پزشکی 1 - medical
عنوان انگلیسی مقاله:
Pathophysiology of Advanced Heart Failure
ترجمه فارسی عنوان مقاله:
پاتوفیزیولوژی نارسایی پیشرفته قلب
ScienceDirect- Elsevier- Heart Failure Clinics, 17 (2021) 519-531: doi:10:1016/j:hfc:2021:06:001
Jan Biegus MD PhD
The pathophysiologyof advanced heart failure (HF) can be characterized asa complex interplay ofdysregulated mechanisms comprising impaired hemodynamics, neurohormonal and proinflammatory
activation, dysfunctional cardiorespiratory reflex control, and inadequate energy handling, all of which
ultimately lead to multiorgan dysfunction; at the later stage of HF, numerous comorbidities, whose underlying pathophysiologiesoftenamplifyHFprogression,tendtodominatetheclinicalpicture and therapeutic approach, and some of these mechanisms have been identified as therapeutic targets in HF.
Blockade of the renin-angiotensin-aldosterone system (preferably with an angiotensin receptorneprilysin inhibitor, but alternatively with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers together with mineralocorticoid receptor antagonist) and sympathetic nervous system (with b-blockers) is now considered a fundamental element of pharmacologic therapy for all patients with advanced HF and reduced ejection fraction.
Autonomic modulation (vagal nerve stimulation or baroreflex stimulation) in advanced HF tends to benefit functional variables (qualityof life,NewYork HeartAssociation class, 6-minutewalking distance), whereas improvement in the outcomes (total mortality, HF hospitalizations) still remains uncertain.
Fluid overload with central and/or peripheral congestion characterize the clinical picture of advanced HF and is the main reason for hospital admission in these patients; distinction of different clinical patterns of congestion with different underlying mechanisms may improve the management of fluid overload in advanced HF.
Recent clinicaltrials have shown that the following novel therapiestargeting impairedpathophysiologic pathways in advanced HF seem to improve patients’ outcomes: (1) vericiguat, a soluble guanylate cyclase stimulator; (2) omecamtiv mecarbil, a selective cardiac myosin activator; (3) sodium-glucose cotransporter 2 inhibitors; (4) ferric carboxymaltose, for patients with concomitant iron deficiency.
Better understanding of the pathophysiology underlying HF progression may allow characterization of novel mechanisms that can be targeted in order to revert to a natural pathway of HF development and progression.
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