…development of pathological Q waves after infarction. The sensitivity of fragmented QRS for myocardial infarction was 86%, as compared with 36% for pathological Q waves…

…patient's usual saturation. Previous exacerbations and hospital admissions. Current inhaled treatment and adherence. Opioids, benzodiazepines and other sedating drugs. Thromboembolic risk, for example immobilisation…

…or any excipient. Active bleeding. Previous intracranial hemorrhage. Severe liver impairment. Concurrent administration of ticagrelor with strong CYP3A4 inhibitors (e.g., ketoconazole, clarithromycin, nefazodone, ritonavir…

…Familial and genetic screening in cardiovascular medicine is the systematic assessment of relatives and other individuals who may carry an inherited predisposition to cardiovascular disease…

…to LDL and other apoB containing particles. Cardiovascular risk categories Primary prevention For adults aged 40–75 years without diabetes and with LDL C between…

…and infarction Myocardial ischemia: cellular changes, ECG signs and development of infarction Like all other cells in the human body, cardiac myocytes use ATP (adenosine…

…NSTEMI and unstable angina. Management begins in parallel with the diagnostic work up. Obtain an interpretable 12 lead ECG within 10 minutes of first medical…

…drugs . The diagnosis rests on the history, a positive Dix–Hallpike test and the absence of other neurological findings. The treatment is a repositioning manoeuvre…

…when combined with ACE inhibitors. Corticosteroids and other NSAIDs: Increased risk of gastrointestinal bleeding when combined with acetylsalicylic acid. Uric acid excretion agents (e.g…

…cardiovascular death, and progression of atherosclerotic disease in patients with established coronary or other atherosclerotic vascular disease. Antiplatelet therapy is a central component because platelet…