Microvascular Angina | How Does It Happen?

The term “angina” is derived from Latin, and the literal translation means “to choke.” The diagnosis of this condition was originally based on symptoms and careful evaluation of the pattern of pain until the advent of investigations such as angiography and cardiac MRI. The heart’s main blood supply comes from the blood inside of the heart after its contraction, where it passes through the aortic valves and into the coronary sinuses to the right and left coronary arteries. It reaches the heart muscle through a complex network of small blood vessels “microvasculature.” Lesions or narrowing of those blood vessels causes the characteristic pain, also known as “ischemic pain.”

In most cases, this narrowing affects the large blood vessels. It causes stable, unstable angina or -in case of narrowing due to the contraction of smooth muscles of the walls of blood vessels- vasospastic angina. In microvascular angina, however, it mainly affects the small branches. It was previously believed that microvascular angina is a benign disease that doesn’t have the fatal effects of other kinds of angina. However, it is now estimated that about 10% of MVA patients present with deadly heart attacks.

Who does it affect?

Coronary artery disease is generally more common in males. It affects them at a younger age, owing to their chief sex hormone “testosterone” in raising the cholesterol level and causing what we call “visceral obesity,” where fat accumulates around the abdominal organs. The level of LDL-C rises and deposits in the arteries at an earlier age.

In the case of microvascular angina, however, the prevalence of the disease in women clearly exceeds that of men’s. An estimated 30% of all stable angina patients have microvascular angina in the absence of damage to the large coronary arteries.

How does it happen?

A delicate balance controls the flow of blood to the heart muscle. Various factors contribute, either local in the blood vessel itself or neurogenic under the control of the autonomic nervous system. Multiple theories explain the mechanism of microvascular angina, but the most accepted is the endothelial dysfunction theory.

In microvascular angina, the amount of dilator substances released by the endothelium is reduced, and the balance shifts towards the vasoconstrictor substances. The primary vasodilator is nitric oxide, and a defective release, whether at rest or during exercise, reduces the blood flow to the heart, producing ischemia.