Lipoprotein (a) is not a risk factor for restenosis after percutaneous transluminal coronary angioplasty.
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Biomedical subjects
Publications and source records attributed to W Klein.
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Increases of triglycerides and total cholesterol have been reported during treatment with antihypertensive drugs, most notably with beta blockers and diuretics. ACE inhibitors, on the other hand, are not known for having a negative effect on lipid profile. To evaluate the effects of a fixed combination of captopril and hydrochlorothiazide on lipid metabolism, blood pressure, and quality of life, we performed an open prospective study. A total of 2,154 patients with or without hypercholesterolemia, but not receiving lipid lowering drugs, were enrolled. Of the 1891 evaluable patients at baseline, 34.1% had a moderate risk with total cholesterol between 5.2 and 6.5 mmol/l (mean 5.8 mmol/l) and 41.3% had a high coronary heart disease (CHD) risk with total cholesterol higher than 6.5 mmol/l (mean 7.3 mmol/l). After six months of treatment, the median cholesterol level in the moderate risk group decreased from 5.8 to 5.4 mmol/l (p less than 0.0003) and in the high risk group from 7.3 to 6.3 mmol/l (p less than 0.0001). Triglycerides also decreased, whereas high density lipoprotein (HDL) increased in both risk groups. Systolic and diastolic blood pressure fell as expected and quality of life improved. The fixed combination was well tolerated. We observed a significant improvement of lipid profile in patients with mild to moderate hypertension while undergoing treatment with the fixed combination of captopril and hydrochlorothiazide. We suggest that captopril may balance the negative effects of hydrochlorothiazide on lipid metabolism in patients with hypertension and concomitant hyperlipidemia.
Microalbuminuria is known to be associated with an increased risk for cardiovascular disease. It is detectable in acute myocardial infarction and could therefore also be a risk factor for reocclusion after percutaneous transluminal coronary angioplasty (PTCA). In our study follow-up coronary angiography was performed in 50 consecutive patients with a mean age of 56 years (38-70) on average 14 months after successful PTCA. Restenosis was defined as a decrease in diameter of 25% or more of the original result and one of at least 50% in vessel diameter. In the restenosis group there were 23 patients, and 27 showed no restenosis. The family history and anamnestic risk profile, results of the initially performed coronary angiography, and laboratory risk factors were comparable in the two groups. Median microalbumin was 11.2 mg/g creatinine in those with restenosis and 9.8 mg/g creatinine in those without. Using a cut-off of 10.0 mg/g creatinine, 12 of 23 patients with restenosis (52%) and 10 of 27 patients without (37%) were positive for microalbuminuria (NS). The incidence of microalbuminuria was higher in both groups compared to historical controls. Thus, in the restenosis group the incidence of microalbuminuria tended to be higher than in the nonrestenosis group, but since this difference did not reach statistical significance, it cannot be used to predict the risk of reocclusion after PTCA.
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Sixty anterior cruciate Dacron prosthetic ligaments were placed arthroscopically in 57 patients from 1983 to 1985. Fifty-five of the 57 patients were followed for an average of 4.4 years. The complication rate at 13 months was 29%; at 4.4 years, 43%. There were 34 reoperations. In 16 knees (28%) the prosthesis had to be removed due to abrasion and arthritis with rupture of the prosthesis. Thirteen knees had chronic synovitis and one knee had bacterial infection, all of which were managed with arthroscopic debridement. Four knees required removal of the extraarticular staple. Clinical testing in 42 knees with the Dacron prosthesis still in place showed the Lysholm score improved from a preoperative score of 43 points to a score of 82 points after 5 years. Of the knees, 58% had a pivot shift of 2(+)-3+: a trace pivot shift in 30%; a negative pivot shift in only 12%. The KT-1000 arthrometer verified those pivot shifts. The results of this study are discouraging. The procedure was complicated by a high reoperation rate, usually secondary to arthritis. The impression was that although stability of the knee was improved by use of an artificial anterior cruciate ligament, the end result of the therapeutic procedure was the development of an iatrogenic model of degenerative arthritis in the human knee.
