Effectiveness of vasopressin regulation of coronary blood flow in congestive heart failure secondary to idiopathic dilated or ischemic cardiomyopathy.
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Adult↗
Biomedical subjects
H Ikram
Publications and source records attributed to H Ikram.
Acute hemodynamic, hormonal and electrolyte effects of ramipril in severe congestive heart failure.
The response to ramipril, 10 and 20 mg on consecutive days, in 9 patients with severe (New York Heart Association functional class III or IV) chronic congestive heart failure was measured. Hemodynamic cannulae were placed more than 2 days before ramipril administration to ensure a stable baseline. Dietary sodium (40 mmol daily) and potassium (80 mmol daily) were constant before and during the study, and maintenance doses of digoxin and furosemide (80 to 1,000 mg daily) were continued unchanged. Ramipril induced pronounced, sustained decreases in angiotensin converting enzyme activity, angiotensin II and aldosterone levels, and a reciprocal increase in plasma renin activity. Plasma catecholamines, antidiuretic hormone and cortisol levels were not altered. Urinary sodium and potassium excretion diminished, plasma sodium decreased and plasma potassium increased. Plasma urea and creatinine levels increased. Ramipril treatment resulted in a decrease in systemic arterial pressure that was sustained for 24 hours, a decrease in heart rate and an increase in cardiac index, but little change in pulmonary artery pressure or right atrial pressure. Three patients were drowsy after ramipril administration, and 1 patient had a marked, temporary reduction in urine output. It was concluded that ramipril is a potent, long-acting angiotensin converting-enzyme inhibitor that is likely to be beneficial in patients with severe cardiac failure.
Adult↗
Flecainide acetate for conversion of acute supraventricular tachycardia to sinus rhythm.
The efficacy of intravenous flecainide acetate (maximum 2 mg/kg or 150 mg given at a rate of 15 mg/min) was assessed in patients with acute supraventricular tachycardia (SVT) (within 24 hours). Fifty patients were studied, 46 with spontaneous SVT and 4 with induced SVT at electrophysiologic assessment. Conversion to sinus rhythm was achieved within 45 minutes in 76%: in 25 patients with atrial fibrillation (76% conversion), 15 with atrioventricular (AV) nodal or AV reentrant tachycardia (100% conversion) and 10 with atrial flutter or atrial reentrant tachycardia (40% conversion). Adverse effects were noted in 21 patients (42%): paresthesia in 9, drowsiness in 8, nausea in 2, accelerated ventricular rate in 5, ventricular tachycardia in 1, sinus bradycardia in 1 and hypotension in 5. Adverse effects were associated with larger dosage and atrial flutter or atrial reentrant tachycardia. Thus, flecainide acetate is effective in converting to sinus rhythm acute atrial fibrillation and AV nodal and AV reentrant tachycardias, but not atrial flutter or atrial reentrant tachycardia.
Acute Disease↗
Myocardial function in alcoholic cardiac beriberi.
A case of alcoholic beriberi is described. Left ventricular systolic function as measured by the radionuclide ejection fraction showed an abnormal fall with exercise. Subsequent return to normal with the administration of thiamine suggests myocardial involvement in the condition.
Adult↗
Atrial natriuretic peptide in human hypertension.
Preliminary reports are that plasma levels of immunoreactive atrial natriuretic peptide (IR-ANP) are higher in essential hypertensive patients than in normotensive controls, and that the urinary response to injected alpha human atrial natriuretic peptide (alpha-hANP) is augmented in essential hypertension. Further, there are reports of positive relationships between IR-ANP levels and arterial pressure. Confirmation is needed, however, with larger numbers of patients and with careful matching of diet electrolytes, age and sex, body posture, time of day, and other factors which may alter release or plasma clearance of atrial peptides. If indeed IR-ANP levels are raised in essential hypertension, it is possible that increased demands on the atria as a consequence of altered left ventricular structure and function lead to augmented secretion of atrial peptides. Whether the observed minor increases in plasma IR-ANP could have biologic effects to oppose pressor systems, to sustain glomerular filtration rate, and to suppress vasoactive hormone secretion, is unclear since the threshold level of IR-ANP which has biologic actions in man, is unknown. Plasma IR-ANP levels are raised in primary aldosteronism, and fall with treatment. These early reports suggest that atrial peptides might play a role in the pathophysiology of primary aldosteronism and perhaps essential hypertension, but much more information is needed.
Atrial Natriuretic Factor↗
Plasma immunoreactive atrial natriuretic peptide levels after subcutaneous alpha-hANP injection in normal humans.
The plasma hormone and urine effects of 100 micrograms of alpha-human atrial natriuretic peptide (alpha-hANP) given by subcutaneous (s.c.) injection, were studied in eight healthy male volunteers. A control s.c. injection was administered on a separate day, and the study was single-blind. The peak immunoreactive atrial natriuretic peptide (IR-ANP) level of 29.4 +/- 4.4 pmol/L reached at 5 min was threefold higher than on the control day. Area under the IR-ANP response curve was approximately 1/32 of that after the same dose of alpha-hANP given by intravenous (i.v.) injection. alpha-hANP s.c. injection was not associated with significant effects on plasma renin activity (PRA), plasma aldosterone, or urine electrolyte excretion. It was concluded that only a small percentage of intact alpha-hANP is absorbed into the circulation after s.c. injection. With the dose of peptide and the injection vehicle chosen, alpha-hANP had little or no biological effect.
