Measurement of Myocardial Lactate Production for Diagnosis of Coronary Microvascular Spasm

Assessment of myocardial lactate production during Ach-provocation testing is essential and viable for diagnosing coronary microvascular spasms. This procedure is generally safe and straightforward for detecting the occurrence of a microvascular spasms, which is typically not visible on any other imaging device Before starting the procedure, ensure that myocardial lactate production is measured in patients undergoing acetylcholine provocation testing to diagnose vasospastic angina or microvascular angina due to vasospasm. Additionally, ensure that the patients have discontinued all vasoactive agents at least 48 hours before the catheterization.

Next, shave the patient's hair at puncture sites including both inguinal regions and wrists. After anesthetizing, the puncture sites place two five French venous sheaths through the right or left femoral vein with ultrasound guidance. Then place a five or six French arterial sheath through the radial or femoral artery.

Next, administer intravenous heparin to achieve therapeutic anticoagulation before coronary instrumentation. Cannulate a five or six French Judkins left catheter into the left coronary artery or LCA through the radial or femoral artery. Next advance a coronary sinus or CS catheter from a venous sheath placed at the right femoral vein to the right atrium.

Then confirm the configuration of the CS and the location of its orifice in the right atrium in advance by detecting the CS image in the venous phase of LCA angiography. Next, cannulate an Amplatz left catheter into the CS by turning the catheter counterclockwise at the right atrium with the left anterior oblique view. Then verify whether the catheter is cannulated into the CS and its position in the CS is adequate by contrast injection from the catheter end.

Next, take a pair of blood samples from the CS and the osteum of LCA simultaneously to examine myocardial lactate metabolism at baseline. Finally, measure the lactate levels in the samples using blood gas analysis equipped with an automatic lactate measurement function. Perform the baseline left coronary angiography in an appropriate projection that ensures the best separation of the branches of each coronary artery.

Next, administer acetylcholine into the coronary artery in a cumulative manner over 20 seconds with careful monitoring of blood pressure and 12 lead ECG. Perform a coronary angiography when chest pain or any ECGST segment change occurs or routinely after completing each acetylcholine injection, collect paired samples of one milliliter blood from the LCA osteum and the CS to measure lactate concentrations at one minute after each dose of acetylcholine is given to the LCA and determine lactate concentrations with a calibrated automatic lactate analyzer. Calculate the lactate extraction ratio or LER by dividing the coronary arteriovenous difference in the lactate concentration by the arterial lactate concentration.

If epicardial coronary spasms are induced, administer five milligrams of isosorbide dinitrate into the LCA and promptly perform coronary angiography while the coronary artery is maximally dilated. Simultaneously collect one milliliter of blood from the LCA osteum and the CS to measure lactate concentrations after relieving the acetylcholine induced spasm. Shown here are the coronary angiograms, ECG changes, and lactate levels during acetylcholine provocation testing of a 56-year-old female patient suffering from transient chest discomfort at rest.

Baseline coronary angiogram of LCA and ECG findings appeared normal. Chest pain ischemic ECG changes and negative LER were noted immediately after 100 micrograms of acetylcholine administration into the LCA. Still no relevant epicardial coronary spasm was observed on angiography.

Thus, she was diagnosed as having a microvascular spasm. Interestingly, persistent negative LER was observed even after isosorbide dinitrate was administered into the LCA suggesting that myocardial ischemia attributable to impaired bioavailability of nitric oxide in coronary pre arterials was prolonged. The location of CS orifice must be confirmed in advance by detecting the CS image in the venous face of LCA angiography.