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Biomedical subjects

O Bertel

Publications and source records attributed to O Bertel.

At least 109 records · Page 6Linked to original sources
PubMed1985

Treatment of hypertensive emergencies with the calcium channel blocker nifedipine.

The severe elevations in blood pressure that occur in hypertensive emergencies pose a serious threat to life or vital organ functions. However, use of antihypertensive agents to acutely reduce blood pressure during hypertensive emergencies may cause deficits in the perfusion of the central nervous system or the heart. Therefore, a knowledge of cerebral blood flow regulation during acute treatment of hypertensive emergencies is indispensable. Experience with the calcium channel blocker nifedipine in the acute treatment of patients with hypertensive emergencies has shown that this agent has a pronounced vasodilatory effect, especially in vessels with a high vasoconstrictor tone, and that it does not reduce cardiac output or cerebral blood flow. The drug is highly efficacious and safe, and reports of serious side effects are rare. However, nifedipine should be used with caution in patients with suspected or proved critical arteriosclerotic stenosis of the cerebral arteries, because a reduction in perfusion pressure with any drug places these patients at risk for development of ischemic symptoms. Nifedipine can be used as a first-line drug for acute reduction of blood pressure in patients with hypertensive emergencies.

Blood Pressure↗
PubMed1985

[Diagnostic clarifications and follow-up of 105 patients with syncope].

105 patients with syncope (56 males and 49 females aged 15-87 years) were followed up for 15 +/- 8 months after their first visit in an outpatient clinic. Diagnosis after initial evaluation was syncope of unknown origin (n = 24), vasodepressor syncope (n = 18), orthostatic syncope (n = 18), syncope of cardiac origin (n = 16), seizure disorder (n = 13), syncope occurring during hyperventilation (n = 6), micturition syncope (n = 6), cough syncope (n = 2), and vertebrobasilar transient ischemic attack (n = 2). In 55% of patients the diagnosis was based on the patient's history alone and only in 23 patients was additional laboratory workup of diagnostic importance. During follow-up 4 patients died, but only in one was death related to the syncope (recurrent ventricular tachycardial). In 1 patient the initial diagnosis after follow-up had to be changed (from syncope of unknown origin to cardiogenic syncope) due to sick sinus syndrome. In patients with syncope the history should be carefully evaluated, since it is diagnostic in more than half of the cases. An additional diagnosis workup including resting and 24-hour ECG, as well as EEG examinations, should be ordered not as screening but only in selected patients.

Adolescent↗
PubMed1984

Calmodulin X (Ca2+)4 is the active calmodulin-calcium species activating the calcium-, calmodulin-dependent protein kinase of cardiac sarcoplasmic reticulum in the regulation of the calcium pump.

Calcium-, calmodulin-dependent phosphorylation of cardiac sarcoplasmic reticulum increases the rate of calcium transport. The complex dependence of calmodulin-dependent phosphoester formation on free calcium and total calmodulin concentrations can be satisfactorily explained by assuming that CaM X (Ca2+)4 is the sole calmodulin-calcium species which activates the calcium-, calmodulin-dependent, membrane-bound protein kinase. The apparent dissociation constant of the E X CaM X (Ca2+)4 complex determined from the calcium dependence of calmodulin-dependent phosphoester formation over a 100-fold range of total calmodulin concentrations (0.01-1 microM) was 0.9 nM; the respective apparent dissociation constant at 0.8 mM free calcium, 1 mM free magnesium with low calmodulin concentrations (0.1-50 nM) was 2.60 nM. These results are in good agreement with the apparent dissociation constant of 2.54 nM of high affinity calmodulin binding determined by 125I-labelled calmodulin binding to sarcoplasmic reticulum fractions at 1 mM free calcium, 1 mM free magnesium and total calmodulin concentration ranging from 0.1 to 150 nM, i.e. conditions where approximately 98% of the total calmodulin is present as CaM X (Ca2+)4. The apparent dissociation constant of the calcium-free calmodulin-enzyme complex (E X CaM) is at least 100-fold greater than the apparent dissociation constant of the E X CaM X (Ca2+)4 complex, as judged from non-saturation 125I-labelled calmodulin binding at total calmodulin concentrations of up to 150 nM, in the absence of calcium.

