Acute heart failure is a condition when the cardiac output (the amount of blood pumped by heart every minutes) is not sufficient to meet the needs of the body. Cardiac output depends on how much blood is in the heart before it starts contracting (cardiac pre-load), how strongly hear contracts (cardiac contractility), how much resistance heart faces when pumping blood into the arteries (cardiac after-load, or peripheral vasoconstriction), and how many times heart beats in a minutes.
For a failing heart, increasing the force of contraction and decreasing the pressure against which it pumps blood (after-load or vasoconstriction) are important factors. In fact, peripheral vasodilators such as ACE inhibitors or ARB are standards of care for heart failure patients. One may ask, what if we decrease the pressure against which heart pumps blood really low, in other words, if we cause high (intensive) vasodilation with drugs. This particular hypothesis was tested in The GALACTIC Study recently published in JAMA.
Interestingly, authors found no benefit of intensive vasodilatation on composite endpoint of death or rehospitalization. Further, the intensive vasodilation arm had higher risk of adverse effects such as worsening renal function, hypokalemia, dizziness, and hypotension.
The results are important because they suggest that while we focus on cardiac output, blood flow to individual organ (or fraction of cardiac output received by various organs may be as important, if not more important. Intensive vasodilatation likely results in poor perfusion to various organ resulting in increased adverse effects.
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