ACE*D and cardiovascular disease.
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Cardiovascular Diseases↗
Biomedical subjects
B R Winkelmann
Publications and source records attributed to B R Winkelmann.
Overview of clinical trials with glycoprotein IIb-IIIa receptor antagonists in the prevention and management of coronary.
Platelet aggregation is mediated by the glycoprotein IIb-IIIa receptor, a member of the integrin superfamily of membrane-bound adhesion molecules. In the activated platelet, binding to the major adhesive proteins, fibrinogen and von Willebrand, occurs due to a conformational change of the glycoprotein IIb-IIIa receptor. Glycoprotein IIb-IIIa receptor antagonists effectively block the binding of these adhesive proteins and thus inhibit platelet aggregation. Large-scale clinical trials have demonstrated the benefits of these agents in patients undergoing percutaneous coronary angioplasty and with acute coronary syndromes compared to conventional antiplatelet therapy. Furthermore, trials are in progress in patients with acute myocardial infarction. The beneficial effects of these agents was first demonstrated with abciximab, a monoclonal antibody to the glycoprotein IIb-IIIa receptor, in patients at risk of coronary arterial thrombosis, and was further illustrated in trials with other IIb-IIIa receptor blocking agents, both with synthetic peptide and non-peptide receptor antagonists. This review focuses on the glycoprotein IIb-IIIa receptor antagonists most advanced in clinical development.
Journal Article↗
Diuretics and sudden cardiac death.
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Adrenergic beta-Antagonists↗
Deletion polymorphism of the angiotensin I-converting enzyme gene is associated with increased plasma angiotensin-converting enzyme activity but not with increased risk for myocardial infarction and coronary artery disease.
BACKGROUND: Previous research has shown that the insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene is a major determinant of plasma ACE activity. It has been suggested that persons with the DD genotype (those who express, on average, the highest levels of circulating ACE) have an increased risk for myocardial infarction and coronary artery disease, particularly if they are otherwise at low risk. Subsequent studies, however, have not confirmed that ACE I/D gene polymorphism is a risk factor for coronary artery disease and myocardial infarction. OBJECTIVE: To investigate the association between the I/D polymorphism of the ACE gene and the risk for coronary artery disease and myocardial infarction in patients in whom coronary artery disease status was documented by angiography. DESIGN: Cross-sectional study. SETTING: University medical center. PATIENTS: 209 male case-patients with coronary artery disease and 92 male controls without coronary artery disease, as documented by coronary angiography. MEASUREMENTS: Assessment of the cardiac risk profile by questionnaire; classification of patients by the degree of coronary artery stenosis; levels of lipoproteins, apolipoproteins, and fibrinogen; and ACE I/D gene polymorphism assessed by polymerase chain reaction amplification. RESULTS: Plasma ACE activity was significantly associated with ACE I/D gene polymorphism. The ACE genotype was not associated with the presence of coronary artery disease or myocardial infarction. If a recessive effect of the D allele was assumed (DD compared with DI and II), the relative risk was 1.00 (95% CI, 0.76 to 1.30) for coronary artery disease and 1.03 (CI, 0.77 to 1.38) for myocardial infarction. Results of analyses were also negative when a dominant effect of the D allele was assumed and when low-risk subgroups were examined. The established risk factors age and apolipoprotein B level emerged as the most important risk predictors in multivariate analyses, followed by diastolic blood pressure and fasting glucose levels. CONCLUSIONS: In an angiographically defined study sample, ACE I/D gene polymorphism was not associated with an increased risk for coronary artery disease or myocardial infarction, despite its effects on plasma ACE activity.
Aged↗
Experimental application of controlled limb reperfusion after incomplete ischaemia.
