Assessing stroke risk in atrial fibrillation guides whether to start and continue long-term anticoagulation. The CHA2DS2-VASc score is the standard tool for this purpose because it combines multiple risk factors into a single estimate of annual stroke risk and helps determine if the potential benefit of anticoagulation justifies treatment. It assigns points for congestive heart failure, hypertension, age 75 or older (2 points), diabetes, prior stroke/TIA/thromboembolism (2 points), vascular disease, age 65–74, and female sex. A higher total means a higher stroke risk and a greater likelihood that anticoagulation will be beneficial, whereas a score of zero often leads to withholding anticoagulation. Other scoring systems serve different purposes: HAS-BLED estimates bleeding risk to help gauge safety and monitoring needs; APACHE II measures illness severity in critical care; Framingham risk estimates general cardiovascular risk rather than AF-specific stroke risk.

In sensing systems, sensitivity isn’t tied to a single knob. The device uses a sensing window defined by a lower threshold and an upper threshold, and those two values are programmable separately. So changing the minimum threshold from 0.8 mV to 1.2 mV does not automatically make the device less sensitive by itself—the overall sensing behavior is determined by both thresholds and the detection logic, which remain unchanged if everything else stays the same. This is why the concept tested is that upper and lower thresholds are set independently.

After cardioversion, the risk of thromboembolism can persist because thrombi may have formed during atrial fibrillation and the atrial myocardium can stay functionally abnormal (stunned) for weeks. If the AF has lasted more than 48 hours or the duration is unknown, stopping anticoagulation right away would leave a window of high stroke risk during the period when the heart rhythm has just been restored but the atrial’recovery isn’t complete. The recommended approach is to continue anticoagulation for at least three weeks after cardioversion in these cases, and to consider using a transesophageal echocardiogram to look for left atrial thrombus and guide further decisions about stopping anticoagulation. This reflects the principle that rhythm control does not immediately eliminate embolic risk, so protection with anticoagulation is still needed in the early post-cardioversion period.

Class IC antiarrhythmics slow conduction very strongly by blocking sodium channels. In hearts with structural disease—scar tissue from a prior heart attack, cardiomyopathy, or other remodeling—this marked slowing can create or worsen reentrant circuits and provoke dangerous ventricular arrhythmias. The classic evidence comes from the CAST trial, where flecainide (and encainide) increased mortality in patients after myocardial infarction with structural damage. Propafenone is in the same Class IC category and carries similar proarrhythmic concerns in structurally abnormal hearts, so both are avoided in this setting. The other options include drugs from different classes and do not carry the same level of risk for proarrhythmia in structural heart disease. Thus the pair to avoid is flecainide and propafenone.