calf peak reactive hyperemic flow is reduced in patients with congestive heart failure, whereas forearm peak reactive hyperemic flow is identical to that of age- and gender-matched normal subjects. Calf peak reactive hyperemic flow is linearly related to peak oxygen consumption in patients with congestive heart failure, but forearm peak reactive hyperemic flow is not.

Case-Control Studies↗
PubMed2002

Diaphragmatic function after intense exercise in congestive heart failure patients.

Respiratory muscle strength and endurance is reduced in patients with congestive heart failure, making these patients susceptible to diaphragmatic fatigue during exercise. In order to determine whether or not contractile fatigue of the diaphragm occurs in patients with congestive heart failure following intense exercise, twitch transdiaphragmatic pressures (twitch Ptdi) were measured during unpotentiated and potentiated cervical magnetic stimulation (CMS) of the phrenic nerves before and at intervals after cycle endurance exercise. Ten patients aged 65.7+/-6.0 yrs (mean+/-SD) with an ejection fraction of 31.2+/-9.8% performed a constant-load symptom-limited exercise test at 60% of their peak work capacity. Twitch Ptdi at baseline were 15.9+/-6.3 cmH2O (unpotentiated CMS) and 28.8+/-10.7 cmH2O (potentiated CMS) and at 10 min postexercise were 16.4+/-4.7 cmH2O (unpotentiated CMS) and 27.6+/-10.1 cmH2O (potentiated CMS). One patient demonstrated a sustained fall in twitch Ptdi of > or = 15%, considered potentially indicative of diaphragmatic fatigue. Contractile diaphragmatic fatigue is uncommon in untrained patients with congestive heart failure following high-intensity constant-workload cycle exercise. Therefore, diaphragmatic fatigue is an unlikely cause of exercise-limitation during activities of daily living in heart failure patients.

Activities of Daily Living↗
PubMed1993

Diurnal blood pressure profile in patients with severe congestive heart failure: dippers and non-dippers.

Patients with severe congestive heart failure (CHF) have increased sympathetic nervous activity and altered baroreceptor function, which may influence the diurnal blood pressure rhythm. The 24-h blood pressure profile was measured in 25 patients with severe CHF (mean ejection fraction: 17%) and 25 control subjects. Systemic blood pressure was measured automatically at the arm by a non-invasive blood pressure monitoring system every 15 min. The mean +/- SD systolic blood pressure in CHF patients and controls was during day-time 105 +/- 10 and 130 +/- 11 mm Hg and night-time 97 +/- 10 and 112 +/- 10 mm Hg, i.e. the nocturnal decrease was 9 +/- 6 and 18 +/- 8 mm Hg, respectively (p < 0.0005 for all). The subjects could be divided into two groups: dippers and non-dippers, with and without a relative decrease in nocturnal systolic blood pressure > 10%. There was significantly more non-dipping CHF patients (16) than controls (5) (p < 0.01). Systolic blood pressure was in CHF dippers vs. non-dippers during day-time: 108 +/- 7 vs. 104 +/- 12 mm Hg (NS) and night-time: 92 +/- 7 vs. 99 +/- 11 mm Hg (p = 0.08). The nocturnal decrease was 16 +/- 3 vs. 5 +/- 4 mm Hg and the relative nocturnal decrease 15 +/- 3 vs. 5 +/- 3% (p < 0.00001 for both). It is concluded that patients with severe congestive heart failure can be divided into two groups: dippers and non-dippers, with and without a normal decrease in nocturnal blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Pharmacokinetics of milrinone in patients with congestive heart failure during continuous venovenous hemofiltration.

