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Biomedical subjects

P Thürmann

Publications and source records attributed to P Thürmann.

At least 19 recordsLinked to original sources
PubMed2005

[Cardiorespiratory effects of heliox using a model of upper airway obstruction].

Heliox is a mixture of Oxygen and Helium. The low density of Helium allows this mixture to flow in a laminar pattern where oxygen, nitrogen or air flow would be turbulent. Therefore the force necessary to move a volume of gas (e.g. Heliox) is greatly reduced in comparison to a turbulent gas flow. In a respiratory loading experiment we investigated the effects which Heliox exerts on hemodynamic as well respiratory variables. 10 volunteers were breathing spontaneously and through three different endotracheal (ET-) tubes (ID 4.0, 4.5, 5.0 mm). The subjects were switched from room air to Heliox and differences in the variables heart rate (HR), blood pressure (BP), stroke volume (SV), stroke index (SI), peripheral vascular resistance (TPRI) and left ventricular work index (LVWI) were measured. Furthermore the (PhAng) between abdomen and thorax was detected using respiratory inductance plethysmography (n=2) and the sense of dyspnoe under the different conditions was assessed by the use of a dyspnea score (DS). The means of BP, SV, SI, TPRI and LVWI did not significantly differ between the resting and the different loading conditions irrespective of the gas that was used. The variability of hemodynamic measures was significant larger during loaded vs. unloaded breathing. Heliox could significantly reduce this degree of variability. In two subjects Heliox could also significantly reduce the PhAng as well as DS. Heliox showed effects on hemodynamic as well as respiratory and subjective variables. These effects can be interpreted as a reduction of the extent of pressure variations in the intrapleural space leading to less impact on hemodynamic variables while breathing Heliox vs. room air in a resistive loading experiment. In the future the combined measurement of hemodynmic variables as well as non-invasive assessment of respiration might shed new light on cardio-respiratory interaction and effects of Heliox during airway obstruction.

Administration, Inhalation↗
PubMed2000

[Guidelines Clearing House Statement "Hypertension". Summary and recommendations for a rational hypertension guideline in Germany].

BACKGROUND: In order to promote quality of hypertension management in Germany, a national hypertension guidelines clearing project was initiated in 1999 by the German Guidelines Clearinghouse. OBJECTIVES: To identify and review published German- and English language hypertension guidelines. To establish criteria for future guideline development and implementation. To familiarize stakeholders in Germany with state-of-the-art hypertension guidelines. To identify key topics for a future national evidence-based guideline. METHODS: Search procedure, formal appraisal: Systematic search using literature databases and English-/German-language databases, published between 1990 and 1999. Abstract screening of the search results according to the inclusion criteria (n = 132 of a total of 548 hits). Systematic guideline evaluation using checklist with predefined criteria. APPRAISAL OF GUIDELINES' CONTENTS: Peer review of guidelines with the following inclusion criteria: hypertension--general, German and English language, published later than 1994, original or primary guideline or update, issued for nationwide use. Peer review was performed by a multidisciplinary focus group of EBM experts (primary and secondary care physicians, clinical pharmacologist, clinical epidemiologist). None of these was involved in hypertension guideline development during the review period. DOCUMENTATION OF CRITICAL APPRAISAL RESULTS: Systematic documentation of methodological appraisal and peer review results using a structured abstract form. The focus group wrote a final report (clearing report) including methodological abstracts for each guideline, essential topics for a future German hypertension guideline based on examples from the appraised guidelines, comments and recommendations for health care policy markers in Germany. RESULTS: 11 out of 132 guidelines were in accordance with the formal minimal standard with a wide range range within the following domains: "description of the development process", "declaration of authors' independence", "explicit link between recommendations and the supporting evidence", "management options", "tools for implementation". None of the guidelines identified all the key identified by the focus group, such as: (1) definition of hypertension--epidemiology--health care problems--intended guideline users/goals, (2) blood pressure measurement, (3) medical history and physical examination, (4) case-finding/screening, (5) indications for referral, (6) risk-stratification, (7) diagnostic procedures, (8) therapeutic goals/indications for therapy, (9) nonpharmacological measures, (10), pharmacotherapy, (11) follow-up/patient education/motivation/compliance, (12) comorbidity, hypertension in childhood/elderly, pregnancy, (13) primary prevention, (14) quality assurance/quality management, (15) dissemination/implementation, (16) open questions/challenges for the future. SUMMARY POINTS: To improve the quality of hypertension management in Germany, the expert panel suggested to develop a national evidence-based guideline. This should follow internationally agreed criteria and procedures. The experts identified and reviewed 11 out of 132 hypertension, which might make useful contributions for a future German Hypertension guideline. The expert group identified 16 key topics for a national hypertension guideline.

