Current discharge management of acute coronary syndromes: data from the Rijnmond Collective Cardiology Research (CCR) study.

BACKGROUND: Medical discharge management of acute coronary syndromes (ACS) remains suboptimal outside randomised trials and constitutes an essential quality benchmark for ACS. We sought to evaluate the rates of key guideline-recommended pharmacological agents after ACS and characteristics associated with optimal treatment at discharge. METHODS: The Rijnmond Collective Cardiology Research (CCR) registry is an ongoing prospective, observational study in the Netherlands that aims to enrol 4000 patients with ACS. We examined discharge and 1-month follow-up medication use among the first 1000 patients enrolled in the CCR registry. Logistic regression was performed to identify patient and hospital characteristics associated with collective guideline-recommended pharmacotherapy at hospital discharge. RESULTS: At discharge, 94 % of patients received aspirin, 100 % thienopyridines, 80 % angiotensin-converting enzyme inhibitors/angiotensin-II receptor blockers, 87 % ß-blockers, 96 % statins, and 65 % the combination of all 5 agents. ST-segment elevation myocardial infarction, hypertension, hypercholesterolaemia, and enrolment in an interventional centre were positive independent predictors of 5-drug combination therapy at discharge. Negative independent predictors were unstable angina and advanced age. CONCLUSION: Current data from the CCR registry reflect a high quality of care for ACS discharge management in the Rotterdam-Rijnmond region. However, potential still remains for further optimisation.

Normalisation of the ECG in a patient with right bundle branch block by cardiac pacing.

Right ventricular apical pacing (RVA) appears to have potential deleterious effects on myocardial systolic and diastolic left ventricular function, especially in patients with intact AV conduction. Therefore, new pacing sites in the right ventricle are being explored to overcome these detrimental effects. Alternative pacing sites in the right ventricle are the right ventricular outflow tract (RVOT) and the right ventricular septum (RVS). In this case report, we demonstrate an exceptional form of ventricular fusion, namely normalisation of the QRS complex in a patient with pre-existing right bundle branch block by RVS pacing. To our knowledge, this is the first report in the literature where right ventricular pacing could restore a complete RBBB to a normal QRS complex by stimulating distally from the anatomical position of the RBBB, due to fusion between artificial right ventricular stimulation and intrinsic conduction over the left bundle of the specific His-Purkinje system.

A giant pseudoaneurysm becoming apparent after cardiac resynchronisation therapy.

A 57-year-old male patient with coronary artery disease developed a pseudoaneurysm after an inferior infarct in 1997. He underwent coronary bypass surgery and resection of the pseudoaneurysm located at the inferior wall. Unfortunately, the pseudoaneurysm recurred due to dehiscence of the patch, necessitating a second surgical intervention. After six years he developed progressive heart failure due to severe left ventricular dysfunction. He was referred to our institution for cardiac resynchronisation therapy (CRT) because of drug refractory heart failure which was associated with a left bundle branch block, ejection fraction of 12%, and a NYHA class IV status. After successful implantation of a biventricular pacemaker, a remarkable clinical recovery was observed. Left ventricular function improved and echocardiography now demonstrated that the pseudoaneurysm at the inferior wall had recurred for the third time. This diagnosis could not be established by preoperative echocardiography.

Hemodynamic effects of pimobendan given orally in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

Pimobendan (UD-CG 115 BS) was administered orally to 23 patients with congestive heart failure (functional class IV) caused by coronary artery disease (11 patients) or idiopathic dilated cardiomyopathy (12). All patients received maintenance doses of digoxin, furosemide and warfarin. Baseline data, collected during 15 hours, stayed within a 10% range. A 10-mg oral dose of pimobendan increased the heart rate from 95 +/- 20 to 109 +/- 24 beats/min (p less than 0.003). The pulmonary artery wedge pressure decreased from 23.0 +/- 5.9 to 10.1 +/- 5.2 mm Hg (p less than 0.0001), the cardiac index increased from 1.9 +/- 0.4 to 3.3 +/- 0.7 liters/min/m2 (p less than 0.0001) and the left ventricular stroke work index increased from 2,005 +/- 927 to 3,065 +/- 1,161 ml/mm Hg/m2 (p less than 0.0001). Statistically significant improvements in hemodynamic variables were still present 10 hours after the administration of pimobendan. Most patients felt better and reported no angina or other side effect, the incidence of ventricular arrhythmias was unchanged and no electrocardiographic changes suggesting ischemia were observed. Patients with severe congestive heart failure experienced a prolonged improvement of their cardiovascular condition after a single dose of pimobendan.

Prevalence of retrograde conduction in heart block after DDD pacemaker implantation.

