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PubMedDate not supplied

[Usefulness of enalapril in congestive heart failure].

The usefulness of vasodilating agents in congestive heart failure depends on their ability to diminish left ventricular afterload; this effect does not necessarily persist with long-term treatment. The present study reports the clinical response of 16 patients in heart failure; the trial was double blind with enalapril and/or placebo during 24 weeks. Diagnoses were dilated cardiomyopathy in six, rheumatic heart disease in five, ischemic heart disease in four und hypertensive heart disease in one. Two patients on enalapril died of non cardiac causes and one was withdrawn from the study due to pregnancy. In those patients treated with enalapril the NYHA functional class improved from 2.9/0.8 to 1.1/0.4 (p less than 0.001), and the effort capacity increased from 545/171 to 888/160 seconds (p less than 0.01). Left ventricular systolic function evaluated by echocardiogram and Tc 99 m ventriculogram, radiologic size of the heart and echocardiographic left ventricular diameters showed no significant changes. There were no adverse clinical effects nor laboratory abnormalities. It is concluded that in this study, enalapril produced sustained clinical improvement in patients with heart failure and it was well tolerated during long-term treatment.

Adult↗
PubMed1986

Biochemistry and pathophysiology of congestive heart failure: is there a role for magnesium?

Congestive heart failure (CHF) represents a pathophysiologic state in which cardiac output is inadequate to meet the metabolic needs of multiple organ systems. The primary pathologic event in CHF is a marked, sustained reduction in the intrinsic contractility of the heart. A review of the current knowledge regarding the etiology and progression of CHF reveals that it is associated with profound biochemical, peripheral hemodynamic (increased peripheral vascular resistance), and electrolyte disturbances. In addition to sodium and water retention, CHF is often associated with hypokalemia and hypomagnesemia as well as tissue deficits in K and Mg. Cardiac glycosides and diuretics (loop and distal types) often exacerbate, or result in, hypokalemia and hypomagnesemia, which may lead to cardiac arrhythmias and sudden cardiac death. Deficits in extracellular and vascular tissue Mg lead to peripheral vasoconstriction; this together with K deficits and the release of neurohumoral substances may be responsible in large measure for the increase in peripheral vascular resistance commonly noted in CHF. More attention must be paid to the careful monitoring of electrolyte levels (Na, K, Mg) in tissues (possibly lymphocytes) and plasma of CHF patients. Deficits in either K or Mg must be corrected in CHF. The nonspecific vasodilator properties of Mg2+ together with its ability to unload the heart should be considered as an important adjunct tool in the management of CHF.

Adenosine Triphosphate↗
PubMed1984

[Long-term therapy of congestive heart failure and dilatative cardiomyopathy].

Although therapy of congestive heart failure has to remain symptomatic in many cases, diagnostic evaluation should always precede initiation of therapy. Goals are (1) improvement of contractility (digitalis; other positive inotropic substances are in evaluation) and (2) decrease of preload and afterload by diuretics and vasodilators. Those therapeutic principles are briefly discussed. Symptomatic therapy certainly improves quality of life, but it remains unclear whether survival is improved as well.

Cardiomyopathies↗
PubMedDate not supplied

The acute effect of perindopril upon effort capacity in congestive heart failure.

A number of 21 patients with congestive heart failure (CHF) of various etiologies were studied. All patients were subjected to a classical exercise testing (ET) on cycloergometer. The ET was repeated 24 hrs later, 6 hrs after the administration of 2 mg Perindopril (Coversyl). No statistically significant differences in duration and intensity of ET before and after Perindopril were noted for the whole group. But in 9 patients (42.8%) at least one effort level was gained. In these patients the peak double product (DP) was similar before and after Perindopril, but at submaximal effort DP was, at each level, lesser after Perindopril, suggesting a mechanism of afterload reduction in the improvement of effort capacity.

Adult↗
PubMed1993

[Short-term prognosis in patients with congestive heart failure and normal left ventricular systolic function].

