Determining the etiologies of left ventricular hypertrophy (LVH) can be challenging due to the similarities of the different manifestations in clinical presentation and morphological features. Depending on the underlying cause, not only left ventricular mass but also left ventricular cavity size, or both, may increase. Patients with LVH remain asymptomatic for a few years, but disease progression will lead to the development of systolic or diastolic dysfunction and end-stage heart failure. As hypertrophied cardiac muscle disrupts normal conduction, LVH predisposes to arrhythmias. Distinguishing individuals with treatable causes of LVH is important for prevention of cardiovascular events and mortality. Athletic’s heart with physiological LVH does not require treatment. Frequent causes of hypertrophy include etiologies due to pressure/volume overload, such as systemic hypertension, hypertrophic cardiomyopathy, or infiltrative cardiac processes such as amyloidosis, Fabry disease, and sarcoidosis. Hypertension and aortic valve stenosis are the most common causes of LVH. Management of LVH involves lifestyle changes, medications, surgery, and implantable devices. In this review we systematically summarize treatments for the different patterns of cardiac hypertrophy and their impacts on outcomes while informing clinicians on advances in the treatment of LVH due to Fabry disease, cardiac amyloidosis, and hypertrophic cardiomyopathy.
22 June 2018 in American Journal of Cardiovascular Drugs
The corner stone of atrial fibrillation therapy includes the prevention of stroke with less adverse effects. The Global Anticoagulant Registry in the FIELD-Atrial Fibrillation (GARFIELD-AF) study provided data to compare treatment strategies in Turkey with other populations and every-day practice of stroke prevention management with complications. GARFIELD-AF is a large-scale registry that enrolled 52,014 patients in five sequential cohorts at >1,000 centers in 35 countries.This study initiated to track the evolution of global anticoagulation practice, and to study the impact of NOAC therapy in AF. 756 patients from 17 enrolling sites in Turkey were in cohort 4 and 5.Treatment strategies at diagnosis initiated by CHA2DS2-VASc score, baseline characteristics of patients, treatment according to stroke and bleeding risk profiles, INR values were analyzed in cohorts.Also event rates during the first year follow up were evaluated. AF patients in Turkey were mostly seen in young women.Stroke risk according to the CHADS2 score and CHA2DS2-VASc score compared with world data. The mean of risk score values including HAS-BLED score were lower in Turkey than world data.The percentage of patients receiving FXa inhibitor with or without an antiplatelet usage was more than the other drug groups. All-cause mortality was higher in Turkey. Different form world data when HAS-BLED score was above 3, the therapy was mostly changed to antiplatelet drugs in Turkey. The data of GARFIELD-AF provide data from Turkey about therapeutic strategies, best practices also deficiencies in available treatment options, patient care and clinical outcomes of patients with AF.