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Summary Background Bivalirudin, with selective use of glycoprotein (GP) IIb/IIIa inhibitor agents, is an accepted standard of care in primary percutaneous coronary intervention (PPCI). We aimed to compare antithrombotic therapy with bivalirudin or unfractionated heparin during this procedure. Methods In our open-label, randomised controlled trial, we enrolled consecutive adults scheduled for angiography in the context of a PPCI presentation at Liverpool Heart and Chest Hospital (Liverpool, UK) with a strategy of delayed consent. Before angiography, we randomly allocated patients (1:1; stratified by age [ vs ≥75 years] and presence of cardiogenic shock [yes vs no]) to heparin (70 U/kg) or bivalirudin (bolus 0·75 mg/kg; infusion 1·75 mg/kg per h). Patients were followed up for 28 days. The primary efficacy outcome was a composite of all-cause mortality, cerebrovascular accident, reinfarction, or unplanned target lesion revascularisation. The primary safety outcome was incidence of major bleeding (type 3–5 as per Bleeding Academic Research Consortium definitions). This study is registered with ClinicalTrials.gov, number NCT01519518. Findings Between Feb 7, 2012, and Nov 20, 2013, 1829 of 1917 patients undergoing emergency angiography at our centre (representing 97% of trial-naive presentations) were randomly allocated treatment, with 1812 included in the final analyses. 751 (83%) of 905 patients in the bivalirudin group and 740 (82%) of 907 patients in the heparin group had a percutaneous coronary intervention. The rate of GP IIb/IIIa inhibitor use was much the same between groups (122 patients [13%] in the bivalirudin group and 140 patients [15%] in the heparin group). The primary efficacy outcome occurred in 79 (8·7%) of 905 patients in the bivalirudin group and 52 (5·7%) of 907 patients in the heparin group (absolute risk difference 3·0%; relative risk [RR] 1·52, 95% CI 1·09–2·13, p=0·01). The primary safety outcome occurred in 32 (3·5%) of 905 patients in the bivalirudin group and 28 (3·1%) of 907 patients in the heparin group (0·4%; 1·15, 0·70–1·89, p=0·59). Interpretation Compared with bivalirudin, heparin reduces the incidence of major adverse ischaemic events in the setting of PPCI, with no increase in bleeding complications. Systematic use of heparin rather than bivalirudin would reduce drug costs substantially. Funding Liverpool Heart and Chest Hospital, UK National Institute of Health Research, The Medicines Company, AstraZeneca, The Bentley Drivers Club (UK).

475 patients with suspected uncomplicated myocardial infarction (MI) were divided into 3 groups based on their entry ECG: group 1--significant ST elevation; group 2a--ST depression or T inversion; group 2b--normal ECG. Infarction was confirmed in 99.7% of group 1, 68.5% of group 2a and 39.7% of group 2b patients. Despite similar clinical, haemodynamic and historical variables at presentation, group 1 patients had significantly larger MI, more in-hospital complications and a higher short-term and long-term mortality (P less than 0.005) than group 2 patients. The entry ECG of patients with suspected MI is an excellent and simple predictor of those who are most likely to have an MI confirmed and identifies a group of patients at high risk of death or developing complications.

With advancing technology and ever-expanding indications for implantable cardiac pacing and defibrillation devices, this article reviews modern day practice in this field. This article focuses on topics pertinent not only to cardiologists but also to general physicians, medical trainees and allied medical specialties.

Objective To establish the associations and prognostic utility of angiographic, clinical and HRV parameters in a large cohort of patients undergoing diagnostic cardiac catheterisation (CC). Methods Patients undergoing CC as elective day cases were enrolled at a single tertiary center from September 2001 to January 2003. Patient data, serum biochemistry, current drug therapy, catheter reports and five minute high resolution electrocardiograph (ECG) recordings were prospectively recorded and validated in an electronic archive. ECG recordings were used to generate time domain (SDNN (standard deviation of NN intervals)) and spectral HRV parameters (low frequency (LF) and high frequency (HF) power). Significant associations between dichotomized HRV variables and covariates were investigated using binary logistic regression. The independent prognostic ability of clinical markers was evaluated using the Cox proportional hazard model. Results 841 consecutive consenting patients of mean age 61±10 years were recruited into the study with a mean follow-up period of 690±436 days. In multivariate analysis decreasing LF spectral power was independently associated with proximal right coronary stenosis OR (odds ratio)=1.65 (95% CI=1.16–2.36), P =0.006 and to all cause mortality OR=5.01 (95% CI=1.47–17.01), P =0.010. Increasing LF power was also independently associated with normal coronary angiograms in patients investigated suspected coronary disease without a confirmed prior history of a coronary ischaemic event OR=2.16 (95% CI=1.26–3.73), P =0.002. Conclusions Reduced LF power independently predicts all cause mortality in a large cohort of patients receiving medical therapy after elective CC. LF power was also independently associated with >75% proximal RCA stenosis.

