Inefficacy of daily single bolus dose atrial natriuretic factor in chronic congestive heart failure.
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Aged↗
Biomedical subjects
H Ikram
Publications and source records attributed to H Ikram.
Congenital long QT syndrome in adults.
A family with the Romano-Ward syndrome is presented. This family showed typical features of this syndrome with QT prolongation, torsades de pointes ventricular tachycardia, sudden death and an autosomal dominant inheritance pattern. The index case presented with an exacerbation of torsades de pointes ventricular tachycardia from diuretic induced hypokalaemia, and responded to diuretic withdrawal and beta blocker therapy.
Adolescent↗
Atrial natriuretic factor inhibits proliferation of vascular smooth muscle cells stimulated by platelet-derived growth factor.
The effect of atrial natriuretic factor (Isoleucine-ANF 101-126) on basal and platelet-derived growth factor (PDGF)-stimulated proliferation of rat aortic vascular smooth muscle cells (VSMC) was assessed by microscopy and measurement of incorporation of tritiated thymidine by cells cultured with or without addition of PDGF in the presence of various concentrations (10(-8)-10(-6) molar) of ANF. ANF had little effect on proliferation of cells grown in media supplemented with 2% fetal calf serum (FCS) alone but exhibited clear dose-related inhibition of PDGF-stimulated thymidine incorporation.
Animals↗
The role of selenium deficiency in occidental dilated cardiomyopathy.
The whole blood selenium concentrations were measured in 14 consecutive cases of catheter-proven dilated cardiomyopathy. The mean range of selenium was 59 ng/mL (SD 14). Patients with coronary heart disease had a mean value of 44 ng/mL (9.7) and normal controls had 78 ng/mL (20.1). These results would not support the hypothesis that selenium deficiency is an important causative agent in dilated cardiomyopathy in New Zealand.
Beriberi↗
Hemodynamic and hormone changes during induced ventricular tachycardia secondary to coronary artery disease.
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Aged↗
Chronic and acute volume expansion in normal man: effect on atrial diameter and plasma atrial natriuretic peptide.
Plasma levels of immunoreactive alpha human atrial natriuretic peptide (IR-ANP) and left atrial diameter were measured in 6 normal subjects before and after 6 days of sodium loading using salt supplements and 9-alpha-fluorohydrocortisone. During chronic sodium loading, which increased mean body weight by 1.5 kg and markedly reduced plasma renin and aldosterone levels, plasma IR-ANP increased from 21 +/- 3 to 36 +/- 7 pmol/l (P less than 0.02). Increase in atrial diameter correlated with gains in body weight (r = 0.93, P less than 0.01) but not with increase in plasma IR-ANP. After chronic sodium loading for 6 days, further volume expansion (2 litres of saline infused over 2 hours) significantly increased left atrial diameter but did not affect plasma IR-ANP levels. We conclude that chronic sodium loads increase plasma IR-ANP. However, the failure of further acute atrial distension to increase hormone levels suggests that factors in addition to atrial stretch are important in regulating atrial peptide secretion in man.
Adult↗
Global and regional hemodynamic effects of ramipril in congestive heart failure.
Global and regional hemodynamic changes were assessed in 11 patients with congestive heart failure following the introduction of the novel angiotensin-converting enzyme inhibitor (ACEI), ramipril. All patients were stabilized on digitalis, furosemide, and a fixed diet, central hemodynamics and hormones having been stable over 2 control days. Ramipril resulted in significant falls in converting enzyme activity, angiotensin II, and aldosterone, with a rise in renin. Changes in regional blood flow were assessed 2 h following the first dose of ramipril at the time of maximal increase in global cardiac output (+27%, p less than 0.05), but prior to the maximal fall in systemic arterial pressure. Despite the fall in systemic arterial pressure, blood flow increases were noted in the renal (+93%, p less than 0.05), coronary (+10%), and cerebral (+5%) regions, while forearm blood flow was unchanged. Glomerular filtration rate fell (29%) and was associated with small rises of plasma creatinine and acute sodium retention. After 7 weeks of therapy we noted improvement in functional class (p less than 0.05), exercise time, and left ventricular ejection fraction. We conclude that during inhibition of angiotensin-converting enzyme activity by ramipril in patients with congestive heart failure, blood flow to the kidneys, heart, and brain is increased or preserved despite hypotension. Long-term therapy is associated with beneficial clinical effects.
