real-time-pressure-volume-analysis-acute-myocardial-infarction

Real-time Pressure-volume Analysis of Acute Myocardial Infarction in Mice

Acute myocardial infarction can lead to acute heart failure and cardiogenic shock. The evaluation of hemodynamics is critical for the evaluation of any ...

University Hospital Essen

S-nitrosation of macrophage migration inhibitory factor (MIF) has been shown to be cytoprotective in myocardial ischaemia/reperfusion (I/R) injury. Since the exact mechanism of action is unknown, we here characterise the cardioprotective effects of targeted intracellular accumulation of MIF in myocardial I/R injury. We used different in vivo, ex vivo and in vitro models of myocardial I/R and hypoxia/reoxygenation (H/R) injury to determine MIF levels by immunoblots and ELISA in different phases of reperfusion and reoxygenation, respectively. We discovered a rapid decrease of cardiac MIF that was specific to the early phase of reperfusion. Posttranslational modification of MIF via S-nitrosation--proofed by a modified version of the Biotin Switch Assay--prevented this rapid decrease, leading to a targeted intracellular accumulation of MIF in the early phase of reperfusion. Intracellular MIF accumulation preserved the intracellular ability of MIF to reduce oxidative stress as shown by hydrogen peroxide and aconitase activity measurements. Infarct size measurements by TTC staining showed an overall enhanced cardioprotective effect of this protein by reduction of reperfusion injury. In summary, we have unravelled a novel mechanism of MIF-mediated cardioprotection. Targeted intracellular accumulation of MIF by S-nitrosation may offer a novel therapeutic approach in the treatment of myocardial I/R-injury.

Targeted intracellular accumulation of macrophage migration inhibitory factor in the reperfused heart mediates cardioprotection.

Endothelial dysfunction with impaired bioavailability of nitric oxide (NO) is the hallmark in the development of cardiovascular disease. Endothelial dysfunction leads to atherosclerosis, characterized by chronic inflammation of the arterial wall and stepwise narrowing of the vessel lumen. Atherosclerosis causes deprivation of adequate tissue blood flow with compromised oxygen supply. To overcome this undersupply, remodeling of the vascular network is necessary to reconstitute and sustain tissue viability. This physiological response is often not sufficient and therapeutic angiogenesis remains an unmet medical need in critical limb ischemia or coronary artery disease. Feasible approaches to promote blood vessel formation are sparse. Administration of pro-angiogenic factors, gene therapy, or targeting of microRNAs has not yet entered the daily practice. Nitric oxide is an important mediator of angiogenesis that becomes limited under ischemic conditions and the maintenance of NO availability might constitute an attractive therapeutic target. Until recently it was unknown how the organism provides NO under ischemia. In recent years it could be demonstrated that NO can be formed independently of its enzymatic synthesis in the endothelium by reduction of inorganic nitrite under hypoxic conditions. Circulating nitrite derives from oxidation of NO or reduction of inorganic nitrate by commensal bacteria in the oral cavity. Intriguingly, nitrate is a common constituent of our everyday diet and particularly high concentrations are found in leafy green vegetables such as spinach, lettuce, or beetroot. Evidence suggests that dietary nitrate supplementation increases the regenerative capacity of ischemic tissue and that this effect may offer an attractive nutrition-based strategy to improve ischemia-induced revascularization. We here summarize and discuss the regenerative capacity of dietary nitrate on the vascular system. 

Potential of dietary nitrate in angiogenesis.

Hemodialysis (HD) per se entails vascular dysfunction in patients with ESRD. Endothelial dysfunction is a key step in atherosclerosis and is characterized by impaired flow-mediated dilation (FMD). Interventional studies have shown that cocoa flavanol (CF)-rich supplements improve vascular function. Aim of this study was to investigate the effect of flavanol-rich bioactive food ingredients on acute and chronic HD-induced vascular dysfunction in ESRD.

Vasculoprotective Effects of Dietary Cocoa Flavanols in Patients on Hemodialysis: A Double-Blind, Randomized, Placebo-Controlled Trial.

Following successful resuscitation from cardiac arrest (CA), neurological impairment and other types of organ dysfunction cause significant morbidity and mortality-a condition termed post-cardiac arrest syndrome. Whole-body ischemia/reperfusion with oxygen debt activates immunologic and coagulation pathways increasing the risk of multiple organ failure and infection. We here examined the role of the pro-inflammatory cytokine macrophage migration inhibitory factor (MIF) in post-cardiac arrest syndrome.