Background: There are limited data on the impact of successful chronic total occlusion (CTO) revascularization by percutaneous coronary intervention (PCI) on survival. We performed a retrospective study comparing the survival between patients with a successful and a failed CTO revascularization by PCI. Methods: Between January 1, 2000 and June 30, 2004, 543 of 5803 (9.4%) patients underwent PCI for a CTO at our center. A CTO was defined as an occlusion of the artery present for at least 3 months with Thrombolysis in Myocardial Infarction flow grade 0 or 1. Patient records were linked to a national database to monitor all deaths during follow up. Propensity matching was used to balance out case mix differences. Results: Technical success for CTO was 377 of 543 (69.4%). In-hospital mortality was 0.3% and 1.2% for the CTO success and CTO failure patients, respectively. During a mean (SD) follow up of 1.7 (0.5) years, the mortality rate was 2.5% in the CTO success patients and 7.3% in the CTO failure patients. The crude hazard ratio for death with CTO failure was 3.92 (95% confidence intervals 1.56–10.07; P = 0.004). The rates of coronary artery bypass were 3.2% vs. 21.7% (P < 0.001) for the CTO success and CTO failure patients, respectively. Our propensity matched 157 CTO success to CTO failure patients and the associated hazard ratio for death with CTO failure was 4.63 (95% confidence interval 1.01–12.61; P = 0.049). Multivariate analysis showed that CTO failure was an independent predictor of death. Conclusion: Patients with a successful revascularization of a CTO by PCI have an increased survival rate compared to patients with a failed CTO procedure. © 2007 Wiley-Liss, Inc.

Aortic dissection is an acute medical emergency with a high mortality. Crucial to improving survival is early recognition and appropriate treatment. This review describes the presenting clinical features and imaging techniques used in the diagnosis of aortic dissection and outlines the treatment modalities.

Superior vena caval (SVC) obstruction following permanent pacemaker lead extraction is a serious but uncommon complication. This report describes the case of an 83-year-old man treated by balloon angioplasty and femoral pacemaker implantation.

BACKGROUND: Coronary artery stenting is particularly useful during percutaneous coronary intervention for long lesions previously associated with a low procedural success rate and a high complication rate of dissection and occlusion. Current treatment options include implantation of a single long stent, multiple contiguous stents, or 'spot' stenting. However, multiple stent implantation may result in sections of overlapping stent or gaps of unstented segments and is an independent predictor of restenosis. The early and intermediate clinical outcome of single and multiple long stent (/= 30 mm) implantation is not established. METHODS AND RESULTS: The authors retrospectively identified 123 consecutive patients who had undergone stenting using one or more long coronary stents. Baseline clinical data, procedural outcomes and completed clinical follow-up to 52 weeks were obtained by case-note review. The majority (69%) required intervention for stable coronary disease. Seventy-seven per cent of lesions were either type B2 or C and only 2% were in saphenous vein grafts. The procedural success rate was 94%. A total of 15 major events occurred in 13 patients (11%). Ten acute events occurred and five events were during the follow-up period from 30 days to 52 weeks. Two patients died, one from uncontrolled bleeding secondary to the use of antithrombotic agents and one at four weeks due to sudden death. One patient had a postprocedural infarct. Two patients required in-hospital repeat revascularization for acute vessel closure and eight required revascularization during follow-up (three cases of occlusion/thrombosis and five cases of restenosis). CONCLUSIONS: The use of long coronary stents (/= 30 mm) for the treatment of long diffuse native vessel disease, saphenous vein graft disease and long coronary dissections is associated with a reasonable procedural success rate and acceptable early and intermediate-term clinical outcomes.

Pericardial cysts are rare. We provide high-quality imagery demonstrating a giant cyst using plain radiography, ultrasound and magnetic resonance imaging (MRI).

