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Imagine the moment when the heart ventricles begin to contract. At this moment, what is happening...

Imagine the moment when the heart ventricles begin to contract. At this moment, what is happening with ECG, the heart sounds, the ventricular blood volume, and the tricuspid/bicuspid as well as the semilunar valves? Also, describe how ventricular contraction and blood ejection are affected by mitral regurgitation and by aortic stenosis.

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Heart failure with reduced ejection fraction (HFrEF) happens when the left side of your heart doesn't pump blood out to the body as well as normal.

It's sometimes called systolic heart failure. This is because your left ventricle doesn't squeeze forcefully enough during systole, which is the phase of your heartbeat when your heart pumps blood.

The types of heart failure are based on a measurement called the ejection fraction. The ejection fraction measures how much blood inside the ventricle is pumped out with each contraction. The left ventricle squeezes and pumps some (but not all) of the blood in the ventricle out to your body. A normal ejection fraction is more than 55%. This means that 55% of the total blood in the left ventricle is pumped out with each heartbeat.

Heart failure with reduced ejection fraction happens when the muscle of the left ventricle is not pumping as well as normal. The ejection fraction is 40% or less.footnote1

The amount of blood being pumped out of the heart is less than the body needs. A reduced ejection fraction can happen because the left ventricle is enlarged and cannot pump normally.

Examples of ejection fractions of a healthy heart and a heart with reduced ejection fraction:

  • A healthy heart with a total blood volume of 100 mL that pumps 60 mL has an ejection fraction of 60%.
  • A heart with an enlarged left ventricle that has a total blood volume of 140 mL and pumps 60 mL has an ejection fraction of 43%.
  • Coronary artery disease causes gradual heart damage over time. Ischemia is the medical term for what happens when your heart muscle doesn't get enough oxygen. Ischemia may happen only once in a while, such as when you are exercising and your heart muscle needs more oxygen than it normally does. Ischemia can also be ongoing (chronic) if your coronary arteries are so narrowed that they limit blood flow to your heart all the time. This chronic lack of oxygen can gradually damage portions of your heart muscle. Your heart can slowly lose its ability to pump blood to your body.

    Chronic ischemia can allow your heart muscle to get just enough oxygen to stay alive but not enough oxygen to work normally. Ongoing poor blood flow to the heart muscle reduces the heart's ability to contract and causes it to pump less blood during each beat. The less blood your heart pumps out to your body, the less blood it is actually pumping back to itself through the coronary arteries. The end result is that heart failure makes ischemia worse, which in turn makes heart failure worse.

    Mitral valve regurgitation can gradually lead to heart failure. With this problem, the mitral valve doesn't close properly, and blood leaks back into the left atrium when the left ventricle contracts. Over time, the left ventricle pumps harder to move the extra blood that has returned to it from the left atrium. The ventricle stretches and gets bigger to hold the larger volume of blood. Gradual weakening of the left ventricle may cause heart failure.

    High blood pressure can also gradually lead to heart failure. To pump against your high blood pressure, your heart has to increase the pressure inside your left ventricle when it pumps. After years of working harder to pump blood, your ventricle may begin to weaken. When this happens, the pressure inside the weakened left ventricle will cause the ventricle to expand, stretching out the heart muscle. This damaging process is called dilation, and it impairs your heart's ability to squeeze forcefully. The result is heart failure.

Patients with severe aortic stenosis (AS) with tight valve area and preserved left ventricular (LV) ejection fraction (EF) should present with high aortic jet velocity.1 However, different haemodynamic patterns have been described.2 Discordance between aortic valve area (AVA) and aortic jet velocity is frequently encountered in clinical practice,3,4 even in patients with preserved EF and severely stenotic valve.5 This discordance is often related to low flow, documented by stroke volume indexed to body surface area (SV index) lower than 35 mL/m2.3,5 The presence of low flow is important because patients with this type of AS may encounter high mortality whether symptomatic or asymptomatic6,7 often in the context of delayed referral to surgery. Understanding this haemodynamic pattern is particularly important because surgical benefit provided by aortic valve replacement to these patients appear similar to that of patients with normal flow AS.6,8

However, there is little information regarding pathophysiologic processes determining the low-flow AS state. This condition is associated with increased global ventricular afterload, concentric LV hypertrophy and intrinsic myocardial contractility impairment.9 It is well known that moderate or severe mitral regurgitation (MR) can decrease forward stroke volume (SV) and potentially contributes to the low-flow state.10 However, the role of co-existing MR in determining these inconsistencies in AS patients has not yet been explored in a quantitative manner, covering the entire spectrum of severity, including mild MR. In particular, there are no quantitative data to assess the link between the degree of MR and the reduced aortic flow.


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