Early administration of thrombolysis can prevent myocardial necrosis: time is myocardium.

A case is presented in which a 66-year-old man received thrombolysis for an acute ST elevation myocardial infarction (STEMI) within 6 minutes of developing chest pain. An ECG performed 10 minutes after thrombolysis showed complete resolution of the ST segment elevation and showed no other abnormality. An echocardiogram showed normal left ventricular function and there was no detectable myocardial necrosis, as evidenced by two negative troponin assays. The case clearly reinforces the benefits of the rapid delivery of thrombolysis when appropriate for patients with STEMI. Clinicians need to be aware of the benefits of early thrombolysis as laid out in the national service framework. Evidence for the early administration of thrombolysis, data from the Myocardial Infarction National Audit Project and the future with regard to improving thrombolysis times are discussed.

Diagnosing Paroxysmal Atrial Fibrillation: Are Biomarkers the Solution to This Elusive Arrhythmia?

Atrial fibrillation (AF) is the commonest sustained arrhythmia globally and results in significantly increased morbidity and mortality including a fivefold risk of stroke. Paroxysmal atrial fibrillation (PAF) constitutes approximately half of all AF cases and is thought to represent an early stage of the disease. This intermittent form of atrial arrhythmia can be a challenge to identify and as a result many affected individuals are not prescribed appropriate antithrombotic therapy and hence are at risk of stroke and thromboembolism. Despite these adverse outcomes there have been relatively few diagnostic advances in the field since the introduction of the Holter monitor in 1949. This review aims to establish the available evidence for electrophysiological, molecular, and morphological biomarkers to improve the detection of PAF with reference to the underlying mechanisms for the condition.

Compliance and effectiveness of 1 year's home telemonitoring. The report of a pilot study of patients with chronic heart failure.

UNLABELLED: Patients with a diagnosis of heart failure, registered at the study practice, were recruited into the study. First, they had a cardiologist's assessment. They were then randomised into telemonitored patients who measured pulse, BP, weight and video consulted, and controls. AIM: To examine the acceptability, effectiveness and reliability of home telemonitoring. RESULTS: A high proportion of those invited took part (n=20/24). Compliance with measuring weight, pulse and BP remained high throughout the study. The data collection system and secure web-server were reliable. The telemonitoring group complied better with collecting prescriptions for their cardiac drugs. Video consulting started with enthusiasm, but became less useful. There were no significant differences in the quality of life (GHQ) and Chronic Heart Failure (Guyatt) questionnaire scores between the telemonitored group and the controls. CONCLUSIONS: Home telemonitoring is an acceptable reliable intervention. Baseline rates for compliance with self-monitoring are set out in this study. Benefit in terms of compliance with medication and self-monitoring is still seen after 1 year. Video consulting over ordinary telephone lines did not show sustained benefit, and was not complied with.

Class III antiarrhythmics in overdose. Presenting features and management principles.

Class III (Vaughan-Williams classification) antiarrhythmic drugs prolong the cardiac action potential without affecting depolarisation. The 3 class III drugs currently in general use are amiodarone, sotalol and bretylium. The presenting features of acute toxicity are different for each agent and are, therefore, discussed separately. Several new class III antiarrhythmic agents are under development, including dofetilide and d-sotalol, but specific data on overdoses of these potent class III drugs are not yet available. Amiodarone toxicity following acute overdose is rare because poor bioavailability and a large volume of distribution limit the peak serum concentration. Toxicity is low even if high serum concentrations are reached. The major risks from acute overdose are hypotension (intravenous administration only) and arrhythmia if other factors, such as hypokalaemia or additional antiarrhythmic agents are present. Management is chiefly directed at reducing absorption with activated charcoal or cholestyramine, and monitoring for arrhythmia. Sotalol is a beta-blocker with additional class III activity. Oral bioavailability is high, and overdosed patients can present with bradycardia, hypotension and major haemodynamic collapse. The combination of bradycardia and prolongation of the QT interval is associated with malignant arrhythmias such as torsade de pointes. Management principles include observation and correction of bradycardia with endocardial pacing, intravenous adrenergic drugs and glucagon. The risk of arrhythmia can be substantially reduced by intravenous potassium and magnesium supplements. d-Sotalol is a potent class III drug devoid of beta-blocking activity and may be expected to share the proarrhythmic affects of the racemic mixture in overdose, without pronounced hypotension and bradycardia. Intravenous bretylium in overdose causes an initial hypertensive effect, followed by profound hypotension from systemic vasodilation. Management is directed at controlling hypotension with volume expansion and norepinephrine (noradrenaline).

