The cardiovascular system is markedly affected by stress after stroke. There is a complex interaction between the brain and heart, and the understanding of the mutual effects has increased in recent decades. Stroke is accompanied by pathological disturbances leading to autonomic dysfunction and systemic inflammation, which leads to changes in cardiomyocyte metabolism. Cardiac injury after stroke may lead to serious complications and long-term cardiac problems. Evidence suggests that blood biomarkers and electrocardiogram analyses can be valuable for estimating the severity, prognosis, and therapy strategy in patients after stroke. It is necessary to distinguish whether these abnormalities presenting in stroke patients are caused by coexisting ischemic heart disease or are caused by brain injury directly. Distinguishing the origin can have a great impact on the treatment of patients after acute stroke. In this article, we focus on epidemiology, pathophysiological mechanisms, and the presentation of cardiac changes in patients after stroke.

• Publication type
• Journal Article MeSH
• Review MeSH

The mammalian ventricular myocardium forms a functional syncytium due to flow of electrical current mediated in part by gap junctions localized within intercalated disks. The connexin (Cx) subunit of gap junctions have direct and indirect roles in conduction of electrical impulse from the cardiac pacemaker via the cardiac conduction system (CCS) to working myocytes. Cx43 is the dominant isoform in these channels. We have studied the distribution of Cx43 junctions between the CCS and working myocytes in a transgenic mouse model, which had the His-Purkinje portion of the CCS labeled with green fluorescence protein. The highest number of such connections was found in a region about one-third of ventricular length above the apex, and it correlated with the peak proportion of Purkinje fibers (PFs) to the ventricular myocardium. At this location, on the septal surface of the left ventricle, the insulated left bundle branch split into the uninsulated network of PFs that continued to the free wall anteriorly and posteriorly. The second peak of PF abundance was present in the ventricular apex. Epicardial activation maps correspondingly placed the site of the first activation in the apical region, while some hearts presented more highly located breakthrough sites. Taken together, these results increase our understanding of the physiological pattern of ventricular activation and its morphological underpinning through detailed CCS anatomy and distribution of its gap junctional coupling to the working myocardium.

• MeSH
• Connexin 43 physiology   MeSH
• Gap Junctions physiology   MeSH
• Cell Communication * MeSH
• Mice MeSH
• Pericardium cytology   physiology   MeSH
• Purkinje Fibers cytology   physiology   MeSH
• Heart Ventricles pathology   MeSH
• Muscle Cells cytology   physiology   MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Mice MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

The atrial septum enables efficient oxygen transport by separating the systemic and pulmonary venous blood returning to the heart. Only in placental mammals will the atrial septum form by the coming-together of the septum primum and the septum secundum. In up to one of four placental mammals, this complex morphogenesis is incomplete and yields patent foramen ovale. The incidence of incomplete atrial septum is unknown for groups with the septum primum only, such as birds and reptiles. We found a low incidence of incomplete atrial septum in 11 species of bird (0% of specimens) and 13 species of reptiles (3% of specimens). In reptiles, there was a trabecular interface between the atrial septum and the atrial epicardium which was without a clear boundary between left and right atrial cavities. In developing reptiles (four squamates and one crocodylian), the septum primum initiated as a sheet that acquired perforations and the trabecular interface developed late. We conclude that atrial septation from the septum primum only results in a low incidence of incompleteness. In reptiles, the atrial septum and atrial wall develop a trabecular interface, but previous studies on atrial hemodynamics suggest this interface has a very limited capacity for shunting.

• MeSH
• Heart Septal Defects, Atrial epidemiology   etiology   MeSH
• Incidence MeSH
• Reptiles abnormalities   MeSH
• Birds abnormalities   MeSH
• Atrial Septum embryology   growth & development   pathology   MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH