Pharmacokinetics and pharmacodynamics of various glucagon dosages at different blood glucose levels.

AIMS: To evaluate the pharmacokinetics and pharmacodynamics of different doses of glucagon administered subcutaneously (s.c.) at different blood glucose levels. METHODS: This study was an open-label, randomized, three-period, cross-over experiment in 6 patients with type 1 diabetes. During each of the three periods, different blood glucose levels were established in four consecutive steps (8, 6, 4 and 2.8 mmol/l) and glucagon was given at each blood glucose level in doses from 0.11 to 0.44 mg and 0.33, 0.66 and 1 mg at the lowest glucose concentration. RESULTS: Maximum glucagon concentration and area under the curve increased with increasing glucagon dose. Maximum glucagon concentration was reached after 10-20 min. Glucagon raised blood glucose in a dose-dependent manner at different baseline blood glucose levels. The median glucose excursion ranged from 2.6 to 6.2 mmol/l. Time to maximum glucose concentration was dose-dependent for the glucagon doses at 2.8 mmol/l, with median values from 40 to 80 min. CONCLUSIONS: Glucagon administered s.c. produces a stable pharmacokinetic and pharmacodynamic response at lower doses than the usual rescue dose and across a range of hypo- to hyperglycaemic blood glucose levels. This supports the use of small glucagon doses in the artificial pancreas to correct and prevent hypoglycaemia.

Relevance of hemostasis on restenosis in clinically stable patients undergoing elective PTCA.

BACKGROUND: Secondary coronary thrombus formation is considered to be co-factor in the pathogenesis of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Therefore systemic factors indicating a hypercoagulable disease state may be relevant for the process of coronary renarrowing. Even though experimental data suggest that in particular thrombin may be of major relevance for restenosis induced by mechanical injury, only little clinical data has been presented so far. METHODS AND RESULTS: In 60 consecutive patients, who had been clinical stable for at least 2 months, and who underwent elective and primarily successful PTCA, follow-up films were evaluated by means of quantitative coronary angiography in respect to a categorical and a continuous definition of restenosis, luminal narrowing >50% and late luminal loss respectively. Of the chosen laboratory variables prothrombin fragment 1+2 (1.3+/-0.5 vs. 0.9+/-0.4 mmol/l, p<0.001) red blood cell aggregation at low shear stress (13.5+/-2.9 vs. 11.6+/-2.8 units, p<0.05), and plasminogen-activator inhibitor (3.7+/-1.8 vs. 5.3+/-3.2 U/ml p<0.05) differentiated between patients with (n=18) and without restenosis (n=42). Late luminal loss correlated positively with prothrombin fragment 1+2 (r=0.41, p<0.001), plasminogen-activator inhibitor (r= -0.28, p<0.05) and plasmin-alpha2-antiplasmin complex (r=0.39, p<0.01). CONCLUSIONS: A hypercoagulable disease state and in particular thrombin generation characterize a high-risk group prone for restenosis in clinically stable coronary artery disease.

The effects of angiotensin receptor neprilysin inhibition by sacubitril/valsartan on adipose tissue transcriptome and protein expression in obese hypertensive patients.

Increased activation of the renin-angiotensin system is involved in the onset and progression of cardiometabolic diseases, while natriuretic peptides (NP) may exert protective effects. We have recently demonstrated that sacubitril/valsartan (LCZ696), a first-in-class angiotensin receptor neprilysin inhibitor, which blocks the angiotensin II type-1 receptor and augments natriuretic peptide levels, improved peripheral insulin sensitivity in obese hypertensive patients. Here, we investigated the effects of sacubitril/valsartan (400 mg QD) treatment for 8 weeks on the abdominal subcutaneous adipose tissue (AT) phenotype compared to the metabolically neutral comparator amlodipine (10 mg QD) in 70 obese hypertensive patients. Abdominal subcutaneous AT biopsies were collected before and after intervention to determine the AT transcriptome and expression of proteins involved in lipolysis, NP signaling and mitochondrial oxidative metabolism. Both sacubitril/valsartan and amlodipine treatment did not significantly induce AT transcriptional changes in pathways related to lipolysis, NP signaling and oxidative metabolism. Furthermore, protein expression of adipose triglyceride lipase (ATGL) (Ptime*group = 0.195), hormone-sensitive lipase (HSL) (Ptime*group = 0.458), HSL-ser660 phosphorylation (Ptime*group = 0.340), NP receptor-A (NPRA) (Ptime*group = 0.829) and OXPHOS complexes (Ptime*group = 0.964) remained unchanged. In conclusion, sacubitril/valsartan treatment for 8 weeks did not alter the abdominal subcutaneous AT transcriptome and expression of proteins involved in lipolysis, NP signaling and oxidative metabolism in obese hypertensive patients.

