Interests:Cardioprotection in chronic and acute myocardial ischemia/reperfusion; Mechanism of left ventricular remodeling in cardiovascular disease
Special Issue Information
Indices of myocardial morphology and function should fall within physiological ranges at both the macroscopic and microscopic levels for stable cardiac performance. Accordingly, cardiac chamber sizes together with the characteristics of cardiomyocytes and their subcellular micro-organelles are to be analyzed in combination for the correct interpretation of cardiac health and disease.
Upon various different stress conditions (i.e. hemodynamic pressure- or volume-overload, genetic predispositions, etc.) cardiac muscle enters a transformation process, commonly referred to as cardiac hypertrophy. Thickening of the heart muscle often appears as a compensatory mechanism, nevertheless, concomitant alterations in cardiomyocyte signaling can also limit systolic and/or diastolic functions and evoke life-threatening arrhythmias. In this context, concentric left ventricular hypertrophy has been mostly associated with diastolic dysfunction, leading potentially to heart failure with preserved ejection fraction (HFpEF), while heart failure with reduced ejection fraction (HfrEF) is more often seen in conditions with left ventricular dilation. Nevertheless, making pathophysiological distinctions between HFpEF, HFrEF and the relatively novel category of heart failure with mid-range ejection fraction (HfmrEF) are not without problems. This is due to the high number of overlapping comorbidities and risk factors (e.g. hypertension, atherosclerosis, metabolic derangements, infective-immunological factors, etc.) rarely resulting in pure forms of cardiac pathologies.
Our current view on cardiac remodeling links over-activated neuro-humoral pathways (e.g. the renin-angiotensin-aldosterone system and the beta-adrenergic system) to exhaustive levels of cardiomyocyte receptor stimulations, to an aphysiological function of the intracellular signaling cascades, and ultimately to a modified epigenetic control over cardiomyocytes. One of the hurdles of present time cardiology is the difficulty in finding effective medications acting closer to the distal end of the above chain (i.e. cardiomyocyte nuclei) than to the proximal, like current heart failure medications. In this issue, entitled “Cardiac Hypertrophy: from Basic Science to Clinical Application” we present recent advances in the field of cardiac remodeling and its management to foster preclinical and clinical efforts for the preservation of cardiac integrity and function.
Prof. Dr. Zoltán Papp and Dr. Attila Kiss
Manuscript Submission Information
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