Search

Among the most common causes of death worldwide, ischemic heart disease (IHD) is recognized to rank first. Even if atherosclerotic disease of the epicardial arteries is known as the leading cause of IHD, the presence of myocardial infarction with non-obstructive coronary artery disease (MINOCA) is increasingly recognized. Notwithstanding the increasing interest, MINOCA remains a puzzling clinical entity that can be classified by distinguishing different underlying mechanisms, which can be divided into atherosclerotic and non-atherosclerotic. In particular, coronary microvascular dysfunction (CMD), classifiable in non-atherosclerotic mechanisms, is a leading factor for the pathophysiology and prognosis of patients with MINOCA. Genetic susceptibility may have a role in primum movens in CMD. However, few results have been obtained for understanding the genetic mechanisms underlying CMD. Future studies are essential in order to find a deeper understanding of the role of multiple genetic variants in the genesis of microcirculation dysfunction. Progress in research would allow early identification of high-risk patients and the development of pharmacological, patient-tailored strategies. The aim of this review is to revise the pathophysiology and underlying mechanisms of MINOCA, focusing on CMD and actual knowledge about genetic predisposition to it.

Aims Significant concern has been raised about the effect of pre-existing cardiovascular diseases (CVD), cardiovascular (CV) risk factors and CV therapies on COVID-19 course. On the other hand, COVID-19 could worse pre-existing CVD or trigger the development of new-onset CVD. The aim of this study was to evaluate the relationship between pre-existing CVD, CV risk factors, and CV therapy with the clinical course of hospitalized COVID-19 patients. Methods and results Consecutive hospitalized COVID-19 patients admitted to the Cardiovascular COVID-19 Unit at Policlinico Umberto I of Rome between December 2020 and April 2021 were enrolled. All patients underwent a cardiovascular evaluation including troponin, electrocardiogram (ECG), and echocardiogram. Data on medical history, pre-existing CVD, CV risk factors, and therapy were collected. Admission to the Intensive Care Unit (ICU) or Cardiac Intensive Care Unit (CICU), as well as the development of new-onset CVD, were considered as endpoint of the study. Among n = 229 patients enrolled, 22 (10%) died. Nearly half of patients (112, 49%) were admitted to the ICU/CICU. The presence of prior ischaemic heart disease nearly doubled the probability of hospitalization in the ICU/CICU (HR: 2.09, 95% CI: 1.132–3.866, P 0.018). In regards of therapy, beta blockers reduced the likelihood of admission in the ICU/CICU (HR: −1016, 95% CI: 0.192–10.682, P 0.002). However, neither the use of RAAS blockers, heparin or dexamethasone influenced the risk of ICU/CICU admission (respectively, HR: 0.85, 95% CI: 0.498–1.450, P 0.551; HR: 0.768, 95% CI: 0.435–1.356, P 0.363; HR: 0.861, 95% CI: 0.453–1.635, P 0.647). N = 89 patients (39%) experienced a new onset CVD including arrythmias (18.3%) with nearly half experiencing atrial fibrillation, acute coronary syndrome (10.9%), acute pulmonary embolism (5.3%), heart failure (HF) (3%), and myocarditis and pericarditis (1.3%). A pre-existing diagnosis of HF substantially increased the likelihood of new onset CVD (HR: 2.380, 95% CI: 1.004–5.638, P 0.049). However, treatment with heparin or dexamethasone reduced the risk of new onset CVD (HR: 0.482 95% CI: 0.268–0.867, P 0.015; HR: 0.487, 95% CI: 0.253–0.937, P 0.031, respectively). Conclusions Our study found that hospitalized COVID-19 patients who have at least one CV risk factor or pre-existing CVD had a greater likelihood of being admitted to the ICU/CICU and experiencing new onset CVD.