Philip C. Adams

NICE guidance. Chest pain of recent onset: assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin

Chest pain is a very common symptom; 20% to 40% of the general population will experience chest pain during their lives,1 and in the UK, up to 1% of visits to a general practitioner are because of chest pain.2 Approximately 700 000 visits (5%) to the emergency department in England and Wales and up to 25% of emergency hospital admissions are because of chest pain.3 There are many causes of chest pain, some of which are benign, while others are potentially life threatening. Importantly, in patients with chest pain caused by an acute coronary syndrome (ACS) or angina, there are effective treatments to improve symptoms and prolong life, emphasising the importance of making timely and accurate diagnoses in patients in whom chest pain may be of cardiac origin. This guideline4 addresses the assessment and diagnosis of patients with recent onset chest pain/discomfort that may be of cardiac origin. Unlike many other National Institute for Health and Clinical Excellence (NICE) clinical guidelines it does not make recommendations for the management of the condition once the diagnosis is made. The NICE unstable angina and NSTEMI clinical guideline5 was published at the same time as the chest pain guideline, and a NICE clinical guideline for the management of angina is currently being prepared.6 The guideline has two separate diagnostic pathways. The first is for patients with acute chest pain who may have an ACS and the second for those with intermittent stable chest pain who may have stable angina. The guideline deals with chest pain of suspected cardiac origin. Thus, for example, the guideline does not apply to patients with pain considered to be caused by recent trauma to the chest. However, many patients presenting with chest pain do not have such clearly apparent alternative explanations and need …

Pacemaker-Induced Superior Vena Cava Syndrome: Report of Four Cases and Review of the Literature

GOUDEVENOS, J.A., et al.: Pacemaker‐Induced Superior Vena Cava Syndrome: Report of Four Cases and Review of the Literature Superior vena cava syndrome due to transvenous pacing leads is a rare event. We describe four cases. One occurred among 3,100 primary pacemaker insertions performed at our institution. In the other three cases the primary insertion had been performed elsewhere. Over 30 cases have been reported previously. Local infection, which preceded the development of superior vena cava syndrome in each of our four cases, and the presence of a severed retained lead, as in three of our cases, are important predisposing factors. There is no strong evidence that multiple lead insertion, if each lead remains intact, significantly increases the risk. The pathology at the site of obstruction includes thrombosis and in some cases fibrotic narrowing. Venous angiography is useful to show the site of obstruction, the extent of collateral circulation and to assess the response to treatment. Treatment should include removal of any infected pacemaker apparatus, anticoagulation and, if symptoms are of recent onset, thrombolytic therapy. Most patients improve but in those who do not angioplasty or surgical relief of the obstruction may be helpful.

Complications Associated with Retained Pacemaker Leads

Retention of functionless pacemaker leads may occur following mechanical or infective problems (potentially or definitely infected) or after electrical failure of the lead. One hundred nineteen patients with a pacemaker lead for leads) retained between 1970 and 1990 were reviewed retrospectively. Lead retention after an intervention dictated by potential or definite infection of the pacing system resulted in complications in 27 of 53 patients (51%), which in 22 patients (42%) were major (septicemia, superior vena cava syndrome, and further surgery under general anesthesia for recurrent “infective” problems) including three deaths. Complications were less likely if lead retention occurred after electrical failure with three minor and two major (surgery under general anesthesia, superior vena cava syndrome) complications in 66 patients (P < 0.001). Bacteriology of swabs taken at the time of retention in the patients with potential or definite infection was unhelpful in predicting future complications: 8/18 patients (44%) whose swabs were negative had complications of which 5/18 (28%) were major. In our experience retention of functionless pacemaker leads after an intervention dictated by potential or definite infection of the pacing system, is associated with significant morbidity and mortality and should be avoided.

Rescue thrombolysis: alteplase as adjuvant treatment after streptokinase in acute myocardial infarction.