Severe local and systemic complications may occur after revascularization of extremities exposed to prolonged complete or incomplete ischaemia. These complications may be reduced by controlling the reperfusate and the circumstances of the reperfusion period. Ten adult German domestic pigs were exposed to 6 h of incomplete limb ischaemia by occlusion of the left iliac artery. To simulate the clinical situation of embolectomy, the occlusive snares were released after the ischaemic period in five pigs and normal blood flow developed with systemic pressure (uncontrolled reperfusion). In the other five pigs, a controlled reperfusate was delivered at controlled pressure before establishing normal blood reperfusion (controlled reperfusion). At the end of the observation period (90 min after start of reperfusion), the group with controlled reperfusion had a lower mean(s.e.m.) tissue water content (81.8(0.7) versus 84.3(0.7) per cent, P < 0.05, a greater increase in tissue adenosine 5'-triphosphate compared with values at the end of ischaemia (6.2(1.5) versus -2.5(1.8) mumol per g protein, P < 0.03), a higher tissue pH (7.2(0.1) versus 6.8(0.1), P < 0.03), a smaller temperature decrease (0.3(0.2) versus 1.2(0.3) degrees C, P < 0.05), lower concentrations of creatine kinase (355.0(87.5) versus 624.4(73.4) units/l, P < 0.05) and lactate dehydrogenase (LDH) (369.5(42.5) versus 538.4(39.2 units/l, P < 0.03) in the femoral vein blood and lower LDH concentrations (356.5(48.9) versus 546.0(37.8 units/l, P < 0.03) in central venous blood. These data indicate that severe local and systemic damage occurs with uncontrolled (normal blood) reperfusion even after incomplete limb ischaemia, and that these changes can be reduced by delivering a controlled reperfusate under controlled conditions.
Adenosine Triphosphate↗
Hormonal modifications in patients admitted to an internal intensive care unit for acute hypoxaemic respiratory failure.
To clarify which endocrine modifications can be observed in acute hypoxaemic respiratory failure, 15 severely ill male patients [PAT; median age: 61 (range: 48 years); median height: 173 (range: 12) cm; median mass: 73 (range 31) kg] were investigated immediately upon admission to an intensive care unit (ICU) for this clinical disorder. Before starting treatment, the blood gases were measured and a number of selected hormones with special relevance for an ICU setting were determined. These are known to be modified by acute hypoxaemia in healthy subjects and to possess glucoregulatory properties, or an influence upon cardiocirculation or the vascular volume regulation: insulin, cortisol, adrenaline, noradrenaline, atrial natriuretic peptide, renin, aldosterone, angiotensin converting enzyme, and endothelin-I (ET). To elucidate whether potential endocrine changes resulted from acute hypoxaemia alone, the underlying disease, or unspecific influences connected with the ICU setting, all measurements were compared to those of a completely healthy reference group (REF) with comparable acute experimental hypoxaemia. The latter state was achieved by having the REF breathe a gas mixture with the oxygen content reduced to 14% (H). In the REF, neither the medians nor the distribution of endocrinologic measurements were modified significantly by acute hypoxaemia. In the PAT, the medians were increased considerably, yet with a slight diminution of ET. The distribution of individual values was considerably broader than in the REF with H. In conclusion, considerable increases in the means of the above hormones, with the exception of ET, can be registered in severely ill patients admitted to ICUs with acute hypoxaemic failure. However, such modifications cannot be considered attributable exclusively to acute arterial hypoxaemia. The underlying clinical disorders, such as septicaemia or an unspecific endocrine epiphenomenon, including severe and not only hypoxaemic stress, seem to be predominant.
Acute Disease↗
Clinical pharmacokinetics of molsidomine.
Molsidomine is a prodrug for the formation of nitric oxide (NO). Its pharmacokinetics are characterised by rapid absorption and hydrolysis, taking a short time to achieve maximal systemic concentrations of both the parent compound and its active metabolite, SIN-1. The time to peak plasma drug concentration (tmax) is 1 to 2 hours. The bioavailability of the parent compound after oral administration in tablet form is 44 to 59%, but further metabolism to release NO and form polar metabolites is rapid; the half-life (t-1/2) of SIN-1 is 1 to 2 hours. Urinary excretion accounts for more than 90% of the part of the administered dose of molsidomine which is not excreted unchanged. Protein binding of the parent compound is very low (3 to 11%) and its volume of distribution (Vd) corresponds to the range of bodyweight. Single-dose studies (1, 2 and 4 mg) have revealed linear pharmacokinetics, and multiple dose studies in healthy individuals (2 mg 3 times daily for 7 days) and coronary artery disease (CAD) patients (4 mg 4 times daily for 4 weeks) do not show any accumulation of the drug. A study in young and elderly individuals indicated that the first-pass effect is decreased and t-1/2 prolonged with age, resulting in an increased area under the concentration-time curve (AUC) of molsidomine and SIN-1. In patients with liver disease and congestive heart failure similar changes were observed, but much less so in patients with CAD. Clearance was also impaired in patients with liver disease, but the pharmacokinetics of molsidomine were not markedly altered by impaired renal function. In general, due to a large therapeutic dose range, dosage adjustments are not required on the basis of clinical experience. In certain patients a lower starting dose may be recommended, such as in those with impaired liver or kidney function, in congestive heart failure or in the presence of concomitant treatment with other vasoactive compounds. A linear dose-effect relationship is observed with counterclockwise hysteresis, i.e. a greater effect associated with the decrease of plasma concentrations than during their increase, which may be at least partly due to the metabolic delay in the formation of NO from SIN-1. Accordingly, the duration of action of molsidomine is longer than would be expected on the basis of the elimination half-life. The pharmacokinetics of molsidomine support the recommended dosages for use in angina pectoris.