Monocyte expression of tissue factor and adhesion molecules: the link with accelerated coronary artery disease in patients with chronic renal failure.

OBJECTIVE: To investigate the expression of monocyte tissue factor (MTF) and adhesion molecules in patients with chronic renal failure (CRF) and to look for any correlation with thrombin generation and Lp(a) lipoprotein. DESIGN: A study of MTF expression and adhesion molecules, prothrombin fragments 1+2 (PTf1+2), an index of thrombin generation, and lipoproteins in patients with CRF and in normal control subjects. BACKGROUND: Patients with end stage renal failure have an increased risk of coronary artery disease despite advances in therapy. Stimulated monocytes are potent activators of blood coagulation through the generation of MTF, which was recently implicated in the aetiology of acute coronary ischaemic syndromes. METHODS: MTF expression and adhesion molecules were measured in whole blood using immunofluorescence of monocytes labelled with anti-tissue factor antibody and CD11b and c by flow cytometry. PTf1+2 and Lp(a) lipoprotein in plasma were measured by enzyme linked immunosorbent assay (ELISA). PATIENTS: 70 patients with CRF without documented coronary artery disease (30 patients with CRF undialysed, 20 patients undergoing chronic ambulatory peritoneal dialysis (CAPD), and 20 undergoing haemodialysis (HD)), together with 20 normal controls, were studied. RESULTS: The (mean (SD)) increased MTF of CRF (48.0 (29) v 33.3 (7.2) mesf unit/100 monocytes in controls, p = 0.04) was more pronounced in patients undergoing dialysis (HD 73.1 (32.8) (p < 0.003) and CAPD 62.8 (28.9) mesf unit/100 monocytes, p < 0.04). MTF activity showed a positive correlation with both PTf1+2 and serum creatinine (p < 0.003) but not with Lp(a) lipoprotein. Lp(a) lipoprotein was significantly increased in both dialysis groups compared with controls (p < 0.005) and non-dialysis CRF groups (p < 0.02). Monocyte adhesion molecule (CD11b) was significantly higher in all three CRF groups than in the controls (p = 0.006). CONCLUSION: This study has demonstrated a hypercoagulable state in patients with CRF. This was especially pronounced in the dialysis patients. These findings provide a possible explanation for the increased cardiovascular and cerebrovascular morbidity and mortality in these patients.

Factor V Leiden polymorphism (FV Q506) in patients with ischaemic heart disease, and in different populations groups.

A point mutation in the factor V gene (FV Q506) renders factor V resistant to inactivation by activated protein C. The frequency of this mutation is known to be significantly increased in patients with thrombophilia. There are conflicting reports on the significance of the polymorphism in patients with ischaemic heart disease. We determined the frequency of FV Q506 in a control Caucasian population, and compared it with 192 Caucasian patients admitted to coronary care and assessed as having myocardial infarction (MI) or unstable angina plus previous MI. There was no significant difference between the two groups. A cohort of 105 asymptomatic Afro-Caribbeans showed a much reduced frequency of the polymorphism.

Angiotensin-1 converting enzyme (ACE) polymorphism in patients presenting with myocardial infarction or unstable angina.

A deletion/insertion polymorphism in the ACE gene has been reported previously as a potent factor for myocardial infarction. We have tested the frequency of the deletion (D) allele of the ACE gene in 308 consecutive patients admitted to coronary care with chest pain. The gene frequencies were compared with those of 348 controls recruited from the London area. Of 108 Caucasian patients with myocardial infarction, the DD genotype was found more frequently than the combined DI and II genotypes (Chi-square, chi 2 = 5.07, 2P = 0.024). The overall D gene frequency was higher in myocardial infarction patients (125 of 216, 58%) than in controls (347 of 696, 49.9%) (chi 2 = 3.79, 2P = 0.052). In contrast, the DD genotype and D allele frequencies in patients with unstable angina were similar to those found in our normal population. A nonsignificant difference in allele frequency between myocardial infarction and unstable angina patients was observed but the small numbers of subjects studied precludes a more formal comparison. Since unstable angina and myocardial infarction represent a spectrum of coronary thrombosis, it is possible that the DD genotype favours the development of myocardial infarction, perhaps through the presence of higher serum ACE concentrations.

