Subjective and objective assessment of enalapril in primary Raynaud's phenomenon. Controlled double-blind trial of dazoxiben and nifedipine in the treatment of Raynaud's phenomenon. The effect of captopril on cutaneous blood flow in patients with primary Raynaud's phenomenon. [Treatment of systemic scleroderma with ketanserin. Randomized, double-blind 6-months study of 27 cases]. Skin temperature biofeedback for Raynaud's disease: a double-blind study. The effectiveness of ketanserin in patients with primary Raynaud's phenomenon. A randomized, double blind, placebo controlled study. Successful treatment of Raynaud's syndrome with Iloprost, a chemically stable prostacyclin analogue. Early vasodilator treatment in myocardial infarction: appropriate for the majority or minority? Placebo controlled study showing therapeutic benefit of iloprost in the treatment of Raynaud's phenomenon.
1. The efficacy and acceptability of enalapril were assessed in a double-blind, randomised, placebo controlled cross-over study in 21 patients with primary Raynaud's phenomenon. 2. Skin temperature was assessed by thermocouples in response to a 15 degrees C cold water challenge as an index of digital blood flow. 3. Following enalapril there were no significant changes in the number and severity of Raynaud's attacks, and no subjective benefit from treatment as measured by visual analogue scales, 5 point rating scales, and skin temperature response to cold challenge when compared with placebo. 4. Enalapril in a dose of 20 mg daily is ineffective in the management of primary Raynaud's phenomenon. The prostaglandin thromboxane A2 causes platelet aggregation and vasoconstriction and may be important in the pathogenesis of Raynaud's phenomenon. Therefore, a randomized, double-blind, placebo-controlled trial was conducted to assess the effectiveness of dazoxiben, a selective thromboxane synthetase inhibitor, in the treatment of Raynaud's phenomenon and to compare it with nifedipine, a calcium channel blocker. Twenty-two subjects who had at least one episode of Raynaud's phenomenon per day entered the study. Three patients withdrew from the study because of side effects while taking nifedipine. There was no difference among the subjects' subjective evaluation of the three treatments. Seven of 19 (44 percent) reported a moderate to marked improvement while taking placebo compared with 12 of 19 (63 percent) taking nifedipine and five of 19 (26 percent) taking dazoxiben (p = NS). Similarly, there was no difference in the mean two-week episode rate among the three treatments: placebo 30.4 +/- 4.5, nifedipine 24.7 +/- 5.6, dazoxiben 32.0 +/- 4.9 (p = NS). Twelve of 22 subjects experienced side effects while taking nifedipine as compared with two of 21 taking placebo and eight of 21 taking dazoxiben (p less than 0.005). These data show that dazoxiben is not effective in the treatment of Raynaud's phenomenon and suggest that thromboxane does not cause the vasoconstriction that characterizes this disorder. Fifteen patients with primary Raynaud's phenomenon received captopril 25 mg or placebo, three times daily for 6 weeks, in a randomized double-blind cross-over study. Compared with placebo, captopril produced a significant improvement in cutaneous blood flow but did not alter the frequency or severity of attacks of Raynaud's phenomenon. Twenty-seven patients with systemic scleroderma and Raynaud's phenomenon underwent a randomised double blind therapeutic trial: monotherapy with Ketanserine (80 mg/day for 6 months) against Placebo. The secondary effects were comparable in both groups as were the withdrawals from the trial for aggravation of Raynaud's phenomenon (one in each group). No significant difference was observed between the two groups as regards the evolution of the Raynaud's phenomenon or skin changes. Dysphagia was improved in the Ketanserine group (p less than 0.05) but not in the Placebo group. Some patients in the Ketanserine group experienced an improvement in the Raynaud's phenomenon at the end of the trial period; there were no improvements in the Placebo group. Three haemorrheological parameters (total blood viscosity, plasma viscosity and thixotropism) were abnormal at the beginning of the trial and did not improve by the end in the Ketanserine group. The K infinity coefficient of Quemada's law was normal at the start of the trial and increased after treatment (p less than 0.05). The lack of control procedures inherent in most of the experiments conducted to assess the effectiveness of skin temperature biofeedback in the treatment of Raynaud's disease renders the results inconclusive. In this study, control groups and a double-blind approach are adopted. Thirty-six patients, carefully screened for a diagnosis of primary Raynaud's disease, were assigned to a skin temperature increase group (N = 12), to an EMG relaxation control group (N = 12), or to a notreatment control group (N = 12). All patients kept records of their symptoms for the duration of the study. Each subject in the two training groups received 20 sessions, the last 2 