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Biomedical subjects

I Heck

Publications and source records attributed to I Heck.

14 recordsLinked to original sources
PubMed1989

[Captopril versus digoxin in the treatment of mild to moderately severe heart failure].

In a randomized and double-blind study of 116 patients with chronic heart failure (NYHA classes II or III) the effectiveness of captopril + hydrochlorothiazide (HCT) (group 1) and of digoxin + HCT (group 2) were compared. Treatment was effected for a 12-month period with a combination of 50 mg captopril (twice 25 mg daily, oral) and HCT, or 0.2 mg digoxin (twice 0.1 mg daily, oral) and HCT. In a pretreatment phase over 3-4 weeks the patients of group 1 were given an average HCT dose of 37.7 mg daily, whereas those of group 2 received 34.9 mg per day. At the end of the 12-month treatment period the patients in the captopril/HCT group had improved significantly more--by the criteria of echocardiographic intracardiac diameters, exercise tolerance and NYHA class--than those in the digoxin/HCT group. Change by a mean of one NYHA class had occurred in 61 patients (51.8%) of group 1 and in 47 (40.7%) of group 2 (P les than 0.01). These findings suggest that treatment of patients with mild to moderately severe chronic heart failure in sinus rhythm best be initiated with an angiotensin-converting enzyme inhibitor together with a diuretic rather than a digitalis-diuretic combination.

Blood Pressure↗
PubMed1987

[Severe periodic hypokalemic paralysis. Prevention using beta-receptor blockade].

For ten years, severe physical exercise in a 24 year old male patient had been an almost constant trigger of frequent attacks of pareses which were mostly accompanied by complete tetraplegia and once by the occurrence of cardiac arrest with atrial fibrillation. During the attack, the serum potassium concentration fell to 1.2 mmol/l, whereas the intraleukocytic potassium concentration rose from 136 mmol/l to 149 mmol/l. The catecholamine excretion in the urine was raised during the first 24 hours after admission as an emergency (189 micrograms noradrenalin and 54 micrograms adrenalin). After intravenous adrenalin infusion (0.01-0.1 microgram/kg X min) during the symptom-free interval, there was a major fall of the serum potassium concentration from 3.9 mmol/l to 3.1 mmol/l. This was not accompanied by a raised insulin excretion and could be prevented by prior administration of the nonselective beta blocker propranolol. On the basis of these results, the patient was treated prophylactically with three times 40 mg/d p.o. propranolol. Pareses requiring treatment no longer occurred under this therapy.

Adrenergic beta-Antagonists↗
PubMed1985

[Reduction of regurgitation in aortic and mitral insufficiency by captopril in acute and long-term trials].

Afterload reduction is an accepted therapeutic principle in the management of acute aortic (Ai) and mitral insufficiency (Mi). The question whether acute and chronic converting-enzyme inhibition by captopril has a beneficial hemodynamic effect in chronic Ai and Mi has been investigated in 17 patients with Ai and 10 with Mi. Ejection and regurgitation fraction (RF) were measured by radionuclide ventriculography (RNV) before, after 25 mg captopril and after 3-5 months of long-term treatment. The humoral response of the renin-angiotensin system (RAS) was quantified by analysis of angiotensin I and II. Captopril lowered under acute and chronic treatment RF in Ai and Mi by 32%. Angiotensin II levels decreased by the same order of magnitude. Acute and chronic vasodilation was followed by a distinct but well tolerated fall in blood pressure, especially in patients with Mi. These favourable hemodynamic effects of captopril make this therapy an adjunct but not an alternative to valve replacement.

Aortic Valve Insufficiency↗
PubMed1985

[Acute and long-term effect of captopril in severe chronic heart failure].

In nine patients with severe, treatment-resistant heart failure (stages IV in the NYHA classification) the acute and long-term effect of captopril were studied. In the acute experiment, peripheral resistance fell by 27% after administration of 25 mg captopril, cardiac index rose by 25%, arterial pressure, pulmonary arterial pressure and mean right atrial pressure fell by a similar amount. This haemodynamic improvement increased slightly in the course of longterm treatment (cardiac index +30%, peripheral resistance -30%, mean pulmonary arterial pressure -42%). The fall in heart rate by 15% and 25%, respectively, was an expression of haemodynamic improvement and reduction in angiotensin II. The fall in peripheral vascular resistance coincided with a 50% reduction in angiotensin II concentration. Over the longer term, 2-42 weeks, the renin system stimulation regressed with the improvement in haemodynamics. Four of the nine patients in stage IV improved to stage II, while the remaining five patients improved from IV to III.