In a randomized, double-blind, crossover study in 10 healthy volunteers the hemodynamic effects, drug plasma concentrations, and thyroid hormone profiles were compared after oral administration for 1 week of 40 mg t.i.d. racemic (R,S)-propranolol versus 20 mg t.i.d. optically pure (S)-propranolol. During exercise, both substances decreased heart rate (-14%, p less than 0.01), as well as the overall rate pressure product (-19%, p less than 0.01) to the same extent, indicating similar beta-blocking effects. After oral application of (R,S)-propranolol the maximal plasma concentration (Cmax) and the area under the plasma concentration-time curve (AUC) of (S)-propranolol were higher than those of (R)-propranolol (eudismic ratios (S)- over (R)-propranolol Cmax, 1.36 [p less than 0.01] and AUC, 1.42 [p less than 0.01]) despite dose-equivalence of both enantiomers in the administered racemic (R,S)-propranolol preparation indicating different pharmacokinetic properties. Mean values of Cmax and the AUC of (S)-propranolol did not differ significantly after 1 week of oral administration of 40 mg (R,S)-propranolol and 20 mg (S)-propranolol t.i.d., respectively. The ratio of triiodothyronine to thyroxine was decreased by (R,S)-propranolol (-25%, p less than 0.01) but not by (S)-propranolol, suggesting that only the (R)-enantiomer inhibits the conversion of thyroxine to triiodothyronine. Thus, half-dosed optically pure (S)-propranolol is an equally effective beta-adrenergic receptor antagonist compared with currently used racemic (R,S)-propranolol. By contrast, the conversion of thyroxine to triiodothyronine is inhibited by (R)-propranolol only.(ABSTRACT TRUNCATED AT 250 WORDS)
Fibrinogen has turned out to be an independent risk factor for coronary heart disease (CHD). It is not known whether or not this parameter could be a prognostic factor for restenosis following percutaneous transluminal coronary angioplasty (PTCA), which represents the main problem limiting the long-term efficacy of this procedure. Therefore, we studied fibrinogen concentrations in a series of 50 males (mean age: 55, range: 38-70 years) with CHD and successful PTCA. Follow-up coronary angiography was performed 12 months following PTCA. Twenty-two patients had restenosis, and 28 patients were without restenosis. Both groups did not differ significantly in medical history (smoking habits, hypertension, positive family history for cardiovascular diseases), in routine lipid profile (total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, apolipoproteins A1 and B). Fibrinogen values were 405 +/- 128 mg/dl (range: 202-725) in patients with restenosis and 352 +/- 94 mg/dl (range: 187-568) in patients without restenosis (not significant). Elevated fibrinogen levels of more than 400 mg/dl were found in 8 patients in each group. Although fibrinogen is a proven marker for CHD in men, fibrinogen is not a risk factor for restenosis following PTCA.
The prognosis of heart failure patients is poor and as many as half of the deaths are sudden and thereby presumably attributable to arrhythmias. In the present study the effect of traditional therapy of mild heart failure with digoxin on arrhythmias was compared with the effect of xamoterol, a cardioselective beta 1 partial agonist, which has in addition beta-blocking properties at higher levels of sympathetic tone. Fifteen patients (NYHA class II-III) were included in the study. After a two-week baseline period they were randomized to digoxin or xamoterol for four weeks followed by a two-week washout and another four weeks of crossover therapy. Heart rate, blood pressure, and the number of complex ventricular premature beats remained essentially unchanged with digoxin. With xamoterol heart rate increased from 86 to 93 (ns) but was significantly higher during the night in comparison with digoxin. The number of ventricular premature beats decreased from 186 +/- 317 to 110 +/- 137 and increased to 130 +/- 175 after treatment. The number of runs decreased from 11 +/- 35 to 2.7 +/- 5 and increased to 5.6 +/- 9 after therapy. In conclusion, no significant effect of digoxin or xamoterol on ventricular arrhythmias was found. However, xamoterol showed a tendency to reduce simple and complex ventricular arrhythmias in patients with mild to moderate heart failure.