Improved Insulin Sensitivity With Angiotensin Receptor Neprilysin Inhibition in Individuals With Obesity and Hypertension.

Natriuretic peptide (NP) deficiency and sustained renin-angiotensin system activation are associated with impaired oxidative metabolism and predispose to type-2 diabetes. We hypothesized that sacubitril/valsartan (LCZ696), which augments NP through neprilysin inhibition while blocking angiotensin II type-1 (AT1 )-receptors, improves insulin sensitivity, lipid mobilization, and oxidation. After 8 weeks of treatment of obese patients with hypertension, sacubitril/valsartan 400 mg q.d., but not amlodipine 10 mg q.d., was associated with a significant increase from baseline in the insulin sensitivity index (hyperinsulinemic-euglycemic clamp), and tended to be higher in patients treated with sacubitril/valsartan compared to amlodipine. Abdominal adipose tissue interstitial glycerol concentrations increased with sacubitril/valsartan, but decreased with amlodipine. Whole-body lipolysis and substrate oxidation did not change with either treatment. Results confirm that sacubitril/valsartan treatment leads to a metabolic benefit in the study population and supports the relevance of neprilysin inhibition along with AT1 -receptor blockade in the regulation of human glucose and lipid metabolism.

Long-term intermittent urokinase therapy in patients with end-stage coronary artery disease and refractory angina pectoris: a randomized dose-response trial.

OBJECTIVES: This dose-response study was designed to test two low dose regimens of urokinase administered over a prolonged time period in patients with chronic refractory angina pectoris with respect to effects on clinical symptoms and objective variables of myocardial ischemia. BACKGROUND: Patients with severe and chronic refractory angina pectoris in end-stage coronary artery disease represent an increasing clinical problem. Favorable therapeutic effects on myocardial ischemia have been reported for long-term application of low dose urokinase. METHODS: Ninety-eight patients with chronic refractory and end-stage coronary artery disease were randomly assigned to two treatment groups: group A (49 patients) received 50,000 IU and group B (49 patients) 500,000 IU of urokinase as an intravenous bolus infection three times a week over a period of 12 weeks. Variables evaluated were number of weekly anginal events, data from ergometric exercise testing with simultaneous electrocardiographic registration, semiquantitative evaluation of Tc-99m 2-methoxy isobutyl isonitrile (MIBI) scans and rheologic variables. RESULTS: After 12 weeks of treatment, anginal symptoms (events/week) were reduced significantly in group B by 70% compared with 24% in group A (p < 0.001). Fibrinogen decreased by 3% in group A and by 33% in group B (p < 0.001). Plasma viscosity and red blood cell aggregation were reduced by 6.4% (p < 0.001) and 19.9% (p < 0.001), respectively, in group B. Objective variables of myocardial ischemia were improved significantly in group B only. No cumulation of coronary ischemic events was observed in group B. CONCLUSIONS: Long-term intermittent urokinase therapy in an applied dose of 3 X 500,000 IU/week represents an effective anti-ischemic and antianginal approach for patients with refractory angina pectoris and end-stage coronary artery disease. Apart from rheologic improvement, antithrombotic properties and plaque regression are likely anti-ischemic mechanisms.

Activation of the fibrinolytic system in patients with coronary artery disease and hyperfibrinogenemia.

