Search PubMed⌕ Search

Biomedical subjects

H Ikram

Publications and source records attributed to H Ikram.

233 records · Page 13Linked to original sources
PubMed1969

Bradycardiac angina: haemodynamic aspects and treatment.

A patient with a sinus bradycardia and angina is described who was unable to increase his heart rate on vigorous exercise by more than a few beats. His severe angina was attributed to the bradycardia. Atrial pacing of his heart abolished his angina and increased his exercise tolerance. Circulatory changes at rest, on exertion, and with atrial pacing are described. The cause of angina in this patient is discussed.

Angina Pectoris↗
PubMedDate not supplied

Moderate sodium restriction and potassium supplementation in essential hypertension.

Continuous 24 h arterial blood pressure and vasoactive hormones were measured in twelve patients with essential hypertension after 4 weeks on a control sodium intake (180 mmol/day) and after similar periods of sodium restriction (80 mmol/day) and potassium supplementation (200 mmol/day). Sodium restriction was associated with variable blood pressure changes in individual patients and a small reduction in 24 h mean pressure of 4/3 mmHg. The greatest fall in blood pressure with sodium restriction was seen in those patients with the least rise in renin. Potassium supplementation was associated with variable individual blood pressure changes and a trivial reduction in mean 24 h pressures (0.1/0.8 mmHg). Mean 24 h plasma aldosterone concentration was significantly higher during sodium restricted and potassium-supplemented diets, compared to control levels, but other vasoactive hormones were unchanged.

Adult↗
PubMedDate not supplied

Stability and inter-relationships of hormone, haemodynamic and electrolyte levels in heart failure in man.

Relationships between clinical status, haemodynamic measurements, hormone and biochemical indices, and maintenance diuretic dose in patients with chronic cardiac failure, are not clear. This study assessed such relationships and their stability under standardized conditions in 21 hospitalized patients. The daily maintenance dose of frusemide correlated closely and in a positive fashion with plasma levels of renin activity, angiotensin II and aldosterone (P less than 0.001), and to a lesser extent with plasma noradrenaline. Although there was some overlap, patients most incapacitated by their heart failure had the highest circulating levels of renin activity, angiotensin II, aldosterone and noradrenaline. Plasma aldosterone correlated closely with concomitant angiotensin II levels (r = 0.70, P less than 0.001) but not with its other secretagogues ACTH (as reflected by plasma cortisol) or plasma potassium. Close positive correlations between angiotensin II and plasma levels of urea and creatinine (P less than 0.01) were observed. Both renin and angiotensin II showed positive relationships with right heart pressures, but were inversely related to cardiac index and arterial pressure. These results show close relationships between clinical and haemodynamic indices on one hand, and hormones on the other. The renin-angiotensin system appears to be the primary regulator of aldosterone under these conditions, and its activity relates closely to haemodynamic measurements and to the degree of azotaemia.

Aged↗
PubMedDate not supplied

Mechanisms in human renovascular hypertension.

To clarify the pathophysiology of renovascular hypertension, we monitored intraarterial pressure continuously and measured hourly hormone levels for 24 hours under carefully controlled conditions in two hypertensive patients with unilateral renal artery occlusion. Comparison of the results with those obtained when the patients were normotensive 3 months after uninephrectomy indicated that, while the renin-angiotensin system played a central role in maintaining the hypertension, the sympathetic nervous system also contributed and, in addition, modulated short-term arterial pressure fluctuations. In the untreated state, the sympathetic regulation of renin secretion was heightened, and angiotensin II/aldosterone dose-responsiveness was augmented. It is suggested that these adaptive changes might serve to offset the tendency to severe sodium depletion and thence exacerbation of the hypertension.

Adult↗
PubMedDate not supplied

Endogenous angiotensin-aldosterone-pressure relationships during sodium restriction.

The effects of moderate restriction of dietary sodium and potassium supplementation on plasma levels of renin, angiotensin II, aldosterone, and cortisol and on arterial pressure were studied in 12 patients with mild essential hypertension. To define hormone-blood pressure relationships, venous hormone levels were measured hourly and intra-arterial pressure continuously for 24 hours after 4 to 6 weeks of sodium restriction, 4 to 6 weeks of potassium supplementation, and a similar period of control diet. Our results show that compared with the control diet, moderate sodium restriction was associated with increased levels of aldosterone but no overall change in renin, angiotensin II, or cortisol levels. Further, slopes of regression lines relating log renin and log angiotensin II to aldosterone were increased, as were log cortisol/aldosterone regression lines. On the contrary, regression lines of log renin and log angiotensin II versus arterial pressure were unaltered by sodium restriction. Hormone and blood pressure relationships were not changed by the potassium supplemented diet. Although confirmatory data are needed, our findings suggest that moderate sodium restriction enhances aldosterone responsiveness to endogenous angiotensin II and adrenocorticotropic hormone without diminishing the pressor activity of endogenous angiotensin II. These results may explain in part the disappointingly small hypotensive effect of modest sodium restriction in mild essential hypertension.

Adult↗
PubMedDate not supplied

Effects of alpha-human atrial natriuretic peptide in essential hypertension.

Because there is little published information on the effects of atrial peptides in hypertensive humans, 100 micrograms of alpha-human atrial natriuretic peptide was injected intravenously into six patients with essential hypertension in a double-blind, placebo-controlled study under standardized conditions of body posture and dietary sodium and potassium intake. The peptide increased urine sodium excretion sixfold in the first 30 minutes. Smaller increments occurred in urine volume and in calcium, magnesium, and phosphorus excretion; the rise in urine potassium concentration was not statistically significant. Most of these indices returned to time-matched placebo values within 1 hour, but urine sodium excretion remained high for 2 1/2 hours. Arterial pressure fell within 2 minutes of alpha-human atrial natriuretic peptide injection, then returned to matching placebo levels by 10 minutes. Conversely, heart rate increased rapidly and remained elevated for 3 hours. The peptide induced a prompt, brief rise in plasma norepinephrine concentration and a more sustained fall in epinephrine and aldosterone levels, but it did not affect plasma renin activity or cortisol concentration. Compared with normotensive volunteers studied previously under the same conditions, the hypertensive subjects had a greater response in urine volume and sodium, calcium, and magnesium excretion but a less sustained fall in arterial pressure.

Adult↗
PubMedDate not supplied

Identifying the patient with heart failure.

Heart failure is becoming an increasing concern to healthcare worldwide, and of particular concern in the Western world where the age of the population continues to rise. Furthermore, it has now become clear that, if heart failure is identified and treated in the earliest stages of ventricular dysfunction, the possibility of recovery from or substantial delay in progression to complete heart failure is extremely good and will give the patient a considerably improved quality of life. Certain signs and symptoms found on routine examination, coupled with knowledge of patient history, can indicate early heart failure. Patients will normally present to their family practitioner, who is likely to have long term, firsthand knowledge of the patient's medical and family history. Consequently, the general practitioner has a key role in identifying individuals with early heart failure. It is essential that the general practitioner is aware of the signs and symptoms of early heart failure, can interpret them correctly and knows what follow-up tests are necessary to confirm the diagnosis. Guidelines are presented here to assist the general practitioner in this task.

Cardiac Output, Low↗