What is Coronary Microvascular Disease (Small Vessel Disease)?
Coronary microvascular disease, also known as small vessel disease, refers to the dysfunction of the heart’s small vessels that supply blood to the myocardium. These small vessels—arterioles and capillaries—are not easily visualized during conventional coronary angiography, making diagnosis more challenging. Microvascular disease can cause angina and ischemia, even when the major coronary arteries appear normal or show only mild narrowing.
Anatomy and Physiology of Coronary Circulation
The coronary arterial system forms a continuous network of functionally distinct vessels with progressively decreasing diameters. Specifically, the major epicardial coronary vessels (>400 μm in diameter) transition into pre-arterioles (100–400 μm), then into smaller intramyocardial arterioles (<100 μm), which connect directly with the capillaries (<10 μm).
The large epicardial coronary vessels and their main branches function primarily as conduits or reservoirs of blood. Under normal conditions, their contribution to total vascular resistance is minimal (5%).
Their diameter depends on shear stress, blood flow, and endothelial function. In contrast, the pre-arterioles and arterioles are the main regulators of vascular resistance and play the most significant role in controlling total myocardial blood flow (80% of total coronary flow is determined by these vessels).
Their diameter is regulated by various endogenous metabolic factors secreted by adjacent myocardial cells, such as adenosine.
Under physiological conditions, myocardial perfusion depends on total myocardial blood flow rather than perfusion pressure. The phenomenon of coronary autoregulation refers to the intrinsic ability of the coronary circulation to adjust to changes in perfusion pressure and myocardial oxygen and blood demands.
Since myocardial viability relies on total coronary blood flow, autoregulation aims to maintain flow at levels corresponding to the myocardium’s needs by adjusting the vasodilation of vessels responsible for determining vascular resistance—namely, the coronary arterioles.
Through this adaptive process, at rest, myocardial blood flow remains independent of perfusion pressure.
During stress, when the metabolic demands of the myocardium increase, such as during exercise, coronary autoregulation ensures that total coronary blood flow meets the elevated myocardial oxygen demands through further dilation of the arterioles.
Under conditions of maximal hyperemia, where vascular resistance is minimized, coronary autoregulation ceases. In this case, the compensatory mechanism of autoregulation no longer functions, and coronary blood flow becomes dependent on perfusion pressure.
Under maximal hyperemia and full vasodilation of the arterioles, the relationship between mean coronary pressure and flow becomes almost linear. This assumption forms the basis for functionally assessing the impact of a stenosis on coronary blood flow through the quantitative evaluation of the pressure gradient caused by the stenosis.
When a stenosis occurs in a segment of the epicardial coronary circulation, blood flow decreases due to the additional resistance caused by the narrowing.
However, thanks to compensatory vasodilation in the microcirculation at the arteriolar level, blood flow and thus myocardial supply are maintained at levels that meet metabolic demand, without inducing ischemia. Clinical studies have shown that stenoses up to 50% do not affect total coronary blood flow, even under stress conditions such as exercise.
What are the symptoms of microvascular disease?
Patients with coronary microvascular disease often experience symptoms such as chest pain (angina), fatigue, shortness of breath, and discomfort. Chest pain may resemble that of classical coronary artery disease, but tests for obstructive disease are often negative. These symptoms can worsen with physical exertion or emotional stress.
What causes the disease?
The exact cause of coronary microvascular disease is not fully understood, but several factors are believed to contribute to its development, including:
Endothelial dysfunction, where the inner lining of the small vessels (endothelium) malfunctions, leading to spasms or poor dilation of the vessels (microvascular endothelial dysfunction).
Inflammation, which causes swelling and thickening, leading to structural changes in the vessel walls.
Other contributing factors: age, sex (women are more commonly affected), hypertension, dyslipidemia, diabetes, physical inactivity, obesity, and smoking.
