- Diastolic heart failure
Diastolic dysfunction Classification and external resources ICD-9 428.3
Diastolic heart failure or diastolic dysfunction refers to decline in performance of one or both ventricles of the heart during the time phase of diastole. Diastole is that phase of the cardiac cycle when the heart is not contracting to propel blood out (systole) to the body, brain and lungs but instead is relaxed and filling with incoming blood that is being returned from the body through the inferior vena cava (IVC) from the lungs through the pulmonary veins and from the brain through the superior vena cava (SVC).
Significance of diastolic dysfunction
Diastolic dysfunction is split into left/systemic/body and right/pulmonary/lungs halves. In optimal left sided performance of the heart, blood mass loads forward 60-80 times per minute in an unobstructed cascade from the lungs, into the pulmonary veins, then into the left atrium, through the mitral valve, and finally into the left ventricle. When the left ventricle cannot be normally filled due to deterioration of preload, compliance and/or E/A ratio during diastole, the pressurized cascade begins to fail and incrementally reverses. Eventually blood then regurgitates back into the left atrium in a backward pathologic spiral gradient towards the lungs. This process then creates a second type of high blood pressure known as pulmonary hypertension or PH. Unchecked PH can lead to pulmonary edema. Physiologically this process results in a higher than normal mismatch pressure gradient of blood within both the large and alveolar vessels of the lungs. Diastolic dysfunction paired with pulmonary hypertension is a significant negative prognostic indicator of heart failure with normal ejection fraction. As a result of hydrostatic forces, this pressure mismatch leads to leaking of fluid (i.e. transudate) from the pulmonary blood vessels into the air-spaces (alveoli) of the lungs. The result of this hydrostatic mismatch is sometimes pulmonary edema, a dreaded condition characterized by difficulty breathing, inadequate oxygenation of blood, and, if severe and untreated, death. Pulmonary edema developed as a result of diastolic dysfunction is not fully imparted by failing pump systolic function of the left ventricle and may be insidious in nature or sudden depending upon the pathophysiology involved. The pressure gradient reversal inherent to diastolic dysfunction may further result from the left and/or right ventricle's pathologic inability to readily accept blood entering the ventricles from the atria. Pressure mismatches then may cause or impart pathologic geometric deformational changes of individual heart chambers leading to a gradual loss of optimal valvular coaptation and subsequent regurgitant (sagging/leaking) valvular heart disease.
Diastolic dysfunction is characterized by elevated diastolic pressure in the left ventricle despite essentially normal/physiologic end diastolic volume or EDV. Histologic evidence supporting diastolic dysfunction demonstrates hypertrophy of the cardiomyocytes, increased interstitial Collagen deposition and/or infiltration of the myocardium. These influences collectively lead to a downhill spiral in distensibility of the myocardium. The ventricle then behaves as a balloon made from abnormally thick rubber. (An old tire does not ride nearly as comfortably as a new tire) Despite filling with high pressure, the volume cannot expand adequately. If the heart cannot readily fill with blood following contraction, one of two things must follow; either the cardiac output becomes diminished or compensation ensues to increase the ventricular diastolic pressure to higher levels. When the left ventricular diastolic pressure is elevated, venous pressure in the lungs must also become elevated to maintain forward flow. Increased pulmonary venous pressure results in alveolar edema causing the patient to be short of breath. Phrased differently, left ventricular stiffness makes it more difficult for blood to enter from the left atrium. As a result, pressure rises in the atrium and is transmitted back to the pulmonary venous system thereby increasing its hydrostatic pressure and thus promoting pulmonary edema.
It is important to note that a normal heart that is overfilled with blood may demonstrate increased stiffness and decreased Compliance characteristics. This is loosely analogous to a balloon that is over-filled with air (except that the multichambered balloon is filled with viscous blood, not gas). Blowing more air (or blood) into the balloon becomes difficult because the balloon acts stiff and non-compliant at a filling volume it wasn't designed to hold. It may be misguided to classify the volume overloaded heart as having diastolic dysfunction if it is behaving in a stiff and non-compliant manner. The term diastolic dysfunction should not be applied to the dilated heart. Dilated (remodeled) hearts have increased volume for the amount of diastlolic pressure and therefore have increased (not decreased) distensibility. The term diastolic dysfunction is sometimes erroneously applied in this circumstance when increased fluid volume retention causes the heart to be over-filled.
