[Therapeutic plasma exchange for the treatment of hypertriglyceridemia-induced pancreatitis : A case report]. / Plasmapherese zur Behandlung einer hypertriglyzeridämiebedingten Pankreatitis : Ein Fallbericht.

A rare but serious form of pancreatitis is caused by severe hypertriglyceridemia. It accounts for up to 10 % of all acute pancreatitis episodes. Despite a pathophysiology that differs distinctly from other forms of pancreatitis, there are no accepted guidelines for the treatment of hypertriglyceridemia-induced pancreatitis. We report a morbidly obese (BMI 45 kg/m²) 36-year-old Caucasian woman with a history of schizophrenic psychosis who was transferred to our tertiary care hospital for further diagnosis and treatment of increasing abdominal pain and hypertryglyceridemia of 2757 mg/dl. Due to rapid clinical deterioration, requiring invasive mechanical ventilation we performed therapeutic plasma exchange (TPE). About 1.5 times of the patient's calculated plasma volume was exchanged using fresh frozen plasma as substitution fluid. After a single TPE the triglyceride levels decreased by 86 % to 387 mg/dl. Concomitantly C­reactive protein decreased from 303 to 179 mg/dl. Despite the paucity of data, TPE may be a beneficial means to lower triglycerides in patients with hypertriglyceridemia-induced pancreatitis, due to the rapid removal of the causative agent leading to pancreatic injury.

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.

Angiographic progression of coronary artery disease in patients with end-stage renal disease.

BACKGROUND: Patients with end-stage renal disease have an increased risk of developing coronary artery disease (CAD). The cardiovascular mortality of dialysis patients is 10-15 times higher compared with the general population. The aim of our study was to evaluate the morphological progression of coronary arteriosclerosis in this cardiovascular high-risk group by visual assessment and quantitative coronary angiography. Methods and results. In 26 patients with chronic renal failure (age, 47+/-11 years; 15 male; duration of dialysis, 23+/-25 months) the severity of CAD and degree of coronary stenoses were assessed in two coronary angiograms after a mean follow-up interval of 30+/-15 months (12-60). Baseline angiography revealed CAD in 13/22 patients (59%). The second angiography was performed as screening procedure prior to renal transplantation (n=20) and/or as follow-up angiography after coronary angioplasty (n=10). Visual assessment showed a progression defined by the development of haemodynamically relevant stenosis of >50% luminal diameter in 13 patients. Quantitative angiographic evaluation was performed in a total of 45 segments showing >25% narrowing at the second angiogram. A progression (>15% luminal reduction) was found in 17 of 45 segments, a new lesion (initial luminal diameter <20%) was detected in nine segments, resulting in progression or new lesion in 16 patients (62%). Patients with or without progression did not differ in age, duration of dialysis treatment, number of cardiovascular risk factors, or serum total cholesterol and fibrinogen levels. After percutaneous transluminal coronary angioplasty (PTCA) a restenosis was seen in seven of 16 primarily successfully dilated segments. After the second angiography, myocardial revascularization was performed in eight patients (1 PTCA, 7 coronary artery bypass graft). CONCLUSIONS: Patients with end-stage renal disease have a high prevalence of CAD. In line with the clinical course, CAD patients on maintenance dialysis undergo rapid angiographic progression of CAD, which results in a high rate of subsequent myocardial revascularizations.

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.

Myocardial revascularization in patients with end-stage renal disease: comparison of percutaneous transluminal coronary angioplasty and coronary artery bypass grafting.

BACKGROUND: Ischemic heart disease is the major cause of death in patients with end-stage renal disease. The high prevalence of coronary artery disease results in a rising number of dialysis patients requiring myocardial revascularisation. OBJECTIVE: The objective of this study was to compare the outcomes of recurrent angina, myocardial infarction, rate of reinterventions and cardiovascular death following percutaneous coronary angioplasty (PTCA) or coronary artery bypass grafting (CABG) in patients with end-stage renal disease. PATIENTS AND METHODS: In a retrospective investigation 40 patients with chronic renal failure undergoing primarily PTCA and 65 patients undergoing CABG were included. Both groups were comparable for gender, duration on dialysis and the number of cardiovascular risk factors per patient. Patients undergoing PTCA were younger (53 +/- 12 years vs. 57 + 8 years; p < 0.05) and more often diabetics (30% vs. 14%; p < 0.05). RESULTS: Most patients in both groups had a multi-vessel disease (95% in the CABG group vs. 74% in the PTCA group), in the CABG group there were significantly more patients with a triple-vessel disease (62% with vs. 40% in the PTCA group; p < 0.01), PTCA was primarily successful in 95% of the patients while complete revascularization was achieved in 88% of patients undergoing CABG. The perioperative mortality after CABG was 4.8% as compared to none after interventional revascularisation. The cumulative freedom of angina after 6, 12 and 24 months after intervention was significantly lower after PTCA (54%, 40%, 29%) than after bypass grafting (97%, 94%, 90%, p < 0.001). The frequency of reinterventions following PTCA was significantly higher compared to patients following CABG (p < 0.001). After PTCA 15 patients needed further revascularisations, 8 of them underwent CABG, whereas after CABG only two patients required additional myocardial revascularisation. There was no significant difference in the overall mortality between both groups; the survival rate after 12 and 24 months was 95% and 82% after PTCA and 93% and 86% after CABG, respectively. CONDITION: Although patients receiving CABG had a more severe coronary artery disease the overall mortality was comparable and clinical and functional outcome was improved compared to patients after coronary angioplasty.

