Systemic markers of inflammation are associated with cardiac allograft vasculopathy and an increased intimal inflammatory component.

We evaluated an extensive profile of clinical variables and immune markers to assess the inflammatory milieu associated with cardiac allograft vasculopathy (CAV) assessed by intravascular ultrasound (IVUS) and virtual histology (VH). In total, 101 heart transplant (HTx) recipients were included and underwent IVUS/VH examination and measurement of plasma C-reactive protein (CRP), soluble tumor necrosis factor receptor-1, interleukin-6, osteoprotegerin, soluble gp130, von Willebrand factor, vascular cell adhesion molecule-1 (VCAM-1) and neopterin. Mean Maximal Intimal Thickness (MIT) was 0.61 +/- 0.19 mm and mean fibrotic, fibrofatty, dense calcified and necrotic core components were 55 +/- 15, 14 +/- 10, 15 +/- 13 and 17 +/- 9%, respectively. In multivariate analysis, CRP > 1.5 mg/L (OR 4.6, p < 0.01), VCAM-1 > 391 ng/mL (adjusted OR 3.2, p = 0.04) and neopterin > 7.7 nmol/L (OR 3.8, p = 0.02) were independently associated with MIT > 0.5 mm. Similarly, CRP > 1.5 mg/L (OR 3.7, p < 0.01) and VCAM-1 > 391 (OR 2.7, p = 0.04) were independently associated with an increased intimal inflammatory component (dense calcified/necrotic core component > 30%). Advanced CAV is associated with elevated CRP, VCAM-1 and neopterin and the two former biomarkers are also associated with an increased intimal inflammatory component. Forthcoming studies should clarify if routine measurements of these markers can accurately identify HTx recipients at risk of developing advanced CAV and vulnerable lesions.

Randomized comparison of coronary stent implantation under ultrasound or angiographic guidance to reduce stent restenosis (OPTICUS Study).

BACKGROUND: Observational studies in selected patients have shown remarkably low restenosis rates after ultrasound-guided stent implantation. However, it is unknown whether this implantation strategy improves long-term angiographic and clinical outcome in routine clinical practice. Methods and Results-- A total of 550 patients with a symptomatic coronary lesion or silent ischemia were randomly assigned to either ultrasound-guided or angiography-guided implantation of

Intensive home-based exercise training in cardiac rehabilitation increases exercise capacity and heart rate variability.

BACKGROUND: Reduced heart rate variability (HRV) is a risk factor for cardiac death. Animal studies have shown increased HRV and reduced mortality after physical training. We evaluated the change in exercise capacity and HRV in cardiac rehabilitation patients, randomised to routine or home-based intensive training. The design was prospective, stratified randomisation with pre-specified subgroup analysis. METHODS: Maximal bicycle exercise test and 24-h Holter were performed 1 (baseline), 4 and 12 months after myocardial infarction (MI) or coronary artery by-pass surgery (CABG). Patients were randomised to physical training either two (N) or six (I) times per week for 3 months Sixty-two patients (43 MI and 19 CABG patients) were evaluated. RESULTS: Exercise capacity increased significantly more after 3 months of training in group I (mean (S.E.)); 29.0 (3.4) vs. 7.2 (2.6) watts, P<0.001). One year later the difference in exercise capacity remained (26.5 (3.3) vs. 11.8 (3.8) watts, P<0.001). Global HRV measurements SDNN and SDANN increased significantly more in group I after training (17.1 (5.6) vs. 1.7 (3.7) and 16.2 (4.9) vs. 2.8 (3.1) ms, P<0.05) and 1 year later the differences were still significant. Subgroup analysis showed more pronounced HRV response in CABG than MI patients. CONCLUSION: Intensive exercise training in cardiac rehabilitation increases exercise capacity and global HRV, which could be of prognostic significance.

Circadian variation of heart rate variability and the rate of autonomic change in the morning hours in healthy subjects and angina patients.