Although the term diastolic heart failure is often used when there are signs and symptoms of heart failure with normal LV systolic function, this is not always appropriate. Diastolic function is determined by relative EDV in relation to EDP and is therefore independent of LV systolic function. Leftward shift of the end-diastolic pressure-volume relationship (ie. decreased LV distensibility) can occur both in those with normal and those with decreased LV systolic function. Likewise, heart failure may occur in those with dilated LV and normal systolic function. This is often seen in valvular heart disease and high output failure. Neither of these situations constitutes a diastolic heart abnormality.
Risk factors and causes
Any condition or process that leads to stiffening of the left ventricle can lead to diastolic dysfunction. Causes of left ventricular stiffening include:
- high blood pressure (i.e. hypertension, where, as a result of left ventricular muscle hypertrophy to deal with the high pressure, the left ventricle has become stiff)
- aortic stenosis of any cause (here as with hypertension, the ventricular muscle has hypertrophied and thence become stiff, as a result of the increased pressure load placed on it by the stenosis)
- scarred heart muscle (e.g. occurring after a heart attack) (scars are relatively stiff)
- diabetes (stiffening occurs presumably as a result of glycosylation of heart muscle)
- severe systolic dysfunction that has led to ventricular dilation (i.e when the ventricle has been stretched to a certain point, any further attempt to stretch it more, as by blood trying to enter it from the left atrium, meets with increased resistance - it has become stiff
- reversible stiffening as can occur during periods of cardiac ischemia
Meaningful criteria suggesting diastolic dysfunction or diastolic heart failure remains imprecise. This has made it difficult to conduct clinical trials of treatments for diastolic heart failure. This problem is compounded by the fact that systolic and diastolic heart failure is a common coexisting presentation in many ischemic and nonischemic etiologies of HF. Narrowly defined, Diastolic Dysfunction has often been described as heart failure with normal systolic function (LVEF>60%) Chagasic heart disease may represent an optimal academic model of diastolic heart failure that spares systolic function. A patient is defined as having diastolic [vagal] dysfunction if they have signs and symptoms of heart failure but the left ventricular ejection fraction is normal. A second approach is to use an elevated BNP level in the presence of normal EF to diagnose diastolic heart failure. Concordance of both volumetric and biochemical measurements/markers lends to even stronger terminology regarding scientific/mathematical expression of diastolic heart failure. These are both probably too broad a definition for diastolic heart failure and this group of patients is more precisely described as heart failure with normal systolic function. Echocardiography can be used to diagnose diastolic dysfunction but is a limited modality unless boosted by stress imaging. MUGA imaging is an earlier mathematical attempt to divide systolic vs. diastolic heart failure.
No one single echocardiographic parameter can make the diagnosis of diastolic heart failure. Multiple echo parameters have been proposed including mitral inflow velocity patterns, pulmonary vein flow patterns, E:A reversal, tissue Doppler measurements, and M-mode echo measurements (ie. left atrial size). Algorithms have been developed which combine multiple echocardiographic parameters to diagnose diastolic heart failure.
There are four basic Echocardiographic patterns of diastolic heart failure, graded I to IV.
- The mildest form is called an abnormal relaxation pattern or grade I diastolic dysfunction. On the mitral inflow Doppler echocardiogram, there is reversal of the normal E/A ratio. This pattern may develop normally with age in some patients and many grade I patients will not have any clinical signs or symptoms of heart failure.
- Grade II diastolic dysfunction is called pseudonormal filling dynamics. This is considered moderate diastolic dysfunction and is associated with elevated left atrial filling pressures. These patients more commonly have symptoms of heart failure and many have left atrial enlargement due to the elevated pressures in the left heart.
Grade III and IV diastolic dysfunction are called restrictive filling dynamics. These are both severe forms of diastolic dysfunction and patients tend to have advanced heart failure symptoms.
- Class III diastolic dysfunction patients will demonstrate reversal of their diastolic abnormalities on echocardiogram when they perform the Valsalva maneuver and are called reversible restrictive diastolic dysfunction.
- Class IV diastolic dysfunction patients will not demonstrate reversibility of their echocardiogram abnormalities and are therefore called fixed restrictive diastolic dysfunction. The presence of either class III and IV diastolic dysfunction is associated with a significantly worse prognosis. These patients will have left atrial enlargement and many will have a reduced left ventricular ejection fraction indicating a combination of systolic and diastolic dysfunction.
Imaged volumetric definition of systolic heart performance is commonly accepted as ejection fraction. Volumetric definition of the heart in systole was first described by Adolph Fick as cardiac output. Fick may be readily and inexpensively inverted to cardiac input and Injection fraction to mathematically describe Diastole. Decline of Injection fraction paired with decline of E/A ratio seems a stronger argument in support of mathematical definition of diastolic heart failure.
Generally, diastolic dysfunction is chronic process (except during acute ischemia - see above). When this chronic condition is well tolerated by an individual, no specific treatment may be indicated. Rather, therapy should be directed at the root cause of the stiff left ventricle with things like high blood pressure and diabetes treated appropriately. Conversely, and as noted above, diastolic dysfunction tends to be better tolerated if the atrium is able to pump blood into the ventricles in a coordinated fashion. This does not occur in atrial fibrillation where there is no coordinated atrial activity. Hence, atrial fibrillation should be treated aggressively in people with diastolic dysfunction. In the same light, and also as noted above, if the atrial fibrillation persists and is leading to a rapid heart rate, treatment must be given to slow down that rate. The use of a self-expanding device that attaches to the external surface of the left ventricle has been suggested yet still awaits FDA approval. When the heart muscle squeezes, energy is loaded into the device, which absorbs this energy, and releases it to the left ventricle in the diastolic phase, which help retain muscle elasticity 
At this date, the role of specific treatments for diastolic dysfunction per se is unclear. There is some evidence that calcium channel blocker drugs may be of benefit in reducing ventricular stiffness in some cases. Likewise, treatment with angiotensin converting enzyme inhibitors such as enalapril, ramipril, and many others, may be of benefit due to their effect on ventricular remodeling.
A major treatment consideration in people with diastolic dysfunction is when pulmonary edema develops. Unlike treatment of pulmonary edema occurring the setting of systolic dysfunction (where the primary problem is poor ventricular pumping as opposed to poor filling), the treatment of pulmonary edema complicating diastolic dysfunction emphasizes heart rate control (i.e. lowering it). Diuretics are often given as well. The role of afterload reduction in this setting is unknown.
Until recently, it was generally assumed that the prognosis for individuals with diastolic dysfunction and associated, intermittent pulmonary edema was better than those with systolic dysfunction. In fact, in two studies appearing in the New England Journal of Medicine in 2006, evidence was presented to suggest that the prognosis in diastolic dysfunction is the same as that in systolic dysfunction 
- ^ Eric J. Topol; Robert M. Califf (2007). Textbook of cardiovascular medicine. Lippincott Williams & Wilkins. pp. 420–. ISBN 9780781770125. http://books.google.com/books?id=35zSLWyEWbcC&pg=PA420. Retrieved 16 November 2010.
- ^ 
- ^ Owan TE, Hodge DO, Herges RM, Jacobsen SJ, Roger VL, Redfield MM (July 2006). "Trends in prevalence and outcome of heart failure with preserved ejection fraction". N. Engl. J. Med. 355 (3): 251–9. doi:10.1056/NEJMoa052256. PMID 16855265. http://content.nejm.org/cgi/content/abstract/355/3/251.
- ^ Bhatia RS, Tu JV, Lee DS, et al. (July 2006). "Outcome of heart failure with preserved ejection fraction in a population-based study". N. Engl. J. Med. 355 (3): 260–9. doi:10.1056/NEJMoa051530. PMID 16855266. http://content.nejm.org/cgi/content/abstract/355/3/260.
Cardiovascular disease: heart disease · Circulatory system pathology (I00–I52, 390–429) IschaemicActive ischemia LayersValves Conduction/
arrhythmiaPremature contractionWolff-Parkinson-White · Lown-Ganong-LevineFlutter/fibrillationPacemakerOther/ungrouped
Wikimedia Foundation. 2010.