[Clinical course and complications of meningococcal septicemia]. / Klinischer Verlauf und Komplikationen der Meningokokkensepsis.

BACKGROUND: Meningococcal septicemia is still associated with high mortality with most deaths occurring within the first 24 hours. CASE REPORT: We report on 3 patients with severe meningiococcemia. All patients had an aprupt onset of clinical illness with fever and unspecific prodomi like arthralgias, myalgias and abdominal pain. On admission all patients had severe prostration, hypotension and tachycardia. Two patients presented purpuric rash and petechiae, meningitis was found in only 1 patient. Gram-negative diplococci were demonstrated in spinal fluid primarily in 2 patients, in all patients meningococcae could be cultured in serial blood specimens. Because of severe cardiorespiratory distress all patients required mechanical ventilation and catecholamine support within 24 hours of diagnosis. Complications of meningococcemia demonstrated by these patients were coagulopathy, meningitis, myocarditis with alterations of echocardiographic and ECG records and elevations of CK levels and surgical relevant peripheral gangrene. Antibiotic therapy was initiated with penicillin on the day of admission, which resulted in stabilisation and recuperation in all patients. CONCLUSIONS: In patients with aprupt onset of acute illness, which include fever and sudden petechial rash, severe meningococcal septicemia has to be taken in consideration without clinical signs of meningitis. The prompt diagnosis, the use of parenteral antiobiotics in suspected meningococcal disease as well as the management of meningococcemia and its complications in intensive care units is crucial for the prognosis of the individual patient.

[Large pseudoaneurysm of the left ventricle after posterolateral wall infarct]. / Grosses Pseudoaneurysma des linken Ventrikels nach Posterolateralwandinfarkt.

Pseudoaneurysms of the left ventricle are rare complications after acute myocardial infarction. We report on a 69 year old patient with a large false aneurysm located in the posterolateral ventricular wall. It became clinically apparent during an episode of severe left heart failure. Echocardiography and left ventriculography allowed an accurate determination of localization and dimension of the pseudoaneurysm; coronary angiography revealed a proximal occlusion of the left circumflex coronary artery. Because of the high risk of rupture, a rapid surgical repair of the false aneurysm was indicated.

[Angina pectoris in "coronary steal syndrome" caused by a coronary fistula in the left ventricle]. / Angina pectoris bei koronarem Steal-Syndrom aufgrund einer Koronarfistel in den linken Ventrikel.

HISTORY AND CLINICAL FINDINGS: A 55-year-old female patient reported left-sided chest pain at rest as well as during exercise, which recurred during the last three years before admission. Cardiovascular risk factors included hypercholesterolemia and smoking. The physical examination of the patient was unremarkable. INVESTIGATIONS: The ECG at rest showed T-wave inversions in leads I, aVL, V3-V6 and ergometric exercise testing resulted in angina pectoris and descending ST-segments in leads V3-V6. Stress thallium 201 scintigraphy demonstrated a reversible perfusion deficit of the the anterior wall at peak exercise. The left ventricular angiogram and echocardiogram revealed normal end-diastolic dimensions and regular systolic contractions without signs of left ventricular hypertrophy. Selective coronary arteriography excluded hemodynamically relevant stenosis of the coronary arteries. A coronary artery fistula originating from a large, ectatic first diagonal branch with drainage into the left ventricle was observed. TREATMENT AND COURSE: Because the patient rejected interventional therapy she was treated conservatively and follow-up investigations 3 and 4 years after arteriography revealed unchanged clinical symptomatology. CONCLUSION: In this case a "coronary steal" phenomenon caused by the coronary fistula induced myocardial ischemia. Therefore if present congenital coronary anomalies have to be considered in patients with chest pain and normal coronary angiogram.

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.

[Formation, therapy and prevention of false aneurysm of the femoral artery following diagnostic and interventional heart catheterization]. / Entstehung, Therapie und Prävention des Aneurysma spurium der Arteria femoralis nach diagnostischen und interventionellen Herzkatheteruntersuchungen.