BACKGROUND: Incidence of sudden cardiac death peaks during the early morning hours when there is a rapid withdrawal of vagal and an increase of sympathetic tone. The rate of autonomic change could be of prognostic importance. PATIENTS AND METHODS: A total of 65 patients with angina pectoris, free from other diseases and drug free, were Holter monitored for 24 h. A total of 30 patients were also monitored on isosorbide-5-mononitrate (IS-5-MN) and on metoprolol respectively. A total of 33 age-matched healthy subjects served as controls. Spectral components of heart rate variability (HRV) were analysed hourly, with special reference to the rapid changes of autonomic tone during the night and early morning hours. Circadian variation was assessed in two ways: (1) Mean HRV day (8 a.m.-8 p.m.) and night (0-5 a.m.) were compared. (2) For the morning/night hours (0-10 a.m.), individual hourly values for max. and min. HRV, the difference max.-min. (gradient), the rate of change per hour between max. and min. (velocity) and the largest difference between two consecutive hours (max. velocity) were recorded and the mean value for the group calculated. RESULTS: During the night/morning hours, healthy controls demonstrated faster HF max. velocity (P=0.002) and higher HF gradient (P=0.011) than angina patients. Metoprolol and IS-5-MN increased the HF gradient (P=0.008 and P=0.003, respectively), and metoprolol tended to increase the max. velocity (P=0.02). Metoprolol substantially decreased the LF/HF gradient (P=0.001), velocity (P=0.008) and max. velocity (P=0.0001). CONCLUSION: Rapid vagal withdrawal seemed to be a sign of a healthy autonomic nervous system in the control group but was significantly slower in angina patients. IS-5-MN and metoprolol tended to normalise vagal withdrawal and metoprolol slowed down the rapid increase in sympathetic predominance in the morning in patients.

Intensive use of intravascular ultrasound during coronary angioplasty. A six-month campaign.

BACKGROUND: Compared to coronary angiography, intravascular ultrasound (IVUS) gives additional information important for the percutaneous transluminal coronary angioplasty (PTCA) procedure, but is time-consuming and may cause complications. AIM: To evaluate, during a period of intensive use of IVUS, the impact of IVUS on the final decision on balloon/stent diameter, consumption of devices, time-consumption and IVUS-related complications. METHOD: During a 6-month period, IVUS was contemplated in all PTCA procedures and the reason for not using IVUS was specified. We used CVIS during the first, and Endosonics during the last 3 months, and both periods started with 1 week of hands-on practice. All procedures were to be planned according to an initial quantitative coronary angiography (QCA), and the finally achieved result, material used and complications were registered. RESULTS: The proportion of IVUS/PTCA was 37% during, 8% 6 months before and 12% 6 months after the study period. Three hundred and twenty-three patients were included in the study (57% of all patients), 199 of them were subjected to IVUS. The indications for PTCA during the study period were stable angina (58%), unstable angina (32%) and acute myocardial infarction (10%). The main reasons for not doing IVUS were use of 6F guiding catheter (13%), urgent procedure (12%) and occluded vessel (11%). Initial QCA detected 253 stenoses in 199 patients and 64 additional stenoses were treated, most of them probably detected by IVUS. QCA systematically underestimated vessel size, particularly in small vessels. There was a non-significant trend to more accurate estimations towards the end of the study in small vessels. Dissection, probably due to IVUS, occurred in two cases (1%). There were no significant differences in the number of devices used in IVUS compared to non-IVUS patients. The procedural time was 24 min longer in IVUS than in non-IVUS cases and more stenoses were treated per procedure in the IVUS group. CONCLUSION: Coronary angiography often underestimated balloon/stent size but in an unpredictable way, with a substantial proportion of significant stenoses being undetected. IVUS had few serious complications, did not increase device consumption but prolonged procedural time.

