Cardiorespiratory screening for sleep-disordered breathing.
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Diagnostic Techniques, Respiratory System↗
Biomedical subjects
O Oldenburg
Publications and source records attributed to O Oldenburg.
Relevance of the NOS3 T-786C and G894T variants for cholinergic and adrenergic coronary vasomotor responses in man.
OBJECTIVE: We investigated the impact of the -786C allele at the promoter and the 894T allele in exon 7 of the gene encoding the endothelial nitric oxide synthase (NOS3) on coronary vasomotor responses to exogenous and endogenous stimuli. METHODS: In 47 individuals undergoing coronary angiography for chest pain, but without significant stenosis in the left anterior descending artery (LAD), nitroglycerine and acetylcholine were infused intracoronarily, and a cold pressor test (CPT) was performed. Coronary blood flow (CBF) in the LAD was calculated from quantitative coronary angiography and intracoronary Doppler measurements. Aortic and coronary sinus lactate levels were determined in 18 individuals. To analyze the impact of NOS3 genotypes, a logistic regression model was used. RESULTS: In response to acetylcholine (p = 0.002) and CPT (p = 0.015) CBF reduction was associated with homocygosity for the -786C allele. Myocardial lactate uptake was reversed into net lactate production in CC homocygotes. No independent effects of the G894T polymorphism were observed in the present study. Haplotype analysis revealed a significant linkage disequilibrium between both polymorphisms (p < 0.001). CONCLUSIONS: Our findings suggest a pathophysiologically relevant role for the T-786C polymorphism in human coronary vasomotion. The observed linkage disequilibrium between both NOS3 genotypes deserves further research in future studies.
Acetylcholine↗
Improved detection and analysis of sensed and paced events in dual chamber pacemakers with extended memory function. A prospective multicenter trial in 626 patients.
PATIENTS AND METHODS: This prospective study analyzed the incidence of atrial arrhythmias in a population of 626 patients in 173 medical centers of eleven European countries and Japan with indication for a dual chamber pacemaker system. The accuracy of the new Automatic Interpretation for Diagnosis Assistance (AIDA) program which is included in Chorus pacemakers was evaluated and the AIDA analysis was compared to and proven with Holter monitoring. Data stored in the pacemakers' memories for the first 24 hours (D1) were compared with simultaneously recorded 24-hour surface electrocardiograms, and data stored over the following 28 days (D28) were examined against reported intercurrent symptoms. RESULTS: At D1, atrial arrhythmias were detected by AIDA in 60 of 626 patients (12%), consisting of atrial fibrillation (n = 29), atrial flutter (n = 4), and miscellaneous arrhythmias (n = 17), and closely corroborated by Holter monitoring (sensitivity 93.7%, specificity 94.9%). At D28, 149 of 386 patients (49%) had had episodes of automatic mode switch prompted by atrial arrhythmias. Symptoms were reported by 81 patients (54%), 92 (62%) had no histories of atrial arrhythmias, and 57 patients (38%) were neither symptomatic nor had histories of atrial arrhythmias. An inverse relationship was found between the number of atrial paced events and the occurrence of atrial arrhythmias (p < 0.001). A history of atrial arrhythmias and older age were associated with a higher risk of atrial arrhythmias (p < 0.05). In contrast, gender, hypertension, concomitant heart disease, or type of atrial lead fixation system were not related with the occurrence of atrial arrhythmias. CONCLUSION: AIDA allowed to confirm, or disprove, the occurrence of atrial arrhythmias as a source of symptoms reported during long-term follow-up. It could also be used to examine the efficacy of antiarrhythmic therapy, and be of assistance when weighing the needs for anticoagulation in patients experiencing asymptomatic atrial arrhythmias.
Adult↗
Ambulatory norepinephrine treatment of severe autonomic orthostatic hypotension.