Comorbidity↗
PubMed1998

[Structure and activities of drug committees in Germany. Results of a survey of 143 hospitals. Pharmaco-economic Study Group and Rational Drug Therapy of the German Society of Clinical Pharmacology and Therapy].

BACKGROUND: To obtain information on the structure, present activities and decision making process of hospital drug committees in Germany in 1995 a questionnaire with 36 items was designed and sent to 450 hospitals in Germany with more than 400 beds. 143 returned questionnaires could be evaluated. RESULTS: According to hospital size the median value of the annual drug budget 1993 ranged between DM 2.4 Mio for hospitals with less than 500 beds and DM 30.0 Mio for university hospitals with more than 1,000 beds (including blood and blood derived products). In 53% of drug committees a pharmacist held the position of the chairman, followed by medical specialists (32%), (clinical) pharmacologists held this position only in 8% of the hospitals, but in almost 50% of the university hospitals. In most cases all clinical specialties are represented in the drug committee, the number of members ranging between 5 and 40 (median 12). The number of drugs included in the internal drug list ranging between 400 in hospitals with < 500 beds and about 700 in university hospitals was strongly correlated with the number of beds and, interestingly, with the number of drug committee members. Treatment guidelines were implemented mainly for antiinfectives (87%), infusion solutions (30%), antiemetic drugs (5-HT3-receptor antagonists, 27%) and blood and blood-derived products such as intravenous immunoglobulins (23%). However, effective control of these guidelines was only performed in about 50% of the hospitals. A drug information service was provided in most hospitals, where 95% of queries were answered by pharmacists. CONCLUSION: The results of our survey showed, that German hospital drug committees vary considerably with regard to their function and control mechanisms on drug use. Most of the responders would appreciate a more intensive exchange of current problems and treatment guidelines.

Drug Costs↗
PubMed1998

Prescription of cardiovascular drugs in outpatient care: a survey of outpatients in a German university hospital.

AIMS: We evaluated ambulatory prescriptions by general practitioners for outpatients with cardiovascular (CV) disease referred to the cardiology outpatient clinic of the Frankfurt University Hospital in order to prove adherence to generally acknowledged therapy standards for treating CV disease. METHODS AND RESULTS: Appropriateness of current CV medication was assessed according to the following criteria: aspirin or anticoagulants obligatory after myocardial infarction (MI), unless contraindicated; beta-blockers should be prescribed after MI, unless contraindicated or not tolerated; ACE inhibitors should be given in left ventricular dysfunction (LVD) after MI, unless contraindicated; and hypertension should be adequately controlled. 346 patients (28-94 years) received a median of 3 CV drug prescriptions (range 0-7). 240 patients had CAD, 142 patients previous MI, 121 patients had LVD (59 after MI), 143 patients were hypertensive. Aspirin was used appropriately in 80% of all MI patients, 13% received oral anticoagulants due to atrial fibrillation. However, 7% received no antithrombotic therapy. ACE inhibitors were administered in 65% of the MI patients with LVD. beta-blockers were used in 25% of the MI-patients. In the remaining patients, beta-blockers were contraindicated, not tolerated, and/or verapamil had been prescribed. However, in 14% of the patients beta-blockers were withheld without evident reason or alternative drug. In 41% of the hypertensive patients, blood pressure was not sufficiently controlled. CONCLUSION: A considerable number of ambulatory prescriptions for CV drugs are not in accordance with current therapeutic guidelines. The role of a cardiology outpatient clinic to detect the misuse or underuse of CV drugs is emphasised.

