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Biomedical subjects

G Bönner

Publications and source records attributed to G Bönner.

At least 19 recordsLinked to original sources
PubMed2005

[Prevention of arteriosclerosis. Importance of the treatment of arterial hypertension].

In most European countries and Northern America, cardiovascular diseases induced by atherosclerosis are the most common cause of death in older people. People surviving acute myocardial infarction or stroke suffer often by disabilities or handicaps. The lifelong care of such patients is expensive and plays a major role for increment of costs in public health systems. Prevention of atherosclerosis will reduce cardiovascular morbidity and mortality, enhance quality of life and prolong lifetime of patients. Therefore the worldwide accepted risk factors of atherosclerosis have to be treated consequently and early enough within the meaning of primary prevention. Hypertension is one of the six major cardiovascular risk factors and is defined as elevated blood pressure above 140/90 mmHg. In case of hypertension, diagnostic efforts has to be focussed on detection of additional cardiovascular risk factors, secondary forms of hypertension, end organ damage or associated diseases. All therapeutic strategies are based on life style changes, which cover weight reduction, sodium restriction, controlled alcohol consumption and increment in physical activity. Pharmacotherapy will be added in regard to the global risk of the patient and the success of the life style changes. Selection of antihypertensives and their optimal combination will be determined by associated diseases (compelling indication), side effects and individual response in blood pressure. Goal of treatment is the normalization of blood pressure below 140/90 mmHg independent of age or sex. In diabetics and in case of nephropathy the goal is set lower (below 130/80 mmHg).There is strong evidence that reduction in blood pressure is followed by a decrease in the incidence of myocardial infarction, stroke, heart failure, nephropathy, and even in cardiovascular mortality. The success of antihypertensive therapy is greater in high risk patients like older people, patients with isolated systolic hypertension or diabetics. Risk reduction correlates well with the degree in blood pressure reduction. However, to minimize cardiovascular risk in hypertensives all additional risk factors have to be treated too.

Antihypertensive Agents↗
PubMed2004

[Recommendations for statin therapy in the elderly].

Elderly patients are significantly less likely to receive statins than younger patients possibly because of doubts regarding compliance or concerns regarding the increased likelihood of adverse events and drug interactions. Poor compliance can be expected especially in patients suffering from dementia or depression as well as those whose stage of cardiovascular disease exhibits few symptoms. On the other hand, the clinical significance of CHD events is high in the elderly, and 80% of coronary deaths occur in patients aged over 65 years. The average statistical life expectancy of elderly and old patients is often underestimated. The HPS and PROSPER studies showed that statins reduce mortality and morbidity even in very elderly individuals with a high global cardiovascular risk and/or CAD. Patients up to the age of 79 years should be treated according to the same guidelines as younger patients. Statin therapy should only be considered for patients aged 80 years and older who are at a very high risk for cardiovascular events.

Aged↗
PubMed2002

Risk evaluation and therapeutical implications of pulse pressure in primary arterial hypertension.

SUMMARY: Analysis of the results raised in the Framingham and the MRFIT study have clearly shown that increased pulse pressure is an independent cardiovascular risk factor. This is valid for all age groups and both sexes. The risk increases with pulse pressures over 60 - 65 mmHg for office blood pressure and 53 mmHg for 24-h-mean of ambulatory blood pressure. Pulse pressure is strongly correlated with systolic blood pressure and will be highest in case of isolated systolic hypertension. Urinary albumin excretion and left ventricular hypertrophy are closely associated with pulse pressure. With elevated pulse pressure cardiovascular risk is increased 2- to 4-fold in relation to age and endpoint. The risk of myocardial infarction is raised more if pulse pressure is associated with low mean arterial blood pressure while risk of stroke is increased with wide pulse pressure and high mean arterial pressure. The risk of pulse pressure can be seen in normotensives and in early pregnancy. Therapeutic management of pulse pressure will be similar to that of systolic blood pressure, since normalization of systolic blood pressure will also lower or normalize pulse pressure. Results of preliminary studies suggest that diuretics are superior to other drugs in decreasing pulse pressure. An increase of pulse pressure during therapy should be avoided since each 10 mmHg increase in pulse pressure will raise the risk of stroke and myocardial infarction about 24 % and 32 %.

Adult↗
PubMed2002

[Dietary fats, salt and alcohol drive up blood pressure. Educate hypertensive patient on avoidance].

General non-drug measures today form the accepted basis for every antihypertensive treatment. WHO identifies the most important of these as weight reduction, salt restriction and moderation in the use of alcohol. These measures can effectively lower raised blood pressure and normalize grade I hypertension, especially in borderline cases. The target of these efforts is a weight reduction of at least 5%, restriction of salt to 5-6 g/day and alcohol consumption not exceeding 20 g/day for women and 25 g/day for men. No negative effects are to be expected from these restrictions, which are really nothing more than a return to "normal portions" with regard to eating and drinking habits.

Alcohol Drinking↗
PubMed1999

[Fat control--an effective antihypertensive strategy. Special recommendations for therapy of the overweight patient].

