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Biomedical subjects

M Zehetgruber

Publications and source records attributed to M Zehetgruber.

30 records · Page 2Linked to original sources
PubMed1996

Effects of antihypertensive therapy on glucose and lipid metabolism.

Large epidemiological studies demonstrate only moderate reduction in the incidence of coronary artery disease by antihypertensive drug treatment. This is attributed to the prevalence of multiple risk factors in hypertensive patients and to possible adverse metabolic effects of antihypertensive drugs which may counteract their ability to reduce the risk of cardiovascular disease. The choices for pharmacological blood pressure reduction are divided between five classes with similar antihypertensive efficacy but markedly different influence on coronary risk factors. Hence, the clinician has to consider the prevalence of coexisting coronary risk factors, comorbidity as well as the efficacy, side effects, and mechanisms of drug action.

Antihypertensive Agents↗
PubMed1996

The ACE-inhibitor lisinopril affects plasma insulin levels but not fibrinolytic parameters.

There is evidence that ACE-inhibitors exert beneficial effects on endogenous fibrinolysis in patients with previous myocardial infarction. It is still unknown if this effect is restricted to this patient group only and by which mechanisms ACE-inhibitors exhibit the profibrinolytic effects. One possible explanation might be the positive influence of ACE-inhibitors on insulin metabolism by decreasing plasma insulin which in turn could decrease PAI-1, a major regulator of the fibrinolytic system. Therefore the present study examines the relationship between insulin and PAI-1 plasma levels during intravenous glucose tolerance tests before and after administration with the ACE-inhibitor lisinopril in 12 male obese patients with angiographically proven coronary artery disease and borderline hypertension. After a 4-weeks wash-out period glucose tolerance tests were performed before and after lisinopril-treatment (10mgs/d) for 12 weeks. After the treatment period, fasting plasma insulin level decreased from 15.6 +/- 2.1 to 11 +/- 1.8 uU/ml, p < or = 0.01. Stimulated levels of insulin during glucose tolerance test also significantly decreased by lisinopril (peak insulin from 57 +/- 10 to 41.2 +/- 7.3 uU/ml, p < or = 0.02). Basal plasma tissue plasminogen activator antigen, PAI-1 total antigen and PAI-1 "active" antigen were unaffected by therapy (8.4 +/- 0.5 vs 8.6 +/- 0.5 ng/ml, 118 +/- 20 vs 124 +/- 16 ng/ml and 21 +/- 7 vs 30 +/- 7 ng/ml, respectively). Our data confirm a beneficial effect of lisinopril on plasma levels of insulin but failed to demonstrate any profibrinolytic effect in this study population, thus questioning the postulated mechanism of influencing endogenous fibrinolysis by changes of plasma insulin.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Estimation of coronary flow reserve by transesophageal coronary sinus Doppler measurements in patients with syndrome X and patients with significant left coronary artery disease.

OBJECTIVES: This study sought to determine the feasibility of coronary sinus flow velocity analysis by transesophageal Doppler echocardiography for estimation of coronary flow reserve in patients with syndrome X and patients with coronary artery disease. BACKGROUND: Coronary flow reserve provides useful information in patients with coronary artery disease and patients with syndrome X. Current methods of measuring coronary flow reserve are invasive or require extensive laboratory equipment, or both. Transesophageal Doppler recordings of coronary sinus flow velocity before and after vasodilator application may allow noninvasive determination of coronary flow reserve. METHODS: We obtained coronary sinus flow velocity recordings before and after dipyridamole administration (0.6 mg/kg body weight per 5 min) in 9 patients with syndrome X, 14 with significant left coronary artery disease and 22 age-matched control patients. We used the formula anterograde minus retrograde flow velocity time integral times heart rate as an index of coronary sinus flow. Coronary flow reserve was calculated by dividing coronary sinus flow variables after dipyridamole administration by the respective baseline values. RESULTS: Technically adequate recordings were obtained in 44 (98%) of 45 patients. Compared with that in the control group (2.78 +/- 0.95 [mean +/- SD]), coronary flow reserve was significantly lower in patients with syndrome X (1.21 +/- 0.23, p < or = 0.001) as well as in those with coronary artery disease (1.47 +/- 0.7, p < or = 0.001). Using a cutoff coronary flow reserve value of 1.8, sensitivity, specificity and overall predictive value of coronary flow reserve determinations were, respectively, 100%, 91% and 94% for syndrome X and 86%, 91% and 89% for coronary artery disease. CONCLUSIONS: Coronary flow reserve calculation by transesophageal coronary sinus flow velocity recordings is feasible in a large proportion of patients and might be useful for the noninvasive evaluation of patients with syndrome X and patients with severe left coronary artery disease.