Adult↗
PubMed1985

Captopril mediated decrease of aortic regurgitation.

The effect of captopril mediated afterload reduction on aortic regurgitation was investigated in 10 patients. Regurgitation was quantitated by means of the regurgitation fraction and the relation of regurgitant volume to end diastolic volume. These variables were derived from gated radionuclide ventriculography. After captopril treatment the blood concentration of angiotensin I rose whereas that of angiotensin II fell significantly. The conversion of angiotensin I to II was reduced to about 50% of the control value. Whereas blood pressure and heart rate did not change significantly, the regurgitation fraction and the regurgitant volume, normalised to end diastolic volume, were significantly reduced by captopril treatment. The ejection fraction remained essentially unchanged. These findings suggest that captopril reduces aortic regurgitation by reducing afterload.

Angiotensin I↗
PubMed1985

The influence of food intake on pharmacodynamics and plasma concentration of captopril.

The influence of food intake on the acute haemodynamic and humoral effects of captopril has been investigated. Eighteen patients with mild-to-moderate essential hypertension (diastolic blood pressure 95-115 mmHg) were treated in a randomized crossover study with a single oral dose of 25 mg captopril after 2 weeks of placebo. They were randomized to receive captopril either 1 h before or together with a standardized breakfast. Blood pressure, heart rate and plasma concentrations of angiotensin converting enzyme (ACE), angiotensin II (ANG II) and captopril were measured before and every 30 min up to 4 h after drug administration. Angiotensin converting enzyme was significantly more suppressed and plasma concentrations of captopril were significantly higher when the drug was given in the fasting patients. However, there was no significant difference in blood pressure reduction whether captopril was administered in the fasting patients or together with food. The results indicate that the antihypertensive efficacy of captopril is not markedly affected when the drug is administered with food.

Adult↗
PubMed1984

[Reduction of regurgitation in aortic insufficiency by inhibition of the renin-angiotensin converting enzyme].

The effect of captopril-mediated afterload reduction on regurgitation was investigated in 10 patients with aortic insufficiency. Regurgitation was quantitated by the regurgitation fraction and the relation of regurgitant volume to enddiastolic volume, which were derived from gated radionuclide ventriculography. 19 patients with coronary artery disease and no evidence of valvular heart disease served as controls. In patients with coronary artery disease no significant regurgitation was found. In patients with aortic regurgitation the blood concentration of angiotensin I increased whereas that of angiotensin II decreased significantly after captopril-medication; thus, the conversion of angiotensin I to II was reduced to about 50% of the control value. Whereas blood pressure and heart rate did not change significantly, the regurgitation fraction and the normalized regurgitant volume were significantly reduced. The ejection fraction remained essentially unchanged. These findings suggest a favorable influence of captopril-induced afterload reduction on hemodynamics in aortic regurgitation.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

[Angiotensin-converting enzyme activity during cytostatic therapy in patients with primary inoperable bronchial carcinoma].

In 43 patients with inoperable bronchogenic carcinoma--32 small cell and 11 squamous or large cell--Angiotensin-Converting-Enzyme (ACE) activity in serum was determined before and every 3-5 weeks during cytotoxic chemotherapy. ACE-activity prior to therapy was 10.7 U +/- 1.17 SE as compared to the normal values 20.4 U +/- 1.8 SE which was statistically significant (p less than 0.01). There was no significant difference between the basal values of patients with small cell and not small cell-carcinoma of the lung. Only for patients with small cell-carcinoma of the lung a significant rise in ACE-activity could be obtained. Mean values of these patients reached normal levels in case they had complete remission, which was achieved in the limited disease group in 82% of patients. The present data suggest, that ACE-activities in serum correspond well to the clinical course in patients with small cell carcinoma of the lung. The decision on the individual mode of therapy may thus become more substantiated by serial determinations of ACE in the course of treatment.

Adult↗
PubMed1983

[Renin-angiotensin system under extracorporeal circulation during heart valve surgery].

Angiotensin I (A I), angiotensin II (A II) and the activity of angiotensin-converting enzyme (ACE) were measured in 15 patients undergoing cardiopulmonary bypass for mitral or aortic valve replacement. During cardiopulmonary bypass A I, A II, A I/II ratio and arteriovenous A II--difference decreased markedly, whereas the activity of ACE fell only during a small 15 min period after start of extracorporeal circulation. Possible reasons for these effects are discussed.

Angiotensin I↗
PubMed1981

Evidence for participation of kinins in the antihypertensive effect of converting enzyme inhibition.