Adult↗
PubMed1996

Mechanism of angiotensin converting enzyme inhibitor-related anemia in renal transplant recipients.

To delineate the pathogenesis of the reduction in hemoglobin occurring in renal transplant patients treated with angiotensin converting enzyme inhibitors (ACEI) and azathioprine (AZA) a controlled, prospective trial of ACEI withdrawal was conducted. The ACEI was replaced by nifedipine or clonidine in 15 kidney transplant patients immunosuppressed with AZA and prednisone (enalapril in 14 and captopril in 1). Before and during 10 to 12 weeks after withdrawal of the ACEI, AZA metabolites, renal function parameters and hematological parameters including erythropoietin and reticulocytes were evaluated. Enalaprilat levels were measured and compared with 15 similar patients matched for transplant function and enalapril dosage immunosuppressed with cyclosporine and prednisone. AZA metabolites did not differ significantly in the presence or absence of the ACEI. Enalaprilat levels also showed no significant difference between the two patient groups treated with AZA or cyclosporine. Hematocrit and hemoglobin increased significantly from 37.5 +/- 6.4 to 39.7 +/- 3.6% (mean +/- SD, P = 0.02) and 12.8 +/- 2.2 to 13.5 +/- 1.2 g/dl, P = 0.04, respectively, 10 to 12 weeks after ACEI treatment had been discontinued. Simultaneously numbers of reticulocytes and erythropoietin concentrations rose significantly after 2, 4 and 10 weeks, with a peak at two weeks (from 14.1 +/- 3.8 to 20.6 +/- 8.0/1000, P < 0.05 and from 14.3 +/- 12.4 to 29.3 +/- 54.5 mU/ml, P < 0.05, respectively). In conclusion, ACEI-related anemia in renal transplant recipients seems to be due to the erythropoietin-lowering effect of this group of drugs. A pharmacokinetic interaction between AZA and enalapril is not likely since plasma enalaprilat levels were independent of the immunosuppressive regimen and AZA metabolite levels were unchanged in the presence and absence of the ACEI. Several mechanisms by which angiotensin converting enzyme blockade may cause a decrease in circulating erythropoietin are discussed.

Adult↗
PubMed1996

Clinically important drug interactions with anticoagulants. An update.