Some 44% of all patients with elevated blood pressure are overweight. In obesity-related hypertension, sympathicotonia is regularly found, together with elevated intracellular calcium, sodium retention, increased cardiac output (per minute) and a sensitivity to salt. The role played by hyperinsulinemia has apparently been overstated. A primary rise in the minimal vascular resistance suffices to reduce the perfusion of the skeletal musculature and, solely on this basis, to induce insulin resistance. For the treatment of obesity-related hypertension, non-medicinal approaches to weight reduction predominate. Reducing the daily salt intake to 5 g can also bring about a measurable reduction in blood pressure. For the treatment with antihypertensive drugs, beta blockers and diuretics are the initial choice; in the case of pronounced metabolic syndrome, ACE-inhibitors and alpha-1 receptors.

Body Mass Index↗
PubMed1998

Anaphylactoid reactions during hemodialysis in sheep are ACE inhibitor dose-dependent and mediated by bradykinin.

Anaphylactoid reactions (AR) have been attributed to the generation of bradykinin (BK) when AN69 membranes are used together with angiotensin converting enzyme (ACE) inhibitors during hemodialysis. However, conclusive evidence for the involvement of the BK as the mediator of these AR is still lacking. This study examined the degree of contact activation in an animal model caused by three PAN membranes--AN69, PAN DX, and SPAN- and the effects of different doses of the ACE inhibitor enalapril (ENA) and the BK B2-receptor antagonist icatibant on AR during hemodialysis. Six sheep were dialyzed for one hour with or without ENA pre-treatment using the different membranes in random order. Severe AR were observed only during hemodialysis with AN69 dialyzers together with ENA pre-treatment; the severity of AR increased with the ENA dose. Mild hypotension was noted during hemodialysis with AN69 without ACE inhibition and with PAN DX and 20 mg ENA. Compared to pre-dialysis values, maximum generation of BK after blood passage through the dialyzer was found at five minutes: 73-fold (AN69 without ENA), 161-fold (AN69 with 10 mg ENA), 97-fold (AN69 with 20 mg ENA), 108-fold (AN69 with 30 mg ENA), 154-fold (AN69 with 30 mg ENA and 0.1 mg/kg icatibant), 18-fold (PAN DX without ENA), and 42-fold (PAN DX with 20 mg ENA). Elevated BK levels in arterial blood were detected during hemodialysis with AN69 membranes even without ACE inhibition (2.5-fold); pre-treatment with 20 mg ENA further increased arterial BK concentrations (4-fold). Furthermore, a marked decline of prekallikrein and high molecular weight kininogen concentrations was noted for both AN69 and PAN DX membranes. Anaphylactoid reactions during hemodialysis were completely prevented by icatibant even after pre-treatment with ENA and in the presence of high BK concentrations. Concentrations of prekallikrein, high molecular weight kininogen, and BK remained unchanged and no AR were observed during hemodialysis with SPAN and pre-treatment with 20 mg ENA. Our findings confirm that AR during hemodialysis with the negatively charged AN69 membrane are mediated by BK, since they can be prevented by the BK B2-receptor antagonist icatibant.

Acrylic Resins↗
PubMed1997

Effect of bunazosin and atenolol on glucose metabolism in obese, nondiabetic patients with primary hypertension.

Antihypertensive drugs, recommended by the World Health Organization for use in monotherapy, exert different effects on glucose and lipid metabolism. In our study we compared the effects of the beta-blocker atenolol (AT) and the alpha1-blocker bunazosin (BU) on glucose metabolism. The doses administered were chosen to produce similar antihypertensive effects with both drugs. The study was conducted as a bicenter, parallel, controlled, and double-blind study. All patients suffered from mild to moderate primary hypertension, were obese (body mass index > 26 kg/m2), but were nondiabetic. After a drug-free period of 4 weeks, patients were treated either with 6 and 12 mg of bunazosin (n = 15) or with 50 and 100 mg of atenolol (n = 17) once daily for 12 weeks. Glucose metabolism was measured by the iv glucose tolerance test (GTT) and the euglycemic hyperinsulinemic clamp test. The results show a similar blood pressure reduction with both drugs. However, their effects on glucose metabolism were significantly (p < 0.05) different: The area under the curve (AUC) of glucose in the iv GTT increased 26.8% during atenolol treatment but decreased 30% during bunazosin treatment. The same influence on the AUC of insulin was observed [AT +478.5 +/- 441.8 (+22%) vs. BU, -588.5 +/- 411.1 (-22%)]. Similar changes were found in the glucose clamp test. The metabolic clearance rate increased 11.4% during bunazosin use and decreased 8.4% during atenolol use to the same degree that the insulin sensitivity index changed (BU +13.2% vs. AT -21.9%). The differences between the two treatment regimes were statistically significant (p < 0.05). These results in obese hypertensives confirm the well-known negative effects of beta-blockers on glucose metabolism. Additionally, they demonstrate that an alpha1-blocker such as bunazosin develops the same blood pressure-lowering effect as beta-blockers, but with a significantly better profile with regard to glucose metabolism. Therefore, the use of alpha1-blockers can be recommended for obese hypertensives without any special care for glucose metabolism.