In low- and normal- renin hypertensive patients, but not in high-renin patients, the acute antihypertensive response to the angiotensin-converting enzyme (ACE) inhibitor captopril was completely blocked by aprotinin-induced kallikrein inhibition. Blood pressure reduction with long-term ACE inhibition could be overcome only in part by aprotinin. It is proposed that in low- and normal-renin hypertension the vasodepressor effect of acute ACE inhibition is mainly due to kinin accumulation. Conversely, in high-renin patients a fall in angiotensin II concentration accounts for the hypotensive response to captopril. From the pressor effect of aprotinin in chronically captopril treated patients it appears that kinins are also involved in the blood pressure reduction with long-term ACE inhibition. The finding that ACE inhibition and kallikrein blockade produced predictable and opposite effects on blood pressure suggests broad participation of changes in depressor kinin production in the control of vascular tone in essential hypertension.

Adult↗
PubMed1980

[A new principle in long-term treatment of essential hypertension: angiotensin-converting enzyme inhibition (author's transl)].

The blood pressure lowering effect of the orally effective converting-enzyme-inhibitor captopril (SQ 14.225) was investigated in a double-blind study in 20 patients with moderate essential hypertension. During treatment with captopril alone (150 mg t.i.c.) blood pressure dropped from an average of 167/111 to 148/99 mm Hg lying and from 164/113 to 143/99 mm Hg upright whereby 4 patients showed normalisation of their blood pressure (less than 145/95 mm Hg). There was no significant change of pulse frequency. Addition of hydrochlorothiazide led to return to normal of blood pressure in all patients. Even after 6 months of treatment tolerance had not developed. The antihypertensive effect of captopril alone paralleled the one of hydrochlorothiazide and there were no side effects. Activity of the converting enzyme in serum as well as plasma concentrations of angiotensin II and aldosterone were clearly lowered by captopril whereas plasma renin activity increased significantly. Renal sodium and water excretion and glomerular filtration rate were not influenced.

Adult↗
PubMed1980

Altered blood pressure and renin responses to converting enzyme inhibition after aprotinin-induced kallikrein-kinin-system blockade.

1. The effect of aprotinin-induced blockade of the kallikrein-kinin system on haemodynamic and biochemical responses to converting enzyme inhibition by SQ 14 225 was evaluated in 26 patients with essential hypertension. 2. SQ 14 225 lowered blood pressure in high, normal and low renin hypertension. In low and normal renin patients, but not in high renin patients, the acute blood pressure-lowering effect of SQ 14225 could be overcome by aprotinin. Aprotinin infusion produced small vasopressor effects in all groups of patients. 3. Aprotinin lowered the level of circulating active renin but not that of inactive renin. 4. It is concluded that in low and normal, but not in high, renin hypertensive patients activation of the kallikrein-kinin system is responsible for the acute blood pressure reduction observed with converting enzyme inhibitions. 3. Aprotinin lowered the level of circulating active renin but not that of inactive renin. 4. It is concluded that in low and normal, but not in high, renin hypertensive patients activation of the kallikrein-kinin system is responsible for the acute blood pressure reduction observed with converting enzyme inhibition. 5. With long-term converting enzyme inhibition kallikrein-kinin system activation seems to play only a minor role. 6. The kallikrein-kinin system may be involved in the regulation of blood pressure. 7. There is no direct evidence of a participation of kallikrein in the activation of prorenin in vivo.

Aldosterone↗
PubMed1980

[Reaction of stress parameters during electrostimulation analgesia and neuroleptanalgesia (author's transl)].

Surgical interventions produce a stress response in patients. Electrostimulation analgesia (ESA) has been described as a method yielding excellent results in poor-risk patients. The present study was undertaken to investigate the stress response of ESA compared with neuroleptanalgesia (NLA). 30 female patients (16 with ESA, 14 with NLA) ranging from 34 to 55 years without endocrine, hepatic, renal or cardiovascular disease who were undergoing vaginal hysterectomy, were subjected to the study. The concentrations of cortisol, cholesterol and glucose in the plasma, the mean arterial blood pressure, the heart rate and the tension-time-index were measured before and during anesthesia as well as during and after surgery. In patients receiving ESA the stress reaction seems to be more pronounced, judged by the higher level of plasma cortisol. The decrease of cholesterol as well as the increase of plasma glucose, mean arterial pressure, heart rate and tension-time-index supported this interpretation. During anaesthesia but before starting the operation the changes in the parameters showed that ESA induces a higher stress reaction than NLA.

Adrenocorticotropic Hormone↗