For several reasons, increasing numbers of patients with hypertension are treated with angiotensin-converting enzyme inhibitors and calcium channel blockers. In a twenty-four week, double-blind, randomized, parallel study, the antihypertensive effect of lisinopril (20 to 80 mg qd) and nifedipine (20 to 80 mg bid) were compared in 21 patients. Fourteen patients received lisinopril (mean dose 35 mg), and 7 patients received nifedipine (mean dose 54 mg). By the end of week 12, 8 patients had responded (supine diastolic pressure less than or equal to 90 mg) to lisinopril and 5 to nifedipine. At the end of the study supine systolic/diastolic blood pressure was reduced from 172/104 to 149/92 mmHg with lisinopril and from 171/102 to 158/94 mmHg with nifedipine. No significant difference between the two treatments was detected. Three patients were reported to have at least one clinical adverse experience during the active treatment period, 1 in the lisinopril group and 2 in the nifedipine group. No serious clinical adverse experiences were recorded. In conclusion, lisinopril and nifedipine are both effective in reducing blood pressure in patients with mild to severe hypertension. Lisinopril qd and nifedipine slow release bid produce similar decreases in blood pressure after twelve weeks of therapy and the safety profiles of the two drugs are similar.
Nisoldipine represents a new attractive second generation calcium channel blocker of the dihydropyridine-class for the treatment of all types of coronary artery disease. The effect on chronic ischemia is comparable to long-acting nitrates, side-effects have been rarely observed. The advantages will be the high vascular selectivity with only slight negative inotropic effect as well as a long-lasting positive influence on the myocardial metabolism. Up to now, no studies have been reported which compare nisoldipine and long-acting nitrates directly, but this calcium antagonist appears to influence duration and intensity of symptomatic and silent episodes of ischemia similar to the nitrates.
Hyperlipidemia has turned out to be the most important risk factor for coronary heart disease and necessitates frequently lipid lowering long-term treatment. Therefore, efficacy and tolerability of hypolipemic drugs are of great interest. The objective of the present study was to compare the safety, tolerability and effect on plasma lipids of Lovastatin and Bezafibrate retard in patients with hypercholesterolemia. 99 patients with total cholesterol of > or = 250 mg/dl after a 4 week standard lipid-lowering diet were treated another 4 weeks with placebo and then randomized to 400 mg Bezafibrate retard or 20 to 80 mg Lovastatin given once a day for 12 weeks. Mean changes from baseline in total cholesterol, LDL cholesterol and triglycerides were significantly reduced, in HDL cholesterol increased in both treatment-groups (p < or = 0.01). The effects of Lovastatin on total cholesterol and LDL cholesterol were more pronounced than those of Bezafibrate retard (p < or = 0.01), while Bezafibrate had a larger effect on triglycerides (p < or = 0.05). The frequency of clinical adverse experiences was low and similar among treatment groups, the frequency of laboratory adverse experiences was higher in the Lovastatin group. One patient in the Bezafibrate group was withdrawn because of nausea, one patient in the Lovastatin group because of GGT elevation.
Meta-analysis of several large interventional trials in patients with mild to moderate hypertension has shown that coronary events are reduced to a much lesser extent than expected. One of the possible explanations for this are the metabolic side-effects of diuretics and betablockers used in these trials that may counteract their beneficial blood-pressure-lowering effect. Diuretics, especially thiazide, increase total cholesterol (+5%) and LDL-cholesterol (+10%), while betablockers decrease HDL-cholesterol (-5%) and increase triglycerides (+20%). Calcium antagonists and ACE-inhibitors do not affect lipids, and alpha-blockers have some beneficial effects. Regarding the carbohydrate metabolism, diuretics and betablockers decrease insulin sensitivity, increase plasma insulin, LDL-cholesterol, and triglycerides, and reduce HDL-cholesterol. Calcium channel blockers are neutral, while alpha-blockers and ACE-inhibitors improve glucose tolerance and reduce insulin resistance. To date, the clinical relevance of this side-effects is not known. Controlled, long-term trials in hypertensive patients with calcium channel blockers, ACE-inhibitors, and alpha-blockers are needed.