BACKGROUND--In acute myocardial infarction patients who do not reperfuse their infarct arteries shortly after thrombolytic treatment have a high morbidity and mortality. Management of this high risk group remains problematic, especially in centres without access to interventional cardiology. Additional thrombolytic treatment may result in reperfusion and improved left ventricular function. METHODS--Failure of reperfusion was assessed non-invasively as less than 25% reduction of ST elevation in the electrocardiographic lead with maximum ST shift on a pretreatment electrocardiogram. 37 patients with acute myocardial infarction who showed electrocardiographic evidence of failed reperfusion 30 minutes after 1.5 MU streptokinase over 60 minutes were randomly allocated to receive either alteplase (tissue type plasminogen activator (rt-PA) 100 mg over three hours) (19 patients) or placebo (18 patients). 43 patients with electrocardiographic evidence of reperfusion after streptokinase acted as controls. Outcome was assessed from the Selvester Q wave score of a predischarge electrocardiogram and a nuclear gated scan for left ventricular ejection fraction 4-6 weeks after discharge. RESULTS--Among patients in whom ST segment elevation was not reduced after streptokinase, alteplase treatment resulted in a significantly smaller electrocardiographic infarct size (14% (8%) v 20% (9%), P = 0.03) and improved left ventricular ejection fraction (44 (10%) v 34% (16%), P = 0.04) compared with placebo. This benefit was confined to patients who failed fibrinogenolysis after streptokinase (fibrinogen > 1 g/l). In patients in whom ST segment elevation was reduced after streptokinase, infarct size and left ventricular ejection fraction were not significantly different from those in patients treated with additional alteplase. CONCLUSION--Patients without electrocardiographic evidence of reperfusion after streptokinase may benefit from further thrombolysis with alteplase.

Effect of sex, age, and weight on ejection fraction and end-systolic volume reference limits in gated myocardial perfusion SPECT

BackgroundThe left-ventricular ejection fraction (EF) and end-systolic volume (ESV) are strong predictors of prognosis for cardiac death. Gated myocardial perfusion single-photon emission computed tomography (gSPECT) may be used to measure ESV and EF. However, systematic differences may exist between referred populations. Our aim was to derive male and female reference limits for left-ventricular functional parameters, and determine the effect of age, weight, and body surface area (BSA).Methods and ResultsThe ejection fraction and ESV were derived using QGS software for 127 patients with normal gSPECT studies. The lower reference limits of EF were 46.2% and 55.6% for men and women, respectively. The upper reference limits of ESV were 30.4 mL and 21.4 mL, and 15.7 mL/m2 and 11.1 mL/m2, when indexed to BSA for men and women, respectively. There was no correlation between EF and age, weight, or BSA (P>.05). There was a small decrease in ESV with age, and an increase with weight and BSA (P<.05). The sex-specific differences remained after adjusting for confounding variables.ConclusionsWe demonstrated a significant sex difference for all functional parameters measured, and we established the influence of patient age and weight. Local reference limits for ESV and EF have been established, and the latter are transferable to other departments operating similar protocols.

Prospective comparision of unstable angina versus non-Q wave myocardial infarction during antithrombotic therapy ☆

Abstract Objectives. This study was designed to compare the response of unstable angina and non-Q wave myocardial infarction during treatment with antithrombotic therapy. Background. Antithrombotic therapy is beneficial in patients with these two coronary syndromes. Methods. In a multicenter trial of antithrombotic therapy in unstable angina or non-Q wave myocardial infarction, 358 patients admitted within 48 h of chest pain were randomized to antithrombotic therapy with either 1) aspirin alone, or 2) aspirin plus heparin followed by aspirin plus warfarin, and were prospeclively followed up for 12 weeks. Admission cardiac enzyme analyses revealed unstable angina in 268 patients and non-Q wave myocardial infarction in 62. Given an event rate of about 25%, this study has a power of 80% to detect a 50% difference between the two groups. Results. Patients with unstable angina and non-Q wave myocardial infarction were similar with regard to age, gender, coronary risk factors and prior antianginal medication. Primary end points at 12 weeks were recurrent ischemia, infarction and death. In the non-Q wave group, all infarctions and death occurred within the 1st week. Conclusions. Patients with unstable angina or non-Q wave myocardial infarction on antithrombotic therapy haw a similar total number of ischemic events by 12 weeks. However, despite maximal medical therapy with antianginal and antithrombotic medication, patients with non-Q wave infarction have a significantly higher rate of reinfarction and death.

Strikingly Low Prevalence of Atrial Fibrillation in Elderly Tanzanians

To determine the prevalence of atrial fibrillation (AF) in individuals aged 70 and older in a rural African community.

