Expert consensus on the clinical application of enhanced external counterpulsation in elderly people (2019).

Enhanced external counterpulsation (EECP) is a non-invasive assisted circulation technique and a rich pool of evidence has accumulated for its clinical application in the prevention and management of multiple comorbidities in the elderly population, including angina, heart failure, ischemic cerebrovascular diseases, neurodegenerative diseases, sleep disorder, diabetes and its complications, ischemic eye diseases, sudden hearing loss and erectile dysfunction, as well as various psychological and psychiatric conditions. When applying EECP to elderly patients, emphasis should be placed on issues such as safety assessment, risk management and protocol individualization, as well as the monitoring of efficacy during and after treatment.

Protective effect of lipid microspheres 1 on myocardial injury following elective percutaneous coronary intervention in patients with angina pectoris: a pilot study.

BACKGROUND: Prostaglandin E1 incorporated into lipid microspheres (lipo-PGE1) is effective in the treatment of peripheral vascular disorders and diabetic neuropathy. It is unknown whether it has protective effects in patients with angina pectoris undergoing percutaneous coronary intervention (PCI). OBJECTIVES: The goal of this pilot study was to investigate whether lipo-PGE1 has protective effects in patients with angina pectoris undergoing PCI. METHODS: A single-blinded, randomized controlled trial was conducted in 79 patients with stable or unstable angina pectoris. The control group received standard medical therapy, and the Lipo-PGE1 group (n = 40) received 20 µg/day of lipo-PGE1 intravenously, starting at least 48 h before PCI and continuing for 5 days. Cardiac troponin T (cTnT) and creatine kinase myocardial isoenzyme (CK-MB) were measured before lipo-PGE1 infusion and at 6, 12 and 24 h after PCI. RESULTS: The cTnT and CK-MB concentrations were lower in the lipo-PGE1 group than in the control group at 6 h (0.15 ± 0.33 vs. 0.43 ± 0.77; 2.87 ± 3.99 vs. 5.64 ± 6.27, respectively; P < 0.05), 12 h (0.20 ± 0.48 vs. 0.54 ± 0.85; 3.58 ± 5.22 vs. 7.45 ± 9.48; P <  0.05) and 24 h (0.18 ± 0.50 vs. 0.50 ± 0.75; 3.15 ± 4.50 vs. 6.16 ± 6.83; P < 0.05). The incidence of postprocedural myocardial injury, defined as an elevation of cTnT more than 0.1 ng/ml or CK-MB more than 5.0 ng/ml, was less in the PGE1 group than in the control group (30 vs. 54%; 13 vs. 31%, respectively; P < 0.05). Lipo-PGE1 was well tolerated and there were no serious adverse events or side-effects. CONCLUSIONS: Lipo-PGE1 treatment appears to reduce myocardial injury following elective PCI in angina patients.

Effects of therapeutic hypothermia on coagulopathy and microcirculation after cardiopulmonary resuscitation in rabbits.

OBJECTIVE: The aim of this study was to investigate the effects of therapeutic hypothermia (TH) on coagulopathy and cerebral microcirculation disorder after cardiopulmonary resuscitation (CPR) in rabbits. METHODS: Cardiac ventricular fibrillation was induced by alternating current in 24 New Zealand rabbits, and hypothermia was induced by surface cooling or normothermia (NT) was maintained for 12 hours after the return of spontaneous circulation (ROSC). Several physiologic indexes were measured before CPR and at 4, 8, and 12 hours after ROSC. The microcirculation flow in the cerebral cortex was measured with a PERIMED Multichannel Laser Doppler system (Perimid, Sweden), and glomerular fibrin deposition was determined by microscopy. RESULTS: Compared with the NT group, the prothrombin time, activated partial thromboplastin time, and international normalized ratio in the TH group were increased; there were no differences in anti-thrombin-III, protein C, and d-dimer indexes. The microcirculation flow in the cerebral cortex before CPR and after ROSC at 4, 8, and 12 hours was 401.60 ± 11.76, 258.86 ± 34.58, 317.59 ± 23.36, and 371.98 ± 5.79 mL/min, respectively, in the NT group, and 398.18 ± 12.91, 336.19 ± 19.27, 347.76 ± 13.80, and 383.78 ± 3.29 mL/min, respectively, in the TH group. There were apparent disparities at each checkpoint after ROSC in these 2 groups (4 hours: P = .001; 8 hours: P = .011; 12 hours: P = .009). The Pearson correlation test showed that the microcirculation flow in the cerebral cortex was positively correlated with activated partial thromboplastin time after ROSC (4 hours: r = 0.503, P = .033; 8 hours: r = 0.565, P = .035; 12 hours: r = 0.774, P = .009), but not with other coagulation parameters. CONCLUSIONS: Therapeutic hypothermia might cause coagulant dysfunction but concomitantly improves the microcirculation flow in the cerebral cortex, which might be an effect of TH that results in cerebral protection.