Coronary artery stenting minimizes the occurrence of abrupt closure and late restenosis after angioplasty. The range of stents now available allows interventional cardiologists to perform more complex angioplasties at lower risk. In the near future, biologically inert, biodegradable stents coated with antiproliferative and antithrombotic agents may become available.

A 38-year-old man underwent coronary artery bypass graft surgery for angina pectoris following myocardial infarction. During the following 28 years, he required two repeat coronary artery bypass graft surgical procedures, nine percutaneous coronary interventions and 17 coronary angiograms. His treatment included saphenous vein, left internal mammary artery and gastroepiploic artery grafting, percutaneous transluminal coronary angioplasty and intragraft thrombolytic therapy, directional coronary atherectomy, cutting balloon angioplasty, intracoronary stenting with bare-metal and drug-eluting stents, treatment for in-stent restenosis, stenting of the left main and circumflex coronary arteries and saphenous vein graft as well as intracoronary pressure wire diagnostics. In addition to his statin therapy, antiplatelets and angiotensin-converting enzyme inhibitors, he also underwent biventricular automatic implantable cardioverter-defibrillator implantation and atrioventricular node radiofrequency ablation for his impaired left ventricular function, ventricular tachycardia and rapid atrial fibrillation. The present unusual case represents almost 'the whole nine yards' of treatment that has become available to patients with coronary artery disease during the past 30 years of technological development.

Coronary artery perforation is an unusual but well recognised complication of Percutaneous Transluminal Coronary Angioplasty (PTCA) and coronary atherectomy and may lead to hemopericardium and cardiac tamponade. If the perforation cannot be sealed by prolonged inflation with a perfusion balloon catheter, emergency cardiac surgery is usually necessary. This case report describes the potential use of a "covered" coronary artery stent for sealing perforations in the coronary circulation.

Valvular endocarditis after percutaneous coronary intervention is unusual. We report a new case of mitral valve endocarditis after stent implantation to a saphenous vein graft.

In animal models, oxygen-derived free radicals have been found to be important mediators of reperfusion injury to ischemic but viable myocardium. However, in humans, there is no direct evidence of free radical production after the restoration of coronary artery patency in acute myocardial infarction. The purpose of this study was to quantitate and assess the time course of free radical production in coronary venous outflow in patients with acute myocardial infarction undergoing successful recanalization of the infarct-related artery by primary percutaneous transluminal coronary angioplasty (PTCA). Primary PTCA was performed in 17 patients with acute myocardial infarction of < 6 hours duration. Direct free radical production was assessed by coronary venous effluent blood sampling before PTCA and at timed intervals up to 24 hours (or 48 hours in 6 patients) after recanalization. All samples were added to the spin trapping agent alpha-phenyl N-tert butyl nitrone and analyzed by electron paramagnetic resonance spectroscopy. Vessel patency resulted in a sharp increase in free radical signal. Relative to the level before PTCA, the changes reached statistical significance after only 15 minutes (p < 0.05). Peak signals were observed between 1 1/2 and 3 1/2 hours (p < 0.001), then declined up to 5 hours. A second increase in signal level was detected between 18 and 24 hours despite no angiographic evidence of reocclusion. A gradual decline was observed after 24 hours. These findings provide the first direct and quantitative evidence of free radical production in the immediate postrecanalization phase after thrombotic occlusion of a major coronary artery in humans.

OBJECTIVES--To compare transmyocardial ischaemia and oxidative stress, as well as non-infarction myocardial injury, in patients randomised to intermittent hypothermic cardioplegia or continuous normothermic blood-potassium cardioplegia. DESIGN--Prospective randomised trial. SETTING--Tertiary cardiac referral centre. METHODS--24 patients undergoing elective coronary artery bypass surgery were randomised to hypothermic (13 patients, mean (SEM) age 59.5 (2.6) years) or normothermic (11 patients, mean (SEM) age 59.7 (3.3) years) cardioplegia. Transmyocardial oxidative stress and ischaemia were assessed by the difference in plasma concentrations of oxidised glutathione and lactate respectively, from samples taken simultaneously from the coronary sinus and aortic root. Blood samples were taken just before cross clamp application and at intervals up to 15 min after cross clamp release. Non-infarction myocardial injury was assessed by measurement of creatine kinase MB isoenzyme activity from peripheral venous blood taken 2 and 18 h after surgery. RESULTS--Intermittent hypothermic cardioplegia resulted in a significant increase in transmyocardial ischaemia (P < 0.001) and oxidative stress (P < 0.001). Evidence of significantly increased myocyte damage was also present (P < 0.01). No significant corresponding changes were present with normothermic cardioplegia. CONCLUSIONS--Normothermic blood cardioplegia seems to avoid significant changes in myocardial ischaemic status and consequent oxidative stress. This study provides direct evidence that normothermic cardioplegia offers enhanced myocardial protection compared with that of hypothermic cardioplegia. Certain subsets of patients may derive more benefit from normothermic cardioplegia, although it is unclear whether this would be the case for all patients.