Patients with uncomplicated coronary artery disease have reduced heart rate variability mainly affecting vagal tone.

AIM: To investigate whether uncomplicated chronic coronary artery disease causes changes in heart rate variability and if so, whether the heart rate variability pattern is different from that described in patients with acute myocardial infarction. METHODS: Heart rate variability was studied in 65 patients with angina who had no previous myocardial infarcts, no other diseases, and were on no drug that could influence the sinus node. Results were compared with 33 age matched healthy subjects. The diagnosis of coronary artery disease in angina patients was established by coronary angiography in 58, by thallium scintigraphy in six, and by exercise test only in one. Patients and controls were Holter monitored 24 hours outside hospital, and heart rate variability was calculated in the frequency domain as global power (GP: 0.01-1.00 Hz), low frequency peak (LF: 0. 04-0.15 Hz), high frequency peak (HF: 0.15-0.40 Hz), LF/HF in ms(2), and in the time domain as SDNN (SD of normal RR intervals), SDANN (SD of all five minute mean normal RR intervals), SD (mean of all five minute SDs of mean RR intervals), rMSSD (root mean square of differences of successive normal RR intervals) (all in ms), and pNN50 (proportion of adjacent normal RR intervals differing more than 50 ms from the preceding RR interval) as per cent. RESULTS: The mean age in patients and controls was 60.4 (range 32-81) and 59.1 (32-77) years, respectively (NS), the male/female ratio, 57/65 and 24/33 (NS), and the mean time of Holter monitoring, 23.0 (18-24) and 22.8 (18-24) hours (NS). Mortality in angina patients was 0% (0/65) at one year, 0% (0/56) at two years, and 3% (1/33) at three years. Compared with healthy subjects angina patients showed a reduction in GP (p = 0.007), HF (p = 0.02), LF (p = 0.02), SD (p = 0.02), rMSSD (p = 0.01), and pNN50 (p = 0.01). No significant difference was found in RR, LF/HF, SDNN, or SDANN. CONCLUSIONS: Uncomplicated coronary artery disease without previous acute myocardial infarction was associated with reduced high and low frequency heart rate variability, including vagal tone. SDANN and SDNN, expressing ultra low and very low frequencies which are known to reflect prognosis after acute myocardial infarction, were less affected. This is in agreement with the good prognosis in uncomplicated angina in this study.

Reduced heart rate variability in ischemic heart disease is only partially caused by ischemia. An HRV study before and after PTCA.

BACKGROUND: Reduced heart rate variability (HRV) after acute myocardial infarction (AMI) indicates poor prognosis. HRV in patients with uncomplicated coronary artery disease is reduced, and an association with poor prognosis has been suggested. The mechanism of the HRV reduction is not known, but ischemia is a possibility. AIM: To evaluate, in angina patients with no prior AMI, no other disease and drug-free, if complete revascularization and thus important reduction of ischemia by means of PTCA influences HRV. PATIENTS AND METHODS: Twenty-four-hour Holter recordings were performed at baseline prior to PTCA in 48 patients with angina and in 41 age-matched healthy control subjects. The recording was repeated 1 and 6 months after complete revascularization. In addition, HRV was registered during controlled respiration in the supine and standing positions and during cold pressure test at baseline in all angina patients and controls and in 17 consecutive angina patients 6 months after PTCA. RESULTS: Compared to controls, angina patients had a significantly reduced mean RR interval (p = 0.02), SD (p = 0.003), rMSSD (p = 0.03), pNN50 (p = 0.03), total power (p = 0.003), low- (p = 0.004) and high-frequency peak (p = 0.04), but normal SDNN, SDANN and LF/HF. One and 6 months after PTCA, 42/46 and 32/40 follow-up patients, respectively, were free of angina. Six months after PTCA, there was a significant recovery of vagal modulation seen in the frequency domain during controlled respiration, but only nonsignificant trends in HRV parameters analyzed over 24 h. CONCLUSION: Patients with uncomplicated angina had reduced HRV, mainly affecting vagal activity, but normal low frequency variability associated with mortality. Complete revascularization caused a partial normalization of vagal modulation indicating that ischemia may be one of but not the only mechanism of the HRV reduction in uncomplicated chronic coronary artery disease.

