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Approximately 15 to 40% of cerebral infarctions and transient ischemic attacks (TIA) are of cardiac origin. Knowledge of a significant cardiac disease arouses the suspicion of cardiogenic embolism, but its diagnosis requires identification of the source of embolism. Atrial fibrillation is the most common cause of cardiogenic embolism, and should be actively sought after an ischemic cerebrovascular attact. The detection of atrial fibrillation or an intracardiac thrombus in these patients requires initiation of permanent anticoagulant therapy. Transesophageal echocardiography (TEE) has proven to be more sensitive than transthoracic echocardiography (TTE) in detecting certain possible cardiogenic sources of embolism.

Introduction: The recommendation to discharge low-risk pulmonary embolism patients from or after a brief monitoring in the emergency department has not been widely adopted in Finland., Methods: We explored the practices for examination and treatment of patients with pulmonary embolism in a university hospital and a central hospital. An assessment was made on how these practices followed the risk classifications., Results: A very small proportion (3.9%) of the patients were discharged directly from the emergency department. According to the risk classifications, the proportion of patients suited for home care would have been between 30 and 60%., Conclusions: A significant proportion of patients with pulmonary embolism can be treated on the outpatient basis.

AF is associated with the risk of stroke, and this risk is exceedingly high in elderly patients (> or = 75 years) and in patients after a stroke. DOACs are appropriate anticoagulants for AF patients without mechanical heart valves or mitral stenosis. Patients on DOACs do not require routine monitoring of coagulation, but need regular follow-up visits including an assessment of therapy adherence, thromboembolic and bleeding events and measurements of hemoglobin and platelets values as well as renal and liver function.

Platelet inhibitors and anticoagulants are called antithrombotic drugs. New platelet inhibitors prasugrel and ticagrelor are more effective than the traditional clopidogrel, but their use is also accompanied by more frequent bleeding complications. Varfarin has gained true competitors; new oral anticoagulants include dabigatran, rivaroxaban and apixaban. New anticoagulants are easier to use but clearly more expensive. The use of new anticoagulants is also accompanied by several potential problems that the clinician should be aware of.

Clopidogrel inhibits platelet action through the P2Y12-ADP receptor in an irreversible manner. Plasma levels of the active drug and thus the drug effect exhibit large individual variation. Part of the variation is explained by genetic reasons, but drug interactions may also have an effect on the response. The obtained efficacy is lower than anticipated in as many as 30% of the patients. The poor drug response is associated with an increased risk of cardiovascular events. Measurement of clopidogrel resistance with laboratory studies is challenging. Several methods have been developed and are becoming available for clinical use.

A major proportion of cardiac patients use long-time antithromobitic medication. It is not uncommon that these patients require surgery and operations. Discontinuation of antithrombotic therapy may be used to decrease risk of hemorrhage, but on the other hand the medication break will make the patient susceptible to thrombotic and thromboembolic complications. The attending physician must decide which is safer: to break the medication or to continue it. Often the best choice is a compromise of the above, i.e. application of a somewhat reduced compensatory antithrombotic therapy.