Acute ST segment elevation myocardial infarction usually occurs when thrombus forms on a ruptured atheromatous plaque and occludes an epicardial coronary artery. Patient survival depends on several factors, the most important being restoration of brisk antegrade coronary flow, the time taken to achieve this, and the sustained patency of the affected artery. Histological appearance of a ruptured atheromatous plaque (bottom arrow) and occlusive thrombus (top arrow) resulting in acute myocardial infarction There are two main methods of re-opening an occluded artery: administering a thrombolytic agent or primary percutaneous transluminal coronary angioplasty. Effects of treatment with placebo, thrombolytic drugs, or primary percutaneous coronary intervention (PCI) on mortality, incidence of cerebrovascular events, and incidence of non-fatal re-infarction after acute myocardial infarction in randomised studies. Of the 1% incidence of cerebrovascular events in patients undergoing primary percutaneous intervention, only 0.05% were haemorrhagic. In contrast patients receiving thrombolytic drugs had a 1% incidence of haemorrhagic cerebrovascular events (P

The term acute coronary syndrome refers to a range of acute myocardial ischaemic states. It encompasses unstable angina, non-ST segment elevation myocardial infarction (ST segment elevation generally absent), and ST segment elevation infarction (persistent ST segment elevation usually present). This article will focus on the role of percutaneous coronary intervention in the management of unstable angina and non-ST segment elevation myocardial infarction; the next article will address the role of percutaneous intervention in ST segment elevation infarction. Although there is no universally accepted definition of unstable angina, it has been described as a clinical syndrome between stable angina and acute myocardial infarction. This broad definition encompasses many patients presenting with varying histories and reflects the complex pathophysiological mechanisms operating at different times and with different outcomes. Three main presentations have been described—angina at rest, new onset angina, and increasing angina. Spectrum of acute coronary syndromes according to electrocardiographic and biochemical markers of myocardial necrosis (troponin T, troponin I, and creatine kinase MB), in patients presenting with acute cardiac chest pain The process central to the initiation of an acute coronary syndrome is disruption of an atheromatous plaque. Fissuring or rupture of these plaques—and consequent exposure of core constituents such as lipid, smooth muscle, and foam cells—leads to the local generation of thrombin and deposition of fibrin. This in turn promotes platelet aggregation and adhesion and the formation of intracoronary thrombus. Diagram of an unstable plaque with superimposed luminal thrombus Unstable angina and non-ST segment elevation myocardial infarction are generally associated with white, platelet-rich, and only partially occlusive thrombus. Microthrombi can detach and embolise downstream, causing myocardial ischaemia and infarction. In contrast, ST segment elevation (or Q wave) myocardial infarction has red, fibrin-rich, and more stable occlusive thrombus. Distal embolisation of a platelet-rich thrombus causing occlusion of intramyocardial arteriole (arrow). Such …

Patients often ask about what precautions they should take to avoid damaging or affecting the function of their pacemaker. The commonest issues discussed by patients are set out below and are most often seen with unipolar systems. Table 10.1 lists sources of electromagnetic interference and the possible effects on pacemakers.

Sudden cardiac death (SCD) is defined as death from a cardiac cause occurring unexpectedly within a short time of onset of symptoms (usually within 1 h). It accounts for 325,000 deaths per year in the USA – an incidence of 0.1–0.2% per year in the adult population. SCD represents the largest proportion of the deaths attributable to coronary artery disease. Several risk factors have been identified for SCD and include previous myocardial infarction and myocardial scars, active coronary lesions, for example, ulcerated atheromatous plaques with subtotal or total thrombotic occlusion, and compromised left ventricular systolic function. In addition, there are familial cardiac conditions that may increase the risk of SCD such as Long QT syndrome (Fig. 17.1) and Brugada Syndrome (Fig. 17.2).