Aged↗
Atrial natriuretic peptide levels in congestive heart failure in man before and during converting enzyme inhibition.
1. To determine the response of plasma atrial natriuretic peptide (ANP) to treatment with an angiotensin converting enzyme (ACE) inhibitor in heart failure, seven patients (NYHA Functional Class III-IV) were studied before and after the addition of ramipril to maintenance digoxin and diuretic treatment. 2. Baseline arterial ANP levels were raised, but fell during ramipril treatment in parallel with changes in both haemodynamic recordings (arterial pressure, pulmonary artery diastolic pressure, and right atrial pressure) and hormone levels (angiotensin II and aldosterone). 3. Coronary sinus ANP, measured in three patients, was greater than concomitant arterial levels, and the coronary sinus ANP secretion rate was calculated to be between 15 and 119 pmol/min. 4. These results demonstrate that improvement in haemodynamic function during ACE inhibitor treatment is associated with a decline in elevated ANP levels, and support the concept that atrial stretch or pressure regulates the secretion of atrial peptides in man.
Adult↗
Neurohumoral changes during onset and offset of ovine heart failure: role of ANP.
The temporal relationship of changes in atrial natriuretic peptide (ANP) secretion to other pathophysiological changes in heart failure has not been investigated. We studied the hemodynamic, hormonal, and metabolic changes before, during, and after the induction of heart failure in eight sheep using a 14-day period of rapid left ventricular pacing (LVP). Arterial pressure declined 21% on the first day, while cardiac output fell progressively to 48% of base line, and atrial pressures rose to a plateau over the first week. Plasma ANP levels increased 10-fold with a close correlation to left atrial pressure in all sheep. Furthermore, ANP secretion appeared to be sustained throughout the LVP period but did not prevent avid sodium retention. Marked and early activation of the renin-angiotensin system was observed, whereas the major increase in plasma aldosterone commenced 4 days later. On termination of LVP, a prompt natriuresis and diuresis occurred with return of all parameters toward base line. Thus this ovine model is useful for studying pathophysiological changes during the onset and offset of heart failure.
Animals↗
Atrial natriuretic factor in hypertension: bioactivity at normal plasma levels.
To ascertain whether small shifts in plasma atrial natriuretic factor (ANF) exerted biological effects in hypertension, we studied the renal, hemodynamic, and hormonal effects of ANF [human ANF-(99-126)] infused at a dose (0.75 pmol/kg/min for 3 hours) that would induce changes in plasma ANF confined to the normal, resting range, in a group of six young men with uncomplicated, mild essential hypertension. During ANF infusions, the patients excreted 11.8 +/- 2.0 mmol (mean +/- SEM) sodium more than during the time-matched placebo phase natriuresis (p less than 0.001, mean increase of 53% above placebo values). Urinary excretion of cyclic guanosine monophosphate rose to more than double (212%, p less than 0.001) placebo values. Plasma renin activity (0.4 +/- 0.05 vs. 0.9 +/- 0.12 nmol/l/hr, p less than 0.0001) and aldosterone concentrations (102 +/- 4 vs. 184 +/- 47 pmol/l, p less than 0.05) were clearly suppressed during administration of ANF. Plasma norepinephrine also fell significantly below placebo values (268 +/- 17 vs. 439 +/- 35 pg/ml, p less than 0.05). Urine volume, the excretion of electrolytes other than sodium, hematocrit, effective renal plasma flow, glomerular filtration rate, and filtration fraction were unaffected by ANF. Similarly, plasma concentrations of epinephrine, arginine vasopressin, adrenocorticotropic hormone, and cortisol were unchanged. Blood pressure and heart rate were unchanged. Minor perturbations in plasma ANF concentrations exert clear biological effects in patients with mild essential hypertension. These data suggest that such minor shifts in plasma ANF are of physiological relevance in mild hypertension and probably contribute to volume homeostasis in this condition.
Adolescent↗
Blood pressure and vasoactive hormones with improved glycaemic control in patients with diabetes mellitus.
