Purulent pericarditis,an uncommon entity in modern practice: a case report

We report an 82-year-old female with pneumococcal pneumonia. Antimicrobial therapy was started in an early stage of the disease. On the 10th day of admission she developed peripheral pitting oedema with elevated jugular venous pressure and a drop in blood pressure. Her electrocardiogram showed sinus tachycardia and concave upward ST-segment elevation in almost all leads. A transthoracic two-dimensional echocardiogram revealed a large circumferential pericardial effusion, with diastolic collapse of the right atrium and a mitral inflow pattern that suggested cardiac tamponade. Emergency pericardiocentesis was performed, releasing 600 cc of thick green purulent material, followed by good haemodynamic recovery. The haemodynamic state, pneumonic infiltrate and inflammatory parameters responded gradually to antimicrobial therapy and the patient recovered and was discharged after six weeks. We conclude that even susceptible strains of Streptococcus pneumonia in a patient with no predisposing factors may still cause purulent pericarditis, even in the era of adequate antibiotic therapy.     

Left and Right Ventricle Leads Switch as a Solution for T Wave Oversensing - How a Good Idea Turned Out Bad

A 50-year-old male with a CRT defibrillator received inappropriate ICD shocks due to T-wave oversensing. Decreasing the sensitivity to avoid T wave oversensing was not an option due to a suboptimal R-wave sensing amplitude. We decided to re-plug the LV lead in the RV port and the RV lead in the LV port. This however led to intermittent phrenic nerve stimulation due to mandatory bipolar (tip-ring) or unipolar (tip-can) pacing on the LV-lead from the RV port. Re-intervention was necessary with the implantation of an additional pacing/sensing RV lead. A software programmable choice to switch sensing and tachycardia detection from RV to LV lead could be a valuable feature in future CRT devices.     

Exercise related ventricular arrhythmias are related to cardiac fibrosis in hypertrophic cardiomyopathy mutation carriers

Aims

Hypertrophic cardiomyopathy (HCM) is a frequent cause of sudden cardiac death (SCD) due to exercise-related ventricular arrhythmias (ERVA); however the pathological substrate is uncertain. The aim was to determine the prevalence of ERVA and their relation with fibrosis as determined by cardiac magnetic resonance imaging (CMR) in carriers of an HCM causing mutation.

Methods

We studied the prevalence and origin of ERVA and related these with fibrosis on CMR in a population of 31 HCM mutation carriers.

Results

ERVA occurred in seven patients (23%) who all showed evidence of fibrosis (100% ERVA(+) vs. 58% ERVA(-), p = 0.04). No ventricular tachycardia or ventricular fibrillation occurred. In patients with ERVA, the extent of fibrosis was significantly larger (8 ± 4% vs. 3 ± 4%, p = 0.02). ERVA originated from areas with a high extent of fibrosis or regions directly adjacent to these areas.

Conclusions

ERVA in HCM mutation carriers arose from the area of fibrosis detected by CMR; ERVA seems closely related to cardiac fibrosis. Fibrosis as detected by CMR should be evaluated as an additional risk factor to further delineate risk of SCD in carriers of an HCM causing mutation.     

Thrombus in a normal left ventricle

A 47-year-old women known to have mixed connective tissue disease and hypertension, presented with acute right leg pain requiring urgent right common femoral artery embolectomy with fasciotomy. During the immediate postoperative period, full-dose heparin and oral anticoagulant therapy were started. An echocardiogram revealed an echo-dense mass in the left ventricular cavity, but no additional cardiac abnormality (figure 1). On the sixth day of admission the patient developed a cerebrovascular accident with echocardiographic disappearance of the left ventricular mass.