[Therapy of the pilonidal sinus--Primary wound closure or open wound after excision]. / Die Therapie des Sinus pilonidalis - Primärer Wundverschluss versus offene Wundbehandlung nach Exzision.

The postoperative follow up of 177 operations in 162 patients with pilonidal sinus was investigated. After excision of the sinus a primary wound closure was performed in 80 cases; in 83 cases the wound was left open. After primary wound closure 40 % of the patients showed a primary healing of the wound. Although the remaining 60 % of the wounds healed secondarily the patients were not disabled longer and did not demonstrate more frequently recurrences than those with open wound management. As a consequence we recommend a primary wound closure after excision of a pilonidal sinus.

Cytomegalovirus pp65 antigen-guided preemptive therapy with ganciclovir in solid organ transplant recipients: a prospective, double-blind, placebo-controlled study.

BACKGROUND: The aim of this study was to evaluate pp65 antigen-guided antiviral therapy in preventing human cytomegalovirus (HCMV) infection in solid organ transplant recipients. METHODS: Ten kidney and two liver transplant recipients with asymptomatic HCMV infection were randomized either for i.v. ganciclovir or placebo treatment in a prospective, double-blind study. All patients were positive by HCMV pp65 antigen test at levels >5 positive cells/2 x 10(5) investigated cells. RESULTS: No cases of HCMV end-organ disease occurred. In contrast to patients on placebo (5/7), none of the patients on ganciclovir (0/5) developed HCMV-associated symptoms (P=0.01). However, because of the small number of patients, all three high-risk patients (donor seropositive, recipient seronegative) were randomized to placebo and all three developed symptoms. CONCLUSIONS: Preemptive antiviral therapy guided by the pp65 antigen test seems to have a beneficial effect on preventing HCMV-associated symptoms in kidney and liver transplant recipients.

Breathhold unenhanced and gadolinium-enhanced magnetic resonance tomography and magnetic resonance cholangiography in hilar cholangiocarcinoma.

We assessed the imaging characteristics of hilar cholangiocarcinoma in magnetic resonance imaging (MRI) and magnetic resonance cholangiography (MRC). Breathhold MRI (T2-weighted turbo spin echo sequences, unenhanced T1-weighted gradient echo sequences, and gadolinium-enhanced fat-suppressed gradient echo sequences) and breathhold MRC (fat-suppressed two-dimensional projection images) performed in 12 patients with histologically confirmed hilar cholangiocarcinoma were retrospectively reviewed for morphological tumor characteristics and contrast enhancement patterns. MRC demonstrated a significant bile duct stenosis with intrahepatic bile duct dilatation in all cases except in one patient who received an endoprothesis prior to imaging. Hilar cholangiocarcinoma was diagnosed by MRC only in one patient and MRI and MRC in 11. Mass lesions were seen in nine patients and circumferential tumor growth in three, including the patient diagnosed by MRC only. The tumor appeared hypointense relative to liver parenchyma in 10 of 11 patients in unenhanced T1-weighted images. T2-weighted sequences showed isointense or only slightly hyperintense signal in 5 of 11 patients, 3 of whom demonstrated desmoplastic reactions by histology. The other 6 patients revealed strongly hyperintense signal intensities. Contrast enhancement was increased compared to liver in 5 of 11 patients and decreased in 6 of 11 patients. MRI with MRC seem to be a sensitive tools in the detection of hilar cholangiocarcinomas. The variable imaging characteristics are most probably related to the inhomogeneous histological appearance of this tumor entity.

[Prehospital thrombolysis with rt-PS. Reperfusion strategy in a time management concept of acute myocardial infarct]. / Prähospitale Thrombolyse mit rt-PA. Eine Reperfusionsstrategie im Zeitmanagementkonzept des akuten Herzinfarkts.

