XSMDR

I'll assume you are asking about heart failure secondary to hypertension. Typically the initial hypertrophy does lead to an increase in contractile/inotropic force. However in the later stages of heart failure (i.e. when patients become symptomatic and detected), hypertrophy as a mechanism is no longer sufficient to compensate. You cannot infinitely hypertrophy muscle cells because the increased metabolic demand is unsustainable.

Additionally, over time this leads to remodelling of the affected cardiac ventricles. This is a complex process that is multifactorial and occurs at the cellular level and how the myocytes/fibroblasts/other cells express their genes. Unsatisfyingly, we currently do not have a good understanding of how and why it occurs exactly.

However, in animal models we do see that the remodelling that takes place involves dilation of the affected (typically left) ventricle. This dilation leads to increased wall tension needed to pump blood, and since these patients are already at their limit for compensation via hypertrophy, this leads to decompensated heart failure. See again the Law of LaPlace for the relationship between dilation (increased radius) and wall tension.

Thus most of our current treatments are aimed towards reducing the afterload (beta blockers, angiotensin converting enzyme inhibitors, etc.).

Do you know how much the company bills per minute of work (i.e. how much the hospital has to pay the company)?