Blood Flow Velocity↗
PubMed1995

[Antihypertensive therapy and coronary heart disease: significance of the effect of concomitant cardiovascular risk factors].

Antihypertensive therapy as it was performed in the past has not provided the degree of protection against coronary heart disease as was originally predicted by epidemiologic evidence. An improvement of outcome of antihypertensive therapy can only be achieved if coronary risk is maximally reduced. Therefore, in treating hypertensive patients, one has to take care of a diligent search for the presence of other coexisting coronary risk factors, of a vigorous use of life-style modifications (nondrug therapy), and of a greater individual selectivity of antihypertensive agents for initial and chronic use, preferring those that may provide additional benefits for other coexisting coronary risks.

Antihypertensive Agents↗
PubMed1994

Severe complications following thrombolytic therapy of an acute thrombosis of a prosthetic mitral valve.

Thrombosis of prosthetic cardiac valves is a rare but potentially lethal complication. As emergency surgical intervention of thrombotic prosthetic cardiac valves is correlated with high mortality, fibrinolytic therapy has been recently recommended as a therapy with high efficacy and no severe side effects. We report on a patient with thrombosis of a prosthetic mitral valve who developed severe embolic complications following the administration of the thrombolytic agent. On admission the patient showed signs of incipient cardiogenic shock. The diagnosis of thrombotic obstruction of the prosthetic mitral valve was confirmed by transesophageal echocardiography. The effective valve area was 0.41 cm2. Pulmonary arterial blood pressure and wedge pressure were significantly elevated. A fibrinolytic therapy with recombinant tissue-type plasminogen activator according to the Neuhaus scheme was attempted. Within 60 min after start of treatment the effective valve area increased (1.41 cm2), and the pulmonary capillary wedge pressure decreased. However, peripheral and cerebral embolism occurred. Occlusion of the right brachial and right femoral artery was ascertained by Doppler ultrasound. Embolism into the right leg made an embolectomy with a Fogarty catheter necessary. Computed tomography revealed two lesions located in the occipital and left temporal area of the brain. Correlated with the lesions evaluated in computed tomography, right hemiplegia and complete aphasia was observed. The neurological status of the patient has only slightly improved to the present. To our knowledge no severe persistent neurological deficits following thrombolytic therapy have been reported. We therefore assume that the risk of severe neurological complications is underestimated.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1993

Vascular smooth muscle and nitric oxide.

Experiments were performed to investigate the production of endothelium-derived relaxing factor (EDRF or nitric oxide; NO) by vascular smooth muscle cells. The lumen of bovine pulmonary arteries were filled with Krebs-Henseleit solution (incubates). Both endothelium-intact and endothelium-deprived vessels were used. Incubate solutions from the lumen of generator vessels contained a significant amount of nitric oxide (NO). Although the NO concentration was higher in incubates from endothelium-intact vessels, endothelium-deprived vessels also produced NO. The length of incubation did not influence the amount of nitric oxide released. Endothelium-deprived pulmonary arteries also generated NO as detected by chemiluminescence. The amount produced however was not sufficient to relax endothelium-deprived detector vessels in superfusion bioassay experiments. Samples from Krebs-Henseleit (K-H) solution surrounding the preparation (bathing solution) contained NO values which were also significantly higher than the control. Nitric oxide found in the bathing solution also appeared to originate from endothelium and vascular smooth muscle. Oxyhemoglobin attenuated NO signals. The results demonstrate that nitric oxide is released by vascular smooth muscle cells as well as by endothelium. However, the amount of NO released by muscle is insufficient to relax endothelium-deprived vascular preparations.

Animals↗
PubMed1990

A model to study physiological activation of phospholipase A2 and vasorelaxation by lysophosphatidylcholine.