OBJECTIVES: This study was designed to establish a patient-controlled, ambulatory norepinephrine treatment of refractory orthostatic hypotension due to primary autonomic failure. BACKGROUND: Autonomic dysfunction leads to disabling postural hypotension. Particularly in primary autonomic dysfunction, repeated syncope and immobilization can be the result. Medical treatment of orthostatic hypotension often fails in advanced cases. METHODS: Ambulatory, patient-controlled norepinephrine therapy was initiated in six patients with orthostatic hypotension due to primary autonomic failure that had been refractory to conventional treatment. Before this therapy, three patients were bedridden; one was immobilized in a wheelchair. All had recurrent syncope and tolerated upright tilt-table testing for less than 15 min despite extensive medical treatment. For ambulatory treatment, a port-a-cath system was implanted and, using a CADD ambulatory infusion pump, norepinephrine was infused in individually adjusted dosages. RESULTS: Norepinephrine infusion therapy enabled all patients to sit, stay and walk around for more than 45 min. One patient died after a five-year treatment period, another after nine months because of nonhemorrhagic brain stem infarctions, both in the absence of norepinephrine treatment. The remaining four patients are still mobile after a period of 19, 10, 9 and 7 months, respectively. None of them has suffered complications due to arterial hypo- or hypertension, and there has been no infection of the infusion system. CONCLUSIONS: In these selected patients with refractory orthostatic hypotension due to primary autonomic dysfunction, ambulatory norepinephrine infusion therapy has proved to be a promising new therapeutic option. Further long-term studies including more patients are necessary to assess additional indications, reliability and safety of this new method.
Aged↗
Myocardial lactate release after intracoronary verapamil application in humans: acute effects of intracoronary verapamil on systemic and coronary hemodynamics, myocardial metabolism, and norepinephrine levels.
Coronary and systemic hemodynamic effects of verapamil have been investigated previously in detail. The acute impact of intracoronary verapamil on coronary hemodynamics has, however, not been correlated to simultaneously changes in myocardial metabolism or norepinephrine levels in humans. After bolus application of 1 mg verapamil into the left coronary artery of 52 patients scheduled for routine coronary angiography, heart rate (HR) remained unchanged, whereas mean arterial blood pressure (MAP) decreased (93.8 +/- 14.9 mmHg to 85.1 +/- 13.7 mmHg, p = 0.001). Coronary blood flow (CBF), calculated from intracoronary Doppler measurements and quantitative coronary angiography, increased after verapamil administration (28.5 +/- 16.7 ml/min to 66.2 +/- 41.8 ml/min, p < 0.001), whereas coronary vascular resistance index (CVRI) decreased (1.43 +/- 0.92 to 0.46 +/- 0.23, p < 0.001). Blood samples, taken simultaneously from the aorta (Ao) and coronary sinus (CS) at baseline and at maximal flow velocity, showed an increase in norepinephrine concentrations in Ao (209 +/- 151 ng/l to 283 +/- 195 ng/l, p < 0.001) and CS (233 +/- 162 ng/l to 323 +/- 248 ng/l, p = 0.004). Myocardial metabolism of pyruvate and free fatty acids were not affected. Glucose release was augmented and initial lactate consumption changed to a net lactate release into the CS (Ao to CS differences: glucose: -1.92 +/- 9.9 mg/dl to -12.8 +/- 22.8 mg/dl, p < 0.001; lactate: 0.07 +/- 0.2 mmol/l to -0.08 +/- 0.3 mmol/l, p = 0.001). Similar results were obtained for the extraction ratios and flux of these metabolites. There was a weak correlation between the increase in CBF and lactate release into the CS. This is the first report of unexpected myocardial lactate release following intracoronary verapamil administration in humans. This lactate release was paralleled by an increased glucose release into the CS at an unchanged metabolism of free fatty acids and pyruvate. One explanation for this unexplained lactate release during increased coronary blood flow might be a wash out phenomenon of lactate from previous ischemic areas, other explanations might be the induction of paradox myocardial ischemia and/or a steal effect. Further studies are necessary to explain these unexpected findings of increased coronary flow and myocardial lactate release. Until reliable explanations are pending, studies using only lactate release as a marker of myocardial ischemia, without taken coronary and systemic hemodynamic parameters into account, should be interpreted with caution.
Adult↗
[Heart failure as a cardiac symptom of sarcoidosis. Successful treatment of heart failure with steroids, digitalis and an angiotensin-1-receptor antagonist in sarcoidosis].