Absorption↗
[Multiplicity of clinical symptoms and manifestations of unruptured aneurysms of the sinus of Valsalva--3 case reports].
Sinus Valsalva aneurysms belong to the less common congenital or acquired structural cardiac anomalies. However, in patients with known cardiac anomalies and uncertain or uncharacteristic cardiac symptoms the existence of a sinus Valsalva aneurysm must be taken into consideration. A sinus Valsalva aneurysm can be clinically silent as in the case of the 56-year-old patient with an accompanying bacterial endocarditis. An increasing aortic regurgitation after dilatation of a coarctation of the aorta can also proceed with an ecstasy of the ascending aorta and an aneurysm of the sinus Valsalva (case 2). Furthermore, a rapid dilatation of a non-ruptured sinus Valsalva aneurysm can cause a severe compression of coronary arteries with subsequent myocardial infarction, as in the 27-year-old patient with congenital aortic stenosis and acute endocarditis in case 3.
Adult↗
Circulating endothelin in patients undergoing coronary artery bypass grafting.
Increased synthesis of endothelin, (a powerful physiological vasoconstrictor), is a uniform response to endothelial injury and has been associated with myocardial ischemia and reperfusion. This study tests the hypothesis that coronary artery bypass grafting (CABG) affects endothelin plasma concentrations in various vascular beds. Twenty-four CABG patients were included in this study. Endothelin was determined in multiple plasma specimens obtained from superior vena cava, aortic root and coronary sinus (CS). Venous endothelin plasma concentrations collected in CABG patients before surgery were 1.16 +/- 0.18 pg/ml. They increased after sternotomy (1.71 +/- 0.12 pg/ml) and during (2.97 +/- 0.27 pg/ml) and after cardiopulmonary bypass (CPB, 2.72 +/- 0.21 pg/ml). There is no net release of endothelin from the coronary circulation before (aorta 2.26 +/- 0.13 pg/ml vs CS 2.44 +/- 0.17 pg/ml, not significant (n.s.), during (cardioplegia 2.55 +/- 0.17 pg/ml vs CS 2.45 +/- 0.15 pg/ml, n.s.), and after aortic cross-clamping (aorta 2.95 +/- 0.23 pg/ml vs coronary sinus 2.71 +/- 0.18 pg/ml, n.s.). Pulmonary endothelin clearance is preserved on partial bypass (aorta 2.26 +/- 0.13 pg/ml vs vena cava 2.86 +/- 0.18 pg/ml, P < 0.003), but remains inhibited even 10-30 min after release of the aortic cross-clamp (aorta 2.95 +/- 0.23 pg/ml vs vena cava 2.97 +/- 0.27 pg/ml, n.s.). Two out of 24 patients had severe myocardial ischemia. These patients showed particularly high endothelin concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Low-dose almitrine bismesylate in the treatment of hypoxemia due to chronic obstructive pulmonary disease.