MIF reflects tissue damage rather than inflammation in post-cardiac arrest syndrome in a real life cohort.

Diastolic dysfunction is highly prevalent, and ageing is the main contributor due to impairments in active cardiac relaxation, ventriculo-vascular stiffening, and endothelial dysfunction. Nitric oxide (NO) affects cardiovascular functions, and NO bioavailability is critically reduced with ageing. Whether replenishment of NO deficiency with dietary inorganic nitrate would offer a novel approach to reverse age-related cardiovascular alterations was not known.

Impact of dietary nitrate on age-related diastolic dysfunction.

Mitral regurgitation causes left atrial (LA) and left ventricular (LV) dysfunction, dilatation, and remodeling. Following percutaneous mitral valve repair (PMVR) using the MitraClip® approach, reverse cardiac remodeling is desirable. To date, the influence of PMVR on LA and segmental LV function and remodeling has not been investigated in detail.

Left Atrial and Left Ventricular Function and Remodeling Following Percutaneous Mitral Valve Repair.

The precise sizing of the stent graft in thoracic endovascular aortic repair (TEVAR) affects aortic remodeling and hence, further outcome. Covering the proximal entry tear is essential for successful treatment of Type B aortic dissection. Intravascular ultrasound (IVUS) enables real-time aortic diameter assessment, and is especially useful when computed tomography (CT) image quality is poor. IVUS, however, is not routinely utilized due to cost inefficiency. We investigated the impact of IVUS-assisted stent graft sizing on aortic remodeling in TEVAR. In this single-center retrospective study we evaluated patients with Type B aortic dissection undergoing both CT and IVUS before TEVAR. We assessed the aortic diameter at the level of the left subclavian artery via both methods before stent implantation and analyzed due to which method the implanted stent graft was chosen, retrospectively. To determine the degrees of aortic remodeling involved, we evaluated true lumen and false lumen diameters, and total aortic remodeling in CT. We analyzed 45 patients with Type B aortic dissection undergoing TEVAR. The mean ages were 66.9±10.0 years fo0072 IVUS (n = 20) and 62.3±14.2 years for CT-assisted TEVAR (n = 25; p = 0.226). The follow-up time for both groups did not differ between the two groups (IVUS: 22.9±23.1 months, CT: 25.6±23.0 months; p = 0.700). While both methods were associated with advantages regarding aortic remodeling, IVUS-assisted sizing yielded a greater increase in true lumen (30.4±6.2 vs. 25.6±5.3; p = 0.008) and reductions in false lumen (14.4±8.5 vs. 23.9±9.3; p = 0.001) and total aortic diameter (35.5±6.0 vs. 39.9±8.1; p = 0.045). IVUS-guided stent graft sizing in Type B aortic dissection shows beneficial effects on aortic remodeling and might be of additional advantage in aortic diseases, especially when CT image quality is poor.

Intravascular ultrasound assisted sizing in thoracic endovascular aortic repair improves aortic remodeling in Type B aortic dissection.

Radial artery access is the primary approach for coronary interventions due to higher safety profile in comparison to femoral access. Radial artery occlusion (RAO) is the main complication of transradial catheterization that can lead to severe symptoms and a permanent artery occlusion. The incidence of RAO after transradial access ranges from 5 to 38% and data regarding treatment is scarce. Whether anticoagulation and vasoactive medication provides an additional benefit in recovery of radial artery patency (RAP) after catheterization has not been investigated in detail.

Christos Rammos

West German Heart and Vascular Center,
Department of Cardiology and Vascular Medicine,
Medical Faculty,
West German Heart and Vascular Center, Department of Cardiology and Vascular Medicine, Medical Faculty

University Hospital Essen

Real-time Pressure-volume Analysis of Acute Myocardial Infarction in Mice

Christos Rammos

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}West German Heart and Vascular Center,Department of Cardiology and Vascular Medicine,Medical Faculty,West German Heart and Vascular Center, Department of Cardiology and Vascular Medicine, Medical Faculty

University Hospital Essen

Real-time Pressure-volume Analysis of Acute Myocardial Infarction in Mice

West German Heart and Vascular Center,
Department of Cardiology and Vascular Medicine,
Medical Faculty,
West German Heart and Vascular Center, Department of Cardiology and Vascular Medicine, Medical Faculty