Long-term effect of endoscopic transthoracic sympathicotomy on heart rate variability and QT dispersion in severe angina pectoris.

UNLABELLED: We evaluated short and long-term effects on QT dispersion and autonomic balance after endoscopic transthoracic sympathicotomy (ETS). Heart rate variability (HRV) reflects autonomic balance of the heart. QT dispersion is a marker of cardiac electrical instability in patients with ischemic heart disease. Holter recordings for 24 h and a twelve-lead ECG were made prior to, 1 month, 1 year and 2 years after ETS. HRV was analysed in time domain and spectral analysis was performed during controlled respiration in supine position and during head up tilt. Dispersion of QT time and QTc were calculated. Of 88 patients, 62 (60) were eligible for HRV (QT-dispersion) analysis after 1 month, 39 (38) patients after 1 year and 23 (24) patients after 2 years. The HRV analysis showed a significant change of indices reflecting sympatho-vagal balance indicating significantly reduced sympathetic (LF) and increased vagal (HF, rMSSD) tone. These changes still persisted after 2 years. Global HRV increased over time with significant elevation of SDANN after 2 years. QT dispersion was significantly reduced 1 month after surgery and the dispersion was further diminished 2 years later. CONCLUSION: ETS changed HRV and QT dispersion which could imply reduced risk for malignant arrhythmias and death after ETS.

Potential risk of beta-blockade withdrawal in congestive heart failure due to abrupt autonomic changes.

Beta-Blockers reduce mortality in patients with congestive heart failure and a proposed mechanism has been changes of autonomic tone. Heart rate variability is a non-invasive tool to estimate cardiac autonomic tone. The aim was to study changes of heart rate variability in patients with congestive heart failure on placebo, on the beta1-selective antagonist metoprolol or 24 h after metoprolol withdrawal. Forty-five patients with congestive heart failure were studied with Holter recordings. Heart rate variability measurements were performed before, after 6-12 months of treatment with 150 mg metoprolol/placebo, or 24 h after discontinued metoprolol. After treatment, patients on beta-blockade had a significantly longer mean RR interval and changes of heart rate variability, suggesting elevated vagal tone. Patients monitored in the rebound phase of beta-blocker withdrawal had a significant vagal reduction to the level of the placebo group. There was also a nonsignificant trend towards increased sympathetic tone (LF/HF over 24 h), compared with the beta-blockade group. Heart rate variability indicates an elevated vagal tone during treatment with metoprolol but beta-blockade withdrawal shifts the autonomic balance towards lower vagal and higher sympathetic tone within 24 h. These results could imply a potential risk when abruptly discontinuing beta-blockade medication in these patients.

Effects on heart rate variability of isosorbide-5-mononitrate and metoprolol in patients with recent onset of angina pectoris.