STUDY OBJECTIVE: Assessment of acute and chronic effects of low-dose almitrine bismesylate (AB) in stable chronic obstructive pulmonary disease (COPD). STUDY DESIGN: Oral administration of AB, 25 mg three times a day, for 6 months in all patients. Pulmonary function, blood gases, and peripheral nerve conduction velocity were measured at baseline and after long-term administration of AB. In addition, oral pharmacokinetics and effects on pulmonary circulation at rest were studied in half of the patients. Intravenous pharmacokinetics were measured after a single intravenous dose of 60 mg of AB 3 months before the start of oral AB treatment in the other seven patients. SETTING: Outpatient clinic of a community hospital in a coal mining district in southwest Germany. PATIENTS: Fourteen patients with clinically stable COPD and hypoxemia. RESULTS: Acute effects of AB were as follows: a significant increase in arterial oxygen tension (PaO2) from 61 +/- 7 mm Hg to 74 +/- 8 mm Hg (p < 0.001), a decrease in arterial carbon dioxide tension (PaCO2) from 41 +/- 8 mm Hg to 38 +/- 7 mm Hg (p < 0.01), a rise of pH from 7.45 +/- 0.04 to 7.48 +/- 0.04 (p < 0.01), and a transient increase in mean pulmonary artery pressure from 26 +/- 7 to 29 +/- 6 mm Hg (not significant). After long-term treatment, once tissues were saturated with almitrine, improvement in gas exchange persisted with a PaO2 of 70 +/- 10 mm Hg (p < 0.001) and a PaCO2 of 39 +/- 6 mm Hg (not significant) without elevation of pH (7.45 +/- 0.04) or of pulmonary artery pressure (26 +/- 8 mm Hg). The terminal half-life of AB was 56 +/- 45 days after a single intravenous administration, and 55 +/- 16 days after long-term oral dosing. None of the patients developed clinically manifest peripheral neuropathy. Impaired asymptomatic peripheral motor nerve function was prevalent in 4 (29 percent) of the patients and remained unchanged during long-term AB administration. However, asymptomatic impairment of motor nerve conduction velocity developed in two patients with inadequate high AB plasma levels despite low-dose therapy. Both patients were known to have additional conditions predisposing for neuropathy. CONCLUSIONS: Low-dose AB therapy, 75 mg daily, resulted in sustained elevation of arterial oxygen tension in hypoxemic patients with COPD. Although pulmonary artery pressure increased transiently after the first dose, it remained unchanged with long-term treatment despite persistent improvement of pulmonary gas exchange.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Oral↗
Discordance of anti-ischemic and hemodynamic effects of captopril in stable coronary artery disease.
BACKGROUND: The role of angiotensin converting enzyme (ACE) inhibition in patients with coronary artery disease without concomitant disease such as heart failure or hypertension has not been elucidated. In this double-blind, cross-over, randomized trial of the ACE inhibitor captopril, its antianginal and anti-ischemic effects were studied during monotherapy and in the presence of an organic nitrate. METHODS: Thirty-seven patients (34 men, three women) with stable coronary artery disease and exercise-induced ST-segment depression were enrolled. After a washout phase without medication they received placebo, isosorbide dinitrate (ISDN) 20 mg twice daily, captopril 12.5 mg twice daily, and the combination of both for 1 week each, after which exercise tolerance, blood pressure and heart rate (supine, standing and 24 h profile), and peripheral arterial vasodilatation (finger pulse plethysmography) were assessed. RESULTS: Thirty-three patients completed all phases of the study. Exercise-induced anginal symptoms occurred in 17 patients, and asymptomatic ischemia was seen in the other 16 men. In comparison with ISDN, the anti-ischemic effects of captopril were minimal, despite a similar reduction in blood pressure. Compared with baseline, 1 week of placebo reduced the sum of ST-segment depression, the main efficacy parameter, by 10% (NS), captopril by 19% (NS), ISDN by 37% (P < 0.001) and the combination of captopril and ISDN by 42% (P < 0.001; NS versus ISDN). No patient remained completely free of exercise-induced angina during treatment with captopril; however, three patients after ISDN and seven patients after the combination did (P < 0.05). Blood pressure at rest decreased at peak effect by 9-10% systolic (P < 0.001) with monotherapy and by up to 7% diastolic (P < 0.001), and during combined therapy with captopril and ISDN by 18% systolic (P < 0.001) and 12% diastolic (P < 0.001). Significantly enhanced circulatory effects of captopril plus ISDN versus ISDN were found for blood pressure (P < 0.001) and peripheral arterial vasodilation (P < 0.01). The reflex tachycardia induced by ISDN in the upright position (5 beats/min) was not blocked by captopril during combined therapy. CONCLUSIONS: The antianginal and anti-ischemic effects of captopril alone were marginal, despite significant circulatory effects after short-term administration. Although captopril in combination with ISDN resulted in a significant further blood-pressure-lowering effect and increased peripheral arterial vasodilatation, the magnitude of potentiation of the anti-ischemic nitrate effects was, in contrast, small. Only exercise-induced angina was further improved by the use of the combination. No paradoxical worsening of ischemia or angina was seen after captopril. Thus, although captopril has no place as first-line therapy for ischemia, its use in combination with ISDN could be advantageous for long-term prognosis.