Elevated fibrinogen levels as well as an impaired activity of the fibrinolytic system are regarded as important cardiovascular risk factors. To elucidate a potential interrelation between fibrinogen as an indicator of a hypercoagulable state and the endogenous fibrinolytic function hemostatic and rheological as well as lipid parameters were determined in 224 consecutive patients, who underwent elective coronary angiography. In the selected study population of 81 men and 19 women with fibrinogen concentration either > or = 3.5 g/l (n = 70) or < or = 2.5 g/l (n = 30) hyperfibrinogenemia was found to be significantly associated with increased concentrations of plasmin-alpha 2-antiplasmin complex [PAP [median (25.-75. percentile)], 534 (361-680) micrograms/l vs. 289 (243-440) micrograms/l; p < 0.001] and tissue plasminogen activator (t-PA) antigen [9 (6-11) micrograms/l vs 8 (5-9) micrograms/l; p < 0.05] while this association was lost in the subgroup of patients with angiographically normal coronary arteries (n = 26). In addition to these findings fibrinogen was significantly correlated with PAP (r = 0.40, p < 0.001; n = 224) and t-PA antigen (r = 0.2, p < 0.01; n = 224) after adjustment for age, diabetes mellitus, lipid parameters and leucocyte counts. It can be argued that elevated fibrinogen levels in patients with coronary artery disease are concomitant with an activation of the fibrinolytic system.

Acute myocardial infarction with origin of the left circumflex coronary artery from the right (anterior) aortic sinus with retroaortic course to the left atrioventricular sulcus.

The case of a 17-year-old boy is described, who had myocardial infarction during scholastic sports 15 minutes after scrotal trauma. Cardiac catheterization revealed a nonstenosed aberrant left circumflex artery originating from the right (anterior) sinus of Valsalva with retroaortic course, which has to be regarded the infarct vessel according to electrocardiographic, ventriculographic, and scintigraphic findings.

Vineberg graft: flow reserve of bilateral implantation after 27 years.

We report a patient who underwent bilateral internal thoracic artery implantation into the myocardium known as a Vineberg procedure 27 years ago. Coronary angiography and Doppler echocardiography revealed patent grafts with total occlusion of all native coronary arteries. We measured flow velocities at rest and under stress conditions with noninvasive ultrasonic Doppler echocardiography. The flow patterns in both grafts were biphasic as in native coronary arteries. Under stress conditions no increase in flow was detectable as a marker of end-stage coronary artery disease with refractory angina pectoris.

Antithrombotic treatment in stable coronary syndromes: long-term intermittent urokinase therapy in end-stage coronary artery disease and refractory angina pectoris.

Interventions that modify lipid metabolism and blood coagulation have been shown to favourably influence the natural course of coronary artery disease in terms of the primary prevention and treatment of acute cardiovascular events. Various findings suggest that such interventions may also preserve and enhance myocardial perfusion in the chronic stage of the disease. Long-term intermittent urokinase therapy was developed for patients with end-stage coronary artery disease and refractory angina pectoris. A dose of 500,000 IU of urokinase given intravenously as a bolus three times a week for of 12 weeks reduced symptoms by 70% and was accompanied by objective improvements in myocardial perfusion and an increase of ergometric exercise capacity. The possible therapeutic mechanisms of long-term intermittent urokinase therapy-improvement of rheological blood properties mediated by fibrinogen reduction, thrombolysis of non-occlusive subclinical thrombi, and regression of atherosclerotic plaques-are discussed in the context of other antithrombotic approaches.

Restenosis after elective coronary balloon angioplasty in patients with end stage renal disease: a case-control study using quantitative coronary angiography.