BACKGROUND: Beta-blockers reduce sympathetic tone, increase vagal tone and improve prognosis in ischaemic heart disease. Nitroglycerin, being a vasodilator, may theoretically have an opposite effect and worsen the prognosis. The purpose of the present study was to analyse heart rate variability (HRV), which reflects autonomic tone, in angina patients on isosorbide-5-mononitrate (IS-5-MN) and/or metoprolol. METHODS AND RESULTS: Thirty-two patients (32-81 years old), with recently developed angina (median duration: 3 months), showing no other disease and on no drugs, were Holter-monitored 24-48 h at baseline and after 4-5 days on IS-5-MN (mean daily dose: 33 mg), on metoprolol (mean daily dose: 184 mg) and on the combined treatment. Recordings were analysed on the Marquette Series 8000 Holter scanner. Both IS-5-MN and metoprolol significantly reduced myocardial ischaemia (ST integral) and ventricular tachycardias. Metoprolol induced significant changes in the following parameters (baseline versus metoprolol): high-frequency peak 9 +/- 4 versus 11 +/- 4 ms (p < 0.001), low-to-high frequency ratio 2.5 +/- 0.6 versus 1.9 +/- 0.6 (p < 0.0001), root mean square of RR interval difference 23 +/- 7 versus 31 +/- 9 ms (p < 0.0001), RR intervals differing more than 50 ms from the preceding one 4.8 +/- 3.9 versus 10.0 +/- 7.0% (p < 0.0001), mean of all 5-min standard deviations 50 +/- 12 versus 56 +/- 11 ms (p < 0.001) and mean RR interval 819 +/- 90 versus 1,019 +/- 120 ms (p < 0.00001). The combined treatment caused approximately the same HRV changes as metoprolol alone. IS-5-MN had no significant effect on any HRV parameter, neither alone nor in combination with metoprolol. CONCLUSION: A clinically effective dose of metoprolol had potentially positive effects on HRV with increase in vagal and decrease in sympathetic tone while IS-5-MN had no effect on HRV, neither positive nor negative, neither alone nor in combination with metoprolol.

Anti-ischemic and anti-anginal effects of thoracic epidural anesthesia versus those of conventional medical therapy in the treatment of severe refractory unstable angina pectoris.

BACKGROUND: Cardiac sympathetic blockade by thoracic epidural anesthesia (TEA) dilates stenotic coronary arteries and has been used to control pain in patients with unstable angina. The aim of the present study was to evaluate the potential anti-ischemic effects of cardiac sympathetic blockade by TEA in severe, refractory, unstable angina. METHODS AND RESULTS: Forty patients with unstable angina refractory to standard anti-anginal therapy were randomized to receive either continuous epidural infusion of bupivacaine (TEA, Th1 to Th5) or to standard anti-anginal therapy including beta-blockers, calcium antagonists, aspirin, heparin, and nitroglycerin infusion (control group). The primary end points were number of anginal attacks and severity of myocardial ischemia assessed by 48-hour ambulatory Holter monitoring. The incidence of myocardial ischemia was lower in the TEA group (22% versus 61%; P<.05). The number of ischemic episodes per patient was 1.0+/-0.6 in the TEA group and 3.6+/-0.9 in the control group (P<.05). The episode duration per patient was 4.1+/-2.5 minutes and 19.7+/-6.2 minutes in the TEA and the control groups, respectively (P<.05). The mean area-under-the-ST-time-curve was 6.8+/-4.3 and 32.2+/-14.3 (mm-min) in the TEA and the control groups, respectively (P<.05). Fifteen anginal attacks were recorded in the control group and one attack in the TEA group (0.83+/-0.21 versus 0.06+/-0.06/patient, respectively, P<.01). CONCLUSIONS: The anti-ischemic and anti-anginal effects of continuous TEA are superior to those of conventional therapy in the treatment of refractory unstable angina.

Heart rate variability after acute myocardial infarction in patients treated with atenolol and metoprolol.

