Hypertrophic cardiomyopathy with paroxysmal atrial fibrillation misdiagnosed as WPW syndrome

Hypertrophic cardiomyopathy (HCM) is associated with an increased incidence of Wolff–Parkinson–White (WPW) syndrome and atrial fibrillation. However, a delta-like wide QRS can be observed in the hypertrophied myocardium. When considering the rarity of the paraseptal bypass tract (BT), the normal QRS axis suggests a higher possibility of HCM origin. Otherwise, there is no known electrocardiographic clue indicating a wide QRS differentiation between HCM and WPW syndrome. Moreover, the atriofascicular, nodofascicular/ventricular or fasciculoventricular BT should be differentiated. In this case, atrioventricular conduction system incidental injury revealed a wide QRS origin from the HCM, but this method should be avoided except in some selected cases.

The problem of hypertensive heart disease regression in patients with arterial hypertension

The review presents data from the domestic and foreign literature on the prevalence, pathogenesis, modern methods of verification of hypertensive heart disease (left ventricular hypertrophy) in patients with arterial hypertension and conditions associated with it: coronary heart disease, atrial fibrillation, metabolic syndrome, diabetes mellitus. Methods of non-drug and drug correction of hypertensive heart disease, as well as factors that prevent the reverse regression of hypertrophied myocardium are considered.

The Molecular and Cellular Mechanisms Associated with a Microvascular Inflammation in the Pathogenesis of Heart Failure with Preserved Ejection Fraction

Heart failure withpreserved ejection fraction (HFpEF) is a severe disease with an often unfavorable outcome. The prevalence of HFpEF continues to increase, while effective treatment options remain elusive. All the medical strategies used toimprove the outcome in a heart failure with reduced ejection fraction proved ineffective in HFpEF, which was probably due to the different mechanisms ofdevelopment of these two types of heart failure and the diversity of the HFpEF phenotypes. According to the current paradigm of HFpEF development, a chronic mild pro-inflammatory statecauses a coronary microvascular endothelial inflammation, with further myocardial fibrosis and diastolic dysfunction progression. This inflammatory paradigm of HFpEF has been confirmed with someevidence, and suppressing the inflammation may become a novel strategy for treating and managing HFpEF. This review summarizes current concepts about a microvascular inflammation in hypertrophied myocardium and provides a translational perspective of the anti-inflammatory and immunomodulatory approaches in HFpEF.

The Molecular and Cellular Mechanisms Associated with a Microvascular Inflammation in the Pathogenesis of Heart Failure with Preserved Ejection Fraction

Heart failure withpreserved ejection fraction (HFpEF) is a severe disease with an often unfavorable outcome. The prevalence of HFpEF continues to increase, while effective treatment options remain elusive. All the medical strategies used toimprove the outcome in a heart failure with reduced ejection fraction proved ineffective in HFpEF, which was probably due to the different mechanisms ofdevelopment of these two types of heart failure and the diversity of the HFpEF phenotypes. According to the current paradigm of HFpEF development, a chronic mild pro-inflammatory statecauses a coronary microvascular endothelial inflammation, with further myocardial fibrosis and diastolic dysfunction progression. This inflammatory paradigm of HFpEF has been confirmed with someevidence, and suppressing the inflammation may become a novel strategy for treating and managing HFpEF. This review summarizes current concepts about a microvascular inflammation in hypertrophied myocardium and provides a translational perspective of the anti-inflammatory and immunomodulatory approaches in HFpEF.