Aged↗
Left main coronary artery stenosis after aortic valve replacement: genetic disposition for accelerated arteriosclerosis after injury of the intact human coronary artery?
BACKGROUND: Left main coronary artery stenosis is a rare but life-threatening complication after aortic valve replacement because of coronary perfusion-related trauma to the vessel wall with cannulation of the coronary ostia. We investigated whether this complication still occurs in the 1990s despite the use of more advanced catheter materials and modern surgical preservation techniques. METHODS: Four years after identification of the first two cases in 1987, five further patients had developed left main coronary artery stenosis after aortic valve replacement (incidence, 0.9%) at the cardiothoracic clinic of the J.W. Goethe University and were studied for contributing factors. RESULTS: Severe coronary ostial stenosis developed within 1 to 6 months after aortic valve replacement. In one such case, intimal proliferation was seen in a biopsy specimen that was comparable to the restenosis induced by coronary angioplasty. The clinical characteristics of the patients developing the complication, the surgical technique, and the intraoperative course did not differ from the other patients. However, five of the seven patients (71%) had a common genetic trait concerning their apolipoprotein E genotype (the epsilon 4 allele) that is normally present in only 10% to 15% of patients screened (P < 0.01). CONCLUSIONS: These lesions seem to result from a uniform response of the vessel wall to injury. Their incidence is probably related in part to the degree of injury after trauma to the coronary ostia during cannulation for myocardial protection. Patients with the epsilon 4 allele might be genetically predisposed for a pathologically increased response of proliferative repair mechanisms after arterial injury. The complication can be avoided by not instrumenting the coronary ostia for direct antegrade cardioplegia but using retrograde delivery as an alternative method of myocardial protection.
Adult↗
[Cholesterol--a marker for multiple risk factors? A comparison between coronary disease and coronary health].
Comparison was made in a cross-sectional study between 658 patients in whom coronary arteriography had shown (n = 304) or excluded coronary artery disease (CHD) (n = 354) and a clinically healthy group as controls (n = 1658), to assess possible risk factors. Patients aged 31-40 years with CHD had the highest total cholesterol levels (286 +/- 43 mg/dl) and the highest number of risk factors (3.6 +/- 0.9) compared to patients without CHD of the same age (204 +/- 30 mg/dl; 2.0 +/- 0.5) and healthy controls (216 +/- 45 mg/dl; 1.7 +/- 0.5) (P less than 0.001). In older patients with CHD, total cholesterol levels were lower (age group 61-70 years: 231 +/- 49 mg/dl), reaching about the same level as that of patients without CHD (232 +/- 54 mg/dl) or healthy controls of the same age (228 +/- 55 mg/dl). Furthermore, it was demonstrated that increased total cholesterol concentration can indicate the presence of other risk factors. It would thus appear that the level of total cholesterol in patients with CHD is decisively influenced by age and the presence of other risk factors.
Adult↗
Acute and chronic effects of low dose almitrine bismesylate in the treatment of chronic bronchitis and emphysema.
