Focal and diffuse myocardial fibrosis both contribute to regional hypoperfusion assessed by post-processing quantitative-perfusion MRI techniques

IntroductionIndications for stress-cardiovascular magnetic resonance imaging (CMR) to assess myocardial ischemia and viability are growing. First pass perfusion and late gadolinium enhancement (LGE) have limited value in balanced ischemia and diffuse fibrosis. Quantitative perfusion (QP) to assess absolute pixelwise myocardial blood flow (MBF) and extracellular volume (ECV) as a measure of diffuse fibrosis can overcome these limitations. We investigated the use of post-processing techniques for quantifying both pixelwise MBF and diffuse fibrosis in patients with clinically indicated CMR stress exams. We then assessed if focal and diffuse myocardial fibrosis and other features quantified during the CMR exam explain individual MBF findings.MethodsThis prospective observational study enrolled 125 patients undergoing a clinically indicated stress-CMR scan. In addition to the clinical report, MBF during regadenoson-stress was quantified using a post-processing QP method and T1 maps were used to calculate ECV. Factors that were associated with poor MBF were investigated.ResultsOf the 109 patients included (66 ± 11 years, 32% female), global and regional perfusion was quantified by QP analysis in both the presence and absence of visual first pass perfusion deficits. Similarly, ECV analysis identified diffuse fibrosis in myocardium beyond segments with LGE. Multivariable analysis showed both LGE (β = −0.191, p = 0.001) and ECV (β = −0.011, p < 0.001) were independent predictors of reduced MBF. In patients without clinically defined first pass perfusion deficits, the microvascular risk-factors of age and wall thickness further contributed to poor MBF (p < 0.001).DiscussionQuantitative analysis of MBF and diffuse fibrosis detected regional tissue abnormalities not identified by traditional visual assessment. Multi-parametric quantitative analysis may refine the work-up of the etiology of myocardial ischemia in patients referred for clinical CMR stress testing in the future and provide a deeper insight into ischemic heart disease

Altered blood gas tensions of oxygen and carbon dioxide confound coronary reactivity to apnea

Purpose: Arterial blood gases change frequently during anesthesia and intensive care. Apnea can occur during diagnostic exams and airway and surgical interventions. While the impact of blood gas levels on coronary blood flow is established, their confounding effect on coronary vasoreactivity in response to an apneic stimulus, especially in coronary artery disease, is not known. Methods: Six anesthetized control swine and eleven swine with coronary artery stenosis were examined. Nine different blood gas levels from a combination of arterial partial pressure of oxygen (70, 100, and 300 mmHg) and carbon dioxide (30, 40, and 50 mmHg) were targeted. Apnea was induced by halting controlled positive pressure ventilation for 3–30s, while the left descending coronary artery flow was measured and reported relative to apnea duration, and at the adjusted mean (12s). Results: At normoxemic-normocapnic blood gas levels, apnea increased coronary blood flow in proportion to the duration of apnea in the control (r = 0.533, p < 0.001) and stenosed groups (r = 0.566, p < 0.001). This culminated in a 42% (95% CI: 27–58) increase in controls (p < 0.001) and, to a lesser extent, 27% (15–40) in the presence of coronary artery stenosis (p < 0.001). Vasoreactivity was augmented by mild-hypoxemic levels [81% (65–97), and 66% (53–79) increase in flow respectively, p < 0.001 vs. normoxemia], but markedly reduced during hyperoxia (7.5% (−8.2–23) and 0.3% (−12–13), respectively, p < 0.001 vs. normoxemia). Conclusion: Alterations of blood oxygen and carbon dioxide affect coronary vascular reactivity induced by apnea in swine, which was attenuated further in the presence of coronary stenosis. Especially hyperoxia significantly reduces coronary blood flow and blunts coronary vascular reactivity

Feature tracking strain analysis detects the onset of regional diastolic dysfunction in territories with acute myocardial injury induced by transthoracic electrical interventions.

Electric interventions are used to terminate arrhythmia. However, myocardial injury from the electrical intervention can follow unique pathways and it is unknown how this affects regional ventricular function. This study investigated the impact of transthoracic electrical shocks on systolic and diastolic myocardial deformation. Ten healthy anaesthetized female swine received five transthoracic shocks (5 × 200 J) and six controls underwent a cardiovascular magnetic resonance exam prior to and 5 h after the intervention. Serial transthoracic shocks led to a global reduction in both left (LV, - 15.6 ± 3.3% to - 13.0 ± 3.6%, p < 0.01) and right ventricular (RV, - 16.1 ± 2.3% to - 12.8 ± 4.2%, p = 0.03) peak circumferential strain as a marker of systolic function and to a decrease in LV early diastolic strain rate (1.19 ± 0.35/s to 0.95 ± 0.37/s, p = 0.02), assessed by feature tracking analysis. The extent of myocardial edema (ΔT1) was related to an aggravation of regional LV and RV diastolic dysfunction, whereas only RV systolic function was regionally associated with an increase in T1. In conclusion, serial transthoracic shocks in a healthy swine model attenuate biventricular systolic function, but it is the acute development of regional diastolic dysfunction that is associated with the onset of colocalized myocardial edema

Visualising myocardial injury after noncardiac surgery: a case series using postoperative cardiovascular MRI.

Myocardial injury after noncardiac surgery (MINS) and perioperative myocardial injury are associated with increased morbidity and mortality. Both are diagnosed by a perioperative increase in troponin, yet there is controversy if MINS is a genuine myocardial insult. We applied postoperative cardiovascular magnetic resonance T2 mapping techniques to visualise acute myocardial injury (i.e. oedema) in six patients with multiple cardiovascular risk factors who underwent aortic surgery. The burden of myocardial oedema was substantially higher in four patients with elevated troponin qualifying for MINS, compared with patients without MINS. The data and images suggest that MINS represents genuine myocardial injury