Electrophysiologic studies were performed before DDD pacemaker implantation in 50 patients with symptomatic heart block. The patients were separated into 2 groups. Group I consisted of patients with intact retrograde conduction and group II consisted of patients with blocked retrograde conduction. After pacemaker implantation, postventricular atrial refractory periods in patients in group I were programmed at 50 to 100 ms, in excess of the retrograde conduction times measured during electrophysiologic studies. In group II patients, postventricular atrial refractory periods were routinely programmed at 300 ms. During follow-up, patients visited the outpatient clinic at 3-month intervals for noninvasive assessment of the prevalence of retrograde conduction, and to test the inducibility of pacemaker-mediated tachycardias. The mean follow-up of group I (15 patients) was 27 +/- 10 months, whereas the mean follow-up of group II (35 patients) was 19 +/- 9 months. The mean number of noninvasive tests performed during follow-up was 8 +/- 3 per patient for group I and 5 +/- 3 per patient for group II. In group I, retrograde conduction remained intact in 12 patients (p less than 0.01). In 29 of 31 patients in group II, retrograde conduction remained absent (p less than 0.01). In 4 patients in group II, chronic atrial fibrillation occurred during follow-up. Chronic atrial fibrillation did not occur in any patient in group I. During serial electrophysiologic testing, no pacemaker-mediated tachycardias could be induced in any patient in group I or II.(ABSTRACT TRUNCATED AT 250 WORDS)

[Hemodynamic effects of intravenous perfusion of amrinone in increasing doses in 12 patients with severe heart decompensation]. / Effets hémodynamiques d'une perfusion intraveineuse d'amrinone à doses croissantes chez douze patients en décompensation cardiaque sévère.

Twelve patients with severe heart failure were given amrinone by intravenous infusion in doses rising from 1 to 2, 3 and 4 mg X min-1, the interval between each dose being 30 min. The total cumulative dose was 300 mg over 120 min. Haemodynamic measurements were started the day before treatment to take into account nycthemeral fluctuations in haemodynamics and the possible effects of maintenance treatments and meals, all factors which might influence the baseline values. When given at a rate of more than 2 mg X min-1, amrinone significantly improved cardiac function (p less than 0.001). The mean pulmonary capillary pressure fell from 24.1 +/- 5.3 to 13.7 +/- 8.6 mmHg, and the cardiac index rose from 1.75 +/- 0.40 to 2.51 +/- 0.32 1 X min-1 X m-2. Heart rate and blood pressure were not significantly modified. No adverse reaction was observed during the infusion and the following 24 hours. Thus, intravenous amrinone proved effective in patients with severe heart failure, with maximal effects being obtained in doses of 3 mg X min-1.

Pacemaker safety and long-distance running.

OBJECTIVE: To prove that long-distance running is safe for athletes with pacemaker devices, pacemaker function was evaluated in nine long-distance runners. METHOD: Nine runners participated in a nine-month training programme that involved running for 1000 or 2000 km in preparation for either a full or a half marathon. A professional coach, three cardiologists and a technician - all with running experience - conducted the training and medical checkups. Commercial heart rate monitors were used during training to assess heart rates at rest, and during exercise and long-distance running. Sensing and pacing functions of the pacemaker system were tested during training sessions as well as during the race. In addition, the ChampionChip (a time registration device used in competition) and the Polar heart rate monitor (a widely used self-monitoring device) were tested for possible interference with the pacemaker. RESULTS: All nine athletes completed the Amsterdam 2001 half or full marathon without any pacemaker dysfunction. A short survey after two years showed no pacemaker dysfunction. CONCLUSION: Long-distance running is safe for athletes with pacemaker implants. Overall fitness and sufficient endurance training remain the prerequisites for maintaining the condition necessary for successful completion of a marathon regardless of medical status. In our study, it became clear that for patients who had received a pacemaker because of complete heart block, the upper rate of the pacemaker programme needed to be adjusted to 170 to 180 ppm to insure 1:1 atrio-ventricular synchrony during high atrial rates. It is concluded that there is no a priori reason for cardiologists to advise against long-distance running in athletes with pacemakers. Patients with known or suspected structural heart disease should be screened according the recommendations.

Pacemaker lead endocarditis: A rare diagnosis with a varied presentation.

We present a patient with a pacemaker lead endocarditis who showed no signs of pocket infection but with high fever and signs of infection in the routine laboratory tests. A diagnosis of pacemaker lead endocarditis must be considered in all patients with fever and infection parameters who have a pacemaker inserted, not only in the first weeks after implantation but also late after implantation, as long as no other cause of infection has been found. Transthoracal echocardiography alone is not sensitive enough to establish the correct diagnosis. Transoesophageal echocardiography (TEE) is mandatory to demonstrate the presence or absence of a vegetation on a pacemaker lead.

DDDR pacing for symptomatic patients with hypertrophic obstructive cardiomyopathy: The first experience in the Netherlands with pacing in HOCM.

