Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 229

The coronary arteries normally take an epicardial course over the surface of the heart, but they occasionally have an intramyocardial segment that may get compressed in systole and cause symptomatic ischemia. This is called “myocardial bridging,” and it is characterized by angiographic off-and-on narrowing of the intramyocardial segment by >70%, only during systole (milking effect). This phasic obstruction distinguishes bridging from spasm, which is present throughout the cardiac cycle. Bridging is seen in 2% of coronary angiograms and is almost always limited to the LAD. Intramyocardial coronary segments are even more commonly diagnosed on coronary CT, with a frequency of up to 25%.¹⁴⁰

Since over 80% of the left coronary blood flow occurs during diastole, bridging does not usually cause ischemia and often does not explain chest pain.¹⁴¹ During tachycardia, systolic coronary flow gains more importance as systole occupies a larger part of the cardiac cycle, while stronger inotropism leads to a stronger squeeze of the bridged LAD with a spillover into diastole, which may lead to exertional ischemia. This explains that up to 20% of patients with bridging may have ischemia on stress testing.¹⁴² The combination of exertional angina, ischemia on stress testing, and bridging on angiography without obstructive CAD suggests the diagnosis of symptomatic myocardial bridging. Ischemia correlates with the severity of the narrowing and the intramyocardial depth of the bridge.

The hemodynamic significance of bridging may be assessed via a modified FFR, where dobutamine is used as the stressor (to exaggerate bridging severity), and the distal-to-proximal pressure ratio is calculated in diastole while ignoring systolic pressures (systolic pressure may falsely overshoot past the bridge, because of the direct compression effect). Non-invasively, stress echo may be used: a significant bridge often leads to a unique pattern of isolated mid-septal buckling which spares the apex; unlike fixed LAD stenosis, a bridge results in ischemia that is mostly localized at the bridge level rather than distal to it.

Even when symptomatic, myocardial bridging is a benign condition with a very low risk of MI or arrhythmia,¹⁴³ yet the abnormal stress may cause atheroma 20-30 mm proximal to the bridge. Nitrates and diuretics aggravate bridging as they lead to reflex tachycardia and increased inotropism; the patient may improve enough upon their withdrawal. In fact, NTG administration is a useful diagnostic test during angiography, as it unveils the severity of bridging (opposite effect on vasospasm). β-Blockers are the mainstay of therapy.