OBJECTIVE: To evaluate the pharmocokinetics of intravenous milrinone in patients with severe congestive heart failure during continuous venovenous hemofiltration (CVVH). DESIGN: Prospective study of patients with congestive heart failure admitted to the intensive care unit (ICU). SETTING: ICU between September 1997 and August 1999. PATIENTS AND METHODS: Six patients with severe congestive heart failure during CVVH: all patients received a continuous infusion of milrinone of 0.25 microg x kg(-1) min(-1). The hemodynamics and plasma concentration of milrinone were measured before and after the infusion. Pharmacokinetics were analyzed with one-compartment model featuring constant rate infusion. RESULTS: The steady-state concentration (Css) was 845 +/- 135 (mean +/- SD) ng/ml, and the half-life time (t1/2) was 20.1 +/- 3.3 h. Cardiac index and stroke volume index after the infusion of milrinone increased significantly compared with pre-infusion levels. Other hemodynamic parameters did not change significantly. All patients died within 1 month after the injection of milrinone because of severe forms of arrhythmia, such as ventricular tachycardia and ventricular fibrillation. CONCLUSIONS: We found that the mean Css and the mean t1/2 of milrinone in subjects during CVVH were much higher and longer than those previously reported for subjects with normal renal function. It is therefore essential to adjust the dose or modify the dosing interval of milrinone during renal replacement therapy for patients with severe congestive heart failure. However, further studies are needed to determine the details of pharmacokinetics of milrinone and therapeutic procedures for patients with severe heart failure during CVVH.

Adult↗
PubMed2001

Beta-blockers: a new therapy in congestive heart failure.

BACKGROUND: Until recently, use of beta-blockers was contraindicated in treatment of patients with congestive heart failure. However, empirical evidence suggests that adding beta-blockers to the standard therapy can slow the progression of heart failure and reduce mortality, including sudden cardiac death. PURPOSE: To analyze the results of major, prospective, randomized controlled trials on the effects of beta-blockers in congestive heart failure and to provide recommendations for clinical practice and patients' education. METHODS: MEDLINE (1989-2001) and biomedical databases (1995-2001) were searched for literature on the use of beta-blockers in patients with congestive heart failure. Information on major randomized controlled trials of at least 6 months' duration with mortality as a major end point were reviewed. RESULTS: Both selective and nonselective beta-blockers significantly reduce mortality due to all causes; decrease need for hospitalization due to cardiovascular causes; and improve patients' New York Heart Association functional classification, hemodynamic status, left ventricular ejection fraction, and signs and symptoms of congestive heartfailure. However, clinical use of beta-blockers remains limited. CONCLUSION: Strong empirical evidence supports adding beta-blockers to the standard therapy for congestive heart failure. Future efforts should be directed toward establishing the safety and efficacy of beta-blockers in patients with severe heartfailure.

Adrenergic beta-Antagonists↗
PubMed1995

Lymphocytic and erythrocytic k+, Na+, Ca++, Mg++ content in patients with congestive heart failure.

The content of lymphocytic and erythrocytic K+, Na+, Ca++, Mg++ changed in patients with congestive heart failure, related to clinical treatment and prognosis. The longer the course of disease, the more significant the changes, with no relation to the etiology of heart disease. The changes were partially improved after treatment of the heart failure. The content of electrolytes is not significantly different in patients in NYHA Class III, compared to those in NYHA Class IV. The metabolic changes of electrolytes occur on the myocardial cells, skeletal muscle cells and peripheral erythrocytes in patients with congestive heart failure. However, serum electrolyte content does not reflect precisely overall electrolyte metabolism in the body. Whether similar changes of electrolyte content occur in the peripheral lymphocytes is rarely reported. We studied the lymphocytic and erythrocytic electrolyte content in patients with congestive heart failure, to provide some reference in the clinical treatment and prognosis of congestive heart failure.

Adult↗
PubMed1999

Effects of short-acting and long-acting loop diuretics on heart rate variability in patients with chronic compensated congestive heart failure.

BACKGROUND: We investigated the effects of a short-acting loop diuretic (furosemide) and a long-acting loop diuretic (azosemide) on heart rate variability, fluid balance, and neurohormonal responses in patients with mild to moderate chronic congestive heart failure. METHODS: Nineteen patients with mild to moderate chronic congestive heart failure received furosemide (40 to 60 mg/day) or azosemide (60 to 90 mg/day) for 5 days in a crossover manner. We performed time-domain and frequency-domain analyses of 24-hour Holter electrocardiographic recordings to assess heart rate variability. RESULTS: The 24-hour urinary sodium excretion was similar during the furosemide and azosemide treatment periods but was significantly greater in the first 2 hours after drug administration during furosemide treatment. Plasma renin activity and the hematocrit level increased and high-frequency power significantly decreased 2 hours after the administration of furosemide only. The standard deviation of all normal R-R intervals and the root mean square of successive differences in the R-R interval were lower with furosemide than with azosemide (P <.05). CONCLUSIONS: Furosemide, a short-acting loop diuretic, has a greater influence on heart rate variability and fluid balance than azosemide, a long-acting loop diuretic, in patients with mild to moderate chronic congestive heart failure.