OBJECTIVES: Study of the acute and chronic effects of low-dose almitrine therapy in stable hypoxaemic patients with chronic bronchitis and emphysema. METHODS: A low daily dose of 75 mg almitrine bismesylate was administered for six months in 23 patients with chronic bronchitis and emphysema. Nine patients (group 1) were placed on oral almitrine bismesylate 25 mg t.i.d. after they had received a single intravenous dose of 60 mg almitrine three months earlier. Fourteen additional patients, seven receiving almitrine (group 2) and seven placebo (group 3) were randomized for a 6 month double-blind evaluation of both acute and chronic effects of 75 mg almitrine on pulmonary gas exchange and on pulmonary haemodynamics. All patients were followed-up with regular measurements of blood gases, body plethysmography and with evaluation of peripheral nerve function. RESULTS: Acute effects of almitrine were a significant increase in arterial oxygen tension by 14 mmHg after intravenous (p < 0.001) and by 15 mmHg after oral administration (p < 0.001), amelioration of hypercapnia, a slight transient increase in mean pulmonary artery pressure from 26 +/- 7 to 29 +/- 6 mmHg (NS) and a decrease of shunt due to improvement in ventilation/perfusion mismatching. In contrast, no acute changes in blood gases and pulmonary pressures were seen in the placebo group. A combination of almitrine with oxygen (8-10 L/min) was most effective in amelioration of hypoxaemia and shunt. With chronic almitrine therapy, the improvements in gas exchange persisted without elevation of pulmonary artery pressure (26 +/- 8 mmHg), whereas a negative trend in change of blood gases and pulmonary artery pressure occurred in the placebo treated group (NS). No significant changes in external ventilation, other spirometric parameters or adverse effects concerning peripheral nerve function were seen after almitrine or placebo treatment. The elimination of almitrine was fitted to a three compartment model and the terminal half-life in the patient population was found to be 32 +/- 29 days after intravenous dosing. CONCLUSION: Acute and six-month almitrine bismesylate therapy at a low daily dose of 75 mg is found to be safe, even in severely compromised patients, with regard to pulmonary haemodynamics and peripheral nerve function. The agent is beneficial to pulmonary gas exchange, with reduction of hypercapnia, of intrapulmonary shunt and also with regard to sustained elevation of arterial oxygen tension. A combination with inhaled oxygen seems especially efficacious.
Aged↗
Isometric exercise for the evaluation of vasodilatory therapy in severe congestive heart failure.
There are few data available about the hemodynamic effects of isometric handgrip in severe congestive heart failure and its role in the evaluation of vasodilatory therapy. Therefore, we studied 20 patients with dilated cardiomyopathy at rest, during isometric handgrip, and during supine bicycle exercise before and after a single 25-mg dose of captopril. During handgrip, heart rate (p less than 0.001); systemic vascular resistance (p less than 0.01); systolic, mean, and diastolic pulmonary artery pressure (p less than 0.01) increased significantly; stroke volume index fell (p less than 0.05); whereas mean arterial pressure showed only a small increase, and cardiac index did not change. In contrast, mean arterial pressure and cardiac index increased during dynamic exercise (p less than 0.001), and peripheral resistance decreased (p less than 001). During both handgrip and bicycle exercise, captopril induced a decrease of arterial pressure (p less than 0.01 and p less than 0.001; respectively), peripheral resistance (p less than 0.001 and p less than 0.01; respectively), and systolic (p less than 0.01 and p less than 0.001, respectively) mean (p less than 0.001), and diastolic pulmonary artery pressure (p less than 0.001). Captopril induced and increase in stroke volume index (p less than 0.01) and cardiac index (p less than 0.001 and p less than 0.01 respectively) during both types of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Almitrine bismesylate and hypoxemia.
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Almitrine↗
Life-threatening flecainide toxicity. A pharmacodynamic approach.
Ventricular tachyarrhythmias and severe bradycardia, flecainide acetate's most serious side effects, occur in patients with chronic heart disease or in healthy persons after frank overdose. Toxic effects appear to correlate closely with drug levels in plasma. The surface electrocardiogram can indicate toxicity by demonstrating this drug's electrophysiologic potency to depress all major cardiac conduction pathways with marked prolongation of the PR and QRS intervals. We report the clinical course of a young, healthy person who developed polymorphous ventricular tachycardia after taking a 3800-mg dose of flecainide acetate. Sinus rhythm was restored without pacing or cardioversion after infusion of a beta-sympathomimetic agent, physostigmine, and a sodium load. The initial flecainide serum levels were five times greater than the usual upper therapeutic level. Electrocardiography showed that the lengthened electrocardiographic time intervals decreased in correlation with falling drug levels. Flecainide-associated life-threatening arrhythmias and available therapeutic interventions are discussed.
Adult↗