Despite sophisticated artificial limb devices available today, forequarter amputation following trauma or tumor resection will lead to severe impairment of function. To close the posttraumatic or oncologically required extended defects and to improve prosthetic supplementation coverage of the thoracic wall should be performed by sparing the whole forearm as an osteomyocutaneous flap. In cases of concomitant serial rib resection radius and ulna will serve as stabilizators of the thoracic wall, thus avoiding a flail chest. Indications, technical details and clinical outcome of three salvage replantations after interscapulo-thoracic ablation will be discussed.
Arthroscopy of the ankle joint was limited to the anterior compartments for a long time. The key to the entire diagnostic and therapeutic arthroscopy procedure on the ankle joint was the distension of the joint space through modern distraction techniques. The distraction devices available make arthroscopic surgery of the ankle joint as effective as in other joints like the knee and shoulder. Distension of the joint space allows visualization of all compartments, including the posterior ankle. In the case of hidden cartilage pathology of the posterior talus, an osteotomy linked with hardware removal through a second operation can be avoided today. The indications for arthroscopy of the ankle are pain, swelling, instability, hemarthrosis and joint locking. Generally, arthroscopy of the ankle joint is performed utilizing three general portals: anterolateral, anteromedial and posterolateral. Arthroscopic standard equipment, including the small joint set, is sufficient to treat the major part of ankle pathology through the standard portals. Arthroscopic ankle joint debridement in degenerative arthritis, removal of osteophytes, elimination of loose bodies and the management of soft tissue and bony impingement are possible. A complete synovectomy can be performed, including the posterior compartments. The treatment of osteochondritis dissecans is facilitated through the transmalleolar approach in combination with the distraction device. Arthroscopic ankle arthrodesis is possible and induces less trauma because an arthrotomy can be avoided. In our opinion diagnostic arthroscopy and arthroscopic surgery of the ankle joint is a procedure of great benefit for the patients if the indications are strictly adherred to.
At the present time there is no firm evidence that silent myocardial ischemia (on exercise or Holter ECG) should be treated with anti-ischemic drugs. Silent ischemic episodes obviously are a marker for ischemic activity of coronary artery disease and therefore a bad prognostic sign. However, antianginal drugs (nitrates, calcium-blockers, beta-blockers) have not been shown to improve prognosis. Patients with ischemic episodes should be further evaluated by thallium scintigraphy and coronary angiography. If a significant coronary disease is present, the established therapy with risk factor reduction, lipid lowering drugs and aspirin should be administered. In some instances PTCA or CABG may be indicated.
During the past years, several large trials (Consensus, VHEFT I and II, SOLVD) have shown a significant reduction of mortality in patients with moderate and severe heart failure. However, despite effective treatment with vasodilators, digitalis and diuretics mortality in these patients remains unacceptable high. It seems logic, to state treatment at an earlier stage of the disease to achieve more benefit. The main early pathophysiological disturbance is left ventricular hypertrophy, resulting from hypertension, coronary artery disease, increasing age and obesity. On the long run, LVH may lead to diastolic and systolic heart failure, myocardial ischemia, arrhythmias and sudden death. With ACE-inhibitors LVH can be reduced within 1 month of treatment. The large SAVE- and SOLVD-prevention trials will show, whether this early intervention will improve proposis in patients with asymptomatic heart failure.
In this case report a 30-year-old woman suffering from progressive angina pectoris and dyspnea, having been operated on previously for atrial septum defect at the age of 19 and later aged 24 for coarctation of the aorta, is described. Upon observation, patient showed cardiac symptoms already under mild stress and remained resistant to nitroglycerin. Rest-ECG and serum cardiac enzymes were repeatedly without findings, while stress-ECG at a level of 100 W showed a ST-segment depression of 0.15 mV, at the same time complaining of angina pectoris symptoms. Coronary angiography revealed a left circumflex coronary artery arising from the left atrium being fully supplied by the left anterior descendent artery and the right coronary artery via pronounced collaterals, both originating from the ascending aorta. Despite such severe symptoms patient refused surgery suturing the abnormally arising artery. One year following coronary angiography patient is suffering from stabile angina pectoris without occurrence of myocardial infarction or another cardiovascular event.