To assess the effects of improved glycaemic control on arterial pressure and plasma levels of vasoactive hormones, we studied 5 male insulin dependent (Type 1) diabetic patients before and one month after commencement of rigorous control of blood glucose levels. On each occasion, continuous ambulatory intra arterial pressure monitoring for a 10-hour period, together with hourly venous sampling for plasma glucose and vasoactive hormone determinations, was performed under standardised conditions of diet and posture. Mean (+/- SEM) plasma glucose before and after improved glycaemic control was 9.4 +/- 0.3 and 6.6 +/- 0.4 mmol/l respectively (P less than 0.001). There was a small but significant fall in arterial pressure in each patient as well as for the group overall (mean arterial pressure fall 4.8 +/- 1.2 mmHg, p less than 0.01) after improved glycaemic control. The fall in individual (10 hr mean) diastolic arterial pressure levels correlated with concomitant falls in plasma glucose levels (r = 0.92, p less than 0.05) but not with changes in any of the other variables measured.
Adolescent↗
Cardiac electrophysiological assessment and the natural history of unexplained syncope.
There is little data on cardiac electrophysiological assessment and long term follow-up of unexplained syncope from Australasia. We present 94 patients with unexplained syncope who underwent such assessment and followup for an average of 52 months in 92 patients. Of the 94 investigated 57 were male, the average age was 61 years and average number of syncopal episodes prior to study was 8 (minimum 2). Forty-two patients had heart disease. Patients were divided into 3 groups on results of electro physiological testing. Normal (31 patients), group 1 with intermediate abnormalities of sinus node function or atrioventricular conduction (37 patients) and group 2 in whom the abnormalities were felt likely to represent the cause of syncope (26 patients). Abnormalities detected in group 2 were sinus node dysfunction in 12, abnormal atrioventricular nodal conduction in 8, abnormal infranodal conduction in 2, vagal hypersensitivity in 3 and ventricular tachycardia in two. Follow-up for a mean of 52 months was obtained in 92 patients. Recurrent syncope occurred in 37% of the patients. Treatment reduced recurrent syncope to a level approaching statistical significance in group 2 patients (50% to 13%; 0.01 greater than p greater than 0.05) but had little influence on recurrent syncope in group 1 or normal patients. There were 14 deaths over the follow-up period. Mortality was predicted by group 2 electrophysiological abnormality (p less than 0.02) and the presence of heart disease (p less than 0.05) and was not reduced by specific therapy. Sudden death occurred in 3 patients, all with heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Arrhythmias, Cardiac↗
Atrial natriuretic factor and the heart in health and disease.
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Atrial Natriuretic Factor↗
Converting enzyme inhibitors in heart failure.
The renin-angiotensin system is activated in heart failure in proportion to the severity of the haemodynamic derangement and to diuretic dose. Angiotensin converting enzyme (ACE) inhibitors reduce circulating levels of angiotensin II and aldosterone and, in some patients, plasma noradrenaline, vasopressin and cortisol. Typically there is potassium retention and a minor increase in plasma potassium, but cumulative sodium balance may increase or decrease depending on pretreatment fluid and haemodynamic status and on policy regarding diuretic dose. Circulatory dynamics usually improve and blood flow to the brain, myocardium and kidneys is preserved. Changes in glomerular filtration rate are dictated by haemodynamic characteristics and, again, by diuretic dose and dietary sodium. There are potential hazards with ACE inhibitor therapy but most problems can be anticipated and avoided. Future trends may include the introduction of ACE inhibitors with or without concomitant diuretic therapy in early cardiac failure, and intravenous ACE inhibition immediately after acute myocardial infartion. Whether the ACE inhibitors will prove more successful than alternative antihypertensive agents in preventing cardiac complications (including heart failure) of hypertension, is an intriguing question.
Angiotensin-Converting Enzyme Inhibitors↗
Hormone, calcium and blood pressure relationships in primary hyperparathyroidism.