BACKGROUND: Sarcoidosis is a multisystemic disorder that may involve every organ. A symptomatic manifestation of the myocardium is possible, in these cases arrhythmias are the most common symptoms. CASE REPORT: This case report presents a 26-year-old female with the recurrence of Boeck's sarcoid. Fever, chill and a severe reduction in stress tolerance were the first symptoms. At the time of admission she complained of Grade III dyspnea according to the NYHA classification. The echocardiogram showed a severe impairment of the global and left ventricular function. The left ventricular ejection fraction was reduced to 30% and the Tei index was elevated to 1.0. A specimen taken from a mediastinal tumor confirmed the hypothesis of the recurrence of the sarcoidosis. Myocardial perfusion scintigraphy showed typical lesions for myocardial sarcoidosis. There were signs of an old anteroseptal infarction in the resting ECG without evidence of myocardial ischemia during a stress test. Repeated Holter-ECGs were without signs of severe arrhythmias whereas ventricular late potentials were positive. After the combined therapy with steroids, digitalis and an angiotensin-1 receptor antagonist, mediastinal mass and Tei index were reduced and the ejection fraction moved to 56%. Dyspnoea was classified with Grade II according to the NYHA classification. CONCLUSION: Treatment of asymptomatic sarcoidosis is still controversial, whereas the treatment of life-threatening sarcoidosis, eye involvement or severe hypercalcemia is accepted. This case report presents the successful treatment of severe heart failure with prednisone, glycosides and an angiotensin-1 receptor antagonist. With this combined therapy an improvement of subjective and objective parameters was possible.
Adult↗
Potential embolization by atherosclerotic debris dislodged from aortic wall during cardiac catheterization:: histological and clinical findings in 7,621 patients.
Embolic events during cardiac catheterization have been attributed to atherosclerotic aortic debris dislodged by catheter manipulation. We evaluated the frequency and the histologic morphology of atherothrombotic material retrieved during placement of coronary catheters in patients undergoing diagnostic or interventional cardiac procedures. Over a 4-year period, macroscopically visible aortic debris from coronary catheters, if present after advancement to the ascending aorta, was obtained for histologic examination. In 41 of 7,621 patients (0.54%), visible atherothrombotic material was present in the backflow of catheters. Debris occurred most frequently with 8 Fr guiding catheters (98%). Histologic examination showed foam cells, cholesterol crystals, and amorphic lipoid substance as markers of atheromatous material from atherosclerotic plaques in 38/41 patients (93%) with former plaque hemorrhage in 55% of them. In three patients, fresh thrombus material was observed (7%). None of these patients showed in-hospital ischemic complications. Although visible atheromatous material is a rare phenomenon in cardiac catheterization, an increased risk of scraping debris is associated with large-lumen guiding catheters. In order to avoid vascular embolization, the use of smaller guiding catheters and sufficient free backflow of catheters after advancement are recommended.
Adult↗
Nonsurgical retrieval of embolized coronary stents.
Embolization of coronary stents before deployment is a rare but challenging complication of coronary stenting. Different methods for nonsurgical stent retrieval have been suggested. There were 20 cases (0.90%) of intracoronary stent embolization among 2,211 patients who underwent implantation of 4,066 stents. Twelve of 1,147 manually crimped stents (1.04%) and eight of 2,919 premounted stents were lost (0.27%, P < 0.01) during retraction of the delivery system, because the target lesion could not be either reached or crossed. Percutaneous retrieval was successfully carried out in 10 of 14 patients (71%) in whom retrieval was attempted. In 10 patients, stent retrieval was tried with 1.5-mm low-profile angioplasty balloon catheters (success in 7/10) and in seven cases with myocardial biopsy forceps or a gooseneck snare (success in 3/7). Three patients (15%) underwent urgent coronary artery bypass surgery after failed percutaneous retrieval, but their outcomes were fatal. In two patients, stents were compressed against the vessel wall by another stent, without compromising coronary blood flow. In two patients, a stent was lost to the periphery without clinical side effects; treatment was conservative in these cases. Embolization of stents before deployment is a rare but serious complication of coronary stenting, with hazardous potential for the patient. Manual mounting of stents is associated with a significantly higher risk of stent embolization. Stent retrieval from the coronary circulation with low-profile angioplasty balloon catheters is a readily available and technically familiar approach that has a relatively high success rate.
Aged↗
Percutaneous transluminal laser guide wire recanalization of chronic subclavian artery occlusion in symptomatic coronary-subclavian steal syndrome.