Congestive heart failure (CHF) has been traditionally associated with impairment of the left ventricular systolic function (LVSF). There are few clinical assays that describe the prognosis of patients with CHF and intact LVSF. The aims of this prospective assay are: to describe a group of 70 patients admitted to an internal medicine department with the clinical syndrome of CHF, to determine the contractile state of the left ventricle with echocardiography and to establish the short term prognosis. There were 39 males and 31 females with a mean age of 76.4. The LVSF was impaired in 38 (54.3%) [Group I] and preserved in 32 (45.7%) [Group II] (Table 1). Sex distribution was different between both groups with women predominating in group II (Figure 1). Fourteen patients belonging to Group II had diastolic function impairment according to cardiac Doppler. There was no other evidence of cardiac abnormality that could justify CHF. During an average of 8 months follow-up 20 (28%) patients died. There were no differences in overall mortality between Groups I and II (Figure 2). Multivariate analysis was used to determine the relative risk in prognosis of the covariates age, gender, systolic function and diameters of the LV. None of these were statistically significant (Table 2). In our series 45.7% of the patients with CHF had normal LVSF. The short term prognosis proved to be the same in patients with and without impaired LVSF.

Aged↗
PubMed1989

Acute hemodynamic effects of norepinephrine inhibition in patients with severe chronic congestive heart failure.

The pathophysiologic role of high levels of circulating catecholamines in patients with congestive heart failure remains unclear. To assess the hemodynamic contribution of circulating catecholamines, metyrosine (alpha-methyl-p-tyrosine), an inhibitor of catecholamine synthesis, was administered to nine patients with acutely decompensated chronic congestive heart failure. Baseline left ventricular ejection fraction averaged 23.3 +/- 9.9%, whereas cardiac output averaged 3.69 +/- 1.03 liters/min, with a pulmonary wedge pressure of 27.4 +/- 8.5 mm Hg. After 48 h of metyrosine administration, plasma norepinephrine concentration decreased from 919.4 +/- 810.6 to 335.4 +/- 143.1 pg/ml (p less than 0.05). Plasma epinephrine concentration averaged 176.4 +/- 166.0 pg/ml at baseline, and was unchanged during metyrosine administration. Despite the significant decrease in circulating norepinephrine, no significant hemodynamic changes were observed during metyrosine administration. These results suggest that high levels of circulating norepinephrine may be more a marker of severe congestive heart failure than an important contributor to the underlying pathophysiology at this advanced stage of the disease process.

Adult↗
PubMed1991

Sudden death in congestive heart failure.

Despite significant advances in recent years in the diagnosis and treatment of congestive heart failure, sudden unexpected cardiac death is still considered a major epidemiologic problem among those patients. This article lists some of the predisposing factors to the development of cardiac arrhythmias and sudden death in patients with congestive heart failure. These include electrolyte or autonomic nervous system inbalance, the use of certain anti-arrhythmic drugs, or intermittent myocardial ischemia. This paper shows that an advanced degree of left ventricular dysfunction and the preference frequent or complex ventricular arrhythmias appear to be major predictors of total and sudden mortality among patients with congestive heart failure. A screening of 24 hours ambulatory Holter monitor recording appears to be useful in identifying patients at risk of sudden cardiac death.

Coronary Disease↗
PubMed1986

Hormonal, global, and regional haemodynamic responses to a vascular antagonist of vasopressin in patients with congestive heart failure with and without hyponatraemia.

The pathophysiological role of an increase in circulating vasopressin in sustaining global and regional vasoconstriction in patients with congestive heart failure has not been established, particularly in patients with hyponatraemia. To assess this further, 20 patients with congestive heart failure refractory to digoxin and diuretics were studied before and 60 minutes after the intravenous injection (5 micrograms/kg) of the vascular antagonist of vasopressin [1(beta-mercapto-beta,beta-cyclopentamethylene-propionic acid), 2-(0-methyl) tyrosine] arginine vasopressin. Ten patients were hyponatraemic (plasma sodium less than 135 mmol/l) and 10 were normonatraemic. In both groups of patients the vascular vasopressin antagonist did not alter systemic or pulmonary artery pressures, right atrial pressure, pulmonary capillary wedge pressure, cardiac index, or vascular resistances. Furthermore, there was no change in skin and hepatic blood flow in either group after the injection of the vascular antagonist. Only one patient in the hyponatraemic group showed considerable haemodynamic improvement. He had severe congestive heart failure and a high concentration of plasma vasopressin (51 pmol/l). Plasma renin activity, vasopressin, or catecholamine concentrations were not significantly changed in response to the administration of the vasopressin antagonist in either the hyponatraemic or the normonatraemic groups. Patients with hyponatraemia, however, had higher baseline plasma catecholamine concentrations, heart rate, pulmonary pressure and resistance, and lower hepatic blood flow than patients without hyponatraemia. Plasma vasopressin and plasma renin activity were slightly, though not significantly, higher in the hyponatraemic group. Thus the role of vasopressin in sustaining regional or global vasoconstriction seems limited in patients with congestive heart failure whether or not concomitant hyponatraemia is present. Vasopressin significantly increases the vascular tone only in rare patients with severe congestive heart failure and considerably increased vasopressin concentrations. Patients with hyponatraemia do, however, have raised baseline catecholamine concentrations, heart rate, pulmonary arterial pressure and resistance, and decreased hepatic blood flow.