PATIENTS AND METHOD: Prehospital thrombolysis was performed on 93 patients during a time period of 6 years (3/1992 to 9/1998) in an urban area. Thrombolysis with rt-PA (20 mg rt-PA bolus, 30 minute infusion with 30 mg rt-PA) could be started within 2 hours after the onset of symptoms in 67 patients (73.6%). RESULTS: The time gain from prehospital thrombolysis amounted to 38 +/- 14 minutes. Bleeding complications were not observed in the prehospital setting, but 2 patients suffered from intracerebral hemorrhage subsequently and died in the hospital. An aborted infarction (CKmax < 200 U/l and no new Q-waves) was observed in 18 patients (20%) and another 23 patients (25%) had a limitation of infarct size (CKmax < 500 U/l or no new Q-waves) despite obvious signs of myocardial ischemia in the first ECG. CONCLUSION: Our experience demonstrates a considerable time gain for prehospital thrombolysis even for an urban area. Accelerated rt-PA is a safe and comfortable thrombolysis regime.

[Risk stratification and long-term therapy with amiodarone in patients with idiopathic dilated cardiomyopathy]. / Risikostratifikation und Langzeittherapie mit Amiodaron bei Patienten mit idiopathischer dilativer Kardiomyopathie.

Patients with cardiomyopathy are known to suffer from a high prevalence of tachyarrhythmic complications and sudden cardiac death. In a prospective study, 30 patients (25 men, 5 women, mean age: 52 +/- 12 years) with dilated cardiomyopathy underwent 48-h-Holter monitoring and programmed electrical stimulation and, independent from the results of the diagnostic work-up, were then randomized either to amiodarone or to a conventional or no antiarrhythmic therapy. At baseline, frequent ventricular arrhythmias (> 30 ventricular premature beats/h) were observed in 15/30 patients (50%), 13 patients (43%) had repetitive ventricular arrhythmias, additionally. Four patients suffered spontaneous sustained tachyarrhythmias. During programmed electrical stimulation, sustained monomorphic ventricular tachycardia was induced in 3/3 patients with and in 1/25 patients (4%) without a history of sustained tachycardia. Sustained monomorphic ventricular tachycardia was induced with one to two extrastimuli; three extrastimuli only increased the incidence of inducible ventricular fibrillation (8 patients, 28%). During a mean follow-up of 28 +/- 6 months 10/30 patients (33%) died for cardiac reasons (sudden cardiac death: 4/10 patients). Cardiac death was most likely in patients with a left-ventricular ejection fraction < 35% (5/18 patients, 28% versus 1/12 patients with ejection fraction > 35%, 8%) and further increased in the presence of reduced exercise tolerance and frequent and repetitive ventricular arrhythmias (4/7 patients, 57%). In the amiodarone group 4/15 patients died (27%, sudden cardiac death: one patient), while in patients not treated by amiodarone 8/15 patients died (54%; sudden cardiac death: three patients). Amiodarone therapy was well tolerated in all but one patient.

Short-term and long-term treatment with propafenone: determinants of arrhythmia suppression, persistence of efficacy, arrhythmogenesis, and side effects in patients with symptoms.

OBJECTIVE: To assess the clinical criteria predicting the short and long-term efficacy of propafenone, an agent with class IC antiarrhythmic activity and a broad pharmacological profile. DESIGNS: Prospective study of propafenone at doses of 450 to 900 mg/day during a six week dose titration period (including a placebo phase with two separate 24 Holter recordings). Responders to treatment were followed for one year. PATIENTS: One hundred patients with frequent ventricular arrhythmias (greater than 30 extrasystoles/h) of Lown class III and IVA/B and without evidence of myocardial infarction within the past six months. ANALYSIS: Multivariate regression analysis of spontaneous arrhythmia variability and of different clinical variables to determine the short and long-term efficacy and safety of propafenone. MEASUREMENTS AND MAIN RESULTS: Propafenone 450 mg/day was effective in 30/100 patients (30%), and at 600 mg/day another 14 responded. The efficacy of propafenone correlated with a low spontaneous arrhythmia variability and, as shown by multivariate analysis, with a lower patient age (p less than 0.05). When the dose was increased to 900 mg/day a further six (12%) patients responded. However, with increasing doses of propafenone, the one year probability of effective treatment decreased from 86% (450 mg/day) to 67% (600 mg/day) and to 44% (900 mg/day). After restudying the patients at three, six, and 12 months and after dose adjustment in 11/44 patients (25%), 31 patients (70%) remained responders. Loss of permanent antiarrhythmic efficacy was best predicted by the initial dose that achieved a response. No patient died suddenly or had arrhythmogenic effects during Holter monitoring. Side effects occurred in 36% of patients but these rarely limited long-term treatment. CONCLUSIONS: A younger age, low spontaneous arrhythmia variability, and particularly a low titration dose were the best predictors of the short and long term efficacy of propafenone. All other responders should have repeated Holter recordings during the first year of treatment.

