Intrapulmonary shear stress enhancement: a new therapeutic approach in acute myocardial ischemia

Ischemic heart disease (IHD) is a leading cause of mortality with insufficient results of current therapies, most probably due to maintained endothelial dysfunction conditions. Alternatively, we propose a new treatment that promotes endothelial shear stress (ESS) enhancement using an intrapulmonary pulsatile catheter.

Twelve piglets, divided in equal groups of 6: pulsatile (P) and non-pulsatile (NP), underwent permanent left anterior descending coronary artery ligation through sternotomy. After 1 h of ischemia and heparin injection (150 IU/kg): in P group, a pulsatile catheter was introduced into the pulmonary trunk and pulsated intermittently over 1 h, and irrespective of heart rate (110 bpm). In NP group, nitrates were given (7 ± 2 mg/kg/min) for 1 h.

In P group all 6 animals survived ischemia for 120 min, but in NP group only 2 animals survived. The 4 animals that died during the experiment in NP group survived for 93 ± 14 min. Hemodynamics and cardiac output (CO) were significantly improved in P group compared with NP group: CO was 0.92 ± 0.15 vs. 0.52 ± 0.08 in NP group (L/min; p < 0.05), respectively. Vascular resistances (dynes.s.cm(-5)/kg) were significantly (p < 0.05) lower in P group versus NP group: pulmonary resistance was 119 ± 13 vs. 400 ± 42 and systemic resistance was 319 ± 43 vs. 1857 ± 326, respectively. Myocardial apoptosis was significantly (p < 0.01) lower in P group (0.66 ± 0.07) vs. (4.18 ± 0.27) in NP group. Myocardial endothelial NO synthase mRNA expression was significantly (p < 0.01) greater in P group (0.90 ± 0.09) vs. (0.25 ± 0.04) in NP group.

Intrapulmonary pulsatile catheter could improve hemodynamics and myocardial contractility in acute myocardial ischemia. This represents a cost-effective method, suitable for emergency setting as a first priority, regardless of classical coronary reperfusion.