Blood Pressure↗
PubMed1986

Use of intermittent dobutamine infusion in congestive heart failure.

Dobutamine is a cardiac inotrope useful in the acute treatment of congestive heart failure. Dobutamine improves cardiac output, decreases pulmonary wedge pressure, and decreases total systemic vascular resistance with little effect on heart rate or systemic arterial pressure. Clinical benefit has been observed to continue for weeks to months following the discontinuation of dobutamine. In addition, tolerance to dobutamine has been observed when infusions last 72 hours or longer. This has led investigators to study the effectiveness of chronic intermittent infusions of dobutamine. Studies utilizing dobutamine doses ranging from 1.5 to 15 micrograms/kg/min for 4-48 h/wk have shown sustained clinical and hemodynamic improvement in patients suffering from congestive heart failure. The mechanism by which dobutamine creates this effect is not entirely known; however, studies suggest dobutamine exerts a physical conditioning effect similar to exercise. Dobutamine infusions have also been associated with morphological and metabolic changes in myocardial tissue consistent with improved myocardial structure and function. The intermittent use of dobutamine may be beneficial in the chronic treatment of congestive heart failure in patients who fail to respond to conventional therapy.

Dobutamine↗
PubMed1995

Future approaches to pharmacologic therapy for congestive heart failure.

There have been tremendous advances in our understanding of the pathophysiology of congestive heart failure, and this has led to improvements in its treatment. Nonetheless, the prevalence of congestive heart failure and the associated mortality and morbidity continue to increase. Hence, there remains a need for additional therapeutic approaches that will complement current management with diuretics, angiotensin-converting enzyme inhibitors, other vasodilators, and digoxin. This article reviews a number of potential avenues that are currently being evaluated or remain targets for future investigation. Given our current understanding of the mechanisms of progression of left ventricular dysfunction, therapies that limit neurohormonal activation or interfere with its consequences and those that improve the balance between myocardial energy requirements and supply appear to be the most promising. Agents that improve hemodynamics without altering the underlying pathophysiology may produce short-term symptomatic improvement but have limited potential to alter the natural history of congestive heart failure. Positive inotropic therapies probably fall into this category, but most of these also appear to accelerate progression and increase mortality. In the long-term, specific interventions that reverse changes at the cellular and molecular level offer the greatest promise.

Diuretics↗
PubMed1991

Reversibility of pulmonary hypertension in congestive heart failure patients evaluated for cardiac transplantation: comparative effects of various pharmacologic agents.

Congestive heart failure patients with severe pulmonary hypertension are at risk of death from acute right ventricular failure of the donor heart in the early postoperative period after orthotopic cardiac transplantation. Therefore in the preoperative evaluation of these patients, it is extremely important to determine whether pulmonary hypertension can be reversed by pharmacologic means. Patients with reactive pulmonary hypertension can be considered suitable for orthotopic transplantation and the effective drug utilized postoperatively to reverse pulmonary hypertension and prevent failure of the donor right ventricle. To determine which pharmacologic agent is most effective in reversing pulmonary hypertension in congestive heart failure, the acute pulmonary hemodynamic effects of comparable doses of direct intravenous vasodilators including nitroglycerin, nitroprusside, and prostaglandin E1, and intravenous inotropic agents dobutamine and enoximone, were evaluated in 66 patients undergoing cardiac transplantation evaluation. All drugs significantly increased cardiac output and decreased calculated pulmonary vascular resistance. All drugs except dobutamine significantly lowered pulmonary artery and pulmonary artery wedge pressures. Prostaglandin E1 was the only drug that significantly lowered transpulmonary pressure gradient (pulmonary artery mean pressure minus mean pulmonary wedge pressure). The magnitude of decline of pulmonary vascular resistance and transpulmonary pressure gradient was greatest with prostaglandin E1 compared with other drugs. These observations indicate that prostaglandin E1 may be more effective than the other studied drugs for acute reversal of pulmonary hypertension in congestive heart failure.

Analysis of Variance↗
PubMed1991

Parasympathetic withdrawal is an integral component of autonomic imbalance in congestive heart failure: demonstration in human subjects and verification in a paced canine model of ventricular failure.

Although enhanced sympathetic tone is a well recognized component of the autonomic profile characteristic of congestive heart failure, the contribution of parasympathetic withdrawal to this autonomic imbalance is less well described. The technique of spectral analysis of heart rate variability provides a dynamic map of sympathetic and parasympathetic tone and was thus used to define the nature of sympathetic-parasympathetic interactions in humans with idiopathic dilated cardiomyopathy and in a paced canine model of congestive heart failure. Humans with cardiomyopathy were found to have an augmentation of the sympathetically mediated low frequency area of the power density spectrum. Parasympathetic withdrawal was demonstrated by significant reductions in the parasympathetically mediated high frequency area (p less than 0.05) and the ratio of high to low frequency areas (p less than 0.01). Administration of atropine to normal subjects resulted in a significant reduction in the high frequency area (p less than 0.05) and the high/low frequency area ratio, both of which decreased within the range noted in patients with congestive heart failure. Administration of isoproterenol in normal subjects led to an augmentation of the low frequency area but to only a small decrease in the high/low frequency area ratio. Induction of congestive heart failure in a paced canine model resulted in alterations in the autonomic profile that resembled those seen in humans with ventricular failure. The prominent high frequency region of the spectrum at baseline, indicating a predominance of parasympathetic tone, was absent after the evolution of congestive heart failure, and there was a marked augmentation of the low frequency region of the spectrum.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1999

Potential risk of beta-blockade withdrawal in congestive heart failure due to abrupt autonomic changes.

Beta-Blockers reduce mortality in patients with congestive heart failure and a proposed mechanism has been changes of autonomic tone. Heart rate variability is a non-invasive tool to estimate cardiac autonomic tone. The aim was to study changes of heart rate variability in patients with congestive heart failure on placebo, on the beta1-selective antagonist metoprolol or 24 h after metoprolol withdrawal. Forty-five patients with congestive heart failure were studied with Holter recordings. Heart rate variability measurements were performed before, after 6-12 months of treatment with 150 mg metoprolol/placebo, or 24 h after discontinued metoprolol. After treatment, patients on beta-blockade had a significantly longer mean RR interval and changes of heart rate variability, suggesting elevated vagal tone. Patients monitored in the rebound phase of beta-blocker withdrawal had a significant vagal reduction to the level of the placebo group. There was also a nonsignificant trend towards increased sympathetic tone (LF/HF over 24 h), compared with the beta-blockade group. Heart rate variability indicates an elevated vagal tone during treatment with metoprolol but beta-blockade withdrawal shifts the autonomic balance towards lower vagal and higher sympathetic tone within 24 h. These results could imply a potential risk when abruptly discontinuing beta-blockade medication in these patients.

Adolescent↗
PubMed2003

Rural and urban outcomes after hospitalization for congestive heart failure in Alberta, Canada.

OBJECTIVES: We compare the hospitalization rate, duration, cost, and mortality for newly diagnosed congestive heart failure in patients admitted to rural and metropolitan hospitals in one Canadian province. METHODS: Administrative data for Alberta, Canada, from April 1, 1994, to March 31, 2000. RESULTS: Hospitalizations (16,162) for newly diagnosed congestive heart failure constituted 50% of all hospitalizations for congestive heart failure. Hospitals were distributed as follows: rural with less than 200 cases (21% of hospitalizations), rural with 204 to 646 cases (21% of hospitalizations), regional (13% of hospitalizations), metropolitan with angiography capability (24% of hospitalizations), and metropolitan without angiography capability (21% of hospitalizations). The hospitalization rate per 1000 population was lower for residents of metropolitan regions (1.01; 95% confidence interval [CI] 0.97 to 1.05) compared with residents of rural (1.70; 95% CI 1.65 to 1.75) and regional (1.95; 95% CI 1.90 to 2.00) health regions. Patient comorbidity and severity scores were lower in rural hospitals. Special care unit admissions and cardiac catheterizations were more frequent in patients admitted to metropolitan hospitals. After adjustment, the length of stay and mortality were similar amongst all hospital types. Adjusted hospital total costs were about 23% (900 Canadian dollars) greater in metropolitan hospitals with angiography capability compared to rural hospitals. CONCLUSION: Hospital admission rates for newly diagnosed congestive heart failure were lower for metropolitan residents compared to non-metropolitan residents. Cost per admission was greatest in metropolitan hospitals with angiography capability compared to other hospital types.