Earlier we demonstrated that micellar solutions of LPC caused endothelium-dependent relaxation of rabbit thoracic aorta and bovine intrapulmonary artery and vein through a cyclic GMP-dependent mechanism. The availability of LPC for vasorelaxation depends on its production by deacylation of PC by PLA2. We assessed the possible activation of PLA2 by commonly used vasorelaxants such as acetylcholine, bradykinin, calcium ionophore A23187 and thrombin and vasoconstrictors like histamine and phenylephrine in the presence of indomethacin in a model system where 14C PC was incorporated into bovine intrapulmonary arterial segments. Taking the ratio of 14C PC:LPC formed by exogenous PLA2 as an index of deacylation, we found that while all the agents relaxed the strips in an endothelium-dependent manner, only thrombin caused relaxation followed by an increase in 14C LPC and a concomittant decrease in 14C PC indicating activation of PLA2. Our data show that PC/PLA2 system can be activated to generate LPC for vascular relaxation under specific physiological conditions. This model system can be used to monitor PLA2 activity and LPC production to compensate flow and pressure induced changes in arteries.

Acetylcholine↗
PubMed1989

Effect of lysophosphatidylcholine on atherosclerotic rabbit arteries.

We report here on the effect of an endothelium-dependent vascular smooth muscle relaxant, lysophosphatidylcholine (LPC) on rabbit aortic strips and on hemodynamic changes by LPC in atherosclerotic animals. Cyclic GMP changes induced by LPC in atherosclerotic vessels were also determined. Atherosclerosis was produced by feeding a high cholesterol and saturated fatty acid diet. LPC was injected into the left atrium and coronary flow was measured by radioactive microspheres; in vitro, relaxation of precontracted aortic strips by lysophosphatidylcholine was also recorded. LPC failed to increase coronary flow in the presence of atherosclerosis. In isolated aortic strips, dose-response curves with acetylcholine and LPC showed diminished relaxation in atherosclerotic preparations, and cyclic GMP production following LPC was reduced. The results demonstrate that vascular relaxation by LPC, together with its ability to activate guanylate cyclase is dependent on the functional and morphological integrity of the vascular wall.

Animals↗
PubMed1989

An improved chemiluminescence assay suggests non nitric oxide-mediated action of lysophosphatidylcholine and acetylcholine.

Using a new nitric oxide analyser, we have developed a sensitive chemiluminescence assay to detect trace quantities of NO in aqueous solutions. This improved technique in combination with the bioassay has been employed to verify the theory that NO released by vascular endothelium, accounts for the relaxation produced by acetylcholine, lysophosphatidylcholine and calcium ionophore A23187. Our results show that while calcium ionophore A23187 continuously released NO, acetylcholine and lysophosphatidylcholine relaxed vascular strips without releasing NO over the basal level.

Acetylcholine↗
PubMedDate not supplied

Functional assessment of coronary arteries by poststenotic intravascular Doppler ultrasound.

This study sought to delineate the impact of the rate pressure product on intraluminal Doppler velocity measurements and to determine the relation between poststenotic vasodilator reserve and percent luminal obstruction in coronary vessels. Twenty patients with single-vessel coronary disease were studied prior to coronary angioplasty and at follow-up 6 months later. Intracoronary velocity reserve after administration of adenosine was measured distal to the stenosis with a Doppler-tipped guide wire and was compared to quantitative coronary angiography and adenosine myocardial perfusion scintigraphy. The rate pressure product was confirmed as significant covariate (ANCOVA, p < 0.005) of intracoronary Doppler reserve. When normalized to rate pressure product, poststenotic Doppler velocity reserve in stenosed arteries was significantly lower than in patent arteries as classified by quantitative coronary angiography (1.7 +/- 0.6 vs. 2.9 +/- 0.5, p < 0.001) and perfusion scintigraphy (1.5 +/- 0.4 vs. 2.8 +/- 0.5, p < 0.001). Normalized Doppler velocity reserve showed a nonlinear but highly significant relation to percent area stenosis [y = 3.0.(1 - exp[0.081 (x - 100)]), p < 0.001]. When normalized Doppler velocity reserve was less than 2.0, coronary disease was identified with 95% specificity and 94% sensitivity in comparison to perfusion scintigraphy. Thus, in coronary arteries poststenotic Doppler reserve and percent area stenosis show a significant nonlinear relation. Doppler velocity reserve when normalized to rate pressure product can be used to characterize the hemodynamic impact of coronary obstructions.

Adenosine↗