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The number of local complications after heart catheterization by transfemoral approach can be lowered by optimized compression technique in spite of shortened compression time. It requires a long-term (> 30 minutes) acute compression after removing the sheaths and stable pressure during the following compression period. To achieve this issue the deployment of a novel compression device is superior to the combination of manual compression and conventional pressure dressing. A pressure of 40 to 45 mmHg is sufficient and well tolerated. Local complications as pseudoaneurysms and arteriovenous fistulas are detected by duplexsonography with high sensitivity. Only about 50 percent of pseudoaneurysms are identified by physical examination in contrast to arteriovenous fistulas which are rarely missed because of their characteristic murmur. The early ultrasound-guided compression therapy is considered to be a safe treatment of pseudoaneurysms but is not effective in arteriovenous fistulas. Risk factors of local complications are high blood pressure, multiple arterial puncture and local-anatomical conditions. Compression-related factors are short acute compression (phi 14.3 minutes) and loss of pressure during the following compression period.

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After transfemoral angiography the artery has to be manually compressed in order to stop acute bleeding. Then, to prevent retarded bleeding, a continuous pressure dressing has to be fixed for up to 24 h. To simplify this procedure, we developed a novel compression device and tested it in 133 patients. Color-flow-ultra-sonography was used to scan gross alterations such as hematomas, AV-fistulas or pseudoaneurysms, and changes in tissue consistency as well. By the new device it is possible to perform femoral artery compression and to substitute pressure dressing safely and with significantly less expenditure than by the combination of manual compression and pressure dressing. We found a reduction from 18 to 3 min time requirement for primary sealing of the puncture site. Moreover, 86% of patients experienced in both methods--the conventional and the new device--would prefer the new equipment in recatheterization. It is better tolerated than the combination of pressure dressing and manual compression. The device is reusable and the compression is easily and exactly adjustable in a wide pressure range. In comparison with previously described mechanical compression systems the remarkable advantage of our device is to merge the function of compression for sealing of the puncture site and pressure dressing for prevention of retarded bleeding.

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To determine whether nitroglycerin is just as effective as nifedipine in lowering the blood pressure in excessive hypertension and hypertensive crisis, two groups of 20 patients received in random sequence either 1.2 mg of nitroglycerin sublingually or a 10 mg nifedipine capsule, which was chewed and swallowed. The blood pressure fell after 5 min in the nitroglycerin group from 211/122 mm Hg to 171/95 mm Hg and after nifedipine from 210/118 to 185/102 mm Hg. The greater effect of nitroglycerin results from faster absorption through the oral mucosa than through the small intestinal mucosa where nifedipine is primarily absorbed. After 15 to 20 min a satisfactory reduction in blood pressure was reached in both groups: 157/91 and 158/92 mm Hg, respectively. After 30 min the heart rate in the nitroglycerin group had decreased from 83 to 80/min, but in the nifedipine group it had increased from 84 to 90/min. The reduction in blood pressure persisted up to 6 h. No significant difference in side-effects was determined. Since a hypertensive crisis is usually accompanied by left-ventricular failure, pulmonary edema or angina pectoris and infarction, and nitroglycerin has been definitively shown to positively influence these conditions, preference should be given to nitroglycerin in the treatment of hypertensive crisis.

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To determine whether nitroglycerin is as effective as nifedipine in lowering the blood pressure in severe hypertension and hypertensive crisis, two groups of 20 patients received in random sequence either 1.2 mg nitroglycerin sublingually or a 10-mg nifedipine capsule, which was chewed and swallowed. The blood pressure fell after 5 min in the nitroglycerin group from 211/122 mmHg to 171/95 mmHg and after nifedipine from 210/118 to 185/102 mmHg. The greater effect of nitroglycerin may result from faster absorption through the oral mucosa than through the small intestinal mucosa where nifedipine is primarily absorbed. After 15-20 min a satisfactory reduction in blood pressure was reached in both groups: 157/91 and 158/92 mmHg, respectively. After 30 min the heart rate in the nitroglycerin group had decreased from 83 to 80/min, but in the nifedipine group it had increased from 84 to 90/min. The reduction in blood pressure persisted up to 6 h. No significant differences in side effects were determined. Since a hypertensive crisis is usually accompanied by left ventricular failure, pulmonary edema, angina pectoris, or infarction, nitroglycerin has been definitively shown positively to influence these conditions, and preference should be given to nitroglycerin in the treatment of hypertensive crises.

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The efficacy of beta-blockade after myocardial infarction (MI) has been investigated in a series of studies. When beta-blockers are used during the first hours after the onset of MI, a reduction in infarct size, mortality, and nonfatal reinfarction may occur. Bisoprolol is a highly beta1-selective beta-blocker, without intrinsic sympathomimetic activity (ISA), and with a plasma elimination half-life of 10-12 h, permitting treatment with one daily dose. Because no experience with bisoprolol was available in MI, its safety and efficacy were studied in two open, uncontrolled pilot studies. The first study was a dose-finding study in 37 patients with a 3-day-old MI. Bisoprolol was given intravenously and carefully titrated in steps of 1 mg up to a cumulative maximum dose of 5 mg. Subsequently, the patients received 10 mg of oral bisoprolol once daily (o.d.) until the end of the study. Based on the results of this first pilot study, a second pilot study was performed in which bisoprolol was given within the first 6 h after the onset of MI. Intravenous (i.v.) bisoprolol was titrated in two steps of 2.5 mg each, directly followed by 10 mg of oral bisoprolol o.d. The aim of this study was to investigate the influence of i.v. and subsequent oral bisoprolol on central hemodynamics. The results of these studies demonstrate that i.v. and subsequent oral administration of bisoprolol is well tolerated and indicate that the selected dose regimen is hemodynamically safe.

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Although pacemaker (PM) implantation has developed into a standard therapy in appropriate rhythm disorders the procedure is not free of complications. One of the most common problems is thrombotic alteration in the region of the entry of the pacemaker electrode into the venous system. To obtain more details of the incidence and extent of these complications, we investigated a total of 97 patients in two groups, clinically, phlebographically and by Doppler-ultrasound technique. 56 (30 males, 26 females, mean age 73 years) were examined 1 week, and 41 (18 males, 23 females, mean age 72 years) 1 year after PM implantation. The thrombotic changes were quantified and correlated to various anamnestic and clinical parameters with the following results: 1 week after implantation 25% of patients show thrombi with collaterals, in 15% shorter than, and in 10% longer than 3 cm. One complete obturation of the implantation vessel was recognized. Thrombotic changes without collaterals were found in 36%, in 25% shorter than, and in 11% longer than 3 cm. One year after PM implantation there are organized thrombi in 71%, 41% of these patients show collaterals phlebographically. The others had no hemodynamic changes. Of all the anamnestic and clinical parameters, a significant correlation was found only between development of thrombi and material of electrodes. Polyurethane electrodes have a significantly higher rate of thrombosis than silicone electrodes (p less than or equal to 0.0066).(ABSTRACT TRUNCATED AT 250 WORDS)

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Electrophysiologic studies had been performed before and after pharmacologic autonomic blockade (propranolol 0.2 mg/kg and atropine 0.04 mg/kg body weight) in a 23-year-old female patient with documented sinus arrest of 27 sec duration. Normal electrophysiologic findings before and after autonomic blockade excluded intrinsic sinus node dysfunction. Sinus arrest is therefore though to be due to an intermittent dysregulation of the autonomic nervous system.

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In thyreostatic treatment the loss of taste combined with discreetly increasing hepatic enzymes has been observed as a toxic effect of thiamazole in a female patient. Sense and hepatic enzymes normalized rapidly after discontinuing use of thiamazole.

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Coronary angiograms of 200 patients with coronary artery disease were studied. The distribution of stenoses was analyzed and classified utilizing a special score, taking into account coronary supply pattern (according to Baroldi et al.), localization and severity of stenosis, as well as collateralization. Frank-lead vectorcardiograms were obtained and analyzed by computer. 140 scalar and spatial vector parameters were evaluated. A statistical comparison was made in 36 patients with highgrade stenoses of the left anterior descending branch of the left coronary artery with 37 patients without such vascular narrowing. Utilizing 4 ECG-parameters a mathematical formula can be derived which separates the two groups. Another equation based on 5 parameters allows the calculation of a score from conventional electrocardiograms. By discriminance analysis a specificity of 78.4% and a sensibility of 77.8 in prediction results for the group with stenosis. For the control group a specificity of 75.7% and a sensibility of 77.8% were computed. Correlation between the score obtained by calculation on the one hand, and the score derived from direct analysis of the arteriogram was highly significant with an r = 0.796.

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