Adult↗
PubMed1986

Hemodynamic effects of infused arginine vasopressin in congestive heart failure.

The hemodynamic effects of exogenously administered arginine vasopressin were assessed in 11 patients with chronic congestive heart failure. Infusion rates of 0.1 to 0.8 pmol/kg per min increased plasma arginine vasopressin from 6.5 +/- 2.7 (SD) pg/ml at control to 63 +/- 39 pg/ml at the highest infusion rate. There were progressive decreases in cardiac output and stroke volume, with increases in systemic vascular resistance and pulmonary capillary wedge pressure, but only minimal changes in heart rate and blood pressure. Changes in cardiac output, stroke volume and systemic resistance were evident from the first infusion rate, which increased plasma arginine vasopressin from 6.5 +/- 2.7 to 9.9 +/- 4.6 pg/ml. A paired analysis of baseline hemodynamic data with those measured during infusions producing an arginine vasopressin level averaging 15 +/- 2.6 pg/ml yielded the following changes: cardiac output decreased from 4.6 +/- 1.2 to 4.2 +/- 0.96 liters/min (p less than 0.01), stroke volume decreased from 60 +/- 19 to 54 +/- 16 ml (p less than 0.005) and systemic vascular resistance increased from 1,329 +/- 396 to 1,443 +/- 395 dynes X s X cm-5 (p = 0.01). Thus, small increases in circulating arginine vasopressin cause modest but significant adverse circulatory effects in patients with congestive heart failure. A fall in cardiac output, probably as a result of increased afterload, is seen at levels of arginine vasopressin within the basal range found in congestive heart failure. These data demonstrate that circulating arginine vasopressin in physiologic concentrations is capable of influencing hemodynamics in patients with congestive heart failure and suggest that therapy for this condition directed at inhibition of the vascular effect of arginine vasopressin may be potentially useful.

Adult↗
PubMed1976

Compliance of the peripheral capacitance vessels in patients with congestive heart failure.

A method for measuring compliance of the peripheral capacitance vessels is reported, and the values of compliance in patients with congestive heart failure are compared with those in normal subjects. Peripheral venous compliance and right brachial venous pressure in both patients with congestive heart failure and in normal subjects, when plotted graphically, showed a relationship described by many hyperbolic curves. The mean value of compliance of the peripheral capacitance vessels in patients with congestive heart failure was only half that in normal subjects. This difference was statistically significant (P less than 0.001). After the congestion in the patients with congestive heart failure disappeared following treatment with digitalis and other drugs, the values of compliance became nearly the same as in normal subjects. It seems that the increase of compliance of the peripheral capacitance vessels is not due to an organic change but to a functional change of the vessels caused by distention.

Blood Vessels↗
PubMed1995

Thiamin status, diuretic medications, and the management of congestive heart failure.

