Left atrial thrombus formation after brief interruption of rivaroxaban.

Every year, nearly 250000 atrial fibrillation patients require temporary interruption of anticoagulation therapy for invasive procedures, acute illness, or bleeding events. Rivaroxaban is an oral anticoagulant that works by inhibiting factor Xa leading to a blockage of thrombin production, which inhibits platelet aggregation and thrombus formation. As with other anticoagulants, there is an increased risk of a thrombotic event occurring when rivaroxaban therapy is temporarily interrupted (TI) or prematurely discontinued. The 30-day rate of stroke or systemic embolism for rivaroxaban TI is 0.36%. Possible factors for higher than expected rates of embolic events include a prothrombotic perioperative environment among patients having TI for surgery and a prothrombotic environment associated with TI due to bleeding. The ROCKET AF study showed that there was no detectable difference in the risk of stroke and systemic embolism for participants treated with rivaroxaban vs warfarin undergoing TI. Another analysis suggested that the risk for stroke from TI is probably higher in the rivaroxaban group with 3 to 30 days discontinuation. Alternative anticoagulation therapy such as bridging should always be considered when stopping rivaroxaban.

Cycling Induced Spontaneous Coronary Artery Dissection in a Healthy Male.

INTRODUCTION: Spontaneous coronary artery dissection (SCAD) is a rare but important cause of acute coronary syndrome with a spectrum of disease that can include unstable angina, acute myocardial infarction, or sudden cardiac death. It has also been found in case reports to be caused by shear stress from physical exertion. We present a rare cycling induced SCAD that occurred in our institution in an otherwise healthy male with no cardiac risk factors. CASE PRESENTATION: A 36-year-old male presented to the emergency department with complaints of lightheadedness and diaphoresis after a bicycle fall. In the emergency department, he complained of feeling lightheaded and diaphoretic and having mid back pain. Patient had an ECG performed which showed lateral ST segment elevation and troponin I that was positive. A coronary angiography was subsequently performed demonstrating a spontaneous coronary artery dissection of left anterior descending coronary artery. CONCLUSION: SCAD is a rare cause of myocardial infarction, occurring in healthy individuals, which is rarely reported in the literature. Nearly 70% are diagnosed in postmortem studies after sudden cardiac death. Only 12 cases have been reported from activities involving physical exertion and no studies to our knowledge demonstrate this.

Right ventricular strain rate and strain analysis in patients with repaired tetralogy of Fallot: possible interventricular septal compensation.

BACKGROUND: Indices such as strain rate (SR) and strain (epsilon) are free of geometric assumptions and, thus, may provide new insights into right ventricular (RV) function and compensatory mechanisms in repaired tetralogy of Fallot (TOF). METHODS: All those with postoperative (>1 year) TOF had echocardiography evaluation of SR and epsilon indices along the RV lateral free wall (RVFW) and the interventricular septum (IVS) in the apical 4-chamber view. Pulmonary regurgitation, pulmonary stenosis, QRS duration, RV ejection fraction, and RV dimension were also measured and compared with control subjects. RESULTS: There were 15 patients with TOF (7 +/- 4 years old) 6 +/- 3 years remote from surgical repair and 25 control subjects (10 +/- 5 years old). In the patients with TOF, systolic and diastolic SR and epsilon in the RVFW were significantly reduced but were normal in the IVS. In the RVFW, reduced systolic SR and epsilon correlated with reduced RV ejection fraction (r = -0.7 [P <.01] and -0.6 [P <.03], respectively), and poorer early diastolic SR correlated with poorer RV ejection fraction (r = 0.7, P <.01). CONCLUSIONS: In patients with postoperative TOF, systolic and diastolic RV SR and epsilon were impaired in the RVFW but preserved in the IVS. We speculate that IVS myocardial function is preserved as a compensatory mechanism for impaired RVFW function.

Sleep, inflammation and cardiovascular disease.

In data from prospective cohort studies, self report of insufficient or disturbed sleep is related to increased overall and cardiovascular morbidity. Inflammation is established as a key mechanism in the development of arteriosclerotic heart and vascular disease. Inflammation has been considered a possible link between short sleep and cardiovascular disease and morbidity. Measures of inflammation are increased by experimental sleep deprivation, but in cohort studies a relationship of sleep duration to inflammatory markers is less clear. In these studies the association of self reported short sleep to cardiac morbidity is confounded by many psychological and socioeconomic variables. More studies are needed to explain the link between short sleep duration and cardiac morbidity. Experimental studies of sleep deprivation mimicking habitual shortened sleep over long time intervals, and studies employing sleep extension in habitual short sleepers will allow better characterization of the health benefits of adequate sleep duration. Prospective cohort studies should include objective measures of sleep duration and should to control for the known confounding variables.