Animals↗
PubMed1984

[Treatment of hypertension emergencies].

Hypertensive emergencies are defined as situations where a seriously elevated blood pressure threatens the patients life or vital organ functions. Since treatment of hypertensive emergencies by a rapid reduction of blood pressure can be complicated by serious unwanted effects, the treatment indications should be defined cautiously. In addition the principles of autoregulation of blood flow and vascular resistance in hypertensive patients should be considered as well as the widely differing effects of the drugs used in hypertensive emergencies like alpha- and beta-adrenergic blocking substances, central sympatholytics and vasodilating agents. A reduction of cardiac output as a consequence of betablockade or central sympatholytics may be beneficial in patients with aneurysms, but may result in severe central hypoperfusion in others which can also be induced by vasodilators by local and systemic steal effects. Therefore we propose a treatment scheme for hypertensive emergencies based on pathophysiological considerations with special regard to cerebral perfusion. In many instances calcium-antagonists can be considered as drugs of first choice since they lower blood pressure in relation to pretreatment blood pressure and have only a weak negative inotropic effect. In addition they exert their vasodilating action predominantly in vessels with a high vasoconstrictor tone and do not reduce cerebral perfusion despite a marked reduction of blood pressure within a short time. In every case the initial emergency treatment should be followed by a careful long term management of hypertension.

Administration, Oral↗
PubMed1984

[Treatment of acute coronary heart disease in medical practice].

Despite the recent advances in cardiac intensive care, which have reduced hospital mortality for acute myocardial infarction to below 15%, a substantial decline in overall mortality from myocardial infarction has not been achieved by these therapeutic measures. More effective management of patients with advanced coronary heart disease would include better detection of high risk subgroups, especially of patients with unstable angina, better treatment with rapid adjustment of doses and combination of anti-anginal drugs, and better organisation of medical care in order to reduce hospitalisation delay in patients with impending or suspected myocardial infarction and avoid unnecessary hospital admissions in those with effort angina responsive to medical treatment. We propose a treatment scheme for unstable angina which, for out-patients with recent onset or crescendo angina on effort, is based on betablockers combined with calcium channel blockers and long-acting nitrates as second and third step respectively. In every case an anti-platelet aggregating agent should be added. If medical treatment fails to abolish the ischemic symptoms within days, surgical treatment should be considered.

Acute Disease↗
PubMed1983

[Current aspects of drug treatment of patients with congestive heart failure].

Patients with advanced congestive heart failure are high cost users of medical care, are limited by severe symptoms and have a poor prognosis. Medical treatment should therefore not be based on tradition but on pathophysiological considerations. A rational treatment program should give priority to the principle of unburdening rather than stimulating the failing heart. Unburdening the heart by use of diuretics and vasodilators is most effective in patients with hypertensive heart disease and valvular incompetence, and in acute heart failure. Digoxin remains the basic treatment in patients with tachyarrhythmias, and is valuable additive treatment in most instances. Guidelines are given for a stepwise treatment scheme including diuretics, vasodilators and digoxin.

Blood Pressure↗
PubMed1983

Nifedipine in hypertensive emergencies.

The effects and safety of using oral nifedipine 10-20 mg as acute antihypertensive treatment were studied in a single-blind placebo-controlled study of 25 consecutive patients with very high blood pressure requiring emergency reduction. In addition the effect of this treatment on cerebral blood flow was investigated using xenon-133 in 10 patients randomly allocated to receive oral nifedipine or intravenous clonidine. Whereas placebo did not alter the blood pressure, oral nifedipine significantly reduced the systolic and diastolic blood pressures in all 25 patients (from 221 +/- 22/126 +/- 14 mm Hg to 152 +/- 20/89 +/- 12 mm Hg after 30 minutes, p less than 0.001). Heart rate increased from 74 +/- 11 to 84 +/- 11 beats/minute (p less than 0.01); this effect was inversely related to age (r = -0.65, p less than 0.01). The falls in systolic and diastolic blood pressures were closely related to the blood pressures before treatment ) r = 0.67, p less than 0.001 for systolic, and r = -0.58, p less than 0.01 for diastolic values). No serious unwanted effects were observed. Measurement of cerebral blood flow after nifedipine showed an increase in flow in four out of five patients. Clonidine, by contrast, reduced cerebral blood flow in all patients by up to 28%. Nifedipine is a simple, effective, and safe alternative drug for managing hypertensive emergencies, especially when continuous monitoring of the patient cannot be guaranteed.

