The interactions between cerebrovascular and cardiovascular diseases are complex: while cardiac disease is a risk factor for cerebral ischemia, ischemic stroke may reciprocally induce heart dysfunction.

The aim of this study was to evaluate how prior cerebrovascular lesions may affect myocardial function and to identify the signals involved in these processes.

Adult male Wistar rats underwent cerebral embolization by injection of 90μm microspheres into the left or right common carotid artery. Two or 24h after stroke or sham embolization, each heart was isolated and perfused ex vivo in the Langendorff mode. Two hours after stroke, the baseline left ventricular developed pressure in hearts from both stroke groups was diminished and 24h after surgery, the same alteration was observed. In another set of experiments, echocardiography showed that left ventricular fractional shortening was altered in both stroke groups 2hours, 24hours and 7 days after surgery. Epinephrine, norepinephrine and growth differentiation factor-15 (GDF15) plasma levels were increased 2hours after surgery in rats from both stroke groups compared with the sham group. 24h after surgery, catecholamine and GDF15 levels were also increased in stroke rats. Additionally, an increased gene and protein expression of nitric oxide synthase 3 and glutathione peroxidase 1 was observed in the hearts of stroke rats. Interestingly, decreased protein expression was noticed for beta-1 adrenoceptor and catalase without decreased gene expression which suggests post-translational stroke-induced down-regulations.

To conclude, this study highlighted the deleterious consequences of stroke on cardiac function at different times after stroke both ex vivo, in the isolated heart, and in vivo. The molecular mechanisms involved in these processes need to be further investigated insofar as they may involve the sympathetic nervous system and nitro-oxidative stress.