Coumarin derivatives combine 3 unfavorable properties which make them prone to potentially life threatening drug-drug interactions: (i) high protein binding; (ii) cytochrome P450 dependent metabolism; and (iii) a narrow therapeutic range. An entire list of drugs which are supposed to interact with coumarins (mostly with warfarin) comprises about 250 different compounds. Noteworthy are the interactions with cardiovascular or antilipidaemic drugs which are often coadministered with coumarins: amiodarone, propafenone and fibrates. Cardiovascular drugs which are obviously devoid or proven to be devoid of an interaction are angiotensin converting enzyme (ACE) inhibitors, calcium antagonists, beta-blockers and cardiac glycosides. There are several other drugs which enhance the hypoprothrombinaemic response to coumarins by various mechanisms: inhibitors of the elimination of the eutomer S-(-)-warfarin (e.g. miconazole, phenylbutazone), combined with protein binding displacement (e.g., sulfinpyrazone, phenylbutazone), synergistic hypoprothrombinaemia (e.g. cefazoline). Furthermore, bleeding complications may occur with drugs affecting platelet function [aspirin (acetylsalicylic acid) and several nonsteroidal anti-inflammatories (NSAIDs)]. Strong inducers of coumarin metabolism are rifampicin (rifampin) and carbamazepine. Biphasic interactions may occur where a drug first enhances the hypoprothrombinaemic response to a coumarin but has a sustained inducing effect on coumarin metabolism (e.g. phenytoin or sulfinpyrazone). The complex response of coumarins to concomitant drug therapy makes it difficult to predict the occurrence and degree of a deterioration of anticoagulant control in individual patients. For clinical practice, it seems advisable that one should monitor for changes in prothrombin time when adding or deleting any newly approved drug or any drug suspected (e.g. on the basis of this review) to cause an interaction to patients on coumarin therapy. The onset of the adverse prothrombin time response might be from between 1 to 2 days up to 3 weeks (in case of phenprocoumon) after starting a concomitant drug regimen. With amiodarone, an adverse prothrombin time response might occur up to 2 months after initiating therapy. For heparins, only a drug interaction with aspirin or nitroglycerin seems clinically relevant due to the possibility of coadministration during acute cardiac events. Both drugs are shown to enhance the activated partial thromboplastin time response to heparin.

Anticoagulants↗
PubMed1996

Criteria for the appropriate drug utilisation of immunoglobulin.

Intravenous immunoglobulins (IVIGs) are prepared from human plasma pools and further modified enzymatically or chemically. Despite careful selection of donors and inclusion of effective virus elimination steps in the production process, contamination with hepatitis C virus can still occur. IVIGs possess most of the characteristics of native immunoglobulins, such as antigen neutralisation and complement activation. The serum half-life of native immunoglobulin is about 21 days, and comparable half-lives have been reported for several IVIG preparations. IVIGs have received general approval for the treatment of primary immuno-deficiencies such as agammaglobulinaemia. Of the secondary immuno-deficiencies, only paediatric AIDS, chronic lymphocytic leukaemia and multiple myeloma, as well as allogeneic bone marrow transplantation, are accepted indications for IVIGs. Because of their immunomodulatory action, IVIGs are also recommended for the treatment of idiopathic thrombocytopenic purpura, Kawasaki disease (mucocutaneous lymph node syndrome) and, recently, Guillain Barre syndrome IVIGs have been investigated in a wide range of immunodeficient states (e.g. prematurity) and autoimmune diseases (e.g. multiple sclerosis), but conclusive results are not available. Since IVIGs are associated with a certain risk of transmission of viral infections and, secondly, because they are generally acknowledged as expensive drugs, their use requires careful consideration of risk, benefit and cost.

Animals↗
PubMed1995

Influence of piroxicam coadministration on pharmacodynamic parameters and the plasma concentration/effect relationship of recombinant hirudin (CGP 39393).

Recombinant hirudins are currently under investigation for use in myocardial infarction and unstable angina. In this study the influence of piroxicam on the pharmacodynamics and pharmacokinetics of a recombinant hirudin preparation (CGP 39393) administered intravenously was determined. Twelve healthy, male volunteers received piroxicam 10 mg and matching placebo once daily for 12 days according to a double-blind, randomised cross-over design. On the 12th day, the dose of piroxicam was followed by a 6-hour infusion of hirudin 0.1 mg.kg-1.h-1. Plasma concentrations and urinary excretion of hirudin and repeated measurements of the activated partial thromboplastin time (APTT), bleeding time and platelet adhesion index were assessed up to 24 h after the start of the infusion. The maximum APTT was 83 s (placebo) and 84 s (piroxicam), 3 to 4 h after the start of the infusion, and was comparable on both study days. The AUD0-24 (APTT) came to 913 s.h.kg-1 under placebo and it was slightly increased to 1,017 s.h.kg-1 after piroxicam; the 95%- confidence interval according to MOSES ranged from 0.97 to 1.24, and the point estimator was 1.10. Bleeding time was significantly prolonged from 290 s under placebo to 345 s under piroxicam before the start of the infusion of hirudin. No further prolongation was found during or after the infusion. No change was observed in the platelet adhesion index. Responsiveness parameters according to a sigmoidal Emax-model were obtained from the hirudin-plasma concentration/effect (i.e. APTT-prolongation)-curves after placebo and piroxicam.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

HPLC analysis of azathioprine metabolites in red blood cells, plasma and urine in renal transplant recipients.