OBJECTIVE: To assess the rate of angiographic restenosis in patients with end stage renal disease after elective coronary angioplasty. DESIGN: A retrospective case-control study of 20 patients with end stage renal disease and 20 sex and age matched controls without renal disease, who had undergone primarily successful coronary angioplasty. Control coronary angiography was performed regardless of worsening or renewed incidence of anginal symptoms. MAIN OUTCOME MEASURES: Group comparison of coronary morphology, as evaluated by quantitative coronary angiography, and of cardiovascular risk factors. RESULTS: The rate of angiographic restenosis was 60% in patients with renal disease and 35% in controls. In patients with end stage renal disease the following differences (mean (SD) were found versus controls: raised plasma fibrinogen (483 (101) v 326 (62) mg/dl, p < 0.001); raised plasma triglyceride (269 (163) v 207 (176) mg/dl, p < 0.01); smaller diameter of the coronary reference segment (2.59 (0.87) v 2.90 (0.55) mm, p < 0.10); smaller minimum luminal diameter of the dilated stenosis (0.77 (0.46) v 0.97 (0.27) mm, p < 0.05). Discriminant analysis showed that minimum luminal diameter before angioplasty (r = -0.79) and fibrinogen (r = +0.34) had the highest statistical association with restenosis. CONCLUSIONS: The high rate of angiographic restenosis in patients with end stage renal disease seems to be related to the size of the vessel dilated and to an increased prothrombotic risk, as indicated by higher fibrinogen concentrations.

Morphological differences of the internal thoracic artery in patients with and without coronary artery disease--evaluation by duplex-scanning.

OBJECTIVE: The internal thoracic artery is an established arterial graft for myocardial revascularisation, especially of the left anterior descending artery because of a higher patency rate compared to venous grafts. It has never been investigated, whether there are morphological differences in this vessel between patients with or without coronary artery disease or if they are comparable to morphological changes in the common carotid artery. METHODS: We investigated the internal thoracic artery and the common carotid artery of 24 patients (12 with coronary artery disease, 12 without coronary artery disease) with an ultrasonic system on both sides. The intima-media thickness and the diameter of both vessels were estimated. RESULTS: The intima-media-thickness of the internal thoracic artery was comparable in all patients, independent of the presence of a coronary artery disease (0.51+/-0.11 mm with coronary artery disease, 0.50+/-0.17 mm without coronary artery disease, P>0.05). Compared with this the intima-media-thickness of the common carotid artery was thicker in patients with coronary artery disease (0.84+/-0.13 mm with coronary artery disease, 0.73+/-0.07 mm without coronary artery disease, P< or or =0.014). There was no correlation between the thickness of the internal thoracic artery and the common carotid artery (r=0.018, P>0.05). CONCLUSIONS: It could be demonstrated for the first with non-invasive ultrasound, that the intima-media-complex of the internal thoracic artery is protected of the influence of arteriosclerosis. There are no morphological differences like the intima-media-thickness of the common carotid artery. The proven protective mechanism underlines the widespread use of the internal thoracic artery as a coronary artery bypass graft.

Chronic-intermittent urokinase therapy in patients with end-stage coronary artery disease and refractory angina pectoris--a pilot study.

Patients with coronary artery disease and severe angina pectoris refractory to conventional medical treatment (beta blockers, nitrates, calcium antagonists) and without the option for invasive revascularization procedures represent an increasing clinical problem. For these patients, chronic-intermittent urokinase therapy has been developed. Twenty patients received 500,000 IU urokinase as intravenous bolus injection 3 times a week over a period of 12 weeks. The average reduction in anginal symptoms in 19 patients was 74%, from 23.5 +/- 10.8 to 5.2 +/- 4.8 events/week (p < 0.001); 1 patient was excluded from further treatment because of an increase of > 66% in anginal events. Fibrinogen decreased by 34% from 370 +/- 57 to 244 +/- 44 mg/dl (p < 0.001), the rheological parameters plasma viscosity by 6.1% from 1.39 +/- 0.04 to 1.31 +/- 0.03 mPas (< 0.001), and red blood cell aggregation by 18% from 13.9 +/- 2.4 to 11.2 +/- 2.2 (p < 0.001). Exercise tolerance increased by 51%. Average ST-segment depression decreased from 0.16 +/- 0.10 to 0.12 +/- 0.09 (p < 0.01). After 12 weeks of follow-up, angina pectoris and fibrinogen levels were still significantly reduced compared with baseline values. Chronic-intermittent urokinase therapy represents an effective anti-ischemic and antianginal approach in patients with refractory angina pectoris and end-stage coronary artery disease. Improvement of rheological blood properties and thrombolytic effects are likely therapeutic mechanisms.