OBJECTIVE: As pseudoaneurysm of the femoral artery after catheter introduction is a frequent complication, its causes and therapeutic options were investigated in a large patient collective. PATIENTS AND METHODS: In a prospective study with colour-Doppler duplex sonography of 6928 patients after diagnostic and of 3764 after interventional cardiac catheterisation, pseudoaneurysms were diagnosed in 80 patients (0.75%), 46 after diagnostic (0.66%) and 34 after interventional (0.9%) catheterisation. RESULTS: The incidence was higher in women than men (1.33% vs 0.58%; P < 0.05). Anticoagulation after sheath removal was the leading risk factor (n = 55, 68.8%), especially after interventional coronary intervention 85.3 vs 56.5%, P < 0.05). Local compression under duplex sonography monitoring was undertaken in 69 patients (86.3%), achieving aneurysmal obliteration in 53 (76.8%). Spontaneous thrombosis occurred in 15 of the remaining 27 patients, and surgical closure became necessary in 12. CONCLUSIONS: These data indicate a risk profile for the occurrence of pseudoaneurysm after cardiac catheterisation which can be dealt with by preventive measures. Local compression under duplex sonographic monitoring was the treatment of choice with a high success rate and low incidence of complications.

Relevance of conventional cardiovascular risk factors for the prediction of coronary artery disease in diabetic patients on renal replacement therapy.

BACKGROUND: Diabetic patients undergoing renal replacement therapy have a high cardiovascular mortality. As the rate of patients with diabetic nephropathy rises, adequate risk stratification subsequent to renal transplantation is warranted. It was the aim of our study to elucidate whether conventional risk factors are valid predictors of coronary artery disease in this group of patients with chronic renal failure subsequent to transplantation. METHODS AND RESULTS: Between 1989 and 1993, 105 consecutive diabetic patients (70 men, 35 women, 77 type I and 28 type II diabetics, mean age 43 +/- 12 years) were examined during the first six months of dialysis treatment. Coronary angiography was performed in all patients regardless of clinical symptoms of coronary artery disease (CAD). In 38 patients (36%) CAD was documented (single-vessel disease: 17 patients, double-vessel disease: 6 patients, triple-vessel disease: 15 patients). Manifestations of coronary atherosclerosis were seen in 49 patients (47%). Angina pectoris was present in 9 out of 38 patients (24%), the sensitivity to detect CAD was 43% and 52% for ST-segment depression assessed at rest. Risk factors for atherosclerosis like hypertension, smoking, cholesterol (total cholesterol, HDL-,LDL-cholesterol), triglycerides as well as concentrations of lipoprotein (a) and fibrinogen were not significantly different in patients with or without coronary artery disease. Atherosclerotic manifestations of cerebral and peripheral arteries as well as manifestations of diabetic microangiopathy like retinopathy did not correlate with the prevalence of CAD. In 11 out of 38 patients (29%) cardiac interventions (3 x CA BG, 8 x PTCA) were performed. All of them were defined as transplantable after myocardial revascularisation. CONCLUSIONS: Clinical symptoms as well as the cardiovascular risk profile are not valid predictors of CAD in diabetic patients with chronic renal failure. Therefore coronary angiography should be performed in all diabetic patients prior to renal transplantation.

[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.

[Significance of coronary thrombosis for chronic myocardial ischemia]. / Die Bedeutung der Koronarthrombose für die chronische Myokardischämie.

Apart from the relevance of disorders of lipid metabolism for the clinical and morphological progression of coronary artery disease, coronary thrombosis has received increasing attention in recent years. It is undoubtedly the decisive factor in the pathogenesis of acute coronary syndromes, which is underlined by the therapeutic success of various antithrombotic interventions. Furthermore coronary thrombosis is regarded to be a key factor for morphological disease progression also in stable coronary syndromes, which eventually may lead to critical limitation of myocardial perfusion. This is caused by the formation of subclinical coronary thrombi, which either undergo endogenous lysis or become morphologically fixed as they are incorporated into the plaque. Besides local factors, systemic disturbances of hemostasis and endogenous thrombolysis are of relevance. The concept of thrombotic progression of coronary thrombosis is supported by data on the reduction of morphological disease progression or antiischemic effectiveness of anti-thrombotic interventions like aspirin, low-molecular weight heparin and low-dose intermittent urokinase therapy. Percutaneous transluminal coronary angioplasty results in deep mechanical injury of the vessel wall, which is accompanied by secondary coronary thrombosis in the majority of the cases, not necessarily leading to abrupt vessel closure. Particularly, dilatation of primary thrombus as it has been described as the substrate of the culprit lesion in unstable coronary syndromes, promotes release of thrombin and activation of platelets, which in turn furthers the proliferative processes in the pathogenesis of restenosis. Even though data on the reduction of the rate of restenosis by the use of platelet aggregation inhibitors like aspirin, ticlopidin and dipyridamole have not consistently supported this concept, the EPIC. Study has shown that even in patients with stable angina pectoris clinical restenosis rate may be reduced by a platelet-IIb/IIIa-antagonist.

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.