What is the difference between diastolic dysfunction and systolic dysfunction

In recent years, diastolic heart failure caused by the affected left ventricle has become a clinical issue [ 3 ]. This is because evaluating accurate pathophysiology and diagnosis of diastolic heart failure is in fact difficult. Diastole of the left ventricle is composed of isovolumic relaxation and ventricular filling. Relaxation of the left ventricle is an active process that occurs as a result of energy-dependent uptake of intracellular calcium by the sarcoplasmic reticulum, whose concentration has risen during the systolic phase.

Relaxation of the left ventricle is impaired in a disease state caused by energy metabolism disorders or calcium-handling abnormalities such as myocardial ischemia and myocardial hypertrophy.

Left ventricular filling phase abnormality, namely, elevation of left ventricular stiffness, influences left ventricular flow dynamics during filling phase and is commonly caused by myocardial fibrosis or hypertrophy. When left ventricular diastolic function is impaired, cardiac output is reduced because the left ventricle is not filled enough in diastole due to left ventricular inflow obstruction.

By contrast, to compensate for reduced cardiac output, increasing the inflow pressure to the left ventricle and consequently left ventricular end-diastolic pressure becomes necessary, which in turn increases left atrial pressure. As a result, left ventricular dysfunction easily and directly causes pulmonary congestion. The end-systolic pressure-volume relationship is the same as a normal heart in diastolic heart failure, but the end-diastolic pressure-volume relationship shifts upwards Figure 1 a [ 3 ].

As a result, left ventricular end-diastolic pressure rises. In pathologies with diastolic dysfunction, when an abrupt increase in blood pressure occurs, the pressure-volume loop shifts to the upper right without decrease in absolute index of contractibility. Therefore, pulmonary congestion is induced as a result of the significant increase in left ventricular end-diastolic pressure Figure 1 b. By contrast, in systolic dysfunction, left ventricular contractile function decreases and gets smaller Figure 2.

Meanwhile, the end-diastolic pressure-volume relationship shifts downwards rather than remaining unchanged. To maintain cardiac output, the pressure-volume loop shifts right due to increase in preload.

Therefore, the left ventricular pressure-volume loop operates on the steep part of the end-diastolic pressure-volume curve, consequently causing end-diastolic pressure to rise. In diastolic dysfunction, contractility of whole left ventricle is considered normal. However, the contractile velocity in systole measured with tissue Doppler decreased in both systolic and diastolic dysfunction [ 4 ].

Furthermore, local contractility in longitudinal direction is known to be impaired locally in diastolic heart failure [ 5 ]. Recent findings suggest that contractility decreases even in diastolic heart failure in myocardium level. By contrast, diastolic function is also impaired in systolic heart failure and has been shown to decrease exercise tolerance and be one of the determinants of prognosis [ 6 ].

Therefore, diastolic and systolic heart failure are not considered to be independent and separate entities. The single syndrome hypothesis of heart failure is therefore advocated Figure 3 [ 1 ].

In that hypothesis, heart failure is a single continuous disease spectrum and systolic and diastolic heart failure are phenotypes at two extremes. As shown in Figure 3 , a phenotype of heart failure comprised of some extent of systolic dysfunction and some extent of diastolic function.

By contrast, some researchers have advocated that diastolic function is not something that should only be noted in the pathogenesis of diastolic heart failure, but should be widely viewed as a determinant of pathophysiology in heart failure [ 7 ]. Heart dysfunction that occurs as a result of heart disease causes diastolic dysfunction. Among such cases there exist patients with concurrent systolic dysfunction.

Furthermore, a portion of patients with heart dysfunction clinically exhibit symptoms of heart failure. Among them, those with significant systolic dysfunction where the main pathology is systolic heart failure, and diastolic dysfunction, are said to have diastolic heart failure.

Definition of systolic heart failure is reduction of the left ventricular ejection fraction. Thus, its diagnosis is quite easy. By contrast, diagnosis of diastolic heart failure is difficult since there are no simple and reliable criteria. Therefore, diastolic heart failure can be clinically diagnosed when clinical symptoms and findings of heart failure are exhibited and decrease in left ventricular ejection fraction is none or minimal. The American College of Cardiology Foundation and the American Heart Association define diastolic heart failure as a condition having the typical signs and symptoms of heart failure with a normal left ventricular ejection fraction, without valvular abnormalities on echocardiography [ 8 ].

Currently, accurate diagnosis of 3 needs cardiac catheterization, which could be skipped in a common clinical situation. Diastolic heart failure is strongly suspected probable DHF when conditions 1 and 2 are met [ 9 ]. When diagnosing diastolic heart failure, it is important to perform a careful exclusion of valvular heart disease, pericardial disease, right heart failure, intracardiac tumor, congenital heart disease, and high-output cardiac failure.

Zile et al. The currently accepted criteria for diagnosis of diastolic heart failure are essentially a clinical diagnosis. Thus, it is important to understand that there are possibilities that diastolic heart failure means somewhat broader range than what diastolic heart failure exactly stands for.

According to reports by Owan et al. Compared with systolic heart failure, diastolic heart failure is seen more often in the elderly and women and accompanied by hypertension and anemia. Comorbidity rate of obesity, diabetes, and chronic kidney disease CKD in diastolic heart failure is high, but not particularly higher than in systolic heart disease. In general, both diastolic and systolic heart failure exhibit distinctive subjective symptoms and objective findings of heart failure including dyspnea, edema, and malaise.

Symptoms of diastolic heart failure typically include dyspnea due to pulmonary congestion, particularly shortness of breath, paroxysmal atrial fibrillation, and rapidly developing dyspnea induced by tachycardia, all of which are common initial symptoms. By contrast, in systolic heart failure, symptoms and signs due to general malaise and organ hypoperfusion associated with decreased cardiac output are frequently seen. The main differences between diastolic and systolic heart failure are the presence of contractile dysfunction and left ventricular remodeling Table 1.

In systolic heart failure, progressive ventricular dilatation, or eccentric cardiac hypertrophy, can be seen. By contrast, diastolic heart failure exhibits concentric ventricular remodeling without dilatation or concentric cardiac hypertrophy.

Pattern of pulmonary vein flow and ratio of early to late mitral inflow peak velocity are also established as major diastolic functional indices, though they are rather dependent on hemodynamic status [ 14 ]. In recent years, several reports on important association of various biomarkers for heart failure and subtypes of heart failure have been published [ 15 — 19 ]. On the other hand, growth differentiation factor 15 GDF15 , cystatin C, and urinary albumin excretion were significantly associated with the risk for HFpEF [ 16 , 17 ].

The histological features of systolic heart failure include myocardial hypertrophy, loss of myocardial cells, and restructuring of the extracellular matrix. 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 ].

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. Last Reviewed: May 31, Watch, Learn and Live See your cardiovascular system in action with our interactive illustrations and animations.

Explore the Library. Support That Lifts You Up Our online community of survivors and caregivers is here to keep you going no matter the obstacles. Yancy says. Signs of the condition may include:. The first type is called systolic heart failure, and the second is diastolic heart failure.

The job of the pumping heart is to send oxygen-rich blood to every part of the body. If the heart muscle is weakened or damaged — from hypertension high blood pressure , for instance — it may not be able to contract with enough force to circulate oxygenated and nutrient-filled blood. As part of the pumping cycle, after each contraction, your heart muscle relaxes to allow the heart to fill with blood.