Complications associated with pacemaker implantation are generally uncommon when temporary and permanent pacing is performed by experienced personnel. Unfortunately, temporary pacing (and in some centers even permanent pacing) is carried out by junior doctors who are inexperienced and unsupervised – a scenario for an increased complication rate.

Troubleshooting after pacemaker implantation is the task of both the cardiac physiologist and the cardiologist. It is a process which begins at the time of implantation and should be readdressed not only if the patient re-presents with ongoing or new symptoms post-implant, but also at every routine follow-up appointment. Adherence to these rules not only promotes safe and effective pacemaker function, but also serves to increase device longevity and reduce the adverse effects of unnecessary or inappropriate cardiac pacing.

The implantation and follow-up of pacemakers and ICDs in children poses unique challenges. Less than 1% of all pacemakers and ICDs are implanted in children and the numbers of implants taking place within individual centers are low. In a recent US survey, the mean annual number of new pacemaker implants per center was less than 25. A significant proportion of the pediatric population who require pacemaker and ICD implantation are survivors of palliative surgical procedures for complex congenital heart disease (CHD). Physicians are thus faced with the difficult situation of implanting few devices in complex patients and as a result sometimes adult cardiologists may be asked to implant devices in children. This chapter focuses on the key differences between adults and children in terms of pacemaker and ICD indications, implantation, and follow-up.

Cardiac pacing is indicated for the treatment of both bradyarrhythmias and tachyarrhythmias.

After permanent pacemaker or device implantation, regular follow-up in a pacemaker clinic or transtelephonic follow-up is mandatory. The tests that should be performed include an assessment of battery life and time to elective replacement. The latter is assessed by the elective replacement indicator (ERI) for each device. The latter usually allows 6 months or more to arrange device replacement before end-of-life (EOL) parameters are reached when imminent replacement must take place in order to avoid loss of output and potentially serious clinical events.

Today, approximately three million people worldwide have a pacemaker and more than 600,000 pacemakers are implanted annually.

Although most adult patients requiring pacemaker or ICD implantation will have normal cardiac anatomy, occasionally significant abnormalities will be found only at the time of the procedure, since they had not given rise to symptoms or any obvious physical signs. These include persistent left-sided superior vena cava (SVC) (with or without a right-sided SVC), dextrocardia, atrial septal defect, and patent foramen ovale. Such abnormalities may give rise to practical problems during lead placement and operators should be aware to recognize the problem immediately and know how to deal with it. Patients (adults or children) with congenital structural cardiac abnormalities, such as transposition, corrected transposition, tetralogy of Fallot, univentricular heart, or post-operative “corrected” defects, will require special consideration before proceeding to the pacing theater. In particular, the operator will need to know whether the transvenous approach is feasible, what problems might be encountered during lead implantation, and how to seek the best and most stable of electrode positions. Preoperative investigations, including transthoracic and transesophageal echocardiography, CT and MRI cardiac imaging as well as angiography, for example, left arm venography, should be used to clarify the cardiac and venous anatomy in order to safely embark on transvenous lead placements. Simply reviewing previous surgical notes (following cardiac surgery in earlier life) or previous cardiac catheterization notes may be useful in noting anatomical abnormalities. In recent times with the advent of biventricular pacing, it is relevant also to know the position of the coronary sinus, for example in patients with Ebstein anomaly who have already undergone tricuspid valve replacement.

The rapid developments in technology and pacemaker research have enabled pacemakers and other implantable devices to be become more sophisticated. Devices have numerous programmable features and can store substantial amounts of diagnostic information related to device function, arrhythmia detection, cardiovascular hemodynamic parameters including transthoracic impedance and patient activity. Bi-directional telemetry using encoded and encrypted radiofrequency signals allows transmission of information to the implantable device from the programmer and to the programmer from the device. This process permits review of the programmed parameters and stored diagnostic data and reprogramming of device parameters to correct identified malfunctions and/or to optimize device function (Fig. 9.1).