Treatment of subclavian artery stenosis by percutaneous balloon angioplasty and adjunctive stent placement was shown to be safe and efficacious, but it may be limited in tight stenoses and long occlusions. We describe the case of a patient who experienced progressive angina pectoris associated with signs of cerebrovertebral insufficiency 9 yr after bypass surgery, including left internal mammary artery (LIMA) grafting to the left anterior descending coronary artery. Angiography showed reversed flow through the LIMA graft into the subclavian artery and a 4-cm occlusion beginning at the origin of the left subclavian artery, representing a rare coronary-subclavian steal syndrome. After a conventional approach failed, recanalization was performed successfully using laser guide wire angioplasty with adjunctive stent placement in a combined radial and femoral approach.
Angioplasty, Balloon, Laser-Assisted↗
[Transluminal exclusion of a subclavian artery aneurysm with stent-graft implantation].
In a 73 year-old male patient with generalized atherosclerosis, known infrarenal abdominal aortic aneurysm, renal artery stenosis, and coronary artery disease, an aneurysm of the proximal left subclavian artery was successfully excluded by implantation of a JOSTENT-Peripheral stent graft. Angiographic follow up after 6 and 12 months showed an excellent outcome with complete exclusion of the aneurysm. Intravascular ultrasound showed no neo-intimal hyperplasia within the stent. A computed tomography revealed complete thrombosis of the aneurysm.
Aged↗
Dose-dependent effects of intracoronary verapamil on systemic and coronary hemodynamics.
Calcium antagonists are used in interventional cardiology to prevent coronary vasoconstriction or to overcome the no-reflow phenomenon. The aim of the current study was to evaluate the dose-dependent effects of intracoronary verapamil on systemic and coronary hemodynamics. In 20 patients scheduled for routine coronary angiography, heart rate, blood pressure, and ECG recordings were recorded continuously and intracoronary flow velocity was obtained by intracoronary Doppler measurements in angiographically normal vessels. The cross-sectional area, measured by quantitative coronary angiography, allowed the calculation of coronary blood flow (CBF) and the coronary vascular resistance index (CVRI). Without premedication, increasing dosages of verapamil (0.01 mg, 0.1 mg, 1.0 mg, and 2.0 mg) were injected into the left coronary artery. Intracoronary verapamil administration led to a decrease in systemic blood pressure only after administration of 1.0 mg or 2.0 mg (change in mean arterial pressure: from 87.6 +/-14.6 mmHg to 80.1 +/- 14.9 mmHg and 78.5 +/- 13.9 mmHg, respectively; both P < 0.05) without a change in heart rate. Epicardial diameters of the left coronary artery increased only at dosages of 1.0 mg and 2.0 mg (from 2.14 +/- 0.4 mm to 2.22 +/- 0.3 mm, P < 0.01), whereas the coronary blood flow velocity increased significantly at the smallest dosage of 0.01 mg (from 19.9 +/- 8.7 cm/s to 33.2 +/- 14.9 cm/s, P < 0.001) and was further enhanced with increasing dosages. CBF increased and CVRI decreased at every dosage of verapamil compared with baseline values. CBF increased also after 0.1 mg (from 13.5 +/- 6.5 mL/min to 19.5 +/- 9.3 mL/min; P < 0.05), reaching a maximal effect after administration of 1.0 mg verapamil (26.3 +/- 16.1 mL/min, P < 0.05). Application of 2.0 mg did not further increase CBF compared with 1.0 mg. Intracoronary application of verapamil leads to a decrease in systemic blood pressure at higher dosages, whereas heart rate remains unchanged at any dosage. The maximal increase in coronary blood flow and decrease in vascular resistance can be reached by administration of 1.0 mg verapamil into the left coronary artery.
Adult↗
Safety of intracoronary Doppler flow measurement.