[Cyanosis and dyspnoea in orthostasis]. / Zyanose und Luftnot in Orthostase.

HISTORY AND CLINICAL FINDINGS: A 69-year-old female patient was admitted to a hospital for severe dyspnoea. It was conspicuous that shortness of breath and cyanosis only occurred in upright and completely disappeared in the supine position. This finding was objectified by pulse oximetry which demonstrated a decrease of arterial oyxgen saturation from 96 % in the supine to 86 % in the upright position. INVESTIGATIONS: After exclusion of other diseases the diagnosis of platypnoe- orthodeoxia syndrome as a result of a patent foramen ovale (PFO) was established. TREATMENT AND COURSE: Cardiac catheterization in the upright and the supine position documented a high-grade right-to-left shunt of 31 % proportionally to systemic circulatory volume in the upright position with subsequent critical reduction of pulmonary perfusion to 1.4 l/min/m (2) (reference value > 2.2 l/min/m (2)) as the cause of dyspnoea. Catheter-based occlusion of the PFO was chosen as causal treatment modality. After that arterial oxygen saturation remained constant at 95 % in the supine and upright position and symptoms improved. CONCLUSIONS: Platypnoe-othodeoxia syndrome is a very rare syndrome but it can be substantiated by pathognomonic case history, clinical examination and simple machine-aided examinations. With a causative PFO a causal and save therapy is available.

Successful weaning from milrinone of a patient with severe congestive heart failure using carvedilol.

Congestive heart failure is a major and growing health care concern worldwide, and mortality in patients with severe heart failure is high. Few options are available to patients with New York Heart Association class IV heart failure refractory to oral medical therapy. Over the last 15-20 years milrinone, a phosphodiesterase-III inhibitor, has been used occasionally to treat patients with acute heart failure and as a bridge to heart transplantation and, more recently, has been used intermittently or continuously on an outpatient basis. We report a patient with severe, chronic congestive heart failure, whom we treated successfully with continuous milrinone infusions as an outpatient. We were able to wean him of the milrinone after successful up-titration of carvedilol. Nine months after discontinuation of milrinone the patient remains stable in New York Heart Association class I on high dose carvedilol. Research is required to validate the possibility that patients with severe heart failure may be successfully weaned from milrinone using carvedilol and achieve significant improvement of their functional status and quality of life. This may prove to be an effective strategy for the treatment of selected patients with severe, chronic congestive heart failure. (c)2001 by CHF, Inc.

[Internal thoracic artery bypass--basic principles of Doppler ultrasound for pre- and postoperative diagnosis]. / Arteria thoracica interna-Bypass--Grundlagen der Dopplersonographie für die prä- und postoperative Diagnostik.

During the last 25 years the internal thoracic artery has become a well established conduit for coronary revascularization. Next to angiography, duplex-sonography is increasingly used as a non-invasive imaging procedure for the evaluation of this graft vessel. Preoperative investigation in 117 patients has yielded a high level of agreement between angiography and duplex-sonography. While the preoperative flow-pattern is dominated by systolic flow as it is typical for vessels supplying skeletal muscle, the postoperative findings show an adaptation to the coronary vascular bed as the diastolic flow increases. These non-invasive measurements are well matched with invasive intravascular recordings. Coronary angiography and duplex-sonography of the internal thoracic artery yielded comparable findings in respect to the procedural result. Considering the increasing use of the internal thoracic artery in coronary artery bypass surgery, this non-invasive method should gain increasing relevance.

In vitro bleeding test with PFA-100-aspects of controlling individual acetylsalicylic acid induced platelet inhibition in patients with cardiovascular disease.