Anemia has been frequently reported in renal transplant recipients receiving azathioprine for immunosuppression and enalapril for treatment of hypertension. During the course of a prospective trial in such patients we determined azathioprine metabolites in erythrocytes, plasma, and urine as well as erythropoietin and hemoglobin levels in order to evaluate a potential interaction between these 2 drugs, possibly leading to anemia. Two specific high performance liquid chromatography (HPLC) methods for determination of azathioprine metabolites, both employing a mercurial cellulose resin for extraction, are presented. One method using a strong anion exchange column allows detection of 6-thioguanosine di- and triphosphate (thioguanine nucleotides) in red blood cells (RBC) with a sensitivity of 30 pmol/100 microliters RBC. 6-mercaptopurine (MP) and 6-thiouric acid (TUA) in plasma and urine were analyzed simultaneously by reversed-phase HPLC with a sensitivity of 5 ng/ml. The average (median values are given) steady state concentrations of thioguanine nucleotides in erythrocytes came to 267 pmol/100 microliters RBC (range 53-613) with and to 246 pmol/100 microliters RBC (range 39-629) without concomitant enalapril medication. Mean plasma concentrations of MP and TUA 3 hours after drug intake came to 14.8 +/- 9.9 ng/ml and 398 +/- 262 ng/ml, respectively, during enalapril comedication. Withdrawal of enalapril did not influence these metabolite levels coming to 15.3 +/- 9.1 and 451 +/- 253 after stopping enalapril treatment. Thioguanine nucleotides in RBCs were neither related to the dose of azathioprine given (r = -0.113, p > 0.05) nor to hemoglobin levels (r = 0.278, p > 0.05). However, azathioprine dose/kg body weight seemed to be related to hemoglobin concentration, with and without enalapril comedication. We conclude that enalapril therapy does not influence the measured azathioprine metabolites, the reported cases of anemia may rather be due to a pharmacodynamic interaction as shown by the significant increase in erythropoietin after withdrawal of enalapril. The assays described here are suitable to study the metabolism of azathioprine in patients with various diseases.

Administration, Oral↗
PubMed1994

Drug utilization review on a surgical intensive care unit.

Drug use reviews (DUR) provide information about drug prescription patterns. At the surgical intensive care unit (SICU) of the University Hospital Frankfurt/Main we recorded the indication related administration of blood products and pharmaceuticals (which were responsible for 60% of the total costs at the SICU in the year before) over a 4-month investigation period. Data were recorded and analyzed using a notebook-PC. 207 Patients were included, and recorded total expenditures came to $551,592. The 10 leading substances, represented by antibiotics and blood-products, caused more than 70% of total costs. The usage of these high-cost substances and the most expensive complications are identified and discussed. We concluded that DURs are useful for obtaining information about drug usage patterns and for identifying high cost drugs, which are of economic interest. Furthermore, the indications for the application of these substances can be identified. Our results suggest, that blood and blood-products should always be included in DURs. In our opinion, especially the usage of blood-products represents a field where considerable cost savings may be expected. As certain complications during the postoperative course (e.g. sepsis) may increase costs, they should be considered in the reimbursement negotiations between hospitals and health insurance.

Adult↗
PubMed1994

Effects of flupirtine coadministration on phenprocoumon plasma concentrations and prothrombin time.

