Prevention of coronary microvascular obstruction by addressing ischemia reperfusion injury-part a

Most recently, substantial research efforts were directed to the treatment and prevention of coronary microvascular obstruction (CMVO) by targeting various mechanisms involved in its multifactorial pathophysiology. Among other strategies, antiplatelets and vasodilators were tested in order to reduce thrombus burden and coronary vasospasm potentially resulting in enhanced myocardial perfusion. Furthermore, the impact of intensified statin therapy was evaluated in numerous investigations. Although most of these studies failed to convincingly prove beneficial effects regarding CMVO, especially antiplatelets and statins are indispensable cornerstones of post-infarction medical therapy. This chapter discusses the scientific evidence and guideline recommendations for the use of antiplatelets, statins, and vasodilators in patients with myocardial infarction with a particular focus on their efficacy to treat or prevent CMVO

Impact of Right Atrial Physiology on Heart Failure and Adverse Events after Myocardial Infarction

Background: Right ventricular (RV) function is a known predictor of adverse events in heart failure and following acute myocardial infarction (AMI). While right atrial (RA) involvement is well characterized in pulmonary arterial hypertension, its relative contributions to adverse events following AMI especially in patients with heart failure and congestion need further evaluation. Methods: In this cardiovascular magnetic resonance (CMR)-substudy of AIDA STEMI and TATORT NSTEMI, 1235 AMI patients underwent CMR after primary percutaneous coronary intervention (PCI) in 15 centers across Germany (n = 795 with ST-elevation myocardial infarction and 440 with non-ST-elevation MI). Right atrial (RA) performance was evaluated using CMR myocardial feature tracking (CMR-FT) for the assessment of RA reservoir (total strain εs), conduit (passive strain εe), booster pump function (active strain εa), and associated strain rates (SR) in a blinded core-laboratory. The primary endpoint was the occurrence of major adverse cardiac events (MACE) 12 months post AMI. Results: RA reservoir (εs p = 0.061, SRs p = 0.049) and conduit functions (εe p = 0.006, SRe p = 0.030) were impaired in patients with MACE as opposed to RA booster pump (εa p = 0.579, SRa p = 0.118) and RA volume index (p = 0.866). RA conduit function was associated with the clinical onset of heart failure and MACE independently of RV systolic function and atrial fibrillation (AF) (multivariable analysis hazard ratio 0.95, 95% confidence interval 0.92 to 0.99, p = 0.009), while RV systolic function and AF were not independent prognosticators. Furthermore, RA conduit strain identified low- and high-risk groups within patients with reduced RV systolic function (p = 0.019 on log rank testing). Conclusions: RA impairment is a distinct feature and independent risk factor in patients following AMI and can be easily assessed using CMR-FT-derived quantification of RA strain

Genome-wide association study in takotsubo syndrome - Preliminary results and future directions.

Background: Takotsubo syndrome (TS) is an acute non-ischemic cardiomyopathy characterized by transient regional systolic dysfunction of the left and/or right ventricle with still unknown etiology. The aim of the current study was to conduct for the first time a genome-wide association study (GWAS) in a cohort of TS patients to identify potential genetic risk variants. Methods: This single-center study was conducted at the University Heart Center Lübeck from 2008 to 2016. DNA isolation was done according to standard protocols. Imputation of genotypes were performed at the Michigan Imputation Server (https://imputationserver.sph.umich.edu) using the 1000G Phase 3 v5 reference panel. Results: The study population consisted of 96 TS patients (91 females, 5 males) with a mean age of 71.9±10.4years and 475 healthy controls (268 males, 207 females). The results of GWAS analysis showed several promising candidate loci (68 loci after applying threshold of p<5*10-4 and MAF>5%). Of these 68 loci, 18 loci contained top single nucleotide polymorphisms (SNPs) that were supported by SNPs in high Linkage Disequilibrium (r2>0.8) with p<10-3. Two out of the 18 loci contained SNP with hits in the GWAS catalog (traits: blood pressure, thyroid stimulating hormone). Conclusion: This first GWAS analysis in a larger cohort of patients with TS showed promising preliminary results. Further intensive research efforts of international collaborators are now necessary to enable deep-phenotyping of TS patients to ultimately assess a potential genetic cause of TS