OBJECTIVES: This study investigated the usefulness and practicability of a platelet function analyzer (PFA-100(TM), DADE-Behring, Germany) to determine individual platelet inhibition in patients treated with acetylsalicylic acid (ASA). BACKGROUND: Patients with coronary artery disease (CAD) routinely and during angioplasty (PTCA) receive standard doses of ASA to avoid acute coronary syndromes and abrupt vessel closures without information of the individual efficacy of platelet inhibition. METHODS: With the PFA-100(TM) a standardized bleeding time is measured. Whole-blood anticoagulated with 3.2% sodium citrate is aspirated through a capillary ( solidus in circle 200 microm) and through an aperture ( solidus in circle 147 microm). The time until occlusion of the aperture (closure time, CT) by a stable platelet plug induced by shear stress, collagen and epinephrine (COLL/EPI-CT) or shear stress, collagen and adenosine 5'-diphosphate (COLL/ADP-CT) is determined. To examine the usefulness of the PFA-100(TM) as a rapid bedside test and the individual effect of ASA, closure time was measured in healthy individuals (n=17), in patients with stable CAD (n=19) and in patients undergoing PTCA (n=8). RESULTS: Patients with stable CAD and regular medication with 100 mg ASA per day for at least 3 month showed shorter COLL/ADP-CT in comparison to healthy individuals who took only one single dose of 100 mg ASA. Of the patients with CAD 63% had a COLL/EPI-CT within normal range suggesting a low or no response to ASA. Also only 50% of the patients undergoing PTCA reached the expected COLL/EPI-CT>300 s after an additive single dose of 500 mg ASA intravenously. Neither heparin, phenprocoumon, sex nor different blood sampling methods seem to influence the measurements relevantly. CONCLUSIONS: This pilot study indicates that with the PFA-100(TM) test device a simple and quick measurement of an in vitro bleeding time is possible. It is able to detect an increase in the bleeding time after a single dose of ASA 100 mg in healthy subjects, reflecting a sensitive detection of ASA induced changes in platelet inhibition respective activation. Differences in the individual response to ASA could be observed in healthy subjects, patients with stable CAD and patients undergoing PTCA. Further studies should validate the PFA-100(TM) with standard methods to determine ASA response in patients with cardiovascular disease and investigate implications for treatment and outcome in this patient group.

Non-invasive assessment of graft patency using transcutaneous Doppler echocardiography for the validation of functional improvement after PTCA of the LAD via internal thoracic artery graft.

Percutaneous transluminal coronary angioplasty (PTCA) of a native coronary artery via internal thoracic artery (ITA) graft after bypass surgery is a relatively rare procedure. Our current study evaluates the flow velocity patterns of the graft before and after PTCA. After intervention the mean diastolic flow velocity increased under rest and stress conditions. In addition, the graft patency was proved not before control angiography after 6 months. It could be verified that the measurement of flow velocity patterns under rest and stress conditions is a useful non-invasive procedure for monitoring long-term patency and PTCA-results of this vessel.

[Conservative therapeutic approaches in terminal coronary heart disease. Chronic intermittent urokinase therapy]. / Konservative Therapieansätze bei terminaler koronarer Herzkrankheit. Chronisch-intermittierende Urokinasetherapie.

Despite progress in the invasive revascularization procedures and even though conventional antianginal treatment has improved the quality of life in patients with symptomatic coronary artery disease considerably, an increasing number of patients suffers from end-stage coronary artery disease and refractory angina pectoris. For these refractory patients long-term intermittent urokinase therapy was developed as an antithrombotic intervention, which is based on its capacity to enhance thrombolysis and blood rheology, and may possibly lead to plaque regression. The coronary syndrome of refractory angina pectoris is characterized by a mismatch of severe coronary insufficiency and a relatively large amount of viable myocardium as indicated by an only moderately impaired left ventricular function. Prior to initiation of long-term intermittent urokinase therapy all potential measures to improve myocardial perfusion have to be considered in each patient. These supportive measures include rigorous reduction of LDL-cholesterol, which has proven antiischemic properties due to an improved endothelial function of epicardial conductance vessels possibly resulting in an antianginal effect. Apart from the proven antiischemic properties of long-term intermittent urokinase therapy in patients with refractory angina pectoris, objective signs of ischemic myocardial heart failure improve. Follow-up studies demonstrated a significant increase of left ventricular ejection fraction as evaluated with multi-gated blood pool analysis. Furthermore, left ventricular diastolic function normalized after a treatment period of 12 weeks. As the clinical effects last well beyond the actual treatment period and as they are accompanied by a remarkable increase in the quality of life, a complex approach as this one is justified in this highly symptomatic patient group.