Coronary angiography using a portable super-C-arm imaging system in a district general hospital.

BACKGROUND: New generation portable super-C-arm imaging systems may offer an alternative means of performing coronary angiography at a lower cost compared with a fixed laboratory. We evaluated the use of one such system (GE-OEC 9800) in a district hospital setting. METHODS: The demographics, procedure and screening times, emitted radiation dose and diagnoses of the first 200 consecutive patients were obtained from a prospective database. Comparison between the portable and fixed systems were made by analysing results from similar cohorts of patients who underwent angiography by the same operators. Image quality was assessed in 23 patients, by an independent cardiologist, comparing the GE-OEC 9800 angiograms with repeat images using a fixed laboratory Philips (HM 3000) system within 3 months of the first study. RESULTS: The procedure time (mean (S.D.)) was 18.9 (0.8) min for the 200 cases. The screening time was 255 (15) s with an emitted radiation of 22.8 (1.4) Gy/cm(2). Comparison between the C-arm and fixed systems revealed significantly longer screening time (230.6 (14.6) vs. 157 (12.9) s, p<0.001), whilst the total radiation doses were not significantly different (21.1 (1.5) vs. 18.6 (1.11) Gy/cm(2)). Independently assessed image quality was satisfactory. The main variance in 57 lesions seen in the 23 patients using the angiograms obtained from the fixed laboratory as reference included overestimated stenosis (two lesions), underestimated stenosis (or subsequent disease progression) (four lesions), lack of appreciation of side-branch ostial involvement (two lesions) and vessel calcification (one lesion). CONCLUSIONS: Portable imaging systems can offer a reliable and cost-effective diagnostic coronary angiography service in a district hospital.

The association of germ cell tumours of the testis with sarcoid-like processes.

Sarcoid-type pulmonary lymphadenopathy associated with testicular cancer is a rare condition which has been previously reported in only 14 cases. Earlier case reports have failed to distinguish between generalized sarcoidosis as opposed to a local granulomatous reaction to tumour. We describe a further 8 cases of the association and provide strong supportive evidence for systemic sarcoidosis in 5 of our patients. In 3 of our patients with systemic sarcoidosis there was coexisting testicular cancer requiring additional treatment. We therefore advise caution in the interpretation of the clinical and histological findings in these patients, and recommend thorough investigation of all such cases.

[The diagnosis of myocardial damage during coronary angioplasty by the analysis of the isoforms of the enzyme creatine kinase MB]. / Diagnóstico de daño miocárdico durante la angioplastia coronaria mediante el análisis de las isoformas de la enzima creatincinasa MB.

BACKGROUND: The existence of myocardial damage during percutaneous transluminal coronary angioplasty (PTCA) is controversial. Mild elevations in creatine kinase (CK) activity and its isoenzyme MB (CKMB) in patients who underwent PTCA have been reported. However, other authors failed to confirm these elevations. The low sensitivity of total CK and CKMB activity for the detection of myocardial damage in different settings other than myocardial infarction might account for the controversial findings. Measurement of CKMB isoforms has been shown to have a higher sensitivity than the assessment of CK or CKMB activity for early diagnosis of myocardial infarction. Its sensitivity for the diagnosis of myocardial damage in settings other than infarction is not well described. OBJECTIVES: The aim of our study was two-fold: 1) to assess the incidence of myocardial damage after PTCA and 2) to compare the sensitivity of total CK and CKMB activity and measurement of CKMB isoforms for the detection of myocardial damage. METHODS: 14 patients (11 men and 3 women) with chronic stable angina underwent PTCA. Two electrocardiographic leads were monitored from the beginning of the procedure until 30 minutes after the PTCA. ST segment shifts of at least 1 mm, lasting for more than 1 minute, were considered indicative of myocardial ischemia. The duration of ischemic episodes was measured from the onset of the ST shift until its return to baseline. Total ischemic time, in minutes, was the sum of the duration of every ischemic episode. Blood samples were drawn before PTCA and serially during the first 24 hours post PTCA. CK (normal < 200 U/l) and CKMB (normal < 14 U/l) activities were measured. The CKMB isoforms were separated by electrophoresis, measured by densitometric scanning and their ratio calculated (CKMB2/CKMB1 normal < 1.5). RESULTS: Vessels which underwent PTCA were: the left anterior descending artery (LDA) in 5 patients, the circumflex coronary artery (Cx) in 3 patients, right coronary artery (RCA) in 3 patients, LDA and Cx in 1 patient and Cx and RCA in 2 cases. Eleven patients underwent balloon dilatation, 1 underwent atherectomy (Rotablator) and two patients had treatment with both Rotablator and balloon angioplasty. Ischemic ST segment shifts were found in ten patients and the median of total ischemic time was 13.5 minutes (interquartile range: 2-15 minutes). Total CK and CKMB activities were within the normal range in every patient whereas in 7 patients (50%) the peak ratio CKMB2/CKMB1 was above the normal range. There were no differences in age, sex, number of vessels or lesions treated or in the time of balloon inflation between patients with and without abnormal CKMB2/CKMB1 peak. However, the ischemic time was significantly higher in patients with CKMB2/CKMB1 > 1.5 (median 15 vs 0 minutes; p = 0.023). CONCLUSIONS: Myocardial damage during PTCA is not an uncommon finding. The CKMB isoforms are more sensitive markers of myocardial damage during PTCA than total CK or CKMB activities.