conducted under cold stress. data analysis according to original group assignment, as well as following regrouping of subjects according to several learning criteria, showed that while all patients reported a marked decrease in the number of vasospastic attacks, no significant differences were found among the three groups on the clinical measures used to assess symptomatic relief. The general improvement reported must therefore be attributed to nonspecific factors. In 41 patients with Primary Raynaud's Phenomenon (PRP) the effectiveness of the serotonin receptor blocker ketanserin has been studied in a double blind cross-over study. Subjective assessments included: frequency and duration of the attacks (both per se and combined to a severity score), cold sensation, numbness, paresthesia, pain, cold water and cold weather provocation and the appearance of spontaneous attacks. The objective measurements comprised Digital Skin Temperature (DST), Digital systolic Blood Pressure (DBP) and Doppler Spectral Analysis (DOSA) of the radial and ulnar arteries. All measurements were performed both at room temperature and after instant cold provocation. The severity score, the occurrence of numbness and paresthesia and cold weather provocation improved significantly on ketanserin treatment. All objective measurements with the exception of the end-diastolic blood flow velocity of DOSA did not show significant improvements. Neither blood chemistry nor systemic blood pressure showed any significant change during ketanserin treatment. However, in the 6 (15%) patients with hypertension both systolic and diastolic blood pressure normalized. Although in objective measurements hardly any significant effects of ketanserin could be demonstrated, the results of the study suggest that orally administered ketanserin is effective for minimizing subjective complaints in patients with PRP. Ketanserin did not show any side effects. Twelve female patients with severe secondary Raynaud's phenomenon were treated in a randomized order with both placebo and Iloprost infusions. Infusions were for 5 hours on 3 consecutive days and Iloprost was administered at variable dosage from 1.0 to 3.0 ng/kg/min. A 6-week follow-up period was used between the two sets of infusions. A significant number of patients reported Iloprost had improved Raynaud's symptomatology compared with placebo and this effect lasted for up to 6 weeks. The number of attacks of Raynaud's as recorded by patients in diary books was similarly reduced after Iloprost. Digital and nail-bed blood flows measured by laser-Doppler methods were increased for up to 6 weeks after Iloprost, but not after placebo infusions. Iloprost may be a useful therapeutic agent in the treatment of severe secondary Raynaud's syndrome. To assess the influence of vasodilator treatment started early after myocardial infarction on left ventricular size and function.
                Coronary care unit, Royal Infirmary, Edinburgh.
                105 patients with acute myocardial infarction (systolic blood pressure > 90 mm Hg) were randomised within 24 hours of the start of pain. Unlike previous studies 88% of the patients received thrombolysis.
                Double blind randomised placebo controlled study with either 12.5 mg of captopril three times daily or 20 mg of isosorbide mononitrate three times daily for 28 days.
                Clinical outcome and left ventricular size and function assessed by echocardiography, radionuclide ventriculography, and magnetic resonance imaging.
                There was no difference in left ventricular size or function in either treatment group as measured one week after the end of the trial. Even the placebo group tended to decrease left ventricular diameter over the four week study period (one week: 5.0 (0.1) v, five weeks: 4.8 (0.1) cm, NS). Four patients had an adverse clinical outcome in the placebo group whereas no adverse outcome was seen in the captopril group.
                Vasodilator treatment may be of limited value or of no benefit for most infarct patients, particularly those treated with thrombolytic agents. Captopril, however, may benefit patients at high risk. Iloprost is a chemically stable analog of prostaglandin I2 showing the same properties as the naturally occurring substance, but with advantages of ease of handling and administration to patients. A double blind within patient comparison of intravenous iloprost and placebo was undertaken in 13 patients with Raynaud's phenomenon severe enough to warrant short term hospitalization for intravenous dilator therapy; thermography was used as one form of assessment. Our results, while showing improvements in frequency of Raynaud's attacks after iloprost compared with placebo, show no significant effects on other variables.
Poor methodological quality, small sample sizes and the limited data available resulted in low precision of the statistical results and limited value of the overall results .The overall results show that there is no evidence for an effect of vasodilator drugs on primary Raynaud's phenomenon.