Adult↗
PubMed1987

Left ventricular aneurysm with predominating congestive heart failure. A comparative study of medical and surgical treatment.

From 1979 to 1985, 109 patients were treated for congestive heart failure caused by postinfarction left ventricular aneurysm. Congestive heart failure was predominant in all patients at the time of diagnosis, 73% of whom were in Functional Class III or IV. Left ventricular end-diastolic pressure averaged 23.8 +/- 0.8 mm Hg (mean +/- standard error of the mean), total ejection fraction 29.7% +/- 1.0%, and telediastolic volume of the aneurysm 76.2 +/- 5.8 ml. Aneurysmectomy was performed in 49 patients (45%), whereas the remaining 60 patients were treated medically. The two groups did not differ in regard to clinical and hemodynamic data on admission, except for a more extensive coronary artery disease in the surgical group. Follow-up was obtained for all patients (100%) and averaged 48 +/- 3 months. Actuarial survival curves were similar, and the 5-year survival rates for surgical and medical groups were 70 +/- 7% and 64% +/- 7%, respectively (not significant). However, the 5-year complication-free rate was significantly (p = 0.05) higher among surgical patients (52% +/- 8%) than among the medical group (31% +/- 7%). Multivariate analysis showed the following variables to influence survival independently (p less than 0.05): contractile segment ejection fraction, right ventricular failure, antecedents of cardiac arrest or cardiogenic shock, and corrected contractile score. Independent variables decreasing the risk of cardiac-related complications and death (p less than 0.05) were as follows: surgical treatment, shorter interval between initial infarction and diagnosis of aneurysm, and absence of right ventricular failure. Functional improvement was directly related to surgical treatment and to residual segment contractile score (p less than 0.05). Thus, in patients with congestive heart failure caused by left ventricular aneurysm, surgical treatment improved the quality of life and prognosis for cardiac-related complications, but did not increase overall survival, compared to medical management of similar patients.

Adult↗
PubMedDate not supplied

Atrial fibrillation and congestive heart failure: risk factors, mechanisms, and treatment.

Atrial fibrillation (AF) and congestive heart failure (CHF) are commonly encountered together, and either condition predisposes to the other. Risk factors for AF and CHF include age, hypertension, valve disease, and myocardial infarction, as well as a variety of medical conditions and genetic variants. Congestive heart failure and AF share common mechanisms, including myocardial fibrosis and dysregulation of intracellular calcium and neuroendocrine function. Pharmacological treatments including beta-blockers, digoxin, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can be useful in treating both of these conditions. Antiarrhythmic medications intended to achieve and maintain sinus rhythm may be beneficial in some patients with AF and CHF. Advances in pacemaker and defibrillator therapy, including cardiac resynchronization therapy, may also benefit patients with AF and CHF. Surgical and catheter-based ablation therapy can restore sinus rhythm in patients with AF, with proven benefit in patients with concommitant CHF. Investigational biologic therapy, including cell and gene based therapy, offers promise for the future of reversing the pathophysiological mechanisms that underlie AF and CHF.

Atrial Fibrillation↗
PubMed1995

Occult sleep-disordered breathing in stable congestive heart failure.