Heart failure can potentially complicate all forms of heart disease. Over the last 20 years, there has been a significant increase in both its incidence and prevalence due to the advancing age of the population and improved survival from coronary heart disease – the principal cause of heart failure. Despite improvements in pharmacologic management, many patients with heart failure have severe, resistant symptoms and their prognosis remains poor. Medical therapy consists of angiotensin converting enzyme inhibitors (ACEI), aldosterone antagonists, and β-blockers, all of which have been shown to reduce morbidity and mortality. Digoxin and loop diuretics provide symptomatic benefit only. More recently, however, prospective randomized clinical trials have shown that cardiac resynchronization therapy (CRT), also known as biventricular pacing, results in improvements in LV function, exercise capacity, quality of life and mortality in selected patients with heart failure. This chapter will describe the rationale for CRT, the features that predict a potential benefit from CRT, the technique of implantation and the equipment required for the procedure, the complications that may occur, the follow-up that is required, and finally, the evidence that currently exists that supports its use.

In 1882, von Ziemssen reported that an electrical impulse could activate the exposed human heart! But it was not until almost 50 years later that two doctors reported the first cardiac pacing devices. In 1928, Mark Lidwell, an anesthetist at the Royal Prince Alfred Hospital in Sydney supported by physicist Edgar H. Booth of the University of Sydney, developed a device that delivered an alternating current via a needle inserted into the patient’s ventricle. At the Crown Street Women’s Hospital in Sydney, Lidwell used intermittent electrical stimulation of the heart and saved the life of a newborn child suffering cardiac arrest. He reported his work to the third Congress of the Australian Medical Society in 1929.

Over the past 15 years, training to be a competent implanter of cardiac electrical implantable devices (CEID) and expert in post-implant clinical and technical management has taken a more structured format than previously. However, there are still significant variations on the degree of formality from country to country! Perhaps the most formalized regulations on training come from the USA and these will be presented first. Although the European Society of Cardiology has published guidelines for pacing and cardiac resynchronization therapy, there are none specific to training in pacing. In the UK, most large specialist or tertiary referral centers which boast a large and advanced pacing/device implant and monitoring service will be responsible for teaching specialist fellows or registrars all aspects of cardiac electrophysiology, arrhythmias, pacemaker, and other device implantation as well as the basic techniques for interrogation, programming, and surveillance of pacemakers and ICDs. The Joint Royal Colleges of Physicians Training Board (JRCPTB) in the UK has produced a detailed document on the training requirements for those pursuing a specialist career in pacing. Elsewhere in the world, for example, Australasia, less detailed guidelines have been published by a Specialist Advisory Committee.

A 5-position NBG (NASPE/ BPEG Generic) Code is used internationally to describe the various pacemaker functions (Table 6.1).

Permanent pacemaker implantation is indicated to relieve symptoms of syncope, near syncope, dizziness, or dyspnea in patients with severe bradycardia and to improve prognosis in asymptomatic patients with impaired intracardiac conduction tissue. Indications for permanent pacemaker implantation are shown in Table 4.1. The ECG is the most important guide to whether pacing is indicated.

The day after permanent pacemaker implantation (or just prior to discharge if “day-case” pacing is in operation), lead position should be checked by performing a PA and lateral chest X-ray (see Chap. 7). Pneumothorax and early lead displacement should be excluded. A 12-lead ECG should confirm satisfactory pacing in atrium, ventricle, or both depending on the type of pacemaker implanted, usually by application of the programmer head over the device to produce a “magnet ECG strip.” The pacing threshold should ideally be checked and the pacing parameters set appropriately by the clinical physiologist to ensure satisfactory pacing and sensing, if necessary by adjusting the pulse width (0.1–1.0 ms), output (2.5–7.5 V), and sensitivity (0.25–8 mV) settings (Figs. 8.1, 8.2, and 8.3). The pacemaker’s upper (100–180 bpm) and lower rate (30–100 bpm) limit, pacing mode (e.g., AAI, VVI, VVI, DDD), rate response, polarity (uni- or bipolar), refractory period (200–500 ms), and AVD delay (0–300 ms), etc., should also be confirmed by the clinical physiologist using the programmer and the settings documented in the case notes. For day cases, these checks will be made by the technician before the patient leaves the pacing theater.

A classification of syncope is shown in Table 5.1 and guidelines on the diagnosis and management of syncope have been produced by the ESC in 2009 and are available on the website www.escardio.org.