The cause of hypertension in primary hyperparathyroidism and its response to corrective surgery remains a matter of controversy. We therefore studied blood pressure, vasoactive hormones and plasma calcium responses to parathyroidectomy in six hypertensive and two normotensive patients with primary hyperparathyroidism. Twenty-four-hour intra-arterial pressure recordings, together with hourly blood sampling for plasma renin activity (PRA), aldosterone, cortisol, catecholamines and calcium levels, were undertaken in each patient before surgery and were repeated under identical conditions 3-6 months after parathyroidectomy. Mean plasma calcium was 3.03 +/- 0.1 before, and 2.35 +/- 0.02 mmol/l after, parathyroidectomy. Changes in arterial pressure were small and variable in individual patients. Group mean arterial pressures before and after surgery were identical. Plasma cortisol and PRA were significantly higher in the hypercalcaemic state (P less than 0.01 and P less than 0.05, respectively) but there was no significant difference in plasma aldosterone or catecholamine levels. No correlations between changes in plasma calcium or parathyroid hormone levels and concomitant changes in plasma concentration of other hormones were observed. Our findings show that correction of primary hyperparathyroidism has no systematic effect on arterial pressure in a heterogeneous group, including some patients with probable background essential hypertension, when evaluated 3-6 months after surgery. Compared with values after corrective surgery, mean levels of PRA and cortisol-but not aldosterone or catecholamines--are elevated in patients with primary hyperparathyroidism. These findings are consistent with an inhibitory effect of raised ionic calcium concentration on the response of the adrenal glomerulosa to angiotensin and adrenocorticotrophic hormone.
Aged↗
Atrial natriuretic factor in human pathophysiology.
1. Evidence from numerous experiments incorporating central blood volume expansion and changes in sodium status supports atrial stretch as the prime determinant of ANF release. 2. Plasma ANF levels are the result of both secretion and clearance of the peptide. Clearance is altered by a number of factors, including changes in posture in normal man and is probably impaired in disease states with diminished renal and hepatic blood flow. 3. In normal subjects an inverse relationship exists between plasma ANF values and renin-angiotensin-aldosterone system activity. This relationship is lost and replaced by a positive association in heart failure, presumably reflecting the abnormal concurrence of increased atrial stretch and diminished renal perfusion in this condition. Plasma ANF values rise with increasing severity of heart failure and fall with effective treatment. 4. Plasma ANF values are elevated in hypertension and cardiac tachyarrhythmias possibly reflecting raised central venous and atrial pressures. 5. A variety of other disorders may be associated with abnormal plasma ANF values including cirrhosis and the syndrome of inappropriate ADH secretion. 6. Evidence from low-dose infusions of ANF in normal volunteers suggests that the variations in plasma ANF seen in health and disease are sufficient to exert biological effects. 7. The advent of a specific antagonist is needed to provide further insight into the physiological and pathophysiological roles of ANF.
Atrial Natriuretic Factor↗
Acute thrombotic obstruction of a mitral valve prosthesis: the role of thrombolytic therapy.
An acute thrombotic occlusion of a mitral prosthesis in a hemodynamically compromised patient was successfully lysed with intravenous streptokinase. Unfortunately, the patient had a major cerebral embolus, from which she died several days later. A review of the current literature reveals that thrombolytic therapy successfully relieves the obstructing thrombus in 73% of cases, while it is partially successful in another 16% allowing deferral of surgical repair to a more optimal time. Mortality from thrombolytic therapy is 14% while hemorrhage or cerebral emboli occur in a further 11%. Reports of surgical intervention have shown an operative mortality rate of 25%, in those fit to undergo surgery. If hemodynamically unstable patients unfit for surgery are included on an intention to treat basis, overall mortality is 42%. Thus, thrombolytic therapy should be considered primarily in those compromised patients who have a thrombotic occlusion of a valvular prosthesis with a greater risk of operative mortality. Low dose, prolonged infusions should be favoured over rapid, high concentration infusions currently employed for coronary thrombolysis, as the latter regime could have contributed to the fatal cerebral embolus in our patient.
Aged↗
Atrial natriuretic hormone has biological effects in man at physiological plasma concentrations.
Whether atrial natriuretic hormone (ANH) has biological effects at physiological plasma levels in man is not known. Accordingly, we investigated the effects of a 3-h low dose infusion of human ANF (0.75 pmol/kg.min; i.e. 0.0023 micrograms/kg.min) in six normal men, whose sodium intake was normal while sitting, in a single blind, random order, placebo-controlled study. The ANF infusions induced changes in plasma ANH concentrations entirely within the range for normal subjects. The small increases in plasma ANH values were associated with a significant rise in urinary excretion of sodium, magnesium, calcium, and cGMP. PRA and plasma aldosterone concentrations uniformly decreased to 50% and 64% of placebo values, respectively. Systolic and mean arterial pressures fell significantly from preinfusion values during the ANH infusions. These findings constitute strong evidence that ANH is a hormone of physiological significance in the regulation of body fluid volumes in normal man.
Adult↗