The influence of flupirtine, a non-opioid, centrally acting analgesic agent on phenprocoumon plasma levels and protein binding as well as prolongation of prothrombin time has been investigated in 12 healthy male volunteers. Subjects received phenprocoumon 1.5 mg od over 28 days. From day 15 to 28 oral flupirtine 100mg tid was added. Phenprocoumon plasma levels and prothrombin time (Quick time), measured at trough before the morning drug intake, were chosen as primary pharmacokinetic and pharmacodynamic variables. In addition, phenprocoumon protein binding and the eudismic ratio of phenprocoumon were determined. The mean values from data obtained on day 12 to 15 (i.e. measurements under phenprocoumon alone) and the mean values from those data obtained from day 25 to 28 (i.e. under comedication with flupirtine) were subject to subsequent statistical procedures. Phenprocoumon plasma concentrations came to 1.38 +/- 0.28 micrograms/ml on day 12 to 15 and were not significantly altered under flupirtine coadministration with 1.48 +/- 0.36 micrograms/ml on day 25 to 28 (95% confidence interval: 1.02-1.11, point estimator: 1.06). The average Quick time came to 68 +/- 10% on day 12-15 and 73 +/- 15% on day 25-28. The nonparametric 95%-confidence interval for the ratio ranged between 0.96 and 1.14, the point estimator was determined to 1.04. Protein binding of phenprocoumon was determined to 88.8% +/- 0.5 on day 14 and to 88.9 +/- 0.5% on day 28. The ratio of S/R-phenprocoumon was 1:0.84 on day 14 and 1:0.84 on day 28. These results do not provide any evidence for a pharmacokinetic and/or pharmacodynamic interaction between flupirtine and phenprocoumon.

Administration, Oral↗
PubMed1994

Concentration/effect relationship of bunazosin, a selective alpha 1-adrenoceptor antagonist in hypertensive patients after single and multiple oral doses.

The concentration/effect relationship of bunazosin, a selective alpha-1-adrenoceptor antagonist of the quinazoline class, was established in hypertensive patients after a first dose of bunazosin and after 8 weeks of chronic dosing. The study was part of a placebo controlled, multicenter dose-finding trial with parallel group design. After a wash-out period and a 2-week placebo run-in phase, each 4 patients received either placebo, 3 mg, 6 mg or 12 mg bunazosin o.d. in a slow-release formulation. Concentration/effect analysis based on a sigmoidal Emax-model and the drop in the mean arterial blood pressure application of this model was feasible in 9/11 patients. The EC50 after the first dose was 4.6 +/_ 2.0 ng/ml and increased to 9.1 +/- 7.3 ng/ml at steady-state. The decrease in the average of the responsiveness parameter was mainly due to about three-fold, right-shift in the concentration/effect curves at steady-state in 3 patients, the remaining patients showed no or considerably lesser changes of the EC50. Whereas a significant correlation was observed between the pretreatment mean arterial blood pressure and the height of the maximal effect under bunazosin, no relationship appears between the bunazosin dose, the resulting plasma levels at trough and the corresponding effect.

Administration, Oral↗
PubMed1994

[Anti-ischemia effects of gallopamil and esmolol in an intra-individual comparison in patients with coronary heart disease].

To compare the hemodynamic, antiischemic, metabolic, and neurohumoral effects of intravenous esmolol (beta 1 blocking agent) and gallopamil (verapamil-like calcium channel blocker), 14 patients with angiographically proven CAD and reproducible ST segment depression were studied at rest and during exercise under control conditions and after an intravenous bolus injection of esmolol (0.5 mg/kg/1 min, followed by an infusion with 0.2 mg/kg/min) or gallopamil (0.025 mg/kg/3 min). In contrast to gallopamil, esmolol significantly reduced systolic blood pressure (175.7 vs. 160 mm Hg) and heart rate (107.4 vs. 96.9 min-1) during exercise as well as cardiac output (11.57 vs. 9.38 l/min) and significantly enhanced systemic vascular resistance both at rest (1241 vs. 1479 dynes.s.cm-5) and during exercise (805 vs. 947 dynes.s.cm-5). On the other hand, exercise filling pressures and lactate levels (3.66 vs. 3.05 mmol/l) were significantly reduced by gallopamil only. Thus, the significant improvement of exercise tolerance by both esmolol and gallopamil is based on different mechanisms of action: esmolol improves myocardial ischemia by appreciably reducing myocardial oxygen consumption, whereas gallopamil primarily improves oxygen supply and ventricular performance. Plasma catecholamines, atrial natriuretic factor, and aldosterone levels as well as plasma renin activity were identically influenced by esmolol and gallopamil, respectively. A reflex activation of the sympathetic system did not occur.