Time course and interrelation of reperfusion-induced ST changes and ventricular arrhythmias in acute myocardial infarction.

With the increasing use of thrombolytic therapy, the presence and time course of reperfusion-induced ventricular arrhythmias and ST-segment changes have become of particular interest. Technical improvements in bipolar Holter monitoring offer the opportunity to record both parameters continuously and simultaneously. Time course and interaction of both parameters in dependence on the onset of thrombolysis and time of reperfusion were investigated in 30 patients with acute myocardial infarction. Reperfusion was achieved in 20 patients after 49 +/- 23 minutes and in another 2 patients after 120 minutes (73%, group A). Vascular occlusion persisted in 8 patients for greater than 24 hours (group B). Sudden ST-segment changes (greater than 0.2 mV/15 min) in the bipolar leads indicated reperfusion in 7 of 22 patients (32%). Idioventricular rhythms, most frequent in reperfused patients (group A: 18 of 22 patients, mean 121 beats/hour), were unspecific reperfusion markers (group B: 5 of 8 patients, 1 beat/hour) unless frequent (p less than 0.05) or longer lasting, repetitive (p less than 0.01) episodes were considered. Premature ventricular beats and couplets (p less than 0.05) were also most frequent in group A (peak frequency 3 to 5 hours after thrombolysis). Ventricular tachycardia observed in 21 of 22 patients (95%) in group A and in 3 of 8 (38%) in group B (p less than 0.01) attained their peak frequency 7 to 9 hours after thrombolysis. They occurred most often in anterior myocardial infarction and were often preceded by frequent singular premature beats (r = 0.78).(ABSTRACT TRUNCATED AT 250 WORDS)

Enhanced cardiac angiotensinogen gene expression and angiotensin converting enzyme activity in tachypacing-induced heart failure in rats.

The aim of the study was to analyze changes in myocardial angiotensinogen gene expression and myocardial angiotensin converting enzyme activity in slowly progressing low-output failure. In adult, male Wistar rats, acute ventricular tachypacing by 610 to 620 impulses per minute lowered end-diastolic external diameter of the left ventricle by 2.6% (p less than 0.01), but did not lower cardiac output or abolish coronary reserve, since left-ventricular subendocardial blood flow of paced rats increased under dipyridamole (2 mg/kg i.v.) by 56% (p less than 0.01). Systemic neuroendocrine activation and ventricular dilation without enlargement of ventricular mass developed subsequent to chronic tachypacing, but left-ventricular diameter during pacing never exceeded the value of sham rats on sinus rhythm. After 2 weeks, cardiac output was lowered by 14% (p less than 0.001), cardiopulmonary blood volume was elevated by 30% (p less than 0.001), and angiotensinogen mRNA and angiotensin converting enzyme activity in ventricular myocardium were doubled. We conclude that conditions for an enhanced intracardiac angiotensin II-formation developed in tachypacing-induced heart failure, but that enhanced systolic wall stress or myocardial ischemia are not required for this activation of the local cardiac renin-angiotensin system.