UNLABELLED: Heart rate variability (HRV) reflects autonomous activity that influences the heart. It has been shown that HRV is depressed during acute myocardial infarction (AMI) and that it recovers with time. Beta-blockers reduce mortality after AMI and changes in sympathico-vagal activity have been suggested to be of importance. Under certain animal experimental conditions, metoprolol has been reported to increase vagal tone more than atenolol, which could have clinical implications. The purpose of the present study was to compare the effects of atenolol and metoprolol treatments on HRV during 6 weeks after AMI and to follow the post MI changes in HRV in patients on betablockers. METHODS: In an open, randomised cross-over study, 28 patients were randomised to 3+3 weeks' treatment with atenolol or metoprolol starting 2-5 days after AMI. Twenty-four hour Holter recordings were made before randomisation and after 3 and 6 weeks. HRV was analysed as HR, SDRR, SDANN, SD, rMSSD and pNN50 in the time domain and as coefficient of component variance (CCV) of HF and LF, and as LF/HF ratio in the frequency domain. RESULTS: The average daily dose in our study population was 106 mg of metoprolol and 54 mg of atenolol. There were trends toward lower heart rates daytime, lower LF/HF ratio daytime and higher rMSSD on atenolol compared to metoprolol. In the total group of 28 patients we found during the first 3 weeks, a significant increase of SDNN, SDANN (p<0.0001) and LF/HF ratio daytime and CCV-HF night-time (p<0.01). All differences and trends were unchanged between 3 and 6 weeks. CONCLUSIONS: There was no evidence of more increased vagal tone with metoprolol compared to atenolol as has been suggested from animal models. In patients also on chronic treatment with beta blockers, an increase of HRV was seen during the first weeks post MI.

Effect of endoscopic transthoracic sympathicotomy on heart rate variability in severe angina pectoris.

Endoscopic transthoracic sympathicotomy (ETS) is a recently developed technique to divide sympathetic nerves. ETS has been shown to improve symptoms and reduce ischemia in patients with severe angina pectoris. Low heart rate variability (HRV) in patients with ischemic heart disease carries an adverse prognosis. HRV reflects autonomic response of the heart and a shift in the sympathovagal balance towards parasympathetic dominance could be a marker of improved prognosis. HRV might also be used as an indicator of surgical success in sympathetic heart denervation. Heart rate was recorded in 57 patients before and after ETS. Registration was recorded during controlled respiration in the supine position and at tilt test over 10 minutes and spectral analysis was performed. Twenty-four hour Holter recordings were analyzed in the time domain. During the controlled setting, the high-frequency (HF) component (0.15 to 0.40 Hz) increased significantly whereas the low-frequency (LF) component (0.04 to 0.15 Hz) did not change significantly. The LF/HF ratio at tilt test was reduced from 1.3 to 0.8 (p <0.01). The time-domain analysis showed a significant increase of the mean RR interval (923 to 1,006 ms, p <0.001) and indexes reflecting parasympathetic tone also increased significantly (the root-mean square of difference measured from 24.3 to 29.5 ms, p <0.001 and the proportion of adjacent RR intervals >50% measured from 5.5% to 8.2%, p <0.01), whereas measurements reflecting global HRV did not change. In addition to relief of symptoms and reduced ischemia in severe angina pectoris, ETS caused a shift of sympathovagal balance toward parasympathetic tone. This might explain the anti-ischemic effect and have prognostic implications.

Peripheral muscle training in patients with clinical signs of heart failure.

The aim of the study was to evaluate, in a controlled setting, the effects of a 5-month dynamic peripheral training programme in patients with clinical signs of congestive heart failure with special reference to their anaerobic threshold, muscle function, heart rate variability and quality of life. Twenty-four randomized patients with clinical signs of heart failure in NYHA II-III entered the study. Training resulted in a significant (p = 0.01) change in the anaerobic threshold, the patients' ability to lift weights (p = 0.01) and performance of heel-lift (p = 0.01). The heart rate recorded during the training exercises decreased significantly (p = 0.04). There were no significant differences in peak oxygen uptake, isokinetic and isometric strength, HRV and quality of life except for three items in the control group. The results of this study indicate that peripheral training is beneficial for patients with clinical signs of congestive heart failure.

Lidocaine in out-of-hospital ventricular fibrillation. Does it improve survival?