Adrenergic beta-Antagonists↗
PubMed1994

Angiotensin-converting enzyme inhibition with spirapril in patients with coronary artery disease.

In a randomized double-blind, placebo-controlled, crossover trial, the potential anti-ischaemic action of the angiotensin-converting enzyme (ACE) inhibitor spirapril was studied in 19 patients with coronary artery disease (CAD) and reproducible exercise-induced ST-segment depression, but without hypertension or congestive heart failure. Measurements of blood pressure and heart rate as well as exercise-testing were performed after 2 weeks of treatment each with placebo and spirapril. Anginal attacks and consumption of short-acting nitrates were recorded in the patients' diaries. Resting blood pressure was not significantly reduced (143 +/- 20/89 +/- 10 mmHg vs 138 +/- 17/87 +/- 10 mmHg). The exercise-induced ST-segment depression, the main criterion for anti-ischaemic effect, was 2.17 +/- 1.72 mm after placebo and not significantly affected by spirapril (2.03 +/- 1.47 mm) despite a significant reduction in blood pressure x heart rate product at maximum workload (213 +/- 45.4 vs 197.5 +/- 36.8; p < 0.05). The number of anginal attacks per week and nitrate consumption remained virtually unchanged. A significant reduction of exercise-induced ischaemia in normotensive patients with CAD was not demonstrated with spirapril.

Aged↗
PubMed1994

Antihypertensive efficacy of a slow release nifedipine tablet formulation given once daily in patients with mild to moderate hypertension. A placebo-controlled, double-blind parallel-group trial.

In a double-blind, randomized parallel-group, multi-center study the antihypertensive efficacy of a slow release tablet containing 60 mg nifedipine (Aprical long, CAS 21829-25-4) has been investigated. After two-weeks wash-out of previous antihypertensive medication and a two-weeks placebo run-in period, 88 patients of both gender with a diastolic blood pressure between 95 and 115 mmHg received either nifedipine or placebo for 8 weeks. Blood pressure was measured at the end of the dose interval at rest by a semi-automatic, auscultatory device. Control measurements were recorded using a standard cuff sphygmomanometer. Primary efficacy criterion was the drop in diastolic blood pressure (DBP, measured semi-automatically) after 8 weeks therapy. 88 patients were randomized to nifedipine or placebo. 86 patients completed the protocol (42 nifedipine, 44 placebo). However, only in 73 patients BP measurements were recorded appropriately with the semi-automatic device (36 nifedipine, 37 placebo). In the nifedipine group, blood pressure fell from 152 (+/- 18)/102 (+/- 6) mmHg to 139 (+/- 16)/91 (+/- 10) mmHg. Blood pressure under placebo was determined to 149 (+/- 20)/102 (+/- 8) mmHg before treatment and 146 (+/- 18)/100 (+/- 10) mmHg at the end of the study. Heart rate was not affected under both treatments. The 90% confidence interval of the difference between the mean fall in DBP ranged from 5.0 to 12.5 mmHg, the point estimator was 8.8 mmHg. At the end of the study, 21 of 36 patients under nifedipine and 10 of 37 patients under placebo had a DBP below 90 mmHg and/or a decrease in DBP > 10 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