Positron emission tomographic myocardial viability imaging appears to identify patients at increased risk of having an adverse cardiac event or death. Patients with impaired left ventricular function and positron emission tomographic evidence for jeopardized myocardium appear to have the most benefit from a revascularization procedure.

The SOFA, TMS, and deltaSOFA scores provide the clinician with important information on degree and progression of organ dysfunction in medical, cardiovascular patients. On day 1 both SOFA score and TMS score had a better prognostic value than SAPS II score. The model is closely related to outcome and identifies patients who are at increased risk for prolonged ICU stay.

Coronary hemodynamics in myocardial bridges are characterized by a phasic systolic vessel compression with a localized peak pressure, persistent diastolic diameter reduction, increased blood flow velocities, retrograde flow, and a reduced flow reserve. These alterations may explain the occurrence of symptoms and ischemia in these patients. Intracoronary stent placement abolished all hemodynamic abnormalities and may improve clinical symptoms in otherwise unsuccessfully treated patients with myocardial bridges.

Myocardial bridging is characterized by a delay in diastolic lumen gain and a concomitant increase in diastolic intracoronary Doppler flow velocities, which are enhanced by rapid pacing. In combination with a reduced coronary flow reserve and anginal symptoms these findings support the concept of a haemodynamically significant obstruction to coronary flow due to myocardial bridging in a selected subset of patients.

Background: Oral factor XIa (FXIa) inhibitors may modulate coagulation to prevent thromboembolic events without significantly increasing bleeding. We explored the pharmacodynamics, safety, and efficacy of the oral FXIa inhibitor asundexian for secondary prevention after acute myocardial infarction (MI). Methods: We randomized 1601 patients with recent acute MI to oral asundexian 10, 20, or 50 mg or placebo once daily for 6–2 months in a double-blind, placebo-controlled, phase 2, dose-ranging trial. Patients were randomized within 5 days of their qualifying MI and received dual antiplatelet therapy with aspirin plus a P2Y12 inhibitor. The effect of asundexian on factor XIa inhibition was assessed at 4 weeks. The prespecified main safety outcome was Bleeding Academic Research Consortium type 2, 3, or 5 bleeding comparing all pooled asundexian doses with placebo. The prespecified efficacy outcome was a composite of cardiovascular death, MI, stroke, or stent thrombosis comparing pooled asundexian 20 and 50 mg doses with placebo. Results: The median age was 68 years, 23% were women, 51% had ST-elevation MI, 80% were treated with aspirin plus ticagrelor or prasugrel, and 99% underwent percutaneous coronary intervention before randomization. Asundexian caused dose-related inhibition of FXIa activity with 50 mg resulting in >90% inhibition. Over a median follow-up of 368 days, the main safety outcome occurred in 30 (7.6%), 32 (8.1%), 42 (10.5%), and 36 (9.0%) patients receiving asundexian 10, 20, 50 mg, and placebo (pooled asundexian vs. placebo: HR 0.98, 90% CI 0.71–1.35). The efficacy outcome occurred in 27 (6.8%), 24 (6.0%), 22 (5.5%), and 22 (5.5%) patients assigned asundexian 10, 20, 50 mg, and placebo (pooled asundexian 20 and 50 mg vs. placebo: HR 1.05, 90% CI 0.69–1.61). Conclusions: : In patients with recent acute MI, 3 doses of asundexian, when added to aspirin plus a P2Y12 inhibitor, resulted in dose-dependent, near-complete inhibition of FXIa activity without a significant increase in bleeding and a low rate of ischemic events. These data support the investigation of asundexian at a dose of 50 mg daily in an adequately powered clinical trial of patients following acute MI.

Hibernating myocardium exhibits time-dependent deterioration due to progressive structural degeneration with enhanced fibrosis. Early revascularization should be attempted to salvage the jeopardized tissue and improve postoperative outcome.

Long-term hypoperfusion causes different degrees of morphologic alterations leading to degeneration. Preoperative analysis of regional contractility and perfusion-metabolism imaging does not distinguish the severity of morphologic alterations nor the functional outcome after revascularization. The insufficient act of self-preservation in hibernating myocardium may lead to a progressive structural degeneration with an incomplete and delayed recovery of function after restoration of blood flow.

Background: There is no widely accepted classification to guide therapy in patients with symptomatic myocardial bridging (MB). Methods: A retrospective analysis of 157 patients with chest pain, angiographic MB of the left anterior descending artery without obstructive coronary artery disease (CAD) was performed. Patients were evaluated for clinical symptoms, objective signs of ischemia by stress test, intracoronary Doppler flow measurement and coronary flow reserve. 100 patients without CAD or MB served as controls. Results: There was no difference in clinical symptoms and objective signs of ischemia between controls and patients with MB. The length of MB was 22.6 ± 7.8 mm, maximal systolic luminal diameter reduction 71 ± 16%, and maximal mid-diastolic luminal reduction 34.7 ± 13% as demonstrated by quantitative coronary angiography (QCA). Intracoronary Doppler showed significantly increased average peak flow velocity (APV), average systolic peak velocity (ASPV), average diastolic peak flow velocity (ADPV), and maximal peak velocity (MPV) in MB versus proximal and distal segments at rest and after maximal vasodilatation (p < 0.001 for all parameters). Coronary flow reserve was significantly higher proximally (2.9 ± 0.9) compared with segments distal to the MB (2.0 ± 0.6, p < 0.01). We propose a new MB classification for symptomatic patients with MB:Type A:incidental finding on angiography, no objective signs of ischemia; Type B: objective signs of ischemia, and Type C: with or without objective signs of ischemia and altered intracoronary hemodynamics (by QCA/CFR/intracoronary Doppler). 5-Year follow-up data based on this classification showed that types B and C responded well to β-blockers or calcium channel antagonists. Patients with type C refractory to medical therapy were treated with stenting of the MB. Conclusion: Patients with MB without CAD did not have a higher prevalence of chest pain or abnormal non-invasive stress tests compared to patients without CAD or MB. Intracoronary hemodynamic measurement is a novel approach that may be valuable in defining the functional significance of MB. We propose a classification of symptomatic patients with MB without CAD using non-invasive and invasive parameters to guide therapeutic choices.