BACKGROUND: A large proportion of cardiac arrests outside hospital are caused by ventricular fibrillation. Although it is frequently used, the exact role for treatment with lidocaine in these patients remains to be determined. AIM: To describe the proportion of patients with witnessed out-of-hospital cardiac arrest found in ventricular fibrillation who survived and were discharged from hospital in relation to whether they were treated with lidocaine prior to hospital admission. PATIENTS AND TREATMENT: All the patients with out-of-hospital cardiac arrest found in ventricular fibrillation in Göteborg between 1980 and 1992 in whom cardiopulmonary resuscitation (CPR) was initiated by our emergency medical service (EMS). During the observation period, some of the EMS staff were authorized to give medication and some were not. RESULTS: In all, 1,360 patients were found in ventricular fibrillation, with detailed information being available in 1,212 cases (89%). Lidocaine was given in 405 of these cases (33%). Among patients with sustained ventricular fibrillation, those who received lidocaine had a return of spontaneous circulation (ROSC) more frequently (P < 0.001) and were hospitalized alive more frequently (38% vs. 18%, P < 0.01). However, the rate of discharge from hospital did not significantly differ between the two groups. Among patients who were converted to a pulse-generating rhythm, those who received lidocaine on that indication were more frequently alive than those who did not receive such treatment (94% vs. 84%; P < 0.05). However, the rate of discharge did not significantly differ between the two groups. CONCLUSION: In a retrospective analysis comparing patients who received lidocaine with those who did not in sustained ventricular fibrillation and after conversion to a pulse-generating rhythm, such treatment was associated with a higher rate at ROSC and hospitalization but was not associated with an increased rate of discharge from hospital.

Continuation of CPR on admission to emergency department after out-of-hospital cardiac arrest. Occurrence, characteristics and outcome.

AIM: To describe the occurrence, characteristics and outcome among patients with out-of-hospital cardiac arrest who required continuation of cardiopulmonary resuscitation (CPR) on admission to the emergency department. PATIENTS: all patients in the municipality of Göteborg who suffered out-of-hospital cardiac arrest, were reached by the emergency medical service (EMS) system and in whom CPR was initiated. Period for inclusion in study: 1 Oct. 1980-31 Dec. 1992. RESULTS: of 334 out-of-hospital cardiac arrests, 2,319 (68%) were receiving on-going CPR at the time of admission to hospital. Of these, 137 patients (6%) were hospitalized alive and 28 (1.2%) could be discharged from hospital. Of these patients, 39% had a cerebral performance categories (CPC) score of 1 (no cerebral deficiency), 18% had a CPC score of 2 (moderate cerebral deficiency), 36% had a CPC score of 3 (severe cerebral deficiency) and 7% had a CPC score of 4 (coma) at discharge. Among patients discharged. 76% were alive after 1 year. CONCLUSION: among consecutive patients with out-of-hospital cardiac arrest, CPR was ongoing in 68% of them on admission to hospital. Among these patients, 6% were hospitalized alive and 1.2% were discharged from hospital. Thus, among patients with ongoing CPR on admission to hospital, survivors can be found but they are few in numbers and extensive cerebral damage is frequently present.

Experience of an emergency mobile asthma treatment programme.

In order to reduce mortality and the need for hospital care for patients suffering from acute asthma, an emergency programme was set up. An ambulance crew, trained in coronary-pulmonary resuscitation was instructed in dealing with acute asthma and delegated to give 24 h treatment with bronchodilators (inhaled salbutamol and ipratropium bromide). If there was no, or only slight, improvement with this therapy, nurses (daytime) were delegated to give injections with corticosteroids (terbutaline and theophylline). Over a period of 2 years, 240 patients, 115 women and 125 men, were treated on 367 occasions. In 127 patients (53%), two or more treatments were given. The number of times treatment was given, as well as the proportion of females to males, increased the younger the patients were. Out of all the cases, more than 70% improved after treatment. On arrival, 21 patients (6%) were unconscious. After therapy, 15/21 patients (71%) survived. This may correspond to a similar reduction in mortality (population about 350,000 inhabitants), as it is unlikely that unconscious patients can survive without intensive care.