BACKGROUND: Hypertrophic obstructive cardiomyopathy (HOCM) is a primary cardiac disorder with a heterogeneous expression. When medical therapy fails in patients with symptomatic HOCM, three additional therapeutic strategies exist: ventricular septal myectomy, alcohol-induced percutaneous transluminal septal myocardial ablation (PTSMA) of the first septal branch of the anterior descending artery and pacemaker implantation. In this paper we present the results of seven patients in whom a dual-chamber pacemaker was implanted to reduce the gradient in the left ventricular outflow tract (LVOT) and to relieve their symptoms. METHODS: In patients with drug refractory symptomatic HOCM, not eligible for surgery, pacemaker therapy was recommended. Symptomatic HOCM was defined as symptoms of angina and dyspnoea, functional class NYHA 3-4 and a resting LVOT gradient during Doppler echocardiography of more than 2.75 m/s (30 mmHg). In these patients, a dual-chamber pacemaker was implanted with a right ventricular lead positioned in the right ventricular apex and an atrial lead positioned in the right atrial appendage. In all patients the AV setting was programmed between 50 and 100 ms, using Doppler echocardiography to determine the optimal filling and to ensure ventricular capture. RESULTS: A statistically significant reduction of the LVOT gradient was observed in all patients. The pre-implantation gradient in the LVOT measured by Doppler echocardiography varied from 3-5.8 m/s with a mean of 4.7±1.1 m/s. The post-implantation gradient varied from 1.4-2.6 m/s with a mean of 1.9±0.4 m/s (p<0.001). Symptomatic improvement was present in all patients. NYHA functional class went from 3-4 (mean 3.1±0.5) pre-implantation to 1-2 mean (1.3±0.4) after implantation (p<0.001). During a mean follow-up of 2.3±1.1 years, the improvement in functional class was maintained. CONCLUSION: Our preliminary results demonstrate that dual-chamber pacing is an effective and safe treatment for symptomatic patients with HOCM.

Recommendations for pacemaker implantation for the treatment of atrial tachyarrhythmias and resynchronisation therapy for heart failure: A report from the task force on pacemaker indications of the Dutch Working Group on Cardiac Pacing.

Today, new pacing algorithms and stimulation methods for the prevention and interruption of atrial tachyarrhythmias can be applied on patients who need bradycardia pacing for conventional reasons. In addition, biventricular pacing as additive treatment for patients with severe congestive heart failure due to ventricular systolic dysfunction and prolonged intraventricular conduction has shown to improve symptoms and reduce hospital admissions. These new pacing technologies and the optimising of the pacing programmes are complex, expensive and time-consuming. Based on many clinical studies the indications for these devices are beginning to emerge. To support the cardiologist's decision-making and to prevent waste of effort and resources, the 'ad hoc committee' has provided preliminary recommendations for implantable devices to treat atrial tachyarrhythmias and to extend the treatment of congestive heart failure respectively.

Cell-mediated lipoprotein transport: a novel anti-atherogenic concept.

Lipoprotein transport is thought to occur in the plasma compartment of the blood, where lipoproteins are modulated by various enzymatic reactions. Subsequently, lipoproteins can migrate through the endothelial barrier to the subendothelial space or are taken up by the liver. The interaction between pro-atherogenic (apoB-containing) lipoproteins and blood cells (especially monocytes and macrophages) in the subendothelial space is well known. This lipoprotein-inflammatory cell interplay is central in the development of the atherosclerotic plaque. In this review, a novel interaction is described between lipoproteins and both leukocytes and erythrocytes in the blood compartment. This lipoprotein-blood cell interaction may also be related to the process of atherosclerosis by inducing inflammatory changes in the case of leukocytes (pro-atherogenic) and as an anti-atherogenic transport-system by adherence to erythrocytes. Triglyceride rich lipoprotein (TRL)-mediated leukocyte activation can lead to an inflammatory situation with generation of oxidative stress and the production of cytokines, ultimately resulting in acute endothelial dysfunction. Binding of apoB containing lipoproteins to erythrocytes may be a potential anti-atherogenic mechanism protecting the vessel wall from the pro-inflammatory effects of these lipoproteins and also playing a role in the removal of these particles from the circulation. One of the proposed mechanisms of this interaction implies complement activation on the lipoprotein surface and binding to the Complement Receptor 1 (CR1) on erythrocytes and leukocytes, followed by clearance by the liver.

A severed pacemaker lead entrapped in a hepatic vein.

Complete lead fracture is a uncommon phenomenon in cardiac pacing. Recently we encountered a patient with a severed lead at routine pacemaker follow-up visit. In this case report, the typical ECG changes and noninvasive pacemaker measurements are discussed. The chest roentgengram showed the position of the proximal part of the lead, but this technique could not establish the exact position of the distal part of the lead. Ultrasound recording of the upper abdomen demonstrated that the distal part of lead was entrapped in the great hepatic vein. Since this position was stable with one end in the right ventricular apex and the other end in a hepatic vein, no further action was undertaken to remove this part of lead. The proximal part of the lead and the pulse generator were explanted. So far the clinical course of the patient has been uneventful. Strategies to remove severed leads are discussed based on a review of the literature.

Atrial capture and dual chamber pacing.

During dual chamber pacing it is sometimes impossible to assess atrial capture even on the 12-lead ECG. We developed a strategy to identify atrial capture when it is not possible to do so by ECG, and when the ECG shows no evidence of spontaneous or paced atrial activity.