Adult↗
The pattern of atrial natriuretic peptide release during ventricular tachycardia in man.
1. Plasma levels of atrial natriuretic peptide (ANP) are high in many patients with tachycardia, but patterns of release with onset and termination of tachycardia and relationships to haemodynamic recordings are not clear. Blood for ANP measurements was therefore drawn from the coronary sinus, femoral artery and femoral vein, and simultaneous haemodynamic recordings were made in five patients before, during and after induction of stable ventricular tachycardia for 30 min. 2. Tachycardia induced increases in ANP to peak levels, 2.6 to 5.7 times higher than baseline values at 20 min or later, whereas maximum haemodynamic changes, including a rise in pulmonary artery diastolic pressure, were achieved within 4 min. 3. Reversion to sinus rhythm resulted in immediate changes in haemodynamic recordings, whereas ANP levels in arterial and venous plasma fell sluggishly with an apparent half-life of 9.6 and 7 min, respectively. 4. The results support a central role for atrial pressure in determining ANP secretion, but demonstrate a temporal delay between changes in atrial pressure and ANP secretion.
Aged↗
The course of idiopathic dilated cardiomyopathy in New Zealand.
The course of dilated cardiomyopathy in New Zealand was studied in 72 cases that were followed up for less than or equal to 10 years after cardiac catheterisation and coronary angiography. Eighty one per cent were male and 86% were white; the remainder were Maori. The mean age of patients at the time of investigation was 50 X 15 years. Most patients were unskilled labourers. The commonest presenting symptom was dyspnoea and the commonest physical sign was cardiomegaly. Mean survival time from first hospital presentation was 85 months; half the deaths were sudden. Factors predicting a poor survival included cardiomegaly, age, arrhythmias, cigarette smoking, and subclinical thiamine deficiency. The syndrome of dilated cardiomyopathy in New Zealand appears to be identical with that seen in other European populations.
Adult↗
Atrial natriuretic peptide in spontaneous tachycardias.
Because anecdotal reports suggest that concentrations of atrial natriuretic peptide are raised during tachycardias, plasma immunoreactive atrial natriuretic peptide concentrations were measured in 34 consecutive patients when tachycardia was diagnosed and again five and 15 minutes after conversion to sinus rhythm. Plasma atrial natriuretic peptide concentrations were raised in all but four patients, and were higher in patients with known heart disease than in those without. The concentrations were higher with ventricular tachycardia than with atrial fibrillation or supraventricular tachycardia, and in acute versus chronic tachycardia. There was only a weak positive relation between ventricular rate and atrial natriuretic peptide (r = 0.31); but there was a closer inverse correlation between atrial natriuretic peptide and systolic arterial pressure (r = -0.60). Conversion to sinus rhythm was associated with a definite fall in plasma atrial natriuretic peptide concentrations. Despite very high baseline concentrations of atrial natriuretic peptide only two patients reported polyuria. It is likely that atrial pressure rather than ventricular rate determines atrial natriuretic peptide release during tachycardia. Despite the absence of polyuria in all but two patients in this study atrial peptides could still contribute to, or cause, the polyuria of tachycardias.
Adult↗
Atrial natriuretic peptides in man.
Research on the physiological role of atrial peptides in man is limited, and the potential for these peptides, or more stable analogues, in therapeutics is uncertain. It is clear, however, that plasma levels of immunoreactive atrial natriuretic peptide (IR-ANP) are increased in volunteers taking a high sodium diet, and are elevated in patients with heart failure, chronic renal failure, and primary aldosteronism. There is suggestive evidence that IR-ANP levels are increased also in essential hypertension, although overlap with normotensives is considerable. Injection or infusion of atrial peptides into man results in a diuresis, an increased output of urine electrolytes, a fall in blood pressure and a rise in heart rate, suppression of aldosterone and sometimes of renin also, and stimulation of norepinephrine. In essential hypertensives, urinary effects may be greater than in normotensives. Heart failure patients show a rise in cardiac output and falls in both systemic and pulmonary arterial pressure. Over the next few years and especially if specific antagonists can be developed, the physiologic and pathophysiologic roles of atrial peptides in normal man and in clinical disorders should be clarified. It is possible that stable analogues of atrial peptides will find a place in the treatment of cardiac failure, renal failure, and perhaps hypertension.
Atrial Natriuretic Factor↗
Arrhythmias, electrolytes, and ACE inhibitor therapy in the elderly.