OBJECTIVE: To assess the prevalence of thiamin deficiency in patients with congestive heart failure who are treated with diuretics that inhibit sodium and chloride reabsorption in the thick ascending limb of the loop of Henle (loop diuretic therapy). DESIGN: A cross-sectional investigation of thiamin status of consecutive patients with congestive heart failure being treated with loop diuretic therapy. SETTING: Cardiology clinic of a midwestern tertiary-care medical center. SUBJECTS: Thirty-eight patients were recruited (mean age +/- standard deviation = 55 +/- 14 years). Validation of methodology was conducted with nine age-matched control subjects. MAIN OUTCOME MEASURES: Thiamin status was assessed biochemically by in vitro erythrocyte transketolase activity assay. Assessment of dietary intake of thiamin was accomplished with a semiquantitative food frequency questionnaire. STATISTICAL ANALYSES PERFORMED: Fisher's exact test and logistic regression were used to evaluate relationships between thiamin status and variables of interest. RESULTS: Biochemical evidence of thiamin deficiency was found in 8 of 38 (21%) patients. Evidence of risk for dietary thiamin inadequacy was found in 10 of 38 patients (25%). Seven of the 8 patients with biochemical evidence of thiamin deficiency met study criteria for dietary adequacy, although quantified data suggested that only 4 of the patients achieved two thirds of the Recommended Dietary Allowance. Biochemical evidence of thiamin deficiency tended to be more common among patients with poor left ventricular ejection fractions (P = .07). CONCLUSIONS: Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk.

Adult↗
PubMed1986

Importance of receptor regulation in the pathophysiology and therapy of congestive heart failure.

The available data indicate that the beta-adrenergic receptors that mediate positive inotropic responses undergo "down-regulation," a cellularly mediated decrease in surface receptor number, in congestive heart failure. This decrease in beta-adrenergic receptor number is proportional to the degree of myocardial dysfunction and the loss of contractility that occurs in congestive heart failure. It appears to be chamber-specific, occurring to the greatest degree in the most severely affected ventricular chamber, and is specific to the beta 1-adrenergic receptor subtype. Beta-adrenergic receptor down-regulation may be the result of the excessively high levels of plasma catecholamines seen in congestive heart failure, inasmuch as a similar phenomenon of beta-adrenergic receptor down-regulation is seen in animals treated with high doses of catecholamines. The specific down-regulation in cardiac beta receptors may be, in part, the cause of the decrease in myocardial function observed during long-term beta-adrenergic receptor stimulation, and an actual decrease in beta-adrenergic receptor number has been observed in myocardial tissue from patients with congestive heart failure. Down-regulation of beta receptors in congestive heart failure results in a decrease or loss of efficacy of beta-adrenergic receptor agonists on long-term administration. This is especially evident for partial agonists, which are more dependent on receptor number for their positive inotropic effects than full agonists. Although beta receptors are down-regulated in congestive heart failure, myocardial alpha 1-adrenergic receptors and histamine H2 receptors do not appear to be subject to this same regulatory process. Inasmuch as stimulation of both of these receptors results in a positive inotropic effect, further study should be given to the potential therapeutic utility of selective stimulation of myocardial alpha 1-adrenergic receptors and histamine H2 receptors in congestive heart failure. It is evident that the status of specific receptor subtypes in pathophysiologic states such as congestive heart failure must be considered when assessing the likelihood of success in treating patients with beta-adrenergic receptor agonists.

Adrenergic beta-Antagonists↗
PubMed1989

Pathophysiology and evaluation of severity of congestive heart failure on the basis of venous characteristics.

To elucidate the possibility of grading the severity of congestive heart failure by using venous characteristics, we constructed venous pressure-volume curves (PVR) and calculated venous stiffness constants (K). In addition, effects of vasoactive drugs on venous distensibility were studied. A venous pressure-volume curve could be fit well by an exponential curve (r = 0.98 +/- 0.01). The PVR was shifted to the left with an increase in the clinical severity of congestive heart failure. The exponent of these curves, K, increased as the PVR was shifted to the left. K correlated with heart rate (r = 0.52, p less than 0.01), right atrial pressure (r = 0.54, p less than 0.02) and mean pulmonary arterial pressure (r = 0.47, p less than 0.04). Nitroglycerin and amrinone dilated veins and decreased K by 19.6 +/- 6.9% (p less than 0.03) and 14.0 +/- 4.3% (p less than 0.02), respectively. Changes in K (delta K) during the nitroglycerin and amrinone infusions correlated closely with the baseline K (delta K = -0.41 K + 0.22, r = 0.92, p less than 0.01). Therefore, the venodilating effects of these drugs were greater in patients with more severe congestive heart failure. The venous stiffness constant could be useful to grade the severity of congestive heart failure.

Adult↗