Diastolic dysfunction

Diastolic dysfunction refers to an abnormality in the heart's (i.e. left ventricle's) filling during diastole. Diastole is that phase of the cardiac cycle when the heart (i.e. ventricle) is not contracting but is actually relaxed and filling with blood that is being returned to it, either from the body (into right ventricle) or from the lungs (into left ventricle).

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Significance of Diastolic Dysfunction

Normally, with reference to the left side of the heart, blood flows from the lungs, into the pulmonary veins, into the left atrium, through the mitral valve, and finally into the left ventricle. When the left ventricle cannot be normally filled during diastole, blood will back up into the left atrium and, eventually, into the lungs. The result is a higher than normal pressure of blood within the vessels of the lung. As a result of hydrostatic forces, this high pressure leads to leaking of fluid (i.e. transudate) from the lung's blood vessels into the air-spaces (alveoli) of the lungs. The result is pulmonary edema, a condition characterized by difficulty breathing, inadequate oxygenation of blood, and, if severe and untreated, death.

It is worth re-emphasizing that the pulmonary edema that can develop as a result of diastolic dysfunction is not due to poor pumping function of the left ventricle. Indeed, it has resulted from the left ventricle's inability to readily accept blood trying to enter it from the left atrium.

Pathophysiology

The primary reason for the left ventricle's inability to properly fill with blood during diastole (i.e. diastolic dysfunction) is that it has become stiff (i.e. non-compliant). In the setting of a stiff left ventricle, it is more difficult for blood to flow into it from the left atrium. In such a situation, filling can be maintained by a combination of coordinated left atrial pumping (i.e. beating) and a relatively slow heart rate. The former actively pumps blood into the stiff left ventricle, and the latter can allow for sufficient time for blood to passively enter the left ventricle from the left atrium.

Risk Factors and Causes

Any condition or process that leads to stiffening of the left ventricle can lead to diastolic dysfunction.

Some 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

One miscellaneous but important cause of diastolic dysfunction is mitral stenosis. In this case, the problem is not that the left ventricle is stiff. Rather, in mitral stenosis, blood cannot readily flow out from the left atrium into the left ventricle since the valve between those two heart chambers is blocked. Especially when the heart rate is elevated (as occurs in exercise and pregnancy), there will be insufficient time for blood to traverse the narrowed passageway (i.e. mitral valve) between the left atrium and left ventricle. As a consequence, the blood will back up into the left atrium and, eventually, the lungs. Pulmonary edema may result.

Treatment

By and large, 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.

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.

Prognosis

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 ^{[1] [2]}

References

1. ^ http://content.nejm.org/cgi/content/abstract/355/3/251.
2. ^ http://content.nejm.org/cgi/content/abstract/355/3/260

1. Owan TE, Hodge DO, Herges, RM, Jacobsen SJ, Roger VL, Redfield MM. Trends in Prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med 2006; 355:251-9.

2. Bhatia S, Tu JV, Lee DS, Austin PC, Fang J, Haouzi A, Gong Y, Liu PP. Outcome of heart failure with preserved ejection fraction in a population-based study. N Engl J Med 2006; 355:260-9.