Remote Ischemic Postconditioning in Humans

Percutaneous coronary intervention (PCI) has taken on an important role in the treatment of ischemic heart disease in recent years. However, the beneficial effects of revascularization are partly shadowed by post-reperfusion injury, which accounts for up to half the size of the reperfused myocardial infarct. Several drugs and procedures exist that might protect against this phenomenon. One of the most controversial of these strategies, which has shown promising results in experimental animal models, is remote ischemic post-conditioning. This involves inducing ischemia at a site remote from the heart after an ischemic coronary lesion to reduce the resulting myocardial infarct size.

The myocardial damage produced by ischemia-reperfusion associated with PCI is a known short- and long-term prognostic factor, and is associated with a greater risk of death, myocardial infarction and revascularization during the follow-up.

Our aim is to assess the phenomenon of remote ischemic post-conditioning in patients undergoing PCI, in whom the acute insult on the myocardium is determined by the angioplasty itself. Additionally, we aim to evaluate this phenomenon in a subgroup of diabetic patients, among whom the effectiveness of protective measures against post-reperfusion damage is more questioned.

We have designed a randomized, single-blinded interventional study involving 320 patients (40% diabetics) who are to undergo elective PCI. At the end of the angioplasty procedure, the patients assigned to remote ischemic post-conditioning will undergo three 5-minute cycles of ischemia using a blood-pressure cuff at 200 mmHg, placed on the non-dominant arm, interrupted twice for 5 minutes with the cuff deflated. In the control group the procedure will be limited to placing a deflated blood-pressure cuff (pressure: 0 mmHg) for 25 minutes.

The infarct size will be analyzed from an enzyme curve of troponin I and CK-MB values 0, 8, 16 and 24 hours after the procedure (primary endpoint). Measurements will also be taken of pH and lactate in the baseline sample (0 hours) and at 8 hours, and ultrasensitive C-reactive protein at 0 and 24 hours as a contrasted marker of inflammation in ischemic heart disease.

The follow-up, planned for one year, will seek to determine clinically interesting variables (secondary endpoint), such as readmission due to acute coronary syndrome, heart failure or major arrhythmic events and overall and cardiovascular mortality.