OBJECTIVE: To determine the prevalence and effect of sleep-disordered breathing in ambulatory patients with stable, optimally treated congestive heart failure. DESIGN: A prospective, longitudinal study. SETTING: Referral sleep laboratory of a Department of Veterans Affairs medical center. PATIENTS: 42 of the 48 eligible patients with stable congestive heart failure and left ventricular systolic dysfunction (left ventricular ejection fraction < or = 45%). MEASUREMENTS: After an adaptation night, polysomnography and Holter monitoring were done in the sleep laboratory. Arterial blood gases and pH were measured, and cardiac radionuclide ventriculography and pulmonary, renal, and thyroid function tests were done. RESULTS: Patients were divided into two groups. Group I (n = 23) had an hourly rate of apnea and hypopnea (apnea-hypopnea index) of 20 episodes per hour or less; group II (n = 19 [45%; CI, 30% to 60%]) had an index of more than 20 episodes per hour. In group II, the index varied from 26.5 to 82.2 episodes per hour (mean +/- SD, 44 +/- 13 episodes per hour; CI, 38 to 51 episodes per hour). Group II had significantly more arousals (24 +/- 12 compared with 3 +/- 3 in group I) that were directly attributable to episodes of apnea and hypopnea, longer periods of time with an arterial oxyhemoglobin saturation of less than 90% (23% +/- 24% of total sleep time compared with 2% +/- 4%), lower arterial oxyhemoglobin saturation during sleep (74% +/- 13% compared with 87% +/- 4%), lower left ventricular ejection fraction (22% +/- 9% compared with 30% +/- 10%), and a significantly increased number of episodes of nocturnal ventricular arrhythmias. Multiple regression analyses showed that left ventricular systolic dysfunction was an independent risk factor for sleep apnea in patients with congestive heart failure. CONCLUSIONS: The prevalence of severe occult sleep-disordered breathing is high in ambulatory patients with stable, optimally treated chronic congestive heart failure. The breathing episodes are associated with severe nocturnal arterial blood oxyhemoglobin desaturation and excessive arousals. Severe untreated sleep-disordered breathing may adversely affect left ventricular function, resulting in a vicious cycle that could contribute to death in patients with congestive heart failure. Prospective, longitudinal studies on survival are needed.

Aged↗
PubMed1998

Preventing congestive heart failure.

The morbidity, mortality and health care costs associated with congestive heart failure make prevention a more attractive public health strategy than treatment. Aggressive management of etiologic factors, including hypertension, coronary artery disease, valvular disease and excessive alcohol intake, can prevent the left ventricular remodeling and dysfunction that lead to heart failure. Early intervention with angiotensin converting enzyme inhibitors in patients with chronic left ventricular dysfunction can prevent, as well as treat, the syndrome. Several intervention strategies in patients with acute myocardial infarction can slow or prevent the left ventricular remodeling process that antedates congestive heart failure. The primary care physician must be alert to the need for aggressive intervention to reduce the burden of heart failure syndrome on the patient and on society.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

The N-terminus of the atrial natriuretic factor prohormone in the pleural fluid of congestive heart failure patients.

To investigate the possibility that the prohormone of atrial natriuretic factor might be secreted into the pleural fluid of patients with congestive heart failure who are known to have high concentrations of both the N-terminus and C-terminus of this prohormone circulating in their plasma, six patients with class 2 New York Heart Association classified congestive heart failure had the simultaneous measurement of plasma and pleural fluid N-terminal and C-terminal atrial natriuretic factor prohormone concentrations. The 98 amino acid (aa) N-terminus, the midportion of the N-terminus consisting of aa 31-67 of the 126 aa ANF prohormone (ie, pro ANF 31-67), and the C-terminus (aa. 99-126, ANF) were found in high concentrations in the pleural fluid of all of these patients. The concentrations of the N-terminus (ie, pro ANF 1-98), and pro ANF 31-67 in pleural fluid were nearly equal to their concentration in plasma of these patients. Their plasma levels were more than double the plasma concentrations of pro ANFs 1-98 and 31-67 in 54 persons without congestive heart failure. These preliminary findings demonstrate that all 126 amino acids of the ANF prohormone are present in pleural fluid of patients with congestive heart failure since both the 98 aa N-terminus and the C-terminus (aa 99-126) are present. Whether or not the N-terminus, which contains diuretic and natriuretic peptides, secretion into pleural fluid helps clear the fluid present in the lung in congestive heart failure could not be determined from the present investigation.

Atrial Natriuretic Factor↗
PubMed1988

Peripheral haemodynamic effects of perindopril compared in patients with congestive heart failure and in normal volunteers.

The effects of perindopril, 4 mg orally, on brachial artery blood flow and diameter (pulsed Doppler) and on forearm vascular resistance were investigated and compared in six normal subjects and 10 congestive heart failure patients (New York Heart Association class III or IV). Pre-drug values of brachial artery blood flow and diameter were significantly lower in patients with congestive heart failure than in normal subjects, the reverse being true for forearm vascular resistance. In normal subjects perindopril increased brachial artery blood flow and decreased forearm vascular resistance, while in patients with congestive heart failure the same effects were observed but they were more pronounced and brachial artery diameter was increased. In patients with congestive heart failure, when perindopril effects were maximal, brachial artery blood flow remained below the baseline values of normal subjects but brachial artery diameter was normalized. Finally, there was a correlation between the drug-induced decrease in forearm vascular resistance and basal plasma noradrenaline values in all subjects taken together. These results indicate that: (1) the renin-angiotensin system plays a major role in vasoconstriction in patients with congestive heart failure; (2) this vasoconstriction affects both large arteries and arterioles; (3) perindopril is able to considerably improve peripheral haemodynamics in congestive heart failure; and (4) this improvement is linked to the initial sympathetic tone.

Adult↗
PubMed2005

Cerebrovascular response to carbon dioxide in patients with congestive heart failure.

RATIONALE: Cerebrovascular reactivity to CO(2) provides an important counterregulatory mechanism that serves to minimize the change in H(+) at the central chemoreceptor, thereby stabilizing the breathing pattern in the face of perturbations in Pa(CO(2)). However, there are no studies relating cerebral circulation abnormality to the presence or absence of central sleep apnea in patients with heart failure. OBJECTIVES: To determine whether patients with congestive heart failure and central sleep apnea have an attenuated cerebrovascular responsibility to CO(2). METHODS: Cerebral blood flow velocity in the middle cerebral artery was measured in patients with stable congestive heart failure with (n = 9) and without (n = 8) central sleep apnea using transcranial ultrasound during eucapnia (room air), hypercapnia (inspired CO(2), 3 and 5%), and hypocapnia (voluntary hyperventilation). In addition, eight subjects with apnea and nine without apnea performed a 20-second breath-hold to investigate the dynamic cerebrovascular response to apnea. MEASUREMENTS AND MAIN RESULTS: The overall cerebrovascular reactivity to CO(2) (hyper- and hypocapnia) was lower in patients with apnea than in the control group (1.8 +/- 0.2 vs. 2.5 +/- 0.2%/mm Hg, p < 0.05), mainly due to the prominent reduction of cerebrovascular reactivity to hypocapnia (1.2 +/- 0.3 vs. 2.2 +/- 0.1%/mm Hg, p < 0.05). Similarly, brain blood flow demonstrated a smaller surge after a 20-second breath-hold (peak velocity, 119 +/- 4 vs. 141 +/- 8% of baseline, p < 0.05). CONCLUSION: Patients with central sleep apnea have a diminished cerebrovascular response to PET(CO(2)), especially to hypocapnia. The compromised cerebrovascular reactivity to CO(2) might affect stability of the breathing pattern by causing ventilatory overshooting during hypercapnia and undershooting during hypocapnia.

Aged↗
PubMed1990

Left ventricular filling pattern in congestive heart failure patients with normal sinus rhythm--a decreased ratio of peak mitral flow velocity in atrial systole relative to that in early diastole may reflect markedly increased left ventricular end-diastolic pressure.

The left ventricular filling pattern was studied by pulsed Doppler echocardiography in 13 congestive heart failure patients with normal sinus rhythm. The first study was done when congestive heart failure was present; the second after the signs and symptoms of congestive heart failure disappeared. In 12 of the 13 patients, the peak mitral flow velocity in atrial systole (PFVA) increased after the congestive heart failure disappeared (mean increase from 50.5 cm/sec to 74.8 cm/sec : p = 0.0001, paired t test), and the peak mitral flow velocity in early diastole (PFVE) decreased significantly in all 8 patients in whom secondary mitral regurgitation became less severe after improvement of congestive heart failure (mean decrease from 90.8 cm/sec to 52.0 cm/sec : p = 0.0001, paired t test). The ratio of PFVA to PFVE (PFVA/PFVE) increased in all cases after the congestive heart failure improved (mean increase from 0.59 to 1.33 : p = 0.0001, paired t test). The PFVA/PFVE is a simple index of left ventricular diastolic function. A PFVA/PFVE greater than one indicates disturbed left ventricular diastolic function. However, when the PFVA/PFVE is in a normal range for the patients' age ("pseudo-normalization") and is accompanied by impaired left ventricular systolic function in congestive heart failure, markedly increased left ventricular end-diastolic pressure must be considered.