Accuracy of algorithms for detection of atrial fibrillation from short duration beat interval recordings

Atrial fibrillation (AF) is characterised by highly variable beat intervals. The aims of the study were to assess the accuracy of AF detection algorithms from short analysis durations and to validate prospectively the accuracy on a large community-based cohort of elderly subjects. Three algorithms for AF detection were evaluated: coefficient of variation (CV), mean successive difference (Δ) and coefficient of sample entropy (COSEn), using two databases of beat interval recordings: 167 recordings of 300 s duration for a range of rhythms acquired in a hospital setting and 2130 recordings of 10s duration acquired in the community. Using the longer recordings receiver operating characteristic (ROC) analysis was used to identify optimal algorithm thresholds and to evaluate analysis durations ranging from 5s to 60s. An ROC area of 93% was obtained at recording duration of 60s but remained above 90% for durations as low as 5s. Prospective analysis on the 2130 recordings gave AF detector sensitivities from 90.5% (CV and Δ) to 95.2% (COSEn), specificities from 89.3% (Δ) to 93.4% (COSEn) and accuracy from 89.3% (Δ) to 93.4% (COSEn), not significantly different to those obtained on the initial database. AF detection algorithms are effective for short analysis durations, offering the prospect of a simple and rapid diagnostic test based on beat intervals alone.

Attaining United States and European Guideline LDL-cholesterol Levels with Simvastatin in Patients with Coronary Heart Disease (the GOALLS Study)

Summary The effectiveness and safety of simvastatin in reducing low-density lipoprotein cholesterol (LDL-C) to target levels in patients with coronary heart disease (CHD) were evaluated in the GOALLS (Getting to Appropriate LDL-C Levels with Simvastatin) study. This multinational, multicentre, prospective, open-label, study consisted of a six-week diet washout period followed by a 14-week titrate-to-goal treatment period with simvastatin. One hundred and ninety-eight men and women with documented CHD and a fasting LDL-C level between 115 mg/dl (3.0 mmol/l) and 180 mg/dl (4.7 mmol/l) and triglycerides (TGs) ≤ 400 mg/dl (4.5 mmol/l) were enrolled. The patients were started on 20 mg simvastatin with dose titration up to 80 mg if the LDL-C remained above 100 mg/dl at weeks 6 and 10. The key efficacy parameters were the percentage of patients achieving US and European LDL-C goals [≤ 100 mg/dl (2.6 mmol/l) and ≤ 115 mg/dl (3.0 mmol/l), respectively]. Safety was evaluated by monitoring laboratory tests and recording adverse events. After 14 weeks of simvastatin (20–80 mg) treatment, approximately 90% of the patients achieved LDL-C goals according to US (87%) and European (94%) guidelines. Most patients (72–93%) achieved target LDL-C levels on 20 mg simvastatin. An estimated 14% of the patients required titration to the 80 mg dose. Treatment with simvastatin (20–80 mg) produced statistically significant improvements in all measured lipid variables by the end of the study. The mean reductions in total cholesterol and LDL-C, and the median reduction in TG, were 28%, 41% and 16%, respectively. The increase in high-density lipoprotein cholesterol and apolipoprotein A-1 were 5% and 4%, respectively. Simvastatin was well tolerated across the dosage range. In conclusion, simvastatin, 20–80 mg/day, was safe and highly effective at reducing LDL-C levels. The recommended US and European LDL-C treatment goals were achieved in approximately 90% of the patients. These goals were similarly achieved for a variety of high-risk sub-groups (hypertensives, diabetics and elderly patients).

ATRIAL FLUTTER WITH 1:1 ATRIOVENTRICULAR CONDUCTION CAUSED BY PROPAFENONE

We describe a case of 1:1 atrial flutter in a patient with coronary disease taking propafenone. In atrial flutter, the atrial rate is usually about 300 beciis/min with 2:1 AV conduction and a ventricular rate of 150 beats/min. Class IA antiarrhythmic drugs, especially quinidine and disopyramide, may cause 1:1 AV response because they reduce atrial rate and are vagolytic. However, propafenone is a Class IC agent and has no anticholinergic properties, and the occurrence of 1:1 AV conduction at a rate of about 250 beats/min is an important side, effect that, although uncommon, should be recognized.