Elderly patients have a higher incidence of symptomatic cardiac arrhythmias and greater management problems than younger patients. This is due to the frequency of occult and overt cardiovascular disease, reduction in cardiac reserve as a consequence of the aging process, and coexistence of other disorders which provide a substrate for iatrogenic disease. The last problem is largely due to electrolyte disturbances induced by diuretic therapy for hypertension and heart failure. The major electrolyte disturbance implicated in arrhythmogenesis is diuretic-induced hypokalemia. There is no doubt that arrhythmias are caused by severe hypokalemia (less than 2.5 mEq/l), or by a milder degree of hypokalemia in digitalis-treated patients or those with left ventricular hypertrophy, but the literature contains conflicting data regarding the importance of milder hypokalemia. The most compelling study in support of its importance used a crossover study design in hypertensive patients with coronary disease and showed that mild degrees of hypokalemia induced by thiazide diuretics increased the tendency to arrhythmia when compared with normokalemia on a potassium-sparing diuretic. Diuretic-induced magnesium deficiency is also regarded by some to be as important as hypokalemia, but the evidence is less extensive. Thus, it appears reasonable to avoid hypokalemia and hypomagnesemia. The optimum therapeutic approach in using diuretics is to keep the dose as low as possible, restrict dietary sodium, and add potassium supplements. Since, in many cases of hypertension, hypokalemia is due to secondary hyperaldosteronism, the use of angiotensin-converting enzyme inhibitors is another therapeutic approach that is effective in hypertension and heart failure.
Aged↗
Haemodynamic effects of atrial peptide infusion in heart failure.
The effect of a synthetic analogue of atrial natriuretic peptide (Ileu-ANP) on haemodynamic, hormonal, and electrolyte excretion indices was studied in 7 patients with chronic congestive heart failure. Patients received in random order placebo or Ileu-ANP infusions (5 micrograms/min) for 4 h on 2 separate occasions, at least 1 week apart. Compared with placebo, Ileu-ANP caused significant reductions in mean systemic arterial pressure, mean pulmonary artery pressure, pulmonary diastolic pressure, and right atrial pressure. These changes were sustained for at least 2 h after infusion. Cardiac output increased from 6.2 to 7.4 l/min at 60 min, then returned to pre-infusion levels. Despite considerable falls in systemic pressure there was no significant increase in heart rate or plasma noradrenaline. With Ileu-ANP infusion, plasma renin activity, angiotensin, arginine vasopressin, aldosterone, and cortisol values were not significantly different from placebo values. Plasma cortisol and aldosterone increased after stopping Ileu-ANP. Neither urine volume nor sodium excretion rate was significantly increased by Ileu-ANP.
Aged↗
Relation between left atrial diameter and plasma atrial natriuretic peptide, renin and vasopressin.
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Adult↗
Pericardial constriction following coronary artery bypass surgery: case reports.
Two patients with the rare complication of pericardial constriction following coronary artery bypass surgery are presented. Management was with prednisone but one patient needed a pericardectomy.
Aged↗
Progression of hypertrophic cardiomyopathy to congestive cardiomyopathy.
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Cardiomyopathy, Dilated↗
Thyrotoxic heart disease.
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Arrhythmias, Cardiac↗
Passive hemagglutination for cytomegalovirus antibody: specificity and stability of reagents.
Glutaraldehyde fixed red cells coated with CMV antigen were lyophilized in the presence of stabilizers such as glycerol, lactose, sorbitol and sucrose. These cells maintained their sensitivity for anti-CMV detection for at least 6 mth when held at 4 degrees C. Some rheumatoid factors containing sera react non-specifically with crude CMV antigen coated cells. The agglutinins in these sera could be effectively removed by adsorption with red cells coated with polymerized IgG.
Adsorption↗
Haemodynamic and hormonal responses to exercise: studies in patients with diabetes mellitus and adrenomedullary deficiency.
The haemodynamic and hormonal responses of patients with autonomic neuropathy and others with adrenomedullary deficiency were compared with mild hypertensives (range of blood pressure 90-100 mmHg diastolic and 140-160 mmHg systolic) and uncomplicated diabetics during standard exercise and postural manoeuvres using continuous arterial blood pressure monitoring. There was no difference in these parameters between the groups when at rest or on standing. During exercise there was no significant difference in blood pressure and heart rate between the groups and all showed significant increases in plasma noradrenaline (mean rise for all groups 2730-22 105 pm 1(-1), P less than 0.03) and (in all but the adrenalectomized subjects) adrenaline (mean rise for remaining three groups 946-3384 pm 1(-1), P less than 0.03; adrenalectomized group showed no rise). The group with autonomic neuropathy showed a significant rise in plasma cortisol from basal 450 +/- 40 to 845 +/- 72 nm 1(-1), P less than 0.005 after exercise, but the other groups showed no significant change. The maximum level attained for plasma cortisol in the adrenalectomized subjects after exercise was significantly less (260 +/- 41 nm 1(-1) than in the diabetic groups (696 +/- 68 nm 1(-1) (non-neuropaths), 845 +/- 72 nm 1(-1) (neuropaths), P less than 0.01). We have demonstrated normal blood pressure and pulse responses to posture and sustained exercise in diabetics with autonomic neutropathy. The findings of similarly normal responses in patients with adrenomedullary deficiency suggest that circulating adrenaline is not obligatory to a normal haemodynamic response to exercise.
Adrenal Insufficiency↗