PMC

Changes of in-hospital mortality rate and relative risk of RV infarction for in-hospital mortality between the fibrinolytic and mechanical reperfusion era.
These data were derived from previously published meta-analyses, which included many prospective or retrospective studies, assessing the impact of RV infarction in patients with acute MI up to June 2007,^,–,– and two additional observational studies that met the same inclusion criteria up to June 2012.^,

Contrast-enhanced cardiovascular magnetic resonance image of right ventricular myocardial infarction (a) and cine angiogram before (b) and after (c, d) percutaneous angioplasty in the corresponding case.
Enlarged short-axis view with infarction of the right ventricular wall (red arrows) and the inferior left ventricle. The occluded proximal right coronary artery was recanalized with percutaneous angioplasty, and the major right ventricular branch (white arrows) was recognized.

Responses before and after volume replacement therapy in patients with right ventricular myocardial infarction.
The association between mean right atrial pressure (mRAP) and the right ventricular systolic work index (RVSWI) is shown by a blue line. An mRAP of 10–15 mmHg seems to be an optimal target for right-sided filling pressure. Changes of pulmonary wedge pressure (PWP) and cardiac index from smaller studies are shown by a red line. There is a wide variation in its response, but no clear linear association was noted between PWP and cardiac index with a higher right-sided filling pressure target.^–

Two physiological concepts explaining the detrimental effects of excessive volume loading. (a) Normal ventricle: at end-systole (ES), the right ventricular (RV) free wall moves toward the septum. (b) Pericardial restraining effects (above, before volume loading; below, after excessive volume loading): RV dilatation, as a result of excessive volume loading, can lead to the elevation of intrapericardial pressure, increase in pericardial constraint (red arrow), and change of geometry due to interventricular septum shift. These changes contribute to the low-output state by decreasing left ventricular (LV) distensibility, preload, and ventricular elastance. (c, d) Role of the interventricular septum (c, pure RV infarction; d, RV infarction with septal ischaemia). (c) At ES, the RV free wall moves toward the septum. At end-diastole (ED), the RV dilates during diastole and the septum reverse curves toward the volume-reduced LV. At ES, the septum thickens but moves paradoxically into the RV, displacing the RV volume despite RV free wall dyskinesis. (d) Septal ischaemia depresses septal contraction and global LV function, resulting in LV dilatation. The septum stops thickening and there is increased systolic septal displacement into the RV. Pansystolic septal thinning and more extensive paradoxical displacement are associated with further depression of RV performance.