Adult↗
PubMed1989

Influence of ibopamine on heart rate and arrhythmic pattern in patients with congestive heart failure. A double-blind multicentre study.

Ibopamine is a dopaminergic and adrenergic receptor agonist, which is active in the treatment of congestive heart failure. Since the long-term prognosis for patients with congestive heart failure remains very poor and the incidence of arrhythmic death is high, every new drug to be employed against this disease should be thoroughly tested in order to rule out any possible arrhythmogenic action. This multicentre study was designed to evaluate the effect of ibopamine versus placebo in double-blind conditions on heart rate, rhythm and electrical safety. Ibopamine was employed at a dose of 100 mg t.i.d. in 97 patients (aged 31-83 years) belonging to NYHA class II and III with congestive heart failure of different aetiology, but without any complex ventricular arrhythmias in basal conditions (couplets with R'-R" less than or equal to 400 msec, ventricular tachycardia, R on T phenomena). Using a random cross-over design the patients were submitted to 48 hr. Holter recordings in basal conditions and following 7 days of ibopamine and placebo treatment. No influence on heart rhythm was noted. No significant variations in maximum heart rate (ibopamine 117.7 +/- 20.9; placebo 118.1 +/- 20.7), medium heart rate (ibopamine 71.8 +/- 10.2; placebo 72.6 +/- 10.1) or minimum heart rate (ibopamine 55.3 +/- 11.7; placebo 54.6 +/- 10.6) were observed. The mean number/hr. of ectopic supraventricular beats was 26.1 +/- 61.9 after ibopamine and 21.7 +/- 35.8 after placebo (p = ns). The complexity of ectopic supraventricular beats did not change. The mean number/hr. of ectopic ventricular beats was 31.1 +/- 52.5 after ibopamine and 30.4 +/- 57.8 after placebo (p = ns). Neither the distribution of the patients among Lown classification nor the Final Score of the Italian Lown Classification (26.1 +/- 18.0 and 26.6 +/- 17.9 in the 1st and 2nd day of monitoring after ibopamine and 25.7 +/- 18.6 and 25.7 +/- 18.8 after placebo; p = ns) showed any difference between active treatment and placebo. Similar results were achieved when the patients were sub-divided into subgroups according to sequences of treatment (basal----ibopamine----placebo and basal----placebo----ibopamine), NYHA class II or III, aetiology of congestive heart failure (dilatative cardiomyopathy, ischemic cardiomyopathy and other aetiologies), associated treatment with digitalis or diuretics and the number and complexity of base ectopic ventricular beats. None of the patients experienced sustained ventricular tachycardia.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMedDate not supplied

Role of atrial natriuretic peptide in congestive heart failure due to chronic diabetes.

OBJECTIVE: It is now believed that diabetes sensitizes the myocardium so that superimposed hypertension with its attendant vascular changes results in progressive myocyte damage leading ultimately to congestive heart failure. In this regard, remarkable progress has been made within the past few years with a family of closely related peptides, the atrial natriuretic peptides (ANPs), which are involved in the regulation of plasma volume. Any changes in their levels and/or action can be seen to participate in the development of diabetes-induced congestive heart failure. While the literature reasonably supports the evidence for a defect in the ANP-receptor coupling system in hypertensive and diabetic animals, it is not as clear that this is the cause for heart failure. The present article attempts to demonstrate evidence for causality. DESIGN: The present article summarizes existing knowledge on the involvement of ANP in the induction of fluid imbalance. In particular, the role of ANP in congestive heart failure, hypertension, diabetes and congestive heart failure in diabetes is examined. Recent data in experimental hypertensive-diabetic rats, obtained from this laboratory have also been described here. MAIN RESULTS: There are now several reports which indicate high plasma ANP concentrations in both patients and animals with heart failure, thus implicating a role for this peptide. The present paper deals with ANP-induced molecular changes in kidney basolateral membranes in congestive heart failure due to chronic diabetes. CONCLUSION: Congestive heart failure in diabetes with hypertension may be due to uncoupling of the ANP-receptor effector system in the kidney basolateral membrane. It is possible that other neurohumoral agents through a wide variety of activities may also contribute to the pathophysiology of this disease.

Atrial Natriuretic Factor↗