[Rate of restenosis after PTCA in patients with terminal renal failure. A quantitative coronary angiography study]. / Restenoserate nach PTCA bei Patienten mit terminaler Niereninsuffizienz. Eine quantitativ-koronarangiographische Untersuchung.

Patients with end-stage renal disease (ESRD) have a high incidence of coronary artery disease. In 30-60% of these patients coronary artery disease can be demonstrated by coronary angiography often prompting myocardial revascularization. Previous studies on PTCA in patients with ESRD have suggested a high rate of procedural complications and restenosis. We studied the rate of restenosis after PTCA in 23 patients with chronic renal failure (17 males, 6 females, age: 52.5 +/- 18.3 years). After primarily successful PTCA all patients were restudied angiographically within 6-12 months. Using quantitative coronary angiography 13 patients (56%) demonstrated restenosis (stenosis > 50% luminal diameter). In 11 of these patients further revascularization therapy was indicated (6 x PTCA, 5 x CABG). Before follow-up angiography 12 patients demonstrated recurrence of angina pectoris, the sensitivity of clinical symptoms for angiographic restenosis was 69%. High concentrations of triglycerides (265 +/- 160 mg/dl), total cholesterol (258 +/- 53 mg/dl) with low HDL-levels (34 +/- 14 mg/dl) as well as elevated plasma levels of fibrinogen (481 +/- 114 mg/dl) were measured before PTCA. The mechanisms contributing to the high rate of coronary restenosis in patients with ESRD remain unclear, influence of lipid abnormalities, hemostatic factors and fibrinolytic state as well as primarily uremic factors have to be discussed. Prospective interventional studies are needed to address the relevance of PTCA for myocardial revascularization in this patient group.

[PTCA of the LAD via the internal thoracic artery graft with Doppler ultrasonic control of the results: a case report and review of the literature]. / RIVA-PTCA via Arteria-thoracica-interna-Bypass mit dopplersonographischer Erfolgskontrolle--Eine Kasuistik mit Literaturübersicht.

The report presents a transluminal angioplasty (PTCA) of a severe stenosis of the left anterior descending artery (LAD) behind the anastomosis; the internal thoracic artery (ITA) graft was used as a conduit. Before and after the PTCA the changing of velocity flow patterns under rest and stress conditions with a handgrip-maneuver were measured with a noninvasive transthoracic ultrasound Doppler system. The mean diastolic velocity, which represent coronary perfusion through the ITA graft, increased after successful PTCA at rest and under stress conditions. An additional increasing of the mean diastolic velocity at rest and under stress conditions was seen after six months before the catheterization proposing no signs of restenosis. For this reason the vessel could be classified prospectively patient. This could be confirmed during coronary angiography. We also present a review of the published reports concerning PTCA of ITA grafts and PTCA of the native vessel using the ITA as a conduit. In this review 286 cardiac interventions on 273 patients with a primary rate of success of 87% could be counted, the documented rate of restenosis was 30%, and the rate of complication was approximately 1%. The PTCA in ITA grafts or of the native vessel via ITA grafts, respectively, represent an alternative to reoperation. The ultrasound-duplex measurements are gaining an increasing significance for the noninvasive patency rate and post-interventional monitoring of the long-term PTCA result. With the augmentation of the ITA as a coronary bypass and expected increase of post-operative interventions, a noninvasive tool is necessary.