BACKGROUND: With the introduction of Doppler-tipped guide wires, intracoronary Doppler flow measurement has been increasingly accepted as an additional diagnostic approach in the catheterization laboratory. However, the safety of intracoronary Doppler flow measurement has not been well-investigated. The purpose of our study was to evaluate the safety of intracoronary Doppler flow measurement using the Doppler FloWire (Cardiometrics, Mountain View, Calif). METHODS AND RESULTS: A total of 906 patients were examined by intracoronary Doppler with a 0.014-inch or an 0.018-inch Doppler FloWire. For coronary flow reserve measurement, intracoronary injection of adenosine or papaverine was used. Of the patients studied, 77 were cardiac transplant recipients and 829 were patients who had not received a transplant, of whom 617 had undergone diagnostic coronary procedures and 212 had coronary interventions. In 27 (2.98%) of 906 patients adverse cardiac events were observed. Fifteen (1.66%) of 906 patients had severe transient bradycardia develop (asystole or second- to third-degree atrioventricular block) after intracoronary administration of adenosine, 14 of which occurred in the right coronary artery and 1 in the left anterior descending artery. Nine (0.99%) of 906 patients had coronary spasm during the passage of the Doppler wire (5 in the right coronary artery, 4 in the left anterior descending artery). Two (0.22%) of 906 patients had ventricular fibrillation during the procedure. Hypotension with bradycardia and ventricular extrasystole each occurred in 1 (0.11%) of 906 patients. The incidence of complication was significantly higher in transplant recipients than in patients who underwent either diagnostic or interventional procedures (12.99% vs 2.43% vs 0.94%, P <.001). The Doppler measurements in the right coronary artery were associated with a higher incidence of complications, especially bradycardia, compared with the left anterior descending and the left circumflex arteries (right coronary, 5.87% vs left anterior descending, 1.05% vs left circumflex, 0.17%; P <.001). All complications were cured medically. CONCLUSION: Intracoronary Doppler flow measurement with Doppler wires and intracoronary administration of adenosine is a safe method. However, severe complications such as bradycardia and coronary spasm can occur. Attention should be paid to the examination of the right coronary artery, especially in heart transplant recipients.
Adenosine↗
G protein beta3 subunit 825T allele and enhanced coronary vasoconstriction on alpha(2)-adrenoceptor activation.
Recently, alpha(2)-adrenoceptor activation was shown to play an important role in the vasoconstriction of normal coronary arteries, whereas in the presence of atherosclerosis, the activation of both alpha(1)- and alpha(2)-adrenoceptors reduces coronary blood flow in humans. alpha(2)-Adrenoceptors activate pertussis toxin (PTX)-sensitive G proteins, whereas alpha(1)-adrenoceptors couple to PTX-insensitive G proteins. Thus, the 825T allele of the beta3 subunit of heterotrimeric G proteins, associated with enhanced PTX-sensitive G protein signaling, was expected to determine the alpha(2)-adrenoceptor-, but not the alpha(1)-adrenoceptor-, mediated reduction in coronary blood flow (CBF). Genotyping was performed on 48 individuals. Twelve of the 48 received the alpha(1)-adrenoceptor agonist methoxamine (MTX; 5 mg IC), and 12 received the alpha(2)-adrenoceptor agonist BHT 933 (BHT; 5 mg IC). Twenty-four additional individuals received both MTX and BHT during the same investigational procedure. CBF was calculated on the basis of coronary angiography and intracoronary Doppler flow velocity measurement. Drug-related ischemia was assessed on the basis of ST-segment changes and angina pectoris. In response to BHT, but not to MTX, CBF was reduced to a significantly greater extent in 825T allele carriers (58+/-4%, n=16) than in individuals homozygous for the C825 allele (28+/-4%, n=19, P=0.001). This finding was independent of cholesterol levels, mean arterial blood pressure, and the presence or absence of coronary artery disease. Ischemic events in response to BHT occurred more frequently in 825T allele carriers than in homozygous 825C allele carriers (P=0.01). alpha(2)-Adrenoceptor coronary vasoconstriction is genetically determined and significantly enhanced in GNB3 825T allele carriers.
Adrenergic alpha-Agonists↗
[Therapy of orthostatic hypotension].
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Adrenergic beta-Antagonists↗
[Diagnosis of orthostatic hypotension].
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Humans↗
Can right-sided atrioventricular sequential pacing provide benefit for selected patients with severe congestive heart failure?
This study reports on the methods and results of applying right-sided atrioventricular (AV) pacing in 26 patients with advanced cardiomyopathy. Ten of these patients had ischemic cardiomyopathy. Of the 16 patients with nonischemic cardiomyopathy, 10 were idiopathic and 6 were due to secondary causes. The patients had a mean age of 56 +/- 12 years and a left ventricular ejection fraction of 26 +/- 11%. Two transvenous stimulation electrodes were temporarily placed in the high right atrium and right ventricle, respectively. A Swan Ganz catheter was positioned into the pulmonary artery to determine cardiac output by the thermodilution method and to measure the pressure in the pulmonary artery and right atrium. In addition, aortic pressure was measured through a catheter sheath via the right femoral artery. Systemic and pulmonary vascular resistance were calculated. Stimulation was performed in VVI and DDD pacing modes using different AV intervals (40, 80, 125, 150, 175, 200, and 250 msec). No increase of cardiac output was observed for the overall study cohort (p = 0.51). At VVI pacing, stroke volume significantly decreased from 66 +/- 20 mL to 53 +/- 13 mL (p < 0.01). We distinguished between responders who developed an increase of cardiac output of > 1 L/min (n = 12, 46%) and nonresponders (n = 14, 54%). Etiology of either ischemic or nonischemic cardiomyopathy for responders, as well as conduction disturbances (first-degree AV block, LBBB, RBBB), were equally distributed among both groups. Using an AV delay of 150 and 175 msec, responders to DDD pacing derived a significant increase in cardiac output. An AV delay of 150 msec produced both a significant increase of stroke volume and decrease of systemic vascular resistance. In 46% of patients with dilated cardiomyopathy of either ischemic or nonischemic origin, right-sided AV-sequential pacing brought about an improvement of left ventricular function in terms of enhanced cardiac output. We suggest individual testing in all patients with severe left ventricular dysfunction to find responders.
Adult↗
[Shy-Drager syndrome: a rare cause of orthostatic hypotension].
HISTORY AND ADMISSION FINDINGS: A 71-year-old man was admitted because of treatment-resistant orthostatic hypotension of unknown aetiology. When aged 64 years he developed some impotence and later urinary incontinence and urinary frequency. At 68 years he noted vertigo on physical activity, and a year later he had signs of reversible cerebral ischaemia. At this point the Schellong test demonstrated vasovagal circulatory dysfunction. After his 70th birthday the unsteadiness on walking and standing got worse and he had recurrent syncopes. He was in a wheel-chair when hospitalized and even the unsteady walk he could maintain for only a few seconds. INVESTIGATIONS: Plasma and urinary concentrations of catecholamines were at the lower limit of normal but failed to increase during orthostasis. Hormonal, cardiological and infectious causes of the orthostatic hypotension were excluded. Orthostatic tests after Schellong and with the tilting table showed orthostatic hypotension without increased sympathetic activity but hypertensive blood pressure levels during the recumbent period. Intravenous infusion of norepinephrine produced an excess rise in blood pressure (raised norepinephrine sensitivity). The recurrent urinary infection was shown to be due to a hypotonic bladder detrusor muscle. Neurological examination revealed cerebellar dysfunction, signs of pyramidal tract abnormality and sensory polyneuropathy. A Shy-Drager syndrome was diagnosed on the basis of the history, absent blood pressure rise and lack of catecholamine release during orthostasis with increased epinephrine sensitivity and characteristic neurological signs. TREATMENT AND COURSE: Physiotherapy and elastic stockings with administration of mineralocorticoids as well as of one direct (norfenefrine) and one indirect (amezinium) sympathomimetic drug failed to improve adequately the abnormal orthostatic response. But on additional administration of an alpha 2-receptor antagonist (yohimbine) the patient was able to stand and walk for a few minutes, but the urinary incontinence and the other neurological signs remained treatment-resistant. CONCLUSION: If orthostatic hypotension occurs together with neurological symptoms, a Shy-Drager syndrome should be taken into account.
Adrenergic alpha-Antagonists↗
Skin microcirculation in healthy subjects and patients with arteriosclerosis.
The concept to use the human skin microcirculation as a pharmacological in-vivo test system is old; however, methods developed in the 50s have been abandoned because of side effects and/or use of radioactive substances. We describe a newly developed minimally invasive method that allows in-vivo pharmacology in the human skin microcirculation injecting very low doses of a substance of drug without any systemic effects. The double injection technique (DIT) bears the potential to predict the effects of a drug and/or the vascular reactivity or dysfunction of other less accessible areas of the circulation (e.g. the myocardium). The DIT has been applied for studies in healthy volunteers and patients with atherosclerosis; the focus of interest was endothelial (dys-)function and the effect of exogenous vasoactive drugs. Using endothelin antagonists, we investigated the role of endogenous endothelin under physiological conditions and in atherosclerosis. The NO-synthase inhibitor L-NMMA has been applied to study the L-arginine-NO-pathway and the role of endothelial adrenoceptors. Ongoing studies with the DIT comparing coronary and skin microcirculation may help to develop minimally invasive methods to predict the effects of drugs and vascular function in the heart.
Arteriosclerosis↗