Association of Helicobacter pylori and Chlamydia pneumoniae infections with coronary heart disease and cardiovascular risk factors.

OBJECTIVE: To investigate the relation between seropositivity to chronic infections with Helicobacter pylori and Chlamydia pneumoniae and both coronary heart disease and cardiovascular risk factors. DESIGN: Cross sectional study of a population based random sample of men. Coronary heart disease was assessed by electrocardiography, Rose angina questionnaire, and a history of myocardial infarction; serum antibody levels to H pylori and C pneumoniae were measured, risk factor levels determined, and a questionnaire administered. SETTING: General practices in Merton, Sutton, and Wandsworth, south London. SUBJECTS: 388 white south London men aged 50-69. MAIN OUTCOME MEASURES: Evidence of coronary risk factors and infection with H pylori or C pneumoniae. RESULTS: 47 men (12.1%) had electrocardiographic evidence of ischaemia or infarction. 36 (76.6%) and 18 (38.3%) were seropositive for H pylori and C pneumoniae, respectively, compared with 155 (45.5%) and 62 (18.2%) men with normal electrocardiograms. Odds ratios for abnormal electrocardiograms were 3.82 (95% confidence interval 1.60 to 9.10) and 3.06 (1.33 to 7.01) in men seropositive for H pylori and C pneumoniae, respectively, after adjustment for a range of socioeconomic indicators and risk factors for coronary heart disease. Cardiovascular risk factors that were independently associated with seropositivity to H pylori included fibrinogen concentration and total leucocyte count. Seropositivity to C pneumoniae was independently associated with raised fibrinogen and malondialdehyde concentrations. CONCLUSIONS: Both H pylori and C pneumoniae infectins are associated with coronary heart disease. These relations are not explained by a wide range of confounding factors. Possible mechanisms include an increase in risk factor levels due to a low grade chronic inflammatory response.

A controlled pilot study in the use of telemedicine in the community on the management of heart failure--a report of the first three months.

This is a controlled pilot study of twenty patients to see if heart failure management can be optimised in the community using telemedicine. The study seeks to examine the feasibility, acceptability and reliability of using telemedicine in this context. Heart failure is a common condition. It is an important cause of mortality and morbidity and has large cost implications for the NHS. Most patients are managed in the UK in General Practice based on clinical assessment by the practitioner. Twenty patients with a mean age of 75.1 years and mean New York Heart Association grade of 1.75 were randomised in to two equal groups (telemonitoring and control) and observed for a period of three months. All twenty patients had a Cardiologist assessment and quality of life measurement at the beginning and end of the study. Patients in the telemedicine group had their blood pressure, pulse and weight data collected daily and undertook a weekly video conference with the nurse. Control patients had their blood pressure, weight and pulse measured at six weekly intervals. The study has been extended for a further six months beyond its initial three-month observation period to see if the initial short term benefit in the telemedicine group is maintained.

Increased monocyte tissue factor expression in coronary disease.