Adult↗
PubMed1982

Clinical and hemodynamic improvement of congestive heart failure by long-term vasodilator therapy with postjunctional alpha 1-adrenoceptor blockade.

Eleven of 12 patients with severe congestive heart failure who were pretreated with diuretics and digitalis benefited from long-term therapy with prazosin which was titrated to the individual's maximally tolerated dose. Nine of the 11 patients improved their functional state by one (n = 4) or two (n = 5) New York Heart Association (NYHA) classes. Within 4 weeks the stroke volume index increased from 23 +/- 10 to 29 +/- 9 SD (ml/beat/m2) while pulmonary capillary pressure decreased from 29 +/- 8 +/- 9 mm Hg (p less than 0.05 for both) and peripheral vascular resistance fell from 2,245 +/- 792 to 1,603 +/- 355 dyn/s cm-5 (p less than 0.01). Hemodynamics results were similar on the same regimen in eight patients assessed for 6 months. Death of three patients (week 5 and week 17) was unrelated to prazosin therapy. Prazosin resulted in improved cardiac performance during leg-up-tilt or supine ergometry. Increase in stroke volume index was related to the fall in peripheral vascular resistance (r = -0.79, p less than 0.01). Plasma adrenaline (301 +/- 480 pg/Ml), noradrenaline (1,312 +/- 1,382 pg/ml), and renin activity (22 +/- 30 ng/ml/h) were in the range observed with pheochromocytoma; variables did not change on prazosin. This reflects an important role of alpha-adrenoceptor-mediated vascular regulation in patients with heart failure in whom long-term treatment with prazosin produces a sustained and well-tolerated vasodilator effect without further rise in catecholamines and renin.

Adrenergic alpha-Antagonists↗
PubMed1982

Electrophysiologic changes after tiapamil in coronary and noncoronary patients.

26 patients who had undergone right heart catheterization were enrolled in the study. The average age was 51.7 +/- 15 years. Half the patients showed coronary artery disease at selective coronary angiography. His bundle recordings and atrial pacing were performed before and 10 min after 1 or 1.5 mg/kg i.v. tiapamil. In addition, arterial blood pressure was recorded. P-R interval increased from a mean value of 153 +/- 36 to 168 +/- 49 ms (p less than 0.05) due to an increase in the A-H time from 88 +/- 19 to 97 +/- 23 ms (p less than 0.05). Arterial blood pressure and heart rate decreased significantly. These changes were more pronounced in patients with coronary artery disease. In the groups with the higher dosage, the differences from the control values were greater than in the patient groups receiving 1.0 mg/kg. Sinus node recovery time tended to increase in all groups but the differences did not reach significance. Patients with the 'sick sinus syndrome' were not studied.

Adult↗
PubMed1982

Antiarrhythmic effects of tiapamil on exercise-induced arrhythmias in patients with coronary artery disease.

57 patients were admitted to the study, 3-6 weeks after acute myocardial infarction. They received either placebo or 1 mg/kg tiapamil intravenously according to a randomized, double-blind procedure. The study had two objectives: (a) to assess the effect of tiapamil on work tolerance and exercise-induced myocardial ischemia: (b) to demonstrate possible antiarrhythmic effects against exercise-induced arrhythmias. The duration of exercise and physical work capacity increased slightly in both groups, these effects, however, not reaching statistical significance. On the other hand, the number of exercise-induced extrasystoles did not change significantly under placebo but decreased from 30.9 to 14.8 beats/min after tiapamil (p less than 0.01). No side effects were observed. While the hemodynamic effects of tiapamil in patients with coronary artery disease are yet to be elucidated, our findings confirm the efficacy of this calcium antagonist against exercise-induced ventricular premature beats in patients with coronary artery disease.

Adult↗