Free-radical activity in coronary venous outflow was assessed before and after reperfusion in nine patients with acute infarction who had undergone successful recanalization of the infarct-related artery by primary coronary angioplasty. Free-radical activity was measured in serum samples from coronary venous outflow over a timed period of 24 hours by using (1) the percentage molar ratio (PMR) of the diene conjugate 9,11-linoleic acid, and (2) malonaldehyde concentration. Preangioplasty PMR means lay within the normal range, but showed a marked increase soon after successful recanalization. Relative to baseline, the changes over time reached statistical significance between 2 and 60 minutes. No statistically significant changes in malonaldehyde occurred over the study period. We conclude that successful recanalization of the infarct artery is associated with significantly elevated free-radical activity, as measured by the PMR of conjugated diene, in coronary venous outflow. Such patients may be at risk from free radical mediated reperfusion injury.

A twenty-three-year-old woman had an acute myocardial infarction during the early postpartum period successfully treated with intravenous strepto kinase. The possible mechanisms of postpartum myocardial infarction are re viewed, and the clinical implication for the use of streptokinase in this situation is discussed.

The objective of this blinded, randomized, prospective study was to assess whether supplementation of normal diet with omega-3 polyunsaturated fatty acids can reduce angiographically defined restenosis following coronary angioplasty. The study included all patients undergoing coronary angioplasty in this institution between January 1988 and January 1989. One hundred and twenty patients enrolled, 60 in each treatment group. All were randomized to either supplementation of normal diet with 3 g of omega-3 polyunsaturated fatty acids per day started 1-2 days prior to angioplasty and continued for 6 months (treatment group), or to receive standard therapy only (control group). Quantitative angiographically defined restenosis was assessed at 6 months post angioplasty. Restenosis occurred in 27.8% (95% CI 18.0-37.7%) of lesions in the treatment group and in 28.3% (CI 16.9-39.7%) of lesions in the control group, but the difference was not statistically significant. The study showed that diet supplemented with 3 g of omega-3 polyunsaturated fatty acids started 1-2 days preceding angioplasty does not reduce angiographically defined restenosis rate.

The relationship between family history of ischaemic heart disease and the presence of coronary heart disease was studied in 387 patients undergoing routine coronary arteriography prior to valve replacement. One hundred and seven patients (27.6%) had a family history of ischaemic heart disease. Of these, 52 (48.6%) had significant coronary artery disease compared with 60 of 280 (21.4%) patients without a family history (P < 0.001). The overall severity (coronary score) and extent (number of vessels) of coronary artery disease was greater in those patients with a family history (P < 0.001). Moreover, the incidence of significant coronary disease increases as the number of relatives with ischaemic heart disease also increase (P < 0.001). Multiple logistic regression analysis suggests that family history is an independent predictor of the presence of significant coronary artery disease.

At first glance, this chest X-ray appears to show a standard, right-sided permanent pacemaker. Further scrutiny, however, shows that the right internal jugular vein …

Data on effectiveness and safety following the implantation of very long segments of drug-eluting stents (DES) are lacking.To describe our experience of consecutive patients undergoing implantation of very long segments of DES (50 mm) in de novo coronary lesions.We evaluated major in-hospital complications, target lesion revascularization (TLR) rates and long-term outcomes in 88 consecutive patients (91 procedures) who underwent a single-vessel intervention with implantation of50 mm of overlapping DES to de novo lesions between October 2002 and October 2007. An additional 14 patients with long segments of in-stent restenosis, 10 receiving both DES and bare-metal stents for long-segment disease and 1 with long-segment disease in a saphenous vein graft were excluded from the study. Baseline clinical data, procedural outcomes and completed follow up were collected prospectively.Follow up was 100% complete up to April 30, 2008. The mean follow up was 26.5 months (6-60 months). The mean stent length was 70.6 mm (51-135 mm) and the average number of stents per vessel was 2.7 (2-5 stents). Acute complications included 1 case of acute stent thrombosis which was treated successfully, 1 case of aortic root dissection, and 1 case of retroperitoneal hemorrhage. The rate of non-Q-wave myocardial infarction (CKMB3 times normal) was 8%. During follow up, the rate of TLR was 6.5%. Five patients died, 4 of them due to noncardiac conditions. One death was attributed to possible late stent thrombosis (18 months) occurring suddenly 2 days post keloid repair. Two patients had definite very late stent thrombosis at 14 and 17 months.In our experience, the use of very long segments of DES is effective in treating diffuse de novo coronary artery lesions. However, longer-term follow up is necessary and more data are required to determine the optimum duration of dual antiplatelet therapy.