OBJECTIVE: To investigate whether monocyte expression of tissue factor is increased in patients with acute coronary syndromes and chronic stable angina. DESIGN: Cross sectional study of monocyte tissue factor expression in patients with ischaemic heart disease and control subjects. BACKGROUND: Unstable angina and myocardial infarction are associated with enhanced mononuclear cell procoagulant activity. Procoagulant activity of blood monocytes is principally mediated by tissue factor expression. Tissue factor initiates the coagulation cascade and monocyte tissue factor expression may therefore be increased in these syndromes. METHODS: Monocyte tissue factor expression was measured cytometrically in whole blood flow using a polyclonal rabbit antihuman tissue factor antibody. PATIENTS: 30 patients with acute myocardial infarction, 17 with unstable angina, 13 with chronic stable angina, and 11 normal control subjects. RESULTS: Increased proportions of monocytes expressing tissue factor (> 2.5%) were found in none of 11 (0%) normal subjects, five 13 (38%) patients with stable angina, 11 of 17 (64%) patients with unstable angina, and 16 of 30 (53%) patients with myocardial infarction (2P = 0.006). Blood from all subjects showed similar monocyte tissue factor expression similar monocyte tissue factor expression (46.1 (15.1)%) after lipopolysaccharide stimulation. CONCLUSION: Hypercoagulability associated with acute myocardial infarction, unstable angina, and chronic stable angina may be induced by tissue factor expressed on circulating monocytes.

Aggressive pattern of angina after successful coronary angioplasty: the role of clinical and angiographic factors.

To assess possible clinical and angiographic factors associated with acute coronary events following PTCA, we performed quantitative angiography in 168 consecutive patients who had undergone successful angioplasty in a native vessel (94 for stable angina, 74 for unstable angina), and who were restudied (24 +/- 15 weeks; range 4 to 52) because of recurrent anginal symptoms. Of the 168 patients, 38 (Group 1) were restudied because the pattern of angina was aggressive (unstable angina in 31, myocardial infarction in 7) and 130 because of effort-related angina (Group 2). the two patient groups were well matched for extent of initial disease but patients in Group 1 were younger (P=0.03). PTCA for unstable angina was originally performed more frequently in Group 1 than in Group 2 (27 of 38 patients (71% vs 47 of 130 patients (36%), P=0.0004). Disease progression in non-dilated segments occurred in 10 patients (26%) in Group 1 compared with eight (6%) in Group 2 (P=0.0004). Disease progression in non-dilated segments occurred in nine patients (24%) in Group 1 and in Group 2 (P=0.0004). Disease progression in non-dilated segments occurred in nine patients (24%) in Group 1 and in 10 (8%) in Group 2 (P=0.0006). Our conclusion is that patients who require re-investigation as a result of angina which has become aggressive following PTCA are usually those who originally underwent PTCA for unstable angina. These patients have a higher incidence of occlusive restenosis or disease progression.

Angiographic stenosis progression and coronary events in patients with 'stabilized' unstable angina.

BACKGROUND: Recent studies suggest that angiographically complex coronary stenoses are associated with an adverse short-term outcome. It is not known, however, if this applies to unstable angina patients who stabilize on medical therapy. METHODS AND RESULTS: We prospectively studied 85 consecutive patients with unstable angina who stabilized on medical therapy but were found to require angioplasty for treatment of obstructive coronary disease. Angiography was carried out at admission, and patients were restudied 8 +/- 4 months (mean +/- SD) after the first angiogram. Ischemia-related stenoses were identified and classified as "complex" (irregular borders, overhanging edges, or thrombus) or "smooth" (absence of complex features). Stenosis progression (> or = 20% diameter reduction or new total occlusion) was assessed by automated edge detection. At initial angiography, there were 198 stenoses (> or = 50%, 102), of which 85 (54 complex and 31 smooth) were ischemia related. At restudy, 21 ischemia-related stenoses and 8 non-ischemia-related stenoses progressed (25% versus 7%, P = .001). Seventeen of the 21 ischemia-related stenoses that progressed developed into total occlusion compared with 3 of the 8 non-ischemia-related stenoses (P = .02). Changes in average stenosis severity and in absolute stenosis diameter were significantly larger in ischemia-related stenoses than in non-ischemia-related stenoses (P = .03). Eighteen (34%) complex stenoses progressed, compared with 3 (10%) smooth lesions (P = .02). During follow-up, 1 patient died (myocardial infarction) and 25 patients had nonfatal coronary events that were associated with progression of ischemia-related stenoses in 14 (56%). CONCLUSIONS: In unstable angina patients who stabilize medically, subsequent short-term stenosis progression and coronary events are common. The unstable coronary lesion (particularly complex stenoses) is often not stabilized and will continue to progress over the ensuing months.

Low-energy DC catheter ablation of left atrial ectopic tachycardia that had resulted in reversible cardiomyopathy.

Catheter ablation of automatic atrial tachycardia has been previously reported in a small number of adult cases in which the ectopic focus was predominantly located in the right atrium. We report on a patient with atrial automatic tachycardia originating in the left atrium, in whom successful low-energy DC catheter ablation was performed via a transseptal puncture. The patient presented with severe congestive cardiac failure that resolved following the procedure. Catheter ablation in such cases is feasible, it can reverse tachycardia induced ventricular function impairment, and should be attempted before resorting to open heart surgical ablation.

Heart rate variability depression in patients with unstable angina.

The degree of reduction in heart rate variability (HRV) after myocardial infarction has been shown to have prognostic significance, but HRV has not been studied extensively in patients with unstable angina. We assessed spectral and nonspectral measurements of HRV in 52 patients with unstable angina, 52 patients with acute myocardial infarction, and 41 normal subjects. The spectral bands of 0.04 to 0.15 Hz (low frequency), 0.15 to 0.4 (high frequency), and nonspectral parameters SDNN, SDANN, SDNN index, rMSSD, and pNN50 were calculated from continuous 24-hour ECGs. All measures of HRV were reduced in patients with acute coronary syndromes compared to normal controls (p < 0.001), and there was no significant difference in measure of HRV between unstable angina and myocardial infarction patients. In patients with unstable angina who stabilized after admission, HRV had increased by the second 24 hours of monitoring. In contrast, HRV was further depressed in patients who had episodes of chest pain or transient ST-segment depression during the second 24 hours. rMSSD, pNN50, and SDNN index were lower in patients with unstable angina who had transient silent ischemia compared to those without silent ischemia. Of the patients with unstable angina, 4 died and 1 had nonfatal acute myocardial infarction within 11 months. HRV was lower in these patients than in patients without further cardiac events.

Effect of magnesium sulphate in patients with unstable angina. A double blind, randomized, placebo-controlled study.

AIMS: Administration of intravenous magnesium sulphate has been shown to be protective during acute myocardial ischaemia and it may therefore have beneficial effects in unstable angina. The purpose of this study was to assess the effects of a 24-h infusion of magnesium in patients with unstable angina. METHODS AND RESULTS: Patients who presented with unstable angina with electrocardiographic changes were randomized to receive a 24-h intravenous infusion of magnesium or placebo within 12 h of admission. The primary endpoint was myocardial ischaemia, as assessed by 48 h Holter monitoring. Resting 12-lead ECGs, creatine kinase-MB release and urinary catecholamines were also assessed. Patients were followed for 1 month. Thirty-one patients received magnesium sulphate and 31 placebo. Baseline characteristics and extent of coronary disease were similar in both groups. On 48 h Holter monitoring, 14 patients (50%) had transient ST segment shifts in the magnesium group vs 12 patients (46%) in the placebo group. However, there were fewer ischaemic episodes in the magnesium group (51 vs 101, P < 0.001) and there was a trend towards an increase in the total duration of ischaemia in the placebo group compared to the magnesium group in the second 24 h (2176 min vs 719 min respectively, P = 0.08). Regression of T wave changes on the 24 h ECG occurred more frequently in patients who received magnesium compared to those treated with placebo (11 patients vs 0 patients respectively, P < 0.005). Creatine kinase-MB release was significantly less at 6 and 24 h in patients who received magnesium compared to those treated with placebo. Catecholamine excretion was lower in patients treated with magnesium than in those treated with placebo (adrenaline: 1.05 +/- 0.16 vs 1.61 +/- 0.32 ng.mmol-1 creatinine; noradrenaline: 9.99 +/- 1.82 vs 18.48 +/- 2.41 ng.mmol-1 creatinine respectively in the first 12 h sample, P < 0.05). CONCLUSIONS: Intravenous magnesium reduces ischaemic ECG changes, creatine kinase-MB release and urinary catecholamine excretion in the acute phase of unstable angina. Thus, magnesium may be a beneficial additional therapy for these patients. Further studies are required to confirm these finding.