Echocardiography is currently the most relevant technique for non-invasive differentiation of the two forms. Systolic dysfunction is easily assessable by estimation of global ejection fraction and regional wall motion. Diastolic dysfunction can be diagnosed indirectly by means of a normal or nearly normal ejection fraction and and changes of the mitral filling pattern in the context of LV failure.
Meanwhile, significant myocardial fibrosis together with myocardial hypertrophy is typical in diastolic heart failure. Myocardial fibrosis is thought to be the main factor in increased stiffness [ 14 ]. Mechanical stimulation to the myocardium is the main factor of myocardial hypertrophy, while myocardial fibrosis may be caused by humoral factors such as various cytokines, growth factors, and hormones. In hypertensive HFpEF model rats, oxidative stress was increased and angiotensin II was produced within the arterial walls due to high blood pressure.
The resulting perivascular inflammation is reported to be the cause of reactive fibrosis of myocardium [ 14 — 16 ]. In Dahl salt-sensitive rat HFpEF models, it was found that endothelin, together with angiotensin II, is an important mediator of myocardial fibrosis [ 17 ].
In addition to the quantitative increase in collagen and distribution abnormalities, qualitative changes are also involved in increased myocardial stiffness caused by fibrosis. In Dahl salt-sensitive rat HFpEF models, the increase in the ratio of stiff type I collagen to type III collagen, which is highly distensible, and increased collagen cross-linking are reported to important factors of increased myocardial stiffness [ 18 ]. In diastolic heart failure, myocardial stiffness of cardiomyocytes per se also increases.
Detailed mechanism for this remains unclear but is thought to be due to changes in structural proteins associated with myocardial hypertrophy. Titin, which is a giant sarcomeric protein, acts as a molecular spring and plays a large part in the distensibility of cardiomyocytes during diastole. However, in diastolic heart failure, compared with systolic heart failure, the ratio of large, distensible N2A isoforms small, rigid N2B isoforms to was found to decrease [ 19 ]. CHARM-preserved trial, in which ARB candesartan was tested for cardiovascular mortality and heart failure hospitalizations, failed to demonstrate a beneficial effect on cardiovascular death but observed fewer heart failure hospitalizations in the candesartan group [ 21 ].
Mortality or hospitalization rate for cardiovascular causes was again not improved by irbesartan [ 22 ]. A preliminary report suggested statin therapy to be beneficial in HFpEF with lower mortality rate [ 24 ]. Several compounds seem to be promising for drug target of HFpEF. Phosphodiesterase 5 inhibitors PDE5I increase cGMP level, attenuate adrenergic stimulation, reduce ventricular-arterial stiffening, antagonize maladaptive chamber remodeling, improve endothelial function, and reduce pulmonary vascular resistance [ 26 — 30 ].
Aldosterone antagonists are currently being actively investigated for HFpEF in the clinical situation. Chamber stiffness is altered by the extracellular matrix like collagen.
Alagebrium chloride ALT is a novel agent that breaks glucose cross-links and improves ventricular and vascular compliance in animal experiments and reduces blood pressure and vascular stiffness in humans [ 33 , 34 ]. Small open-label trial revealed that ALT was associated with reduced LV mass and improved diastolic filling [ 35 ]. Diastolic dysfunction in HFpEF may be related to abnormalities in energy availability or utilization in myocytes [ 36 — 38 ]. Recently, abnormal ATP phosphocreatine shuttle kinetics in HFpEF was demonstrated, and similar results were recently also reported [ 37 , 39 ].
Currently, a novel therapy targeting energy utilization is under investigation [ 40 ]. Despite the fact that diastolic heart failure is a common condition of heart failure, its precise definition still remains unclear.
Therefore, the similarities and differences between the pathogenesis and pathophysiology of diastolic and systolic heart failure have not been sufficiently elucidated.
We hope to proceed with future studies on this paper. The author declares that there is no conflict of interests regarding the publication of this article. National Center for Biotechnology Information , U. Journal List Cardiol Res Pract v.
Cardiol Res Pract. Published online Dec Author information Article notes Copyright and License information Disclaimer. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This article has been cited by other articles in PMC. Abstract Pathophysiology of heart failure has been considered to be a damaged state of systolic function of the heart followed by a state of low cardiac output that is, systolic heart failure. Introduction Pathophysiology of heart failure has been considered to be a damaged state of systolic function of the heart followed by a state of low cardiac output systolic heart failure. Diastolic Dysfunction Diastole of the left ventricle is composed of isovolumic relaxation and ventricular filling.
Open in a separate window. Figure 1. Figure 2. Figure 3. The Diagnostic Criteria for Diastolic Heart Failure Definition of systolic heart failure is reduction of the left ventricular ejection fraction. Medically reviewed by Dr. Payal Kohli, M.
Systolic diagnosis Diastolic diagnosis Systolic medications Diastolic medications Other treatments Takeaway Two types of heart failure affect the left side of the heart: systolic and diastolic. Diagnosing systolic heart failure. Diagnosing diastolic heart failure. Medications for systolic heart failure.
Medications for diastolic heart failure. Other treatments for left-sided heart failure. The takeaway. Read this next. Talk to Your Doctor. Heart Failure Personal Stories. Our online community of survivors and caregivers is here to keep you going no matter the obstacles. Types of Heart Failure. Left-sided heart failure The heart's pumping action moves oxygen-rich blood as it travels from the lungs to the left atrium, then on to the left ventricle, which pumps it to the rest of the body.
Heart failure with reduced ejection fraction HFrEF , also called systolic failure: The left ventricle loses its ability to contract normally. The heart can't pump with enough force to push enough blood into circulation. Heart failure with preserved ejection fraction HFpEF , also called d iastolic failure or diastolic dysfunction : The left ventricle loses its ability to relax normally because the muscle has become stiff.
The heart can't properly fill with blood during the resting period between each beat. Protect the Hearts You Love Help fund lifesaving research and prevent heart failure in communities like yours nationwide. Donate now. Congestive heart failure Congestive heart failure CHF is a type of heart failure which requires seeking timely medical attention, although sometimes the two terms are used interchangeably.
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