In HCM increased preload and afterload , results in increase in cavity size and decrease in LVOT obstruction .
But at the same time Post VPC in HCM , increased filling results in stretching and increase in LVOT obstruction.
increase in cavity size(due to increase in preload and afterload) should also result in increased stretching and incresed force of contraction resulting in increase in LVOT obstruction , due to frank sterling law. But why not ?
Hypertrophic Cardiomyopathy (HCM) is a complex cardiac condition characterized by increased thickness of the left ventricular walls (hypertrophy), particularly of the interventricular septum. The relationship between preload, afterload, cavity size, contractility, and left ventricular outflow tract (LVOT) obstruction in HCM can be somewhat counterintuitive due to the unique physiology of the disease.
Let’s break down the mechanisms to address your question:
- Increased Preload and Afterload:
- In HCM, increased preload (end-diastolic volume) and afterload (resistance against which the heart pumps) can lead to an increase in cavity size due to the heart’s attempt to accommodate the increased volume and pressure. This can temporarily reduce LVOT obstruction because the increased cavity size can help open up the LVOT.
- Frank-Starling Law:
- The Frank-Starling law, which describes the relationship between preload and stroke volume (and thus cardiac output), is applicable in HCM. An increase in preload (end-diastolic volume) can lead to increased stretching of myocardial fibers, resulting in a more forceful contraction and, consequently, an increase in stroke volume.
- However, in HCM, this can be limited due to the structural abnormalities in the myocardium and the LVOT obstruction caused by the thickened septum.
- Post-Ventricular Premature Contraction (VPC):
- When a premature ventricular contraction (VPC) occurs in HCM, the increased filling of the ventricle can lead to stretching of the myocardium, including the hypertrophied septum.
- Stretching can worsen the LVOT obstruction by bringing the hypertrophied septum closer to the anterior mitral leaflet, further narrowing the LVOT and impeding blood flow.
In summary, while increased cavity size due to increased preload and afterload may temporarily reduce LVOT obstruction by helping to open up the LVOT, in HCM, this effect is often outweighed by the structural abnormalities and hypertrophy that cause a baseline level of LVOT obstruction. Any additional stretching, such as from a post-VPC, can exacerbate this obstruction and contribute to the symptoms and complications associated with HCM.
It’s important to note that the dynamics in HCM are complex and can vary from patient to patient, necessitating individualized assessment and management.