Adrenergic alpha-Antagonists↗
PubMed1997

The role of kinins in the antihypertensive and cardioprotective effects of ACE inhibitors.

Kinins are highly potent vasoactive peptides. They reduce blood pressure by vasodilation and are cardio- and vasoprotective. ACE inhibitors potentiate the actions of endogenous kinins by about 50-fold. Kinins are involved in the blood pressure-lowering effects of ACE inhibitors in all forms of hypertension associated with stimulation of the renin-angiotensin system. In addition, kinins play an important role in the metabolic, and cardio- and vasoprotective effects of ACE inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Anaphylactoid reactions during haemodialysis in sheep are associated with bradykinin release.

Anaphylactoid reactions have been observed in patients treated with AN69 dialysers and ACE inhibitors. Recently, it has been shown in vitro that AN69 membranes induce the release of high amounts of bradykinin in plasma. To verify the possible role of bradykinin in these shock-like reactions, six sheep were dialysed in a random fashion using AN69 or the new SPAN membrane with and without pretreatment with captopril. All animals were dialysed for 60 min via double-lumen Shaldon catheters. Blood samples were drawn at 0, 5, 10, 15, 30, and 60 min from the venous line. A total of 24 haemodialysis procedures was carried out: group A (n = 6), AN69 without captopril; group B (n = 6), SPAN without captopril; group C (n = 6), AN69 with captopril; group D (n = 6), SPAN with captopril. A significant bradykinin release was observed only in groups A and C, reaching peak values already after 5 min. Animals in group C showed the highest bradykinin values. In four of six animals in group C anaphylactoid reactions with severe hypotension were noted. From this animal model we conclude that dialysis with the AN69 membrane is associated with bradykinin release. Pretreatment with ACE inhibitors results in further increasing bradykinin levels, which lead to anaphylactoid reactions. In contrast, the new SPAN membrane was well tolerated without detectable changes in bradykinin concentrations.

Acrylic Resins↗
PubMed1995

Plasma catecholamines, thrombocyte alpha 2- and lymphocyte beta 2-adrenoceptor densities in hypertensive patients with low or normal plasma renin concentrations.

The sympathetic nervous system is unique in the regulation of plasma renin, for it can stimulate or suppress renin release by activation of either renal beta- or alpha 2-adrenoceptors. The authors studied plasma renin concentration (PRC), noradrenalin and adrenalin levels in plasma, and the densities of lymphocyte beta 2-adrenoceptors and thrombocyte alpha 2-adrenoceptors in 25 hypertensive patients with either normal (11-40 mU/L; n = 9) or low PRC (0-10 mU/L; n = 14). There were no differences in plasma catecholamine levels and adrenoceptor densities between the two patient groups. A positive correlation (r = 0.66; P < 0.005) between beta 2-adrenoceptor density and PRC in the patient group with low PRC, and a negative correlation (r = -0.72; P < 0.01) between alpha 2-adrenoceptor density and plasma renin in patients with normal PRC were found. They conclude that adrenoceptor densities on blood elements and plasma catecholamines do not differ in low and normal renin hypertension. The significant correlations between adrenoceptor densities and PRCs may indicate that adrenoceptors on blood elements mirror adrenoceptor densities in the kidney and that tonic suppression of renin release through alpha 2-adrenoceptors is preserved in hypertensive patients with normal plasma renin levels.

Adult↗
PubMed1994

ACE-inhibition with perindopril in essential hypertensive patients with concomitant diseases. The Perindopril Therapeutic Safety Collaborative Research Group.

PURPOSE: Many hypertensive patients have other, usually long-term diseases. Antihypertensive therapy may interfere with these diseases and their therapies. In the present study, the possible interactions of the ACE-inhibitor perindopril with several of the most common long-term diseases was evaluated. PATIENTS AND METHODS: In a multicenter, double-blind, randomized, placebo-controlled trial, the effect of perindopril was evaluated in 490 patients with mild essential hypertension and any one of the following concomitant diseases: hyperlipidemia, type II diabetes mellitus, ischemic heart disease, cardiac arrhythmia, peripheral arterial occlusive disease, nephropathy with proteinuria, chronic obstructive pulmonary disease, or degenerative joint disease treated with nonsteroidal anti-inflammatory drugs (NSAIDs). After a 3-week single-blind placebo run-in, the patients received either perindopril (4 mg/d) or matching placebo for 6 weeks. RESULTS: Blood pressure was effectively reduced by perindopril irrespective of the associated disease. The rate of spontaneously reported side effects was low. Treatment with perindopril was free from adverse interactions with the concomitant diseases and therapies. Moreover, favorable actions could be observed in patients with ischemic heart disease (reduction of maximal ST-segment depression during peak exercise and decrease in the number of angina attacks), in patients with proteinuria (decrease in albuminuria in patients with normal serum creatinine levels), and in patients with NSAID-treatment (increase in prostaglandin E2 concentration in gastric mucosa suggesting gastric cytoprotection). CONCLUSION: This trial shows that ACE-inhibition with perindopril represents a simple, safe, and effective short-term therapeutic option for the large proportion of patients with mild essential hypertension and concomitant diseases and therapies.

Adult↗