What’s the treatment for a grade 2 LV diastolic dysfunction?

  • I will try my best to explain it in layman terms. In medical language, “secondary to” means “as a result of an underlying illness”, so “heart failure secondary to diastolic dysfunction” means “heart failure as a result of diastolic dysfunction” or in other words “diastolic heart failure”.

    Systole (systolic phase) is the part of the heart cycle where the heart contracts in order to pump blood from the right ventricle to the lungs and from the left ventricle to the rest of the body. Diastole (diastolic phase) is the part of the heart cycle where the heart’s ventricles are filled with blood. Heart failure is a condition in which the function of the heart is not enough to provide the body with blood, either at rest or on exertion.

    The most obvious case of malfunction is when the heart does not pump out during the systolic phase enough of the blood that it gets filled with during the diastolic phase. This is called systolic heart failure. Its defining characteristic is a diminished “ejection fraction”, which means that the heart pumps out less than half of the maximum volume of blood that the heart is filled with during the end of the diastolic phase (ejection fraction less than 50%, normal is 60% or above).

    A heart with an inability to pump out enough blood during the systolic phase has most of the times also a problem getting filled with blood during the diastolic phase, a so called “diastolic dysfunction”. The opposite, however, is not always true. One third of patients with symptoms of heart failure only have a problem in the diastolic phase and seemingly no problem in the systolic phase. This is what we call a “heart failure secondary to diastolic dysfunction” or else a “diastolic heart failure”. It differs from “systolic heart failure” in that the ejection fraction is normal.

    How can it be that a patient gets symptoms of heart failure if their heart has gets filled with difficulty but still manages to pump out seemingly enough? First of all, the ejection fraction is really only a ratio of the volume of blood pumped out to the volume of blood that the heart gets filled with. It says nothing about how much blood actually leaves the heart.

    • Let’s assume that the walls of the heart muscle are thickened (so called hypertrophy, as in arterial hypertension, aortic stenosis or hypertrophic cardiomyopathy). The inner volume of the ventricles (cavum) gets smaller, so that the heart is filled with less blood. The percentage of blood that gets pumped out during the systolic phase may be nominally enough, hence a normal ejection fraction, but the volume is not actually enough to support the body’s needs.
    • The ventricles get dilated (as in severe valvular regurgitation, advanced coronary artery disease or dilatative cardiomyopathy). The volume of blood that gets pumped out is enough to cover the body’s needs at rest, but not at exertion, where there is no “room” for further dilation of the ventricles.

    In reality, it is not as simple as that. You do not need hypertrophy or dilation of the ventricles to have a diastolic dysfunction. The hallmark is an increased tension of the heart walls during its filling phase due to increased stiffness of the walls. Hypertrophy (again, as in arterial hypertension) does make the walls stiffer, but the walls don’ need to be thicker (hypertrophic) in order to be stiffer.

    There are diseases of the heart that alter the composition of its walls making them stiffer. Some of these fall into the category of so called restrictive or infiltrative cardiomyopathy (as in amyloidosis), but any disease that causes systemic inflammation and endothelial dysfunction (dysfunction of the inner layer of the vessels) can cause the walls of the heart to become stiffer: ischaemic heart disease, metabolic disease with diabetes, chronic kidney disease and, lastly, aging (even in the absence of amyloidosis, which is largely a disease of older age).

    Endothelial inflammation and malfunctioning or obliteration of the small vessels (microvascular angiopathy) causes the formation of harmful mediators which further constrict vessels and a reduction in the bioavailability of substances such as nitrogen monoxide (NO), which are supposed to dilate vessels. Increased stiffness of the veins leads to a shifting of blood volume into the systemic circulation, increasing arterial pressure (causing arterial hypertension). Increased stiffness of the arteries causes arterial hypertension, but even without arterial hypertension, it increases the stiffness of both the heart muscle cells themselves and their extracellular matrix.

    The increased stiffness of the walls of the ventricles increases the filling pressure inside the ventricles and this increased pressure is transferred backwards into the pulmonary veins, causing fluid to come out of the veins into the lungs, and backwards into the systemic veins, causing fluid to